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Ջնջվում է էջի ամբողջ պարունակությունը
Պիտակ՝ Դատարկում
Տող 1.
{{short description|Cancer located in the ovary}}
{{Infobox medical condition (new)
| name = Ovarian cancer
| image = mucinous_lmp_ovarian_tumour_intermed_mag.jpg
| caption = [[Micrograph]] of a mucinous ovarian carcinoma [[H&E stain|stained by H&E]].
| field = [[Oncology]], [[gynecology]]
| symptoms = '''Early''': vague<ref name=NCI2014TxPt/><br>'''Later''': bloating, [[pelvic pain]], abdominal swelling, loss of appetite<ref name=NCI2014TxPt/>
| complications =
| onset = Usual age of diagnosis 63 years old<ref name=NCI2016Onset/>
| duration =
| types = Ovarian carcinoma, [[germ cell tumor]], [[sex cord stromal tumor]]<ref name=WCR2014/>
| causes =
| risks = [[Nulliparity|Never having children]], [[hormone therapy]] after [[menopause]], [[fertility medication]], [[obesity]], genetics<ref name=NCI2014PrePt/><ref name=WCR2014/><ref name=NCI2014PrePro/>
| diagnosis = [[Tissue biopsy]]<ref name=NCI2014TxPt/>
| differential =
| prevention =
| treatment = Surgery, [[radiation therapy]], [[chemotherapy]]<ref name=NCI2014TxPt/>
| medication =
| prognosis = [[Five-year survival rate]] c. 45% (US)<ref name=SEER2014/>
| frequency = 1.2 million (2015)<!-- prevalence --><ref name=GBD2015Pre/>
| deaths = 161,100 (2015)<ref name=GBD2015De/>
}}
<!-- Definition and Symptoms -->
Ձվարանի քաղցկեղ ձվարանի մեջ կամ դրա վրա առաջացող քաղցկեղ<ref name = NCI2014PrePt/><ref name=harrisons9th>{{cite web | publisher = MGraw-Hill Medical | title = Gynecologic Malignancies, Chapter 117 | access-date = June 24, 2017 | first = Michael | last = Seiden | date = 2015 | url = https://accessmedicine.mhmedical.com/content.aspx?bookid=1130&sectionid=79730544 | url-status = live | archive-url = https://web.archive.org/web/20170910175639/https://accessmedicine.mhmedical.com/content.aspx?bookid=1130&sectionid=79730544 | archive-date = September 10, 2017 }}</ref>։ It results in abnormal [[cells (biology)|cells]] that have the ability to invade or [[metastasis|spread]] to other parts of the body.<ref>{{cite web|title=Defining Cancer|url=http://www.cancer.gov/cancertopics/cancerlibrary/what-is-cancer|website=National Cancer Institute|access-date=10 June 2014|url-status=live|archive-url= https://web.archive.org/web/20140625220940/http://www.cancer.gov/cancertopics/cancerlibrary/what-is-cancer|archive-date=25 June 2014|date=2007-09-17}}</ref> When this process begins, there may be no or only vague symptoms.<ref name=NCI2014TxPt/> Ախտանիշները ավելի են արտահայտվում քաղցկեղի պրոգրեսիվմանը զուգընթաց<ref name=NCI2014TxPt/><ref>{{cite journal | vauthors = Ebell MH, Culp MB, Radke TJ | title = A Systematic Review of Symptoms for the Diagnosis of Ovarian Cancer | journal = American Journal of Preventive Medicine | volume = 50 | issue = 3 | pages = 384–394 | date = March 2016 | pmid = 26541098 | doi = 10.1016/j.amepre.2015.09.023 }}</ref>։ These symptoms may include bloating, [[pelvic pain]], [[ascites|abdominal swelling]], and [[Anorexia (symptom)|loss of appetite]], among others.<ref name=NCI2014TxPt/> Common areas to which the cancer may spread include the [[peritoneum|lining of the abdomen]], [[lymph node]]s, [[lungs]], and [[liver]].<ref>{{cite book|last1=Ruddon|first1=Raymond W. | name-list-format = vanc |title=Cancer Biology |date=2007|publisher=Oxford University Press |location=Oxford |isbn=9780195175431 |page=223 |edition=4th |url=https://books.google.com/books?id=PymZ1ORk0TcC&pg=PA223|url-status=live|archive-url=https://web.archive.org/web/20150915231411/https://books.google.com/books?id=PymZ1ORk0TcC&pg=PA223|archive-date=2015-09-15}}</ref>
 
<!-- Cause and Diagnosis -->
Ձվարանի քաղցկեղի հանդիպման հաճախականությունը մեծանում է ձվազատման քանակի հետ կյանքի ընթացքում This includes those who have [[Nulliparity|never had children]], those who begin ovulation at a younger age and those who reach menopause at an older age.<ref name=WCR2014/> Other risk factors include [[hormone therapy]] after [[menopause]], [[fertility medication]], and [[obesity]].<ref name=NCI2014PrePt>{{cite web|title=Ovarian Cancer Prevention (PDQ®)|url=http://www.cancer.gov/cancertopics/pdq/prevention/ovarian/Patient/page1/AllPages|website=NCI|accessdate=1 July 2014|date=December 6, 2013|url-status=live|archiveurl=https://web.archive.org/web/20140706002700/http://www.cancer.gov/cancertopics/pdq/prevention/ovarian/Patient/page1/AllPages|archivedate=6 July 2014}}</ref><ref name=NCI2014PrePro>{{cite web|title=Ovarian Cancer Prevention (PDQ®)|url=http://www.cancer.gov/cancertopics/pdq/prevention/ovarian/HealthProfessional/page1/AllPages|website=NCI|accessdate=1 July 2014|date=2014-06-20|url-status=live|archiveurl=https://web.archive.org/web/20140706002711/http://www.cancer.gov/cancertopics/pdq/prevention/ovarian/HealthProfessional/page1/AllPages|archivedate=6 July 2014}}</ref> Factors that decrease risk include [[hormonal birth control]], [[tubal ligation]], and [[breast feeding]].<ref name=NCI2014PrePro/> About 10% of cases are related to inherited genetic risk; women with mutations in the genes ''[[BRCA1]]'' or ''[[BRCA2]]'' have about a 50% chance of developing the disease.<ref name=WCR2014/> Ovarian carcinoma is the most common type of ovarian cancer, comprising more than 95% of cases.<ref name=WCR2014/> There are five main subtypes of ovarian carcinoma, of which [[high-grade serous carcinoma]] (HGSC) is the most common.<ref name=WCR2014/> These tumors are believed to start in the cells covering the ovaries,<ref name=WCR2014/> though some may form at the [[Fallopian tube]]s.<ref>{{cite book | vauthors = Piek JM, van Diest PJ, Verheijen RH | title = Ovarian carcinogenesis: an alternative hypothesis | journal = Adv. Exp. Med. Biol. | volume = 622 | pages = [https://archive.org/details/ovariancancersta00geor/page/79 79–87] | year = 2008 | pmid = 18546620 | doi = 10.1007/978-0-387-68969-2_7 | isbn = 978-0-387-68966-1 | series = Advances in Experimental Medicine and Biology | url-access = registration | url = https://archive.org/details/ovariancancersta00geor/page/79 }}{{closed access}}</ref> Less common types of ovarian cancer include [[germ cell tumor]]s and [[sex cord stromal tumor]]s.<ref name=WCR2014/> A diagnosis of ovarian cancer is confirmed through a [[biopsy]] of tissue, usually removed during surgery.<ref name=NCI2014TxPt/>
 
<!-- Prevention, Treatment and Prognosis -->
[[Screening (medicine)|Screening]] is not recommended in women who are at average risk, as evidence does not support a reduction in death and the high rate of [[false positives and false negatives|false positive tests]] may lead to unneeded surgery, which is accompanied by its own risks.<ref name=Gros2018>{{cite journal | vauthors = Grossman DC, Curry SJ, Owens DK, Barry MJ, Davidson KW, Doubeni CA, Epling JW, Kemper AR, Krist AH, Kurth AE, Landefeld CS, Mangione CM, Phipps MG, Silverstein M, Simon MA, Tseng CW | display-authors = 6 | title = Screening for Ovarian Cancer: US Preventive Services Task Force Recommendation Statement | journal = Jama | volume = 319 | issue = 6 | pages = 588–594 | date = February 2018 | pmid = 29450531 | doi = 10.1001/jama.2017.21926 }}</ref> Those at very high risk may have their ovaries removed as a preventive measure.<ref name=NCI2014PrePt/> If caught and treated in an early stage, ovarian cancer is often curable.<ref name=NCI2014TxPt/> Treatment usually includes some combination of surgery, [[radiation therapy]], and [[chemotherapy]].<ref name=NCI2014TxPt>{{cite web|title=Ovarian Epithelial Cancer Treatment (PDQ®)|url=http://www.cancer.gov/cancertopics/pdq/treatment/ovarianepithelial/Patient/page1/AllPages|website=NCI|access-date=1 July 2014|date=2014-05-12|url-status=live|archive-url=https://web.archive.org/web/20140705232951/http://www.cancer.gov/cancertopics/pdq/treatment/ovarianepithelial/Patient/page1/AllPages|archive-date=5 July 2014}}</ref> Outcomes depend on the extent of the disease, the subtype of cancer present, and other medical conditions.<ref name=Gib2016>{{cite journal | vauthors = Gibson SJ, Fleming GF, Temkin SM, Chase DM | title = The Application and Outcome of Standard of Care Treatment in Elderly Women with Ovarian Cancer: A Literature Review over the Last 10 Years | journal = Frontiers in Oncology | volume = 6 | pages = 63 | year = 2016 | pmid = 27047797 | pmc = 4805611 | doi = 10.3389/fonc.2016.00063 }}</ref><ref name=WCR2014/> The overall [[five-year survival rate]] in the United States is 45%.<ref name=SEER2014>{{cite web|title=SEER Stat Fact Sheets: Ovary Cancer|url=http://seer.cancer.gov/statfacts/html/ovary.html|website=NCI|access-date=18 June 2014|url-status=live|archive-url=https://web.archive.org/web/20140706145616/http://seer.cancer.gov/statfacts/html/ovary.html|archive-date=6 July 2014}}</ref> Outcomes are worse in the developing world.<ref name=WCR2014/>
 
<!-- Epidemiology -->
In 2012, new cases occurred in approximately 239,000 women.<ref name=WCR2014/> In 2015 it was present in 1.2 million women and resulted in 161,100 deaths worldwide.<ref name=GBD2015De>{{cite journal|author=GBD 2015 Mortality and Causes of Death Collaborators |title=Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015.|journal=Lancet |date=8 October 2016|volume=388|issue=10053|pages=1459–1544|pmid=27733281 |pmc=5388903 |doi=10.1016/S0140-6736(16)31012-1 |url= }}</ref><ref name=GBD2015Pre>{{cite journal|author=GBD 2015 Disease and Injury Incidence and Prevalence Collaborators |title=Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015.|journal=Lancet |date=8 October 2016|volume=388|issue=10053|pages=1545–1602|pmid=27733282 |pmc=5055577 |doi=10.1016/S0140-6736(16)31678-6 }}</ref> Among women it is the seventh-most common cancer and the eighth-most common cause of death from cancer.<ref name=WCR2014/> The typical age of diagnosis is 63.<ref name=NCI2016Onset>{{cite web|title=What are the risk factors for ovarian cancer?|url=http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-risk-factors|website=www.cancer.org|accessdate=18 May 2016|date=2016-02-04|url-status=live|archiveurl=https://web.archive.org/web/20160517173135/http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-risk-factors|archivedate=17 May 2016}}</ref> Death from ovarian cancer is more common in North America and Europe than in Africa and Asia.<ref name=WCR2014>{{cite book|title=World Cancer Report 2014|date=2014|publisher=World Health Organization|isbn=978-9283204299|at=Chapter 5.12|url=http://publications.iarc.fr/Non-Series-Publications/World-Cancer-Reports/World-Cancer-Report-2014|url-status=live|archiveurl=https://web.archive.org/web/20160919073553/http://publications.iarc.fr/Non-Series-Publications/World-Cancer-Reports/World-Cancer-Report-2014|archivedate=2016-09-19}}</ref>
{{TOC limit|3}}
 
==Նշաններ և ախտանիշներ==
===Վաղ ախտանիշներ===
[[File:Site of ovarian cancer.png|thumb|upright=1.3|Site of ovarian cancer]]
Early [[Medical sign|signs]] and [[symptoms]] of ovarian cancer may be absent or subtle. In most cases, symptoms exist for several months before being recognized and [[diagnosis|diagnosed]].<ref name="Harrisons" /><ref name="CDCsep2016">{{cite web|url=https://www.cdc.gov/cancer/ovarian/pdf/ovarian_facts.pdf|title=Ovarian Cancer, Inside Knowledge, Get the Facts about Gynecological Cancer|date=September 2016|publisher=Centers for Disease Control and Prevention|accessdate=June 17, 2017|url-status=live|archiveurl=https://web.archive.org/web/20170616220028/https://www.cdc.gov/cancer/ovarian/pdf/ovarian_facts.pdf|archivedate=June 16, 2017}}{{CDC}}</ref> Symptoms can be misdiagnosed as [[irritable bowel syndrome]].<ref name="Jayson">{{cite journal | vauthors = Jayson GC, Kohn EC, Kitchener HC, Ledermann JA | title = Ovarian cancer | journal = Lancet | volume = 384 | issue = 9951 | pages = 1376–88 | date = October 2014 | pmid = 24767708 | doi = 10.1016/S0140-6736(13)62146-7 }}</ref> The early stages of ovarian cancer tend to be painless. Symptoms can vary based on the subtype.<ref name=Harrisons/> Low malignant potential (LMP) tumors, also known as borderline tumors, do not cause an increase in [[CA125]] levels and are not identifiable with an ultrasound. The typical symptoms of an LMP tumor can include [[abdominal distension]] or pelvic pain. Particularly large masses tend to be benign or borderline.<ref name=Hoffman35/><ref name="Harrisons" />
 
The most typical symptoms of ovarian cancer include [[bloating]], abdominal or pelvic pain or discomfort, back pain, [[irregular menstruation]] or postmenopausal vaginal bleeding, pain or bleeding after or during [[sexual intercourse]], [[Anorexia (symptom)|loss of appetite]], [[Fatigue (medical)|fatigue]], [[diarrhea]], [[indigestion]], [[heartburn]], [[constipation]], [[nausea]], [[satiety|feeling full]], and possibly urinary symptoms (including [[polyuria|frequent urination]] and [[Urinary urgency|urgent urination]]).<ref name = CDCsep2016/>
 
===Ուշ ախտանիշներ===
The growing mass may cause pain if [[ovarian torsion]] develops. Symptoms can be caused by a mass pressing on the other abdominopelvic organs or from metastases.<ref name="Harrisons" /><ref name=":0">{{Cite web|url=http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/about/ovarian-cancer-symptoms|title=Ovarian cancer symptoms|website=www.cancerresearchuk.org|accessdate=2015-05-16|url-status=live|archiveurl=https://web.archive.org/web/20150512172659/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/about/ovarian-cancer-symptoms|archivedate=2015-05-12}}</ref><ref name=":7" /> If these symptoms start to occur more often or more severely than usual, especially after no significant history of such symptoms, ovarian cancer is considered.<ref name="Harrisons" /><ref name="Hoffman35" /> Metastases may cause a [[Sister Mary Joseph nodule]].<ref name=":7" /> Rarely, [[teratoma]]s can cause [[growing teratoma syndrome]] or [[peritoneal gliomatosis]].<ref name=":7" /> Some experience [[menometrorrhagia]] and [[Dysfunctional uterine bleeding|abnormal vaginal bleeding]] after menopause in most cases. Other common symptoms include [[hirsutism]], abdominal pain, [[virilization]], and an [[adnexal mass]].<ref name=":8" />
 
===Երեխաներ===
In adolescents or children with ovarian tumors, symptoms can include severe abdominal pain, irritation of the [[peritoneum]], or [[hemorrhage|bleeding]].<ref name="Current" /> Symptoms of sex cord-stromal tumors produce [[hormone]]<nowiki/>s that can affect the development of [[secondary sex characteristics]]. Sex cord-stromal tumors in prepubertal children may be manifested by [[precocious puberty|early puberty]]; abdominal pain and distension are also common. Adolescents with sex cord-stromal tumors may experience [[amenorrhea]]. As the cancer becomes more advanced, it can cause [[ascites|an accumulation of fluid]] in the abdomen. If the malignancy has not been diagnosed by the time it causes ascites, it is typically diagnosed shortly thereafter.<ref name="Harrisons" /> Advanced cancers can also cause abdominal masses, lymph node masses, or [[pleural effusion]].<ref name=":7" />
 
== Ռիսկի գործոններ ==
Ovarian cancer is related to the amount of time spent ovulating. Thus [[Nulliparity|not having children]] is a risk factor for ovarian cancer, likely because ovulation is suppressed via pregnancy. During ovulation, cells are constantly stimulated to divide while ovulatory cycles continue. Therefore, [[Nulliparity|people who have not borne children]] are at twice the risk of ovarian cancer than those who have. A longer period of ovulation caused by early [[menarche|first menstruation]] and late [[menopause]] is also a risk factor.<ref name="Hoffman35" /><ref name="CRUKRisks" /><ref>{{cite journal | vauthors = Gong TT, Wu QJ, Vogtmann E, Lin B, Wang YL | title = Age at menarche and risk of ovarian cancer: a meta-analysis of epidemiological studies | journal = International Journal of Cancer | volume = 132 | issue = 12 | pages = 2894–900 | date = June 2013 | pmid = 23175139 | pmc = 3806278 | doi = 10.1002/ijc.27952 }}</ref> Both obesity and hormone replacement therapy also raise the risk.<ref name=Harrisons/>
 
The risk of developing ovarian cancer is less for women who have fewer menstrual cycles, no menstrual cycles, [[breast feeding]], take oral contraceptives, have multiple pregnancies, and have a pregnancy at an early age. The risk of developing ovarian cancer is reduced in women who have had [[tubal ligation]] (colloquially known as having one's "tubes tied"), both ovaries removed, or [[hysterectomy]] (an operation in which the uterus, and sometimes the cervix, is removed).<ref name="CDCsep2016" /> Age is also a risk factor.<ref name = Harrisons/><ref name="Gib2016"/>
 
=== Հորմոններ ===
Use of fertility medication may contribute to borderline ovarian tumor formation, but the link between the two is disputed and difficult to study.<ref name=Jayson/> Fertility drugs may be associated with a higher risk of borderline tumors.<ref name=":7" /> Those who have been treated for infertility but remain nulliparous are at higher risk for epithelial ovarian cancer; however, those who are successfully treated for infertility and subsequently give birth are at no higher risk. This may be due to shedding of precancerous cells during pregnancy but the cause remains unclear.<ref name=Hoffman35/> The risk factor may instead be infertility itself, not the treatment.<ref name=CRUKRisks/>
 
Hormonal conditions such as [[polycystic ovary syndrome]] and [[endometriosis]] are associated with ovarian cancer, but the link is not completely confirmed.<ref name="Jayson" /> Postmenopausal hormone replacement therapy (HRT) with estrogen likely increases the risk of ovarian cancer. The association has not been confirmed in a large-scale study,<ref name="Hoffman35" /><ref>{{cite book |last1 = Manson |first1 = JoAnn E. |last2 = Bassuk |first2 = Shari S. | name-list-format = vanc |chapter = The Menopause Transition and Postmenopausal Hormone Therapy |veditors = Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J |title = Harrison's Principles of Internal Medicine |publisher = McGraw-Hill |year = 2012 |edition = 18th |isbn = 978-0-07-174889-6|title-link = Harrison's Principles of Internal Medicine }}</ref> but notable studies including the [[Million Women Study]] have supported this link. Postmenopausal HRT with combined estrogen and progesterone may increase contemporaneous risk if used for over 5 years, but this risk returns to normal after cessation of therapy.<ref name="CRUKRisks" /> Estrogen HRT with or without progestins increases the risk of endometrioid and serous tumors but lowers the risk of mucinous tumors. Higher doses of estrogen increase this risk.<ref name=":7" /> Endometriosis is another risk factor for ovarian cancer,<ref name=CRUKRisks/> as is pain with menstruation. Endometriosis is associated with clear-cell and endometrioid subtypes, low-grade serous tumors, stage I and II tumors, grade 1 tumors, and lower mortality.<ref name=":7" />
 
Before menopause, obesity can increase a person's risk of ovarian cancer, but this risk is not present after menopause. This risk is also relevant in those who are both obese and have never used HRT. A similar association with ovarian cancer appears in taller people.<ref name=CRUKRisks/>
 
=== Գենետիկա ===
{{Further|Hereditary breast–ovarian cancer syndrome}}
[[File:PedigreechartC.png|upright=1.3|thumb|People with ovarian or breast cancer in a pedigree chart of a family|link=Special:FilePath/PedigreechartC.png]]
A family history of ovarian cancer is a risk factor for ovarian cancer. People with [[hereditary nonpolyposis colon cancer]] (Lynch syndrome), and those with BRCA-1 and BRCA-2 genetic abnormalities are at increased risk.
 
The major genetic risk factor for ovarian cancer is a mutation in ''BRCA1'' or ''BRCA2'' genes, or in [[DNA mismatch repair]] genes, which is present in 10% of ovarian cancer cases. Only one [[allele]] need be mutated to place a person at high risk. The gene can be inherited through either the maternal or paternal line, but has variable [[penetrance]].<ref name=Harrisons/><ref name=Hoffman35/> Though mutations in these genes are usually associated with increased risk of breast cancer, they also carry a substantial lifetime risk of ovarian cancer, a risk that peaks in a person's 40s and 50s. The lowest risk cited is 30% and the highest 60%.<ref name=Jayson/><ref name=Harrisons/><ref name=Hoffman35/> Mutations in BRCA1 have a lifetime risk of developing ovarian cancer of 15–45%.<ref name=":7" /> Mutations in ''BRCA2'' are less risky than those with ''BRCA1'', with a lifetime risk of 10% (lowest risk cited) to 40% (highest risk cited).<ref name=Harrisons/><ref name=":7" /> On average, BRCA-associated cancers develop 15 years before their sporadic counterparts, because people who inherit the mutations on one copy of their gene only need one mutation to start the process of carcinogenesis, whereas people with two normal genes would need to acquire two mutations.<ref name=Hoffman35/>
 
In the United States, five of 100 women with a [[first-degree relative]] with ovarian cancer will eventually get ovarian cancer themselves, placing those with affected family members at triple the risk of women with unaffected family members. Seven of 100 women with two or more relatives with ovarian cancer will eventually get ovarian cancer.<ref name=Hoffman35/><ref name=NCIPrevention>{{cite web |url=http://www.cancer.gov/cancertopics/pdq/prevention/ovarian/healthprofessional |title=Ovarian Cancer Prevention (PDQ®) |publisher=[[National Cancer Institute]] |year=2013 |accessdate=2013-12-30 |url-status=live |archiveurl=https://web.archive.org/web/20131231100136/http://www.cancer.gov/cancertopics/pdq/prevention/ovarian/healthprofessional |archivedate=2013-12-31 }}</ref> In general, 5–10% of ovarian cancer cases have a genetic cause.<ref name=Hoffman35/> BRCA mutations are associated with high-grade serous nonmucinous epithelial ovarian cancer.<ref name=":7" />
 
A strong family history of [[endometrial cancer]], [[colon cancer]], or other [[gastrointestinal cancer]]s may indicate the presence of a syndrome known as [[hereditary nonpolyposis colorectal cancer]] (also known as Lynch syndrome), which confers a higher risk for developing a number of cancers, including ovarian cancer. Lynch syndrome is caused by mutations in mismatch repair genes, including ''[[MSH2]], [[MLH1]], [[MLH6]], [[PMS1]]'', and ''[[PMS2]]''.<ref name=Harrisons/> The risk of ovarian cancer for an individual with Lynch syndrome is between 10 and 12 percent.<ref name=Harrisons/><ref name=Hoffman35/> People of [[Icelandic people|Icelandic descent]], [[European Jews|European Jewish descent]]/[[Ashkenazi Jews|Ashkenazi Jewish descent]], and [[Hungarian people|Hungarian descent]] are at higher risk for epithelial ovarian cancer.<ref name=Hoffman35/> Estrogen receptor beta gene ([[ESR2]]) seems to be a key to pathogenesis and response to therapy.<ref>{{cite journal | vauthors = Kyriakidis I, Papaioannidou P | year = 2016 | title = Estrogen receptor beta and ovarian cancer: a key to pathogenesis and response to therapy | journal = Arch Gynecol Oncol | volume = 293 | issue = 6 | pages = 1161–8 |doi = 10.1007/s00404-016-4027-8 |pmid=26861465}}</ref> Other genes that have been associated with ovarian cancer are ''[[BRIP1]]'', ''[[MSH6]]'', ''[[RAD51C]]'' and ''[[RAD51D]]''.<ref name=Norquist2015>{{cite journal |vauthors=Norquist BM, Harrell MI, Brady MF, Walsh T, Lee MK, Gulsuner S, Bernards SS, Casadei S, Yi Q, Burger RA, Chan JK, Davidson SA, Mannel RS, DiSilvestro PA, Lankes HA, Ramirez NC, King MC, Swisher EM, Birrer MJ | year = 2015 | title = Inherited mutations in women With ovarian carcinoma | journal = JAMA Oncol | volume = 30 | issue = 4| pages = 1–9 | doi = 10.1001/jamaoncol.2015.5495 |pmid=26720728 |pmc=4845939 }}</ref> ''[[CDH1 (gene)|CDH1]]'', ''[[CHEK2]]'', ''[[PALB2]]'' and ''[[RAD50 (gene)|RAD50]]'' have also been associated with ovarian cancer.<ref name=Kuusisto2011>{{cite journal | vauthors = Kuusisto KM, Bebel A, Vihinen M, Schleutker J, Sallinen SL | year = 2011 | title = Screening for BRCA1, BRCA2, CHEK2, PALB2, BRIP1, RAD50, and CDH1 mutations in high-risk Finnish BRCA1/2-founder mutation-negative breast and/or ovarian cancer individuals | journal = Breast Cancer Res | volume = 13 | issue = 1 | page = R20 | doi = 10.1186/bcr2832 | pmid = 21356067 | pmc = 3109589 | df = }}</ref>
 
Several rare genetic disorders are associated with specific subtypes of ovarian cancer. [[Peutz–Jeghers syndrome]], a rare genetic disorder, also predisposes people to [[sex cord tumour with annular tubules]].<ref name=Jayson/><ref name=Harrisons/> [[Ollier disease]] and [[Maffucci syndrome]] are associated with [[granulosa cell tumor]]s in children and may also be associated with Sertoli-Leydig tumors. Benign fibromas are associated with [[nevoid basal cell carcinoma syndrome]].<ref name=Harrisons/>
 
=== Միջավայրի գործոններ ===
Industrialized nations, with the exception of Japan, have high rates of epithelial ovarian cancer, which may be due to diet in those countries. [[White people|Caucasian]] are at a 30–40% higher risk for ovarian cancer when compared to [[Black people|Black]] and [[Hispanic people]], likely due to socioeconomic factors; white women tend to have fewer children and different rates of gynecologic surgeries that affect risk for ovarian cancer.<ref name=Hoffman35/>
 
[[Cohort study|Cohort studies]] have found a correlation between dairy consumption and ovarian cancer, but [[case-control study|case-control studies]] do not show this correlation. There is mixed evidence regarding the effect of [[red meat]] and [[processed meat]] in ovarian cancer.<ref name=":7" />
 
Tentative evidence suggests that [[talc]], [[pesticides]], and [[herbicides]] increase the risk of ovarian cancer.<ref>{{cite journal | vauthors = Salehi F, Dunfield L, Phillips KP, Krewski D, Vanderhyden BC | title = Risk factors for ovarian cancer: an overview with emphasis on hormonal factors | journal = Journal of Toxicology and Environmental Health. Part B, Critical Reviews | volume = 11 | issue = 3-4 | pages = 301–21 | date = March 2008 | pmid = 18368558 | doi = 10.1080/10937400701876095 }}</ref> The American Cancer Society notes that as of now, no study has been able to accurately link any single chemical in the environment, or in the human diet, directly to mutations that cause ovarian cancer.<ref>{{cite web|title=Do we know what causes ovarian cancer?|url= http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-what-causes|website=www.cancer.org |url-status=live |archive-url= https://web.archive.org/web/20161110052501/http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-what-causes |archive-date=2016-11-10}}</ref>
 
=== Այլ ===
Alcohol consumption does not appear to be related to ovarian cancer.<ref name=":7" /><ref>{{cite journal | vauthors = Hjartåker A, Meo MS, Weiderpass E | title = Alcohol and gynecological cancers: an overview | journal = European Journal of Cancer Prevention | volume = 19 | issue = 1 | pages = 1–10 | date = January 2010 | pmid = 19926999 | doi = 10.1097/CEJ.0b013e328333fb3a }}</ref> Other factors that have been investigated, such as [[smoking]], low levels of [[vitamin D]] in the blood,<ref>{{cite journal |vauthors=Zhang X, Nicosia SV, Bai W |title=Vitamin D receptor is a novel drug target for ovarian cancer treatment |journal=Curr Cancer Drug Targets |volume=6 |issue=3 |pages=229–44 |year=2006 |pmid=16712459 |doi=10.2174/156800906776842939 |df= }}</ref> presence of inclusion [[ovarian cysts]], and infection with [[human papilloma virus]] (the cause of some cases of [[cervical cancer]]), have been disproven as risk factors for ovarian cancer.<ref name=Jayson/><ref name=":7" /> The carcinogenicity of [[Perineum|perineal]] [[talc]] is controversial, because it can act as an irritant if it travels through the reproductive tract to the ovaries.<ref name=":7" /><ref name=Hoffman35/><ref name="CRUKRisks" /> [[Case-control study|Case-control studies]] have shown that use of perineal talc does increase the risk of ovarian cancer, but using talc more often does not create a greater risk.<ref name=":7" /> Use of [[talc]] elsewhere on the body is unrelated to ovarian cancer.<ref name=CRUKRisks/> [[Sitting]] regularly for prolonged periods is associated with higher mortality from epithelial ovarian cancer. The risk is not negated by regular exercise, though it is lowered.<ref name=Biswas>{{cite journal |vauthors=Biswas A, Oh PI, Faulkner GE, Bajaj RR, Silver MA, Mitchell MS, Alter DA |title=Sedentary Time and Its Association With Risk for Disease Incidence, Mortality, and Hospitalization in Adults: A Systematic Review and Meta-analysis |journal=Annals of Internal Medicine |volume=162 |issue=2 |pages=123–32 |year=2015 |pmid=25599350 |doi=10.7326/M14-1651 }}</ref>
 
Increased age (up to the 70s) is a risk factor for epithelial ovarian cancer because more mutations in cells can accumulate and eventually cause cancer. Those over 80 are at slightly lower risk.<ref name=Hoffman35/>
 
[[Smoking]] tobacco is associated with a higher risk of [[mucinous tumor|mucinous ovarian cancer]]; after [[smoking cessation]], the risk eventually returns to normal. A diet high in animal fats may be associated with ovarian cancer, but the connection is unclear. Diet seems to play a very small role, if any, in ovarian cancer risk.<ref name=CRUKRisks/>
Higher levels of [[C-reactive protein]] are associated with a higher risk of developing ovarian cancer.<ref name=":7" />
 
=== Կանխարգելիչ գործոններ ===
Suppression of ovulation, which would otherwise cause damage to the [[ovarian epithelium]] and, consequently, [[inflammation]], is generally protective. This effect can be achieved by [[multiparity|having children]], taking [[combined oral contraceptive]]s, and [[breast feeding]], all of which are protective factors.<ref name=Harrisons/> A longer period of breastfeeding correlates with a larger decrease in the risk of ovarian cancer.<ref name=CRUKRisks/> Each birth decreases risk of ovarian cancer more, and this effect is seen with up to five births. Combined oral contraceptives reduce the risk of ovarian cancer by up to 50%, and the protective effect of combined oral contraceptives can last 25–30 years after they are discontinued.<ref name=Hoffman35/><ref name=CRUKRisks/> Regular use of [[aspirin]] or [[Paracetamol|acetaminophen]] (paracetamol) may be associated with a lower risk of ovarian cancer; other [[NSAIDs]] do not seem to have a similar protective effect.<ref name=":7" />
 
[[Tubal ligation]] is protective because [[carcinogen]]s are unable to reach the ovary and [[fimbria (female reproductive system)|fimbriae]] via the vagina, uterus, and Fallopian tubes.<ref name="Harrisons" /> Tubal ligation is also protective in women with the BRCA1 mutation, but not the BRCA2 mutation.<ref name=":7" /> [[Hysterectomy]] reduces the risk, and removal of both Fallopian tubes and ovaries (bilateral [[salpingo-oophorectomy]]) dramatically reduces the risk of not only ovarian cancer, but breast cancer as well.<ref name="Jayson" /> This is still a topic of research, as the link between hysterectomy and lower ovarian cancer risk is controversial. The reasons that hysterectomy may be protective have not been elucidated as of 2015.<ref name="CRUKRisks" />
 
A diet that includes large amounts of [[carotene]], [[fiber]], and [[vitamin]]s with low amounts of fat—specifically, a diet with non-starchy vegetables (e.g. [[broccoli]] and [[onion]]s)—may be protective,<ref name="Hoffman35" /> though research is still ongoing in this area.<ref name="CRUKRisks" /> Higher caffeine intake and consumption of more than two cups of tea a day have both been associated with lower ovarian cancer risk.<ref name=":7" /> Smoking tobacco is protective for sex cord-stromal tumors.<ref name=":8" />
 
== Ախտաֆիզիոլոգիա ==
{| class="wikitable sortable" align="right" style="width: 50%"
|+Mutations found in ovarian cancer subtypes<ref name=Jayson/><ref name=":7" /><ref name=DeVita100>{{cite book |title = Molecular Biology of Gynecologic Cancers |pages = 1302–1310 |first1 = Kunle |last1 = Odunsi |first2 = Tanja |last2 = Pejovic |first3 = Matthew L. |last3 = Anderson | name-list-format = vanc |work = DeVita, Hellman, and Rosenberg's Cancer: Principles and Practice of Oncology |publisher = Wolters Kluwer/Lippincott Williams & Wilkins | year = 2011 |isbn = 978-1-4511-0545-2}}</ref>
|-
!Gene mutated
!Mutation type
!Subtype
!Prevalence
|-
|''[[AKT1]]''
|amplification
|
|3%
|-
|''[[AKT2]]''
|amplification/mutation
|
|6%,<ref name=Jayson/> 20%<ref name=DeVita100/>
|-
|''[[ARID1A]]''
|point mutation
|endometrioid and clear cell
|
|-
|''[[BECN1]]''
|deletion
|
|
|-
|[[BRAF (gene)|''BRAF'']]
|point mutation
|low-grade serous
|0.5%
|-
|''[[BRCA1]]''
|nonsense mutation
|high-grade serous
|5%
|-
|''[[BRCA2]]''
|frameshift mutation
|high-grade serous
|3%
|-
|''[[CCND1]]''
|amplification
|
|4%
|-
|''[[CCND2]]''
|upregulation
|
|15%
|-
|''[[CCNE1]]''
|amplification
|
|20%
|-
|''[[CDK12]]''
|
|high-grade serous
|
|-
|[[P16 (gene)|''CDKN2A'']]
|downregulation (30%) and deletion (2%)
|
|32%
|-
|''[[CTNNB1]]''
|
|clear cell
|
|-
|[[DICER1]]
|missense mutation (somatic)
|nonepithelial
|29%
|-
|[[DYNLRB1]] (km23)
| mutation
|
|42%
|-
|[[Epidermal growth factor receptor|EGFR]]
|amplification/overexpression
|
|20%
|-
|''[[ERBB2]]'' (Her2/neu)
|amplification/overexpression
|mucinous and low-grade serous
|30%
|-
|[[FMS (gene)|FMS]]
|coexpression with [[CSF-1]]
|
|50%
|-
|[[Forkhead box L2|FOXL2]]
|point mutation (402 C to G)
|adult granulosa cell
|~100%
|-
|''[[JAG1]]''
|amplification
|
|2%
|-
|''[[JAG2]]''
|amplification
|
|3%
|-
|''[[KRAS]]''
|amplification
|mucinous and low-grade serous
|11%
|-
|''[[MAML1]]''
|amplification and point mutation
|
|2%
|-
|''[[MAML2]]''
|amplification and point mutation
|
|4%
|-
|''[[MAML3]]''
|amplification
|
|2%
|-
|[[MLH1]]
|
|
|1%
|-
|[[nuclear factor 1|''NF1'']]
|deletion (8%) and point mutation (4%)
|high-grade serous
|12%
|-
|''[[NOTCH3]]''
|amplification and point mutation
|
|11%
|-
|[[Neuroblastoma RAS viral oncogene homolog|''NRAS'']]
|
|low-grade serous
|
|-
|[[PIK3C3]] (PI3K3)
|amplification/mutation
|
|12–20%
|-
|''[[PIK3CA]]''
|amplification
|endometrioid and clear cell
|18%
|-
|''[[PPP2R1A]]''
|
|endometrioid and clear cell
|
|-
|[[PTEN (gene)|''PTEN'']]
|deletion
|endometrioid and clear cell
|7%
|-
|''[[RB1]]''
|deletion (8%) and point mutation (2%)
|
|10%
|-
|[[TGF-β]]
|mutation/overexpression
|
|12%
|-
|''[[TP53]]''
|mutation/overexpression
|high-grade serous
|20–50%
|-
|[[TβRI]]
|mutation
|
|33%
|-
|[[TβRII]]
|mutation
|
|25%
|-
|[[USP36]]
|overexpression
|
|
|}
Ovarian cancer forms when errors in normal ovarian [[cell cycle|cell growth]] occur. Usually, when cells grow old or get damaged, they [[apoptosis|die]], and new cells take their place. Cancer starts when new cells form unneeded, and old or damaged cells do not die as they should. The buildup of extra cells often forms a mass of tissue called a growth or tumor. These abnormal cancer cells have many [[genetic mutation|genetic abnormalities]] that cause them to grow excessively.<ref name=NCIGenetics>{{cite web |url = http://www.cancer.gov/cancertopics/pdq/genetics/breast-and-ovarian/HealthProfessional |title = Genetics of Breast and Ovarian Cancer (PDQ®) |date = 2 October 2014 |accessdate = 27 October 2014 |publisher = National Cancer Institute |url-status = live |archiveurl = https://web.archive.org/web/20141022060353/http://www.cancer.gov/cancertopics/pdq/genetics/breast-and-ovarian/HealthProfessional |archivedate = 22 October 2014 }}</ref> When an ovary [[ovulation|releases an egg]], the [[Ovarian follicle|egg follicle]] bursts open and becomes the [[corpus luteum]]. This structure needs to be repaired by dividing cells in the ovary.<ref name=CRUKRisks/> Continuous ovulation for a long time means more repair of the ovary by dividing cells, which can acquire mutations in each division.<ref name=Hoffman35/>
 
Overall, the most common gene mutations in ovarian cancer occur in ''[[nuclear factor 1|NF1]], BRCA1, BRCA2, ''and ''[[CDK12]]''. Type I ovarian cancers, which tend to be less aggressive, tend to have [[microsatellite instability]] in several genes, including both oncogenes (most notably ''[[BRAF (gene)|BRAF]]'' and ''[[KRAS]]'') and tumor suppressors (most notably ''[[PTEN (gene)|PTEN]]'').<ref name="Jayson" /> The most common mutations in Type I cancers are ''KRAS, BRAF, ERBB2, PTEN, PIK3CA,'' and ''ARID1A.''<ref name=":7" /> Type II cancers, the more aggressive type, have different genes mutated, including ''[[p53]], BRCA1'', and ''BRCA2''.<ref name=Jayson/> Low-grade cancers tend to have mutations in KRAS, whereas cancers of any grade that develop from low malignant potential tumors tend to have mutations in p53.<ref name=Hoffman35/> Type I cancers tend to develop from precursor lesions, whereas Type II cancers can develop from a [[serous tubal intraepithelial carcinoma]].<ref name=":7" /> [[Serous cancer]]s that have BRCA mutations also inevitably have p53 mutations, indicating that the removal of both functional genes is important for cancer to develop.<ref name="Hoffman35" />
 
In 50% of high-grade serous cancers, homologous recombination DNA repair is dysfunctional, as are the [[notch signaling pathway|notch]] and [[FOXM1]] signaling pathways. They also almost always have p53 mutations. Other than this, mutations in high-grade serous carcinoma are hard to characterize beyond their high degree of [[genomic instability]]. ''BRCA1'' and ''BRCA2'' are essential for homologous recombination DNA repair, and [[germline mutation]]s in these genes are found in about 15% of people with ovarian cancer.<ref name=Jayson/> The most common mutations in BRCA1 and BRCA2 are the [[frameshift mutations]] that originated in a small [[founder effect|founding population]] of Ashkenazi Jews.<ref name=Hoffman35/>
 
Almost 100% of rare mucinous carcinomas have mutations in ''KRAS'' and amplifications of ''ERBB2'' (also known as ''Her2/neu'').<ref name=Jayson/> Overall, 20% of ovarian cancers have mutations in ''Her2/neu''.<ref name=Harrisons/>
 
Serous carcinomas may develop from [[serous tubal intraepithelial carcinoma]], rather than developing spontaneously from ovarian tissue. Other carcinomas develop from [[cortical inclusion cysts]], which are groups of epithelial ovarian cells inside the [[stroma (animal tissue)|stroma]].<ref name=Hoffman35/>
 
== Ախտորոշում ==
 
=== Զննում ===
[[File:POvarianCA.png|thumb|upright=1.3|A very large ovarian cancer as seen on CT]]
[[File:Serous carcinoma cytology.jpg|thumb|[[Micrograph]] of [[serous carcinoma]], a type of ovarian cancer, diagnosed in [[peritoneal fluid]]]]
Diagnosis of ovarian cancer starts with a physical examination (including a [[pelvic examination]]), a blood test (for [[CA-125]] and sometimes other markers), and [[transvaginal ultrasound]].<ref name=Harrisons/> Sometimes a [[rectovaginal examination]] is used to help plan a surgery.<ref name=Hoffman35/> The diagnosis must be confirmed with surgery to inspect the [[abdominal cavity]], take [[biopsies]] (tissue samples for [[histopathology|microscopic analysis]]), and look for cancer cells in the abdominal fluid. This helps to determine if an ovarian mass is [[benign]] or malignant.<ref name=Harrisons/>
 
Ovarian cancer's early stages (I/II) are difficult to diagnose because most symptoms are nonspecific and thus of little use in diagnosis; as a result, it is rarely diagnosed until it spreads and advances to later stages (III/IV).<ref>{{cite journal | vauthors = Rossing MA, Wicklund KG, Cushing-Haugen KL, Weiss NS | title = Predictive Value of Symptoms for Early Detection of Ovarian Cancer | journal = J Natl Cancer Inst | volume = 102 | issue = 4 | pages = 222–9 | date = 2010-01-28 | pmid = 20110551 | pmc = 2826180 | doi = 10.1093/jnci/djp500 }}</ref> Additionally, symptoms of ovarian cancer may appear similar to [[irritable bowel syndrome]]. In patients in whom pregnancy is a possibility, [[BHCG]] level can be measured during the diagnosis process. Serum [[alpha-fetoprotein]], [[neuron-specific enolase]], and [[lactate dehydrogenase]] can be measured in young girls and adolescents with suspected ovarian tumors as younger patients are more likely to have malignant germ cell tumors.<ref name="Harrisons" /><ref name=":7" />
 
A physical examination, including a pelvic examination, and a pelvic ultrasound (transvaginal or otherwise) are both essential for diagnosis: physical examination may reveal increased abdominal girth and/or [[ascites]] (fluid within the abdominal cavity), while pelvic examination may reveal an ovarian or abdominal mass.<ref name="Jayson" /> An adnexal mass is a significant finding that often indicates ovarian cancer, especially if it is fixed, nodular, irregular, solid, and/or bilateral. 13–21% of adnexal masses are caused by malignancy; however, there are other benign causes of adnexal masses, including [[Follicular cyst of ovary|ovarian follicular cyst]], [[leiomyoma]], [[endometriosis]], [[ectopic pregnancy]], [[hydrosalpinx]], [[tuboovarian abscess]], [[ovarian torsion]], [[dermoid cyst]], [[cystadenoma]] (serous or mucinous), [[Diverticular abscess|diverticular]] or [[Appendiceal abscess|appendiceal]] [[abscess]], [[nerve sheath tumor]], [[pelvic kidney]], [[Ureteral diverticulum|ureteral]] or [[bladder diverticulum]], [[benign cystic mesothelioma of the peritoneum]], [[peritoneal tuberculosis]], or [[paraovarian cyst]]. Ovaries that can be felt are also a sign of ovarian cancer in postmenopausal women. Other parts of a physical examination for suspected ovarian cancer can include a [[breast examination]] and a [[digital rectal exam]]. Palpation of the [[Supraclavicular lymph nodes|supraclavicular]], [[Axillary lymph nodes|axillary]], and [[Inguinal lymph node|inguinal]] [[lymph node]]s may reveal [[lymphadenopathy]], which can be indicative of metastasis. Another indicator may be the presence of a [[pleural effusion]], which can be noted on [[auscultation]].<ref name=":7" />
 
When an ovarian malignancy is included in a list of diagnostic possibilities, a limited number of laboratory tests are indicated. A complete blood count and serum electrolyte test is usually obtained;<ref name=Miller/> when an ovarian cancer is present, these tests often show [[thrombocytosis|a high number of platelets]] (20–25% of people) and [[hyponatremia|low blood sodium levels]] due to chemical signals secreted by the tumor.<ref name=Hoffman35/> A positive test for [[inhibin A]] and [[inhibin B]] can indicate a granulosa cell tumor.<ref name=":7" />
 
A blood test for a marker molecule called CA-125 is useful in differential diagnosis and in follow up of the disease, but it by itself has not been shown to be an effective method to screen for early-stage ovarian cancer due to its unacceptable low sensitivity and specificity.<ref name="Miller" /> CA-125 levels in premenopausal people over 200 U/mL may indicate ovarian cancer, as may any elevation in CA-125 above 35 U/mL in post-menopausal people. CA-125 levels are not accurate in early stage ovarian cancer, as fully half of stage I ovarian cancer patients have a normal CA-125 level.<ref name=":7" /><ref name="Hoffman35" /> CA-125 may also be elevated in benign (non-cancerous) conditions, including [[endometriosis]], [[pregnancy]], [[uterine fibroids]], [[menstruation]], [[ovarian cysts]], [[systemic lupus erythematosus]], [[liver disease]], [[inflammatory bowel disease]], [[pelvic inflammatory disease]], and [[leiomyoma]].<ref name=":7" /><ref>{{Cite web|title = Ovarian cancer tests|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/diagnosis/ovarian-cancer-tests|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150518091201/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/diagnosis/ovarian-cancer-tests|archivedate = 2015-05-18}}</ref> [[HE4]] is another candidate for ovarian cancer testing, though it has not been extensively tested. Other tumor markers for ovarian cancer include [[CA19-9]], [[CA72-4]], [[CA15-3]], [[immunosuppressive acidic protein]], [[haptoglobin-alpha]], [[OVX1]], [[mesothelin]], [[lysophosphatidic acid]], [[osteopontin]], and [[fibroblast growth factor 23]].<ref name=":7" />
 
Use of blood test panels may help in diagnosis.<ref name=":7" /><ref name="Miller">{{cite journal | vauthors = Miller RW, Ueland FR | title = Risk of malignancy in sonographically confirmed ovarian tumors. | journal = Clinical Obstetrics and Gynecology | volume = 55 | issue = 1 | pages = 52–64 | date = March 2012 | pmid = 22343229 | doi = 10.1097/GRF.0b013e31824970cf }}</ref> The OVA1 panel includes CA-125, [[beta-2 microglobulin]], [[transferrin]], [[apolipoprotein A1]], and [[transthyretin]]. OVA1 above 5.0 in premenopausal people and 4.4 in postmenopausal people indicates a high risk for cancer.<ref name="Hoffman35" /> A different set of laboratory tests is used for detecting sex cord-stromal tumors. High levels of [[testosterone]] or [[dehydroepiandrosterone sulfate]], combined with other symptoms and high levels of [[inhibin A]] and [[Inhibin-beta subunits|inhibin B]] can be indicative of an SCST of any type.<ref name=":8" />
 
Current research is looking at ways to consider tumor marker [[proteomics]] in combination with other indicators of disease (i.e. radiology and/or symptoms) to improve diagnostic accuracy. The challenge in such an approach is that the disparate prevalence of ovarian cancer means that even testing with very high sensitivity and specificity will still lead to a number of false positive results, which in turn may lead to issues such as performing surgical procedures in which cancer is not found intraoperatively.{{citation needed|date=March 2018}} [[Genomics]] approaches have not yet been developed for ovarian cancer.<ref name=":7" />
 
[[CT scanning]] is preferred to assess the extent of the tumor in the abdominopelvic cavity, though [[magnetic resonance imaging]] can also be used.<ref name="Jayson" /> CT scanning can also be useful for finding [[omental caking]] or differentiating fluid from solid tumor in the abdomen, especially in low malignant potential tumors. However, it may not detect smaller tumors. Sometimes, a [[Chest radiograph|chest x-ray]] is used to detect metastases in the chest or [[pleural effusion]]. Another test for metastatic disease, though it is infrequently used, is a [[barium enema]], which can show if the rectosigmoid colon is involved in the disease. [[Positron emission tomography]], [[bone scan]]s, and [[paracentesis]] are of limited use; in fact, paracentesis can cause metastases to form at the needle insertion site and may not provide useful results.<ref name="Hoffman35" /> However, paracentesis can be used in cases where there is no pelvic mass and ascites is still present.<ref name="Hoffman35" /> A physician suspecting ovarian cancer may also perform [[mammography]] or an [[endometrial biopsy]] (in the case of abnormal bleeding) to assess the possibility of breast malignancies and endometrial malignancy, respectively. [[Vaginal ultrasonography]] is often the first-line imaging study performed when an adnexal mass is found. Several characteristics of an adnexal mass indicate ovarian malignancy; they usually are solid, irregular, multilocular, and/or large; and they typically have papillary features, central vessels, and/or irregular internal septations.<ref name=":7" /> However, SCST has no definitive characteristics on radiographic study.<ref name=":8" />
 
To definitively diagnose ovarian cancer, a surgical procedure to inspect the abdomen is required. This can be an open procedure ([[laparotomy]], incision through the [[abdominal wall]]) or [[keyhole surgery]] ([[laparoscopy]]). During this procedure, suspicious tissue is removed and sent for [[Histopathology|microscopic analysis]]. Usually, this includes a unilateral [[salpingo-oophorectomy]], removal of a single affected ovary and Fallopian tube. Fluid from the abdominal cavity can also be analyzed for cancerous [[Cell (biology)|cells]]. If cancer is found, this procedure can also be used to determine the extent of its spread (which is a form of [[tumor staging]]).<ref name=Harrisons/>
 
==== Ռիսկի գնահատում ====
{{anchor | RMI}}A widely recognized method of estimating the risk of malignant ovarian cancer is the risk of malignancy index (RMI), calculated based on an initial [[Medical diagnosis#Other diagnostic procedure methods|workup]].<ref name=Jayson/><ref name="NICE2011">{{cite web |url = http://publications.nice.org.uk/ovarian-cancer-cg122/appendix-d-risk-of-malignancy-index-rmi-i |work = NICE clinical guidelines |date = April 2011 |title = Guideline CG122. Ovarian cancer: The recognition and initial management of ovarian cancer, Appendix D: Risk of malignancy index (RMI I). |url-status = dead |archiveurl = https://web.archive.org/web/20130922075958/http://publications.nice.org.uk/ovarian-cancer-cg122/appendix-d-risk-of-malignancy-index-rmi-i |archivedate = 2013-09-22 }}</ref> An RMI score of over 200 or 250 is generally felt to indicate high risk for ovarian cancer.<ref name=Jayson/><ref name=":7" />
 
The RMI is calculated as:
 
:RMI = ultrasound score × menopausal score x CA-125 level in U/ml.<ref name=Jayson/>
 
Two methods can be used to determine the ultrasound score and menopausal score, with the resultant scores being referred to as RMI 1 and RMI 2, respectively, depending on what method is used.
 
{| class="wikitable"
|-
! style="width:32%;"| Feature
! style="width:34%;"| RMI 1<ref name=Jayson/>
! style="width:34%;"| RMI 2<ref name=":7" /><ref>{{cite journal | vauthors = Geomini P, Kruitwagen R, Bremer GL, Cnossen J, Mol BW | title = The accuracy of risk scores in predicting ovarian malignancy: a systematic review | journal = Obstetrics and Gynecology | volume = 113 | issue = 2 Pt 1 | pages = 384–94 | date = February 2009 | pmid = 19155910 | doi = 10.1097/AOG.0b013e318195ad17 }}</ref>
|-
|
Ultrasound abnormalities:
 
* multilocular cyst
* solid areas
* ascites
* intra-abdominal metastases
| {{plainlist |
* 0 {{=}} no abnormality
* 1 {{=}} one abnormality
* 3 {{=}} two or more abnormalities }}
| {{plainlist |
* 0 {{=}} none
* 1 {{=}} one abnormality
* 4 {{=}} two or more abnormalities }}
|-
| Menopausal score
| {{plainlist |
* 1 {{=}} premenopausal
* 3 {{=}} postmenopausal }}
| {{plainlist |
* 1 {{=}} premenopausal
* 4 {{=}} postmenopausal }}
|-
| CA-125
| Quantity in U/ml
| Quantity in U/ml
|}
 
Another method for quantifying risk of ovarian cancer is the Risk of Ovarian Cancer Algorithm (ROCA), observes levels over time and determines if they are increasing rapidly enough to warrant transvaginal ultrasound.<ref name="Hoffman35" /> The Risk of Ovarian Malignancy algorithm uses CA-125 levels and [[HE4]] levels to calculate the risk of ovarian cancer; it may be more effective than RMI. The IOTA models can be used to estimate the probability that an adnexal tumor is malignant.<ref>{{cite journal | vauthors = Kaijser J, Bourne T, De Rijdt S, Van Holsbeke C, Sayasneh A, Valentin L, Van Calster B, Timmerman D | display-authors = 6 | title = Key findings from the International Ovarian Tumor Analysis (IOTA) study: an approach to the optimal ultrasound based characterisation of adnexal pathology | journal = Australasian Journal of Ultrasound in Medicine | volume = 15 | issue = 3 | pages = 82–86 | date = August 2012 | pmid = 28191150 | pmc = 5025098 | doi = 10.1002/j.2205-0140.2012.tb00011.x }}</ref> They include LR2 risk model, The Simple Rules risk (SRrisk) calculation and Assessment of Different Neoplasias in the Adnexa (ADNEX) model that can be used to assess risk of malignancy in an adnexal mass, based on its characteristics and risk factors. The QCancer (Ovary) algorithm is used to predict likelihood of ovarian cancer from risk factors.<ref name=":7" />
 
=== Ախտաբանություն ===
[[File:Incidence of ovarian cancers by histopathology.png|thumb|upright=1.3|Ovarian cancers in women aged 20+, with area representing relative incidence and color representing five-year relative survival rate<ref name=SEER6215ch16/>]]
 
Ovarian cancers are classified according to the microscopic appearance of their structures ([[histology]] or [[histopathology]]). Histology dictates many aspects of clinical treatment, management, and [[prognosis]]. The gross pathology of ovarian cancers is very similar regardless of histologic type: tumors have solid and cystic masses.<ref name="Hoffman35" /> According to [[Surveillance Epidemiology and End Results|SEER]], the types of ovarian cancers in women age 20 and over are:<ref name=SEER6215ch16>{{Cite book | contribution=Chapter 16: Cancers of the Ovary | first=Carol L. | last=Kosary | name-list-format = vanc | pages=133–144 | publisher=National Cancer Institute | title=SEER Survival Monograph: Cancer Survival Among Adults: US SEER Program, 1988–2001, Patient and Tumor Characteristics | veditors = Baguio RN, Young JL, Keel GE, Eisner MP, Lin YD, Horner MJ | series=SEER Program | volume=NIH Pub. No. 07-6215 | place=Bethesda, MD | year=2007 | chapterurl=http://seer.cancer.gov/publications/survival/surv_ovary.pdf | url=http://seer.cancer.gov/publications/survival/ | url-status=live | archiveurl=https://web.archive.org/web/20131010123756/http://seer.cancer.gov/publications/survival/ | archivedate=2013-10-10 }}</ref>
 
{| class="wikitable"
! Percent of<br/> ovarian cancers<br/> in women<br/> age 20+
!Percent of<br/> ovarian cancers<br/> in women<br/> age 20+ by
subdivision
! [[Histology]]
! Five-year<br/>[[Relative survival rate|RSR]]
|-
| 89.7
|
| [[Surface epithelial-stromal tumor]] ([[adenocarcinoma]])
| 54.4
|-
|
|26.4
| [[Papillary serous cystadenocarcinoma]]
| 21.0
|-
|
|15.9
| "Borderline" adenocarcinoma <br/>(underestimated - short data collection interval)
| 98.2
|-
|
|12.6
| Adenocarcinoma, not otherwise specified
| 18.3
|-
|
|9.8
| [[Endometrioid tumor]]
| 70.9
|-
|
|5.8
| [[Serous cystadenocarcinoma]]
| 44.2
|-
|
|5.5
| [[Papilloma|Papillary]]
| 21.0
|-
|
|4.2
| [[Mucinous cystadenocarcinoma]]
| 77.7
|-
|
|4.0
| [[Clear-cell ovarian tumor]]
| 61.5
|-
|
|3.4
| [[Mucinous adenocarcinoma]]
| 49.1
|-
|
|1.3
| [[Cystadenocarcinoma]]
| 50.7
|-
| 5.5
|
| [[Carcinoma]]
|
|-
|
|4.1
| Carcinoma not otherwise specified
| 26.8
|-
|
|1.1
| [[Sex cord-stromal tumour]]
| 87.8
|-
|
|0.3
| Other carcinomas, specified
| 37.3
|-
| 1.7
|
| [[Mullerian tumor]]
| 29.8
|-
| 1.5
|
| [[Germ cell tumor]]
| 91.0
|-
|
|0.8
| [[Teratoma]]
| 89.1
|-
|
|0.5
| [[Dysgerminoma]]
| 96.8
|-
|
|0.3
| Other, specified
| 85.1
|-
| 0.6
|
| Not otherwise specified
| 23.0
|-
| 0.5
|
| Epidermoid ([[squamous cell carcinoma]])
| 51.3
|-
| 0.2
|
| [[Brenner tumor]]
| 67.9
|-
| 0.2
|
| Other, specified
| 71.7
|}
 
Ovarian cancers are histologically and genetically divided into type I or type II. Type I cancers are of low histological grade, and include endometrioid, mucinous, and clear-cell carcinomas. Type II cancers are of higher histological grade and include serous carcinoma and carcinosarcoma.<ref name=Jayson/>
 
==== Էպիթելային կարցինոմա ====
[[File:Ovarian carcinoma.JPG|thumb|upright=1.3|A pathological specimen of ovarian carcinoma]]
[[Surface epithelial-stromal tumour]], also known as ovarian epithelial carcinoma, is the most common type of ovarian cancer, representing approximately 90% of ovarian cancers. It includes [[serous tumour]], [[endometrioid tumor]], and [[mucinous]] [[cystadenocarcinoma]]. Less common tumors are malignant [[Brenner tumor]] and [[transitional cell carcinoma of the ovary]]. Epithelial ovarian cancers develop from the [[epithelium]], a layer of cells that covers the ovary.<ref name=":1">{{Cite web|title = Types of ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/about/types-of-ovarian-cancer|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150518091024/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/about/types-of-ovarian-cancer|archivedate = 2015-05-18}}</ref>
 
===== Շճային կարցինոմա =====
Most people with epithelial ovarian carcinoma, about two-thirds, have a [[serous carcinoma]],<ref name=Jayson/> though this proportion is estimated as high as 80%.<ref name=":7">{{Cite web|url = http://www.dynamed.com/topics/dmp~AN~T900705/Ovarian-cancer|title = Ovarian cancer|date = June 18, 2015|publisher = DynaMed|url-access=subscription |url-status = live|archiveurl = https://web.archive.org/web/20150621210904/http://www.dynamed.com/topics/dmp~AN~T900705/Ovarian-cancer|archivedate = June 21, 2015}}</ref><ref name=Levy/> Low-grade serous carcinoma is less aggressive than high-grade serous carcinomas, though it does not typically respond well to chemotherapy or hormonal treatments.<ref name=Jayson/> Serous carcinomas are thought to begin in the [[Fallopian tube]].<ref name=":1" /> Histologically, serous adenocarcinomas have [[Psammoma body|psammoma bodies]]. Low-grade serous adenocarcinomas resemble Fallopian tube epithelium, whereas high-grade serous adenocarcinomas show [[anaplasia]] and [[nuclear atypia]].<ref name="Hoffman35" />
 
50% of the time, serous carcinomas are bilateral, and in 85% of cases, they have spread beyond the ovary at the time of diagnosis. Most have a diameter over 15&nbsp;cm.<ref name="Levy" />
 
===== Մանր բջջային կարցինոմա =====
[[Small-cell carcinoma|Small-cell]] ovarian carcinoma is rare and aggressive, with two main subtypes: hypercalcemic and pulmonary. It is typically fatal within 2 years of diagnosis. Hypercalcemic small cell ovarian carcinoma overwhelmingly affects those in their 20s, causes [[Hypercalcaemia|high blood calcium levels]], and affects one ovary. Pulmonary small cell ovarian cancer usually affects both ovaries of older women and looks like [[Small-cell carcinoma|oat-cell carcinoma of the lung]].<ref name="Hoffman35" />
 
====== Առաջնային պերիտոնեալ կարցինոմա ======
{{Main|Primary peritoneal carcinoma}}Primary peritoneal carcinomas develop from the [[peritoneum]], a membrane that covers the [[abdominal cavity]] that has the same embryonic origin as the ovary. They are often discussed and classified with ovarian cancers when they affect the ovary.<ref name=":1" /><ref>{{Cite web|title = Primary peritoneal carcinoma|url = http://www.cancerresearchuk.org/about-cancer/type/rare-cancers/rare-cancers-name/primary-peritoneal-carcinoma|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150520031318/http://www.cancerresearchuk.org/about-cancer/type/rare-cancers/rare-cancers-name/primary-peritoneal-carcinoma|archivedate = 2015-05-20}}</ref> They can develop even after the ovaries have been removed and may appear similar to [[mesothelioma]].<ref name="Hoffman35" />
 
===== Պարզ բջջային կարցինոմա =====
[[Clear-cell ovarian carcinoma]]s do not typically respond well to chemotherapy and may be related to endometriosis.<ref name=Jayson/> They represent approximately 5% of all endometrial cancers. Japanese women develop clear-cell ovarian cancer more frequently than other groups of women.<ref name=":7" />
 
===== Պարզ բջջային կարցինոմա =====
[[File:Clear cell carcinoma hobnail cells.png|thumb|upright=1.3|Hobnail cells seen in a clear cell carcinoma sample]]
 
Clear-cell adenocarcinomas are histopathologically similar to other [[clear cell carcinoma]]s, with [[clear cell]]s and [[hobnail cell]]s. They represent approximately 5–10% of epithelial ovarian cancers and are associated with endometriosis in the pelvic cavity. They are typically early-stage and therefore curable by surgery, but advanced clear-cell adenocarcinomas (approximately 20%) have a poor prognosis and are often resistant to platinum chemotherapy.<ref name="Hoffman35" />
 
===== Էնդոմետրոիդ =====
Endometrioid adenocarcinomas make up approximately 15–20% of epithelial ovarian cancers. Because they are typically low-grade, endometrioid adenocarcinomas have a good prognosis. These tumors frequently co-occur with [[endometriosis]] or endometrial cancer.<ref name="Hoffman35" />
 
====== Malignant mixed müllerian tumor (carcinosarcoma) ======
Mixed müllerian tumors make up less than 1% of ovarian cancer. They have epithelial and mesenchymal cells visible and tend to have a poor prognosis.<ref name="Hoffman35" />
 
===== Շճային =====
Mucinous tumors include mucinous adenocarcinoma and mucinous cystadenocarcinoma.<ref name="Hoffman35" />
 
====== Շճային ադենոկարցինոմա ======
{{Main|Mucinous adenocarcinoma}}
 
Mucinous adenocarcinomas make up 5–10% of epithelial ovarian cancers. Histologically, they are similar to intestinal or cervical adenocarcinomas, and are often actually metastases of [[appendiceal cancer|appendiceal]] or [[colon cancer]]s. Advanced mucinous adenocarcinomas have a poor prognosis, generally worse than serous tumors, and are often resistant to platinum chemotherapy, though they are rare.<ref name="Hoffman35" />
 
====== Որովայնամզի պսրդոմիքսոմա ======
{{Main|Pseudomyxoma peritonei}}
 
''Pseudomyxoma peritonei'' refers to a collection of encapsulated mucous or gelatinous material in the abdominopelvic cavity, which is very rarely caused by a primary mucinous ovarian tumor. More commonly, it is associated with ovarian metastases of intestinal cancer.<ref name="Hoffman35" />
 
===== Չտարբերակված Undifferentiated epithelial =====
Undifferentiated cancers - those where the cell type cannot be determined - make up about 10% of epithelial ovarian cancers and have a comparatively poor prognosis.<ref name="Hoffman35" /><ref name=":1" /> When examined under the microscope, these tumors have very abnormal cells that are arranged in clumps or sheets. Usually there are recognizable clumps of serous cells inside the tumor.<ref name="Hoffman35" />
 
====== Malignant Brenner tumor ======
{{Main|Brenner tumor}}
 
Malignant Brenner tumors are rare. Histologically, they have dense fibrous stroma with areas of transitional epithelium, and some squamous differentiation. To be classified as a malignant Brenner tumor, it must have Brenner tumor foci and transitional cell carcinoma. The transitional cell carcinoma component is typically poorly differentiated and resembles urinary tract cancer.<ref name="Hoffman35" />
 
====== Transitional cell carcinoma ======
{{Main|Transitional cell carcinoma}}
 
Transitional cell carcinomas represent less than 5% of ovarian cancers. Histologically, they appear similar to [[bladder carcinoma]]. The prognosis is intermediate - better than most epithelial cancers but worse than malignant Brenner tumors.<ref name="Hoffman35" />
 
==== Sex cord-stromal tumor ====
{{Main|Sex cord-stromal tumor}}
 
[[Sex cord-stromal tumour|Sex cord-stromal tumor]], including [[estrogen]]-producing [[granulosa cell tumor]], the benign [[thecoma]], and virilizing [[Sertoli-Leydig cell tumor]] or [[arrhenoblastoma]], accounts for 7% of ovarian cancers. They occur most frequently in women between 50 and 69 years of age, but can occur in women of any age, including young girls. They are not typically aggressive and are usually unilateral;<ref name=Harrisons/> they are therefore usually treated with surgery alone. Sex cord-stromal tumors are the main hormone-producing ovarian tumors.<ref name=":8">{{harvnb|Williams Gynecology|2012}}</ref>
 
Several different cells from the [[mesenchyme]] can give rise to sex-cord or stromal tumors. These include [[fibroblast]]s and endocrine cells. The symptoms of a sex-cord or stromal ovarian tumor can differ from other types of ovarian cancer. Common signs and symptoms include [[ovarian torsion]], [[hemorrhage]] from or rupture of the tumor, an abdominal mass, and hormonal disruption. In children, [[precocious puberty#Isosexual and heterosexual|isosexual precocious pseudopuberty]] may occur with granulosa cell tumors since they produce estrogen. These tumors cause abnormalities in menstruation ([[menometrorrhagia|excessive bleeding]], [[oligomenorrhea|infrequent menstruation]], or [[amenorrhea|no menstruation]]) or postmenopausal bleeding. Because these tumors produce estrogen, they can cause or occur at the same time as [[endometrial cancer]] or [[breast cancer]]. Other sex-cord/stromal tumors present with distinct symptoms. Sertoli-Leydig cell tumors cause [[virilization]] and [[hirsutism|excessive hair growth]] due to the production of [[testosterone]] and [[androstenedione]], which can also cause [[Cushing's syndrome]] in rare cases. Also, sex-cord stromal tumors occur that do not cause a hormonal imbalance, including benign fibromas, which cause ascites and [[hydrothorax]].<ref name=Harrisons/> With germ cell tumors, sex cord-stromal tumors are the most common ovarian cancer diagnosed in women under 20.<ref name=":8"/>
 
===== Հատիկավոր բջջային ուռուցք =====
Granulosa cell tumors are the most common sex-cord stromal tumors, making up 70% of cases, and are divided into two histologic subtypes: adult granulosa cell tumors, which develop in women over 50, and juvenile granulosa tumors, which develop before puberty or before the age of 30. Both develop in the [[ovarian follicle]] from a population of cells that surrounds [[germinal cell]]s.<ref name=":8" />
 
====== Մեծահասակների հատիկավոր բջջային ուռուցք ======
Adult granulosa cell tumors are characterized by later onset (30+ years, 50 on average). These tumors produce high levels of estrogen, which causes its characteristic symptoms: [[menometrorrhagia]]; [[endometrial hyperplasia]]; [[Breast pain|tender]], [[Breast enlargement|enlarged breasts]]; [[Vaginal bleeding|postmenopausal bleeding]]; and [[Amenorrhoea|secondary amenorrhea]]. The mass of the tumor can cause other symptoms, including abdominal pain and distension, or symptoms similar to an [[ectopic pregnancy]] if the tumor bleeds and ruptures.<ref name=":8" />
 
====== Պատանեկան հատիկավոր բջջային ուռուցք ======
 
===== Sertoli-Leydig cell tumor =====
Sertoli-Leydig tumors are most common in women before the age of 30, and particularly common before puberty.<ref name=":8" />
 
===== Sclerosing stromal tumors =====
Sclerosing stromal tumors typically occur in girls before puberty or women before the age of 30.<ref name=":8" />
 
==== Germ cell tumor ====
{{Main|Ovarian germ cell tumors}}
Germ cell tumors of the ovary develop from the ovarian [[germ cells]].<ref name=":1" /> [[Germ cell tumor]] accounts for about 30% of ovarian tumors, but only 5% of ovarian cancers, because most germ-cell tumors are [[teratoma]]s and most teratomas are benign. Malignant teratomas tend to occur in older women, when one of the germ layers in the tumor develops into a [[squamous cell carcinoma]].<ref name=Harrisons/> Germ-cell tumors tend to occur in young women (20s–30s) and girls, making up 70% of the ovarian cancer seen in that age group.<ref name=Current>{{cite book |chapter = Pediatric and Adolescent Gynecology |title = Current Diagnosis & Treatment Obstetrics & Gynecology |isbn = 978-0071638562 |edition = 11th |year = 2012 |first1 = Alan |last1 = DeCherney |first2 = Lauren |last2 = Nathan |first3 = T. Murphy |last3 = Goodwin |first4 = Neri |last4 = Laufer |first5 = Ashley |last5 = Roman | name-list-format = vanc }}</ref> Germ-cell tumors can include dysgerminomas, teratomas, yolk sac tumors/endodermal sinus tumors, and choriocarcinomas, when they arise in the ovary. Some germ-cell tumors have an [[isochromosome]] 12, where one arm of chromosome 12 is deleted and replaced with a duplicate of the other.<ref name=Harrisons/> Most germ-cell cancers have a better prognosis than other subtypes and are more sensitive to chemotherapy. They are more likely to be stage I at diagnosis.<ref name=":8" /> Overall, they metastasize more frequently than epithelial ovarian cancers. In addition, the cancer markers used vary with tumor type: [[choriocarcinomas]] are monitored with [[beta-HCG]] and endodermal sinus tumors with [[alpha-fetoprotein]].<ref name=Harrisons/>
 
Germ-cell tumors are typically discovered when they become large, palpable masses. However, like sex cord tumors, they can cause ovarian torsion or hemorrhage and, in children, isosexual precocious puberty. They frequently metastasize to nearby lymph nodes, especially para-aortic and pelvic lymph nodes.<ref name=Harrisons/> The most common symptom of germ cell tumors is [[Abdominal pain|subacute abdominal pain]] caused by the tumor bleeding, [[Necrosis|necrotizing]], or stretching the [[ovarian capsule]]. If the tumor ruptures, causes significant bleeding, or torses the ovary, it can cause [[Acute abdomen|acute abdominal pain]], which occurs in less than 10% of those with germ-cell tumors. They can also secrete hormones which change the [[menstrual cycle]]. In 25% of germ-cell tumors, the cancer is discovered during a [[Well-woman examination|routine examination]] and does not cause symptoms.<ref name=":8" />
 
Diagnosing germ cell tumors may be difficult because the normal menstrual cycle and [[puberty]] can cause pain and pelvic symptoms, and a young woman may even believe these symptoms to be those of pregnancy, and not seek treatment due to the stigma of [[Teenage pregnancy|teen pregnancy]]. Blood tests for alpha-fetoprotein, [[karyotype]], human chorionic gonadotropin, and liver function are used to diagnose germ cell tumor and potential co-occurring gonadal dysgenesis. A germ cell tumor may be initially mistaken for a benign [[ovarian cyst]].<ref name=":8" />
 
===== Dysgerminoma =====
{{Main|Dysgerminoma}}
Dysgerminoma accounts for 35% of ovarian cancer in young women and is the most likely germ cell tumor to metastasize to the lymph nodes; nodal metastases occur in 25–30% of cases.<ref name=Current/><ref name=":8" /> These tumors may have mutations in [[CD117|the ''KIT'' gene]], a mutation known for its role in [[gastrointestinal stromal tumor]]. [[Swyer syndrome|People with an XY karyotype and ovaries]] ([[gonadal dysgenesis]]) or an X,0 karyotype and ovaries ([[Turner syndrome]]) who develop a unilateral dysgerminoma are at risk for a [[gonadoblastoma]] in the other ovary, and in this case, both ovaries are usually removed when a unilateral dysgerminoma is discovered to avoid the risk of another malignant tumor. Gonadoblastomas in people with Swyer or Turner syndrome become malignant in approximately 40% of cases. However, in general, dysgerminomas are bilateral 10–20% of the time.<ref name=Harrisons/><ref name=":8" />
 
They are composed of cells that cannot [[Cellular differentiation|differentiate]] further and develop directly from germ cells or from gonadoblastomas. Dysgerminomas contain [[syncytiotrophoblast]]s in approximately 5% of cases, and can therefore cause elevated hCG levels. On gross appearance, dysgerminomas are typically pink to tan-colored, have multiple lobes, and are solid. Microscopically, they appear identical to [[seminoma]]s and very close to [[Embryonic germ cell|embryonic primordial germ cells]], having large, polyhedral, rounded [[clear cell]]s. The nuclei are uniform and round or square with prominent [[Nucleolus|nucleoli]] and the [[cytoplasm]] has high levels of [[glycogen]]. Inflammation is another prominent histologic feature of dysgerminomas.<ref name=":8" />
 
===== Խորիոնկարցինոմա =====
{{Main|Choriocarcinoma}}
Choriocarcinoma can occur as a primary ovarian tumor developing from a germ cell, though it is usually a gestational disease that metastasizes to the ovary. Primary ovarian choriocarcinoma has a poor prognosis and can occur without a pregnancy. They produce high levels of hCG and can cause [[Precocious puberty|early puberty]] in children or [[menometrorrhagia]] (irregular, heavy menstruation) after menarche.<ref name=":8" />
 
===== Անհաս տերատոմա =====
{{Main|Immature teratoma}}Immature, or solid, teratomas are the most common type of ovarian germ cell tumor, making up 40–50% of cases. Teratomas are characterized by the presence of disorganized tissues arising from all three embryonic [[germ layer]]s: [[ectoderm]], [[mesoderm]], and [[endoderm]]; immature teratomas also have undifferentiated [[stem cell]]s that make them more malignant than mature teratomas (dermoid cysts). The different tissues are visible on gross pathology and often include bone, cartilage, hair, [[mucus]], or [[Sebaceous gland|sebum]], but these tissues are not visible from the outside, which appears to be a solid mass with lobes and cysts. Histologically, they have large amounts of [[neuroectoderm]] organized into sheets and tubules along with [[Neuroglia|glia]]; the amount of neural tissue determines the histologic grade. Immature teratomas usually only affect one ovary (10% co-occur with dermoid cysts) and usually metastasize throughout the peritoneum. They can also cause mature teratoma implants to grow throughout the abdomen in a disease called [[growing teratoma syndrome]]; these are usually benign but will continue to grow during chemotherapy, and often necessitate further surgery. Unlike mature teratomas, immature teratomas form many [[Adhesion (medicine)|adhesions]], making them less likely to cause ovarian torsion. There is no specific marker for immature teratomas, but [[carcinoembryonic antigen]] (CEA), CA-125, CA19-9, or AFP can sometimes indicate an immature teratoma.<ref name=":8" />
 
Stage I teratomas make up the majority (75%) of cases and have the best prognosis, with 98% of patients surviving 5 years; if a Stage I tumor is also grade 1, it can be treated with unilateral surgery only. Stage II though IV tumors make up the remaining quarter of cases and have a worse prognosis, with 73–88% of patients surviving 5 years.<ref name=":8" />
 
===== Հասուն տերատոմա (դերմոիդ կիստա) =====
{{Main|Dermoid cyst}}
Mature teratomas, or dermoid cysts, are rare tumors consisting of mostly benign tissue that develop after menopause. The tumors consist of disorganized tissue with nodules of malignant tissue, which can be of various types. The most common malignancy is [[Squamous-cell carcinoma|squamous cell carcinoma]], but [[adenocarcinoma]], [[basal-cell carcinoma]], [[Carcinoid|carcinoid tumor]], [[neuroectodermal tumor]], [[Melanoma|malignant melanoma]], [[sarcoma]], [[Sebaceous carcinoma|sebaceous tumor]], and [[struma ovarii]] can also be part of the dermoid cyst. They are treated with surgery and adjuvant platinum chemotherapy or radiation.<ref name=":8" />
 
===== Yolk sac tumor/endodermal sinus tumor =====
{{Main|Yolk sac tumor}}
[[Yolk sac]] tumors, formerly called endodermal sinus tumors, make up approximately 10–20% of ovarian germ cell malignancies, and have the worst prognosis of all [[ovarian germ cell tumors]]. They occur both before menarche (in one-third of cases) and after menarche (the remaining two-thirds of cases). Half of people with yolk sac tumors are diagnosed in stage I. Typically, they are unilateral until metastasis, which occurs within the peritoneal cavity and via the bloodstream to the lungs. Yolk sac tumors grow quickly and recur easily, and are not easily treatable once they have recurred. Stage I yolk sac tumors are highly treatable, with a 5-year disease free survival rate of 93%, but stage II-IV tumors are less treatable, with survival rates of 64–91%.<ref name=":8" />
 
Their gross appearance is solid, friable, and yellow, with necrotic and hemorrhagic areas. They also often contain cysts that can degenerate or rupture. Histologically, yolk sac tumors are characterized by the presence of [[Schiller–Duval body|Schiller-Duval bodies]] (which are pathognomonic for yolk sac tumors) and a reticular pattern. Yolk sac tumors commonly secrete [[alpha-fetoprotein]] and can be [[Immunohistochemistry|immunohistochemically]] stained for its presence; the level of alpha-fetoprotein in the blood is a useful marker of recurrence.<ref name=":8" />
 
===== Էմբրիոնալ կարցինոմա =====
{{Main|Embryonal carcinoma}}
Embryonal carcinomas, a rare tumor type usually found in mixed tumors, develop directly from germ cells but are not terminally differentiated; in rare cases they may develop in dysgenetic gonads. They can develop further into a variety of other neoplasms, including choriocarcinoma, yolk sac tumor, and teratoma. They occur in younger people, with an average age at diagnosis of 14, and secrete both alpha-fetoprotein (in 75% of cases) and hCG.<ref name=":8" />
 
Histologically, embryonal carcinoma appears similar to the [[embryonic disc]], made up of epithelial, [[Anaplasia|anaplastic]] cells in disorganized sheets, with gland-like spaces and papillary structures.<ref name=":8" />
 
===== Պոլիէմբրիոմա =====
{{Main|Polyembryoma}}
Polyembryomas, the most immature form of teratoma and very rare ovarian tumors, are histologically characterized by having several [[embryo]]-like bodies with structures resembling a [[germ disk]], [[yolk sac]], and [[amniotic sac]]. [[Syncytiotrophoblast|Syncytiotrophoblast giant cells]] also occur in polyembryomas.<ref name=":8" />
 
==== Տափակ բջջային կարցինոմա ====
Primary ovarian squamous cell carcinomas are rare and have a poor prognosis when advanced. More typically, ovarian squamous cell carcinomas are cervical metastases, areas of differentiation in an endometrioid tumor, or derived from a mature teratoma.<ref name="Hoffman35" />
 
==== Խառը ուռուցքներ ====
Mixed tumors contain elements of more than one of the above classes of tumor histology. To be classed as a mixed tumor, the minor type must make up more than 10% of the tumor.<ref name=":7" /> Though mixed carcinomas can have any combination of cell types, mixed ovarian cancers are typically serous/endometrioid or clear cell/endometrioid.<ref name="Hoffman35" /> Mixed germ cell tumors make up approximately 25–30% of all germ cell ovarian cancers, with combinations of dysgerminoma, yolk sac tumor, and/or immature teratoma. The prognosis and treatment vary based on the component cell types.<ref name=":8" />
 
==== Ձվարանի երկրորդային քաղցկեղ ====
Ovarian cancer can also be a secondary cancer, the result of [[metastasis]] from a primary cancer elsewhere in the body.<ref name=Harrisons/> About 7% of ovarian cancers are due to metastases, while the rest are primary cancers.{{citation needed|date=November 2014}} Common primary cancers are [[breast cancer]], [[colon cancer]], [[appendiceal cancer]], and [[stomach cancer]] (primary gastric cancers that metastasize to the ovary are called [[Krukenberg tumor]]s).<ref name=Harrisons/> Krukenberg tumors have signet ring cells and mucinous cells.<ref name="Hoffman35" /> Endometrial cancer and lymphomas can also metastasize to the ovary.<ref name=Levy>{{Cite book|title = Premalignant & Malignant Disorders of the Ovaries & Oviducts|last = Levy|first = Gary | name-list-format = vanc |publisher = McGraw-Hill|year = 2013|last2 = Purcell|last3 = Karen|work = CURRENT Diagnosis & Treatment: Obstetrics & Gynecology, 11e| veditors = DeCherney AH, Nathan L, Laufer N, Roman AS |url = http://accessmedicine.mhmedical.com/content.aspx?bookid=498&sectionid=41008645|isbn = 978-0-07-163856-2|url-status = live|archiveurl = https://web.archive.org/web/20170910175639/http://accessmedicine.mhmedical.com/content.aspx?bookid=498&sectionid=41008645|archivedate = 2017-09-10}}</ref>
 
==== Low malignant potential tumors====
Low malignant potential (LMP) ovarian tumors, also called borderline tumors, have some benign and some malignant features.<ref name="Hoffman35" /> LMP tumors make up approximately 10%-15% of all ovarian tumors.<ref name=":7" /><ref name=":1" /> They develop earlier than epithelial ovarian cancer, around the age of 40–49. They typically do not have extensive invasion; 10% of LMP tumors have areas of stromal microinvasion (<3mm, <5% of tumor). LMP tumors have other abnormal features, including increased mitosis, [[pleomorphism (cytology)|changes in cell size or nucleus size]], [[nuclear atypia|abnormal nuclei]], cell stratification, and [[papillary projections|small projections on cells]] (papillary projections). Serous and/or mucinous characteristics can be seen on histological examination, and serous histology makes up the overwhelming majority of advanced LMP tumors. More than 80% of LMP tumors are Stage I; 15% are stage II and III and less than 5% are stage IV.<ref name=Hoffman35/> Implants of LMP tumors are often non-invasive.<ref name=":1" />
 
=== Փուլավորում ===
Ovarian cancer is staged using the [[International Federation of Gynecology and Obstetrics|FIGO]] staging system and uses information obtained after surgery, which can include a total [[Hysterectomy|abdominal hysterectomy]] via [[Laparotomy|midline laparotomy]], [[Salpingoophorectomy|removal of (usually) both ovaries and Fallopian tubes]], [[Omentectomy|(usually) the omentum]], [[pelvic washing|pelvic (peritoneal) washing]]s, assessment of [[Retroperitoneal lymph node dissection|retroperitoneal lymph nodes]] (including the [[Pelvic lymph nodes|pelvic]] and [[Paraaortic lymph node|para-aortic lymph nodes]]), [[appendectomy]] in suspected mucinous tumors, and pelvic/peritoneal biopsies for [[cytopathology]].<ref name=Jayson/><ref name=Harrisons/><ref name=":7" /><ref name=SGO/> Around 30% of ovarian cancers that appear confined to the ovary have metastasized microscopically, which is why even stage-I cancers must be staged completely.<ref name=Harrisons/> 22% of cancers presumed to be stage I are observed to have lymphatic metastases.<ref name=":7" /> The AJCC stage is the same as the FIGO stage. The AJCC staging system describes the extent of the primary tumor (T), the absence or presence of [[metastasis]] to nearby [[lymph nodes]] (N), and the absence or presence of distant metastasis (M).<ref name="A">{{cite web | url=http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-staging | title=How is ovarian cancer staged? | publisher=American Cancer Society | accessdate=June 17, 2017 | url-status=live | archiveurl=https://web.archive.org/web/20161124070854/http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-staging | archivedate=November 24, 2016 }}</ref> The most common stage at diagnosis is stage IIIc, with over 70% of diagnoses.<ref name=Harrisons/>
 
====FIGO====
[[File:Tumor deposet.JPG|thumb|upright=1.3|Ovarian adenocarcinoma deposit in the [[mesentery]] of the small bowel]]
{| class="wikitable"
|+ FIGO stages of ovarian cancer<ref name=Jayson/><ref name=SGO>{{cite web |url = https://www.sgo.org/wp-content/uploads/2012/09/FIGO-Ovarian-Cancer-Staging_1.10.14.pdf |title = Ovarian Cancer Staging |publisher = Society for Gynecologic Oncology |date = 1 January 2014 |url-status = live |archiveurl = https://web.archive.org/web/20141105012607/https://www.sgo.org/wp-content/uploads/2012/09/FIGO-Ovarian-Cancer-Staging_1.10.14.pdf |archivedate = 5 November 2014 }}</ref>
! Stage
!
!
!
! Description
|-
| I
|
|
|
| Cancer is completely limited to the ovary
|-
|
| IA
|
|
| involves one ovary, capsule intact, no tumor on ovarian surface, negative washings
|-
|
| IB
|
|
| involves both ovaries; capsule intact; no tumor on ovarian surface; negative washings
|-
|
| IC
|
|
| tumor involves one or both ovaries
|-
|
| IC1
|
|
| surgical spill
|-
|
| IC2
|
|
| capsule has ruptured or tumor on ovarian surface
|-
|
| IC3
|
|
| positive ascites or washings
|-
| II
|
|
|
| pelvic extension of the tumor (must be confined to the pelvis) or primary peritoneal tumor, involves one or both ovaries
|-
|
| IIA
|
|
| tumor found on uterus or fallopian tubes
|-
|
| IIB
|
|
| tumor elsewhere in the pelvis
|-
| III
|
|
|
| cancer found outside the pelvis or in the retroperitoneal lymph nodes, involves one or both ovaries
|-
|
| IIIA
|
|
| metastasis in retroperitoneal lymph nodes or microscopic extrapelvic metastasis
|-
|
|
| IIIA1
|
| metastasis in retroperitoneal lymph nodes
|-
|
|
|
| IIIA1(i)
| the metastasis is less than 10&nbsp;mm in diameter
|-
|
|
|
| IIIA1(ii)
| the metastasis is greater than 10&nbsp;mm in diameter
|-
|
|
| IIIA2
|
| microscopic metastasis in the peritoneum, regardless of retroperitoneal lymph node status
|-
|
| IIIB
|
|
| metastasis in the peritoneum less than or equal to 2&nbsp;cm in diameter, regardless of retroperitoneal lymph node status; or metastasis to liver or spleen capsule
|-
|
| IIIC
|
|
| metastasis in the peritoneum greater than 2&nbsp;cm in diameter, regardless of retroperitoneal lymph node status; or metastasis to liver or spleen capsule
|-
| IV
|
|
|
| distant metastasis (i.e. outside of the peritoneum)
|-
|
| IVA
|
|
| pleural effusion containing cancer cells
|-
|
| IVB
|
|
| metastasis to distant organs (including the parenchyma of the spleen or liver), or metastasis to the inguinal and extra-abdominal lymph nodes
|}
 
<gallery>
File:Diagram showing stage 1 ovarian cancer CRUK 193.svg|Stage 1 ovarian cancer
File:Diagram showing stage 2A to 2C ovarian cancer CRUK 214.svg|Stage 2 ovarian cancer
File:Diagram showing stage 3A to 3C ovarian cancer CRUK 225.svg|Stage 3 ovarian cancer
File:Diagram showing stage 4 ovarian cancer CRUK 233.svg|Stage 4 ovarian cancer
</gallery>
 
====AJCC/TNM====
The AJCC/TNM staging system indicates where the tumor has developed, spread to lymph nodes, and metastasis.<ref name=":7" />
{| class="wikitable"
|+ AJCC/TNM stages of ovarian cancer<ref name=":7" />
!Stage
!
!
!Description
|-
|T
|
|
|Primary tumor
|-
|
|Tx
|
|Cannot be assessed
|-
|
|T0
|
|No evidence
|-
|
|T1
|
|Tumor limited to ovary/ovaries
|-
|
|
|T1a
|One ovary with intact capsule, no surface tumor, and negative ascites/peritoneal washings
|-
|
|
|T1b
|Both ovaries with intact capsules, no surface tumor, and negative ascites/peritoneal washings
|-
|
|
|T1c
|One or both ovaries with ruptured capsule or capsules, surface tumor, positive ascites/peritoneal washings
|-
|
|T2
|
|Tumor is in ovaries and pelvis (extension or implantation)
|-
|
|
|T2a
|Expansion to uterus or Fallopian tubes, negative ascites/peritoneal washings
|-
|
|
|T2b
|Expansion in other pelvic tissues, negative ascites/peritoneal washings
|-
|
|
|T2c
|Expansion to any pelvic tissue, positive ascites/peritoneal washings
|-
|
|T3
|
|Tumor is in ovaries and has metastasized outside the pelvis to the peritoneum (including the liver capsule)
|-
|
|
|T3a
|Microscopic metastasis
|-
|
|
|T3b
|Macroscopic metastasis less than 2&nbsp;cm diameter
|-
|
|
|T3c
|Macroscopic metastasis greater than 2&nbsp;cm diameter
|-
|N
|
|
|Regional lymph node metastasis
|-
|
|Nx
|
|Cannot be assessed
|-
|
|N0
|
|No metastasis
|-
|
|N1
|
|Metastasis present
|-
|M
|
|
|Distant metastasis
|-
|
|M0
|
|No metastasis
|-
|
|M1
|
|Metastasis present (excluding liver capsule, including liver parenchyma and cytologically confirmed pleural effusion)
|}
 
The AJCC/TNM stages can be correlated with the FIGO stages:<ref name=":7" />
{| class="wikitable"
!FIGO
!T
!N
!M
|-
|I
|T1
|N0
|M0
|-
|IA
|T1a
|N0
|M0
|-
|IB
|T1b
|N0
|M0
|-
|IC
|T1c
|N0
|M0
|-
|II
|T2
|N0
|M0
|-
|IIA
|T2a
|N0
|M0
|-
|IIB
|T2b
|N0
|M0
|-
|IIC
|T2c
|N0
|M0
|-
|III
|T3
|N0
|M0
|-
|IIIA
|T3a
|N0
|M0
|-
|IIIB
|T3b
|N0
|M0
|-
|IIIC
|T3c
|N0/N1
|M0
|-
|IV
|Any
|Any
|M1
|}
 
====Աստիճանավորում====
Grade 1 tumors have well differentiated cells (look very similar to the normal tissue) and are the ones with the best prognosis. Grade 2 tumors are also called moderately well-differentiated and they are made up of cells that resemble the normal tissue. Grade 3 tumors have the worst prognosis and their cells are abnormal, referred to as poorly differentiated.<ref>{{Cite web|title = Stages of ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/stages-of-ovarian-cancer|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150518132114/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/stages-of-ovarian-cancer|archivedate = 2015-05-18}}</ref>
 
Metastasis in ovarian cancer is very common in the abdomen, and occurs via exfoliation, where cancer cells burst through the ovarian capsule and are able to move freely throughout the peritoneal cavity. Ovarian cancer metastases usually grow on the surface of organs rather than the inside; they are also common on the omentum and the peritoneal lining. Cancer cells can also travel through the [[lymphatic system]] and metastasize to lymph nodes connected to the ovaries via blood vessels; i.e. the lymph nodes along the [[Suspensory ligament of ovary|infundibulopelvic ligament]], the [[Broad ligament of the uterus|broad ligament]], and the [[Round ligament of uterus|round ligament]]. The most commonly affected groups include the [[paraaortic lymph node|paraaortic]], [[hypogastric lymph node|hypogastric]], [[external iliac lymph nodes|external iliac]], [[obturator lymph nodes|obturator]], and [[inguinal lymph node]]s. Usually, ovarian cancer does not metastasize to the liver, lung, brain, or kidneys unless it is recurrent disease; this differentiates ovarian cancer from many other forms of cancer.<ref name="Hoffman35" />
 
== Սկրինինգ ==
There is no simple and reliable way to test for ovarian cancer in women who do not have any signs or symptoms. Screening is not recommended in women who are at average risk, as evidence does not support a reduction in death and the high rate of false positive tests may lead to unneeded surgery, which is accompanied by its own risks.<ref name=Gros2018/> The [[Pap test]] does not screen for ovarian cancer.<ref name = CDCsep2016/>
 
Ovarian cancer is usually only palpable in advanced stages.<ref name=Hoffman35/> Screening is not recommended using [[CA-125]] measurements, [[HE4]] levels, ultrasound, or adnexal palpation in women who are at average risk. Risk of developing ovarian cancer in those with genetic factors can be reduced. Those with a genetic predisposition may benefit from screening. This high risk group has benefited with earlier detection.<ref name=Jayson/><ref name=Harrisons/><ref name=Harrisons82>{{cite book |last1 = Croswell |first1 = Jennifer M. |last2 = Brawley |first2 = Otis W. |last3 = Kramer |first3 = Barnett S. | name-list-format = vanc |chapter = Prevention and Early Detection of Cancer |veditors = Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J |title = Harrison's Principles of Internal Medicine |publisher = McGraw-Hill |year = 2012 |edition = 18th |isbn = 978-0-07-174889-6|title-link = Harrison's Principles of Internal Medicine }}</ref>
 
Ovarian cancer has low prevalence, even in the high-risk group of women from the ages of 50 to 60 (about one in 2000), and screening of women with average risk is more likely to give ambiguous results than detect a problem which requires treatment. Because ambiguous results are more likely than detection of a treatable problem, and because the usual response to ambiguous results is invasive interventions, in women of average risk, the potential harms of having screening without an indication outweigh the potential benefits. The purpose of screening is to diagnose ovarian cancer at an early stage, when it is more likely to be treated successfully.<ref name=Harrisons/><ref name=Harrisons82/>
 
Screening with [[transvaginal ultrasound]], pelvic examination, and CA-125 levels can be used instead of preventive surgery in women who have BRCA1 or BRCA2 mutations. This strategy has shown some success.<ref name=Hoffman35/>
 
== Կանխարգելում==
People with strong genetic risk for ovarian cancer may consider the surgical removal of their ovaries as a preventive measure. This is often done after completion of childbearing years. This reduces the chances of developing both breast cancer (by around 50%) and ovarian cancer (by about 96%) in people at high risk. Women with ''BRCA'' gene mutations usually also have their Fallopian tubes removed at the same time (salpingo-oophorectomy), since they also have an increased risk of [[Fallopian tube cancer]]. However, these statistics may overestimate the risk reduction because of how they have been studied.<ref name=Harrisons/><ref name=Harrisons82/>
 
People with a significant family history for ovarian cancer are often referred to a [[genetic counselor]] to see if testing for BRCA mutations would be beneficial.<ref name=Hoffman35/> The use of oral contraceptives, the absence of 'periods' during the menstrual cycle, and tubal ligation reduce the risk.<ref name="CibulaWidschwendter2010">{{cite journal | vauthors = Cibula D, Widschwendter M, Májek O, Dusek L | title = Tubal ligation and the risk of ovarian cancer: review and meta-analysis | journal = Human Reproduction Update | volume = 17 | issue = 1 | pages = 55–67 | year = 2010 | pmid = 20634209 | doi = 10.1093/humupd/dmq030 }}</ref>
There may an association of developing ovarian cancer and ovarian stimulation during infertility treatments. Endometriosis has been linked to ovarian cancers. [[Human papillomavirus infection]], smoking, and [[talc]] have not been identified as increasing the risk for developing ovarian cancer.<ref name=Jayson/>
 
== Management ==
Once it is determined that ovarian, fallopian tube, or primary peritoneal cancer is present, treatment is scheduled by a gynecologic oncologist (a physician trained to treat cancers of a woman’s reproductive system). Gynecologic oncologists can perform surgery on and give chemotherapy to women with ovarian cancer. A treatment plan is developed.<ref name=CDCfeb2017>{{cite web | title = How Is Ovarian Cancer Treated? | publisher = Centers for Disease Control and Prevention | date = February 13, 2017 | url = https://www.cdc.gov/cancer/ovarian/basic_info/treatment.htm | accessdate = June 17, 2017 | url-status = live | archiveurl = https://web.archive.org/web/20170616220128/https://www.cdc.gov/cancer/ovarian/basic_info/treatment.htm | archivedate = June 16, 2017 }}{{CDC}}</ref>
 
Treatment usually involves [[surgery]] and [[chemotherapy]], and sometimes [[radiotherapy]], regardless of the subtype of ovarian cancer.<ref name=":1" /><ref>{{cite journal | vauthors = Marchetti C, Pisano C, Facchini G, Bruni GS, Magazzino FP, Losito S, Pignata S | title = First-line treatment of advanced ovarian cancer: current research and perspectives | journal = Expert Review of Anticancer Therapy | volume = 10 | issue = 1 | pages = 47–60 | date = January 2010 | pmid = 20014885 | doi = 10.1586/era.09.167 }}</ref> Surgical treatment may be sufficient for well-differentiated malignant tumors and confined to the ovary. Addition of chemotherapy may be required for more aggressive tumors confined to the ovary. For patients with advanced disease, a combination of surgical reduction with a combination chemotherapy regimen is standard. Borderline tumors, even following spread outside of the ovary, are managed well with surgery, and chemotherapy is not seen as useful.<ref name=":2">{{Cite web|title = Types of treatment for ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/which-treatment-for-ovarian-cancer|website = www.cancerresearchuk.org|access-date = 2015-05-16|url-status = live|archive-url = https://web.archive.org/web/20150512164129/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/which-treatment-for-ovarian-cancer|archive-date = 2015-05-12}}</ref> [[Second-look surgery]] and [[maintenance chemotherapy]] have not been shown to provide benefit.<ref name="Hoffman35" />
 
=== Վիրահատություն ===
[[Surgery]] has been the standard of care for decades and may be necessary in obtaining a specimen for [[medical diagnosis|diagnosis]]. The surgery depends upon the extent of nearby invasion of other tissues by the cancer when it is diagnosed. This extent of the cancer is described by assigning it a stage, the presumed type, and the grade of cancer. The gynecological surgeon may remove one (unilateral oophorectomy) or both ovaries (bilateral oophorectomy). The Fallopian tubes (salpingectomy), uterus (hysterectomy), and the [[Greater omentum|omentum]] (omentectomy) may also be removed. Typically, all of these organs are removed.<ref name="CanadianCS2017" />
 
For low-grade, unilateral stage-IA cancers, only the involved ovary (which must be unruptured) and Fallopian tube will be removed. This can be done especially in young people who wish to preserve their fertility. However, a risk of microscopic metastases exists and staging must be completed.<ref name="Jayson" /> If any metastases are found, a second surgery to remove the remaining ovary and uterus is needed.<ref name=":2" /> [[Tranexamic acid]] can be administered prior to surgery to reduce the need for blood transfusions due to blood loss during the surgery.<ref name=":7" />
 
If a tumor in a premenopausal woman is determined to be a low malignant potential tumor during surgery, and it is clearly stage I cancer, only the affected ovary is removed. For postmenopausal women with low malignant potential tumors, hysterectomy with bilateral salpingo-oophorectomy is still the preferred option. During staging, the appendix can be examined or removed. This is particularly important with mucinous tumors.<ref name="Hoffman35" /> In children or adolescents with ovarian cancer, surgeons typically attempt to preserve one ovary to allow for the completion of [[puberty]], but if the cancer has spread, this is not always possible. Dysgerminomas in particular tend to affect both ovaries: 8–15% of dysgerminomas are present in both ovaries.<ref name="Current" /> People with low-grade (well-differentiated) tumors are typically treated only with surgery,<ref name="Harrisons" /> which is often curative.<ref name=":1" /> In general, germ cell tumors can be treated with unilateral surgery unless the cancer is widespread or fertility is not a factor.<ref name=":8" />
 
In advanced cancers, where complete removal is not an option, as much tumor as possible is removed in a procedure called [[debulking]] surgery. This surgery is not always successful, and is less likely to be successful in women with extensive metastases in the peritoneum, stage- IV disease, cancer in the [[porta hepatis|transverse fissure of the liver]], [[mesentery]], or diaphragm, and large areas of ascites. Debulking surgery is usually only done once.<ref name=Jayson/> More complete debulking is associated with better outcomes: women with no macroscopic evidence of disease after debulking have a median survival of 39 months, as opposed to 17 months with less complete surgery.<ref name=Harrisons/> By removing metastases, many cells that are resistant to chemotherapy are removed, and any clumps of cells that have died are also removed. This allows chemotherapy to better reach the remaining cancer cells, which are more likely to be fast-growing and therefore chemosensitive.<ref name="Hoffman35" />
 
Interval debulking surgery is another protocol used, where neoadjuvant chemotherapy is given, debulking surgery is performed, and chemotherapy is finished after debulking.<ref name=":2" /> Though no definitive studies have been completed, it is shown to be approximately equivalent to primary debulking surgery in terms of survival, and shows slightly lower morbidity.<ref name="Hoffman35" />
 
There are several different surgical procedures that can be employed to treat ovarian cancer. For stage I and II cancer, laparascopic (keyhole) surgery can be used, but metastases may not be found. For advanced cancer, laparoscopy is not used, since debulking metastases requires access to the entire peritoneal cavity. Depending on the extent of the cancer, procedures may include a bilateral salpingo-oophorectomy, biopsies throughout the peritoneum and abdominal lymphatic system, [[omentectomy]], [[splenectomy]], [[bowel resection]], [[Diaphragm resection|diaphragm stripping or resection]], [[appendectomy]], or even a posterior [[pelvic exenteration]].<ref name="Hoffman35" />
 
To fully stage ovarian cancer, [[lymphadenectomy]] can be included in the surgery, but a significant survival benefit to this practice may not happen.<ref name=Jayson/> This is particularly important in germ cell tumors because they frequently metastasize to nearby lymph nodes.<ref name=Harrisons/>
 
If ovarian cancer recurs, secondary surgery is sometimes a treatment option. This depends on how easily the tumor can be removed, how much fluid has accumulated in the abdomen, and overall health.<ref name=Jayson/> It can be helpful in people who had their first surgery done by a generalist and in epithelial ovarian cancer.<ref name=":7" /> Secondary surgery can be effective in dysgerminomas and immature teratomas.<ref name=":8" />
 
The major side effect of an oophorectomy in younger women is early [[menopause]], which can cause [[osteoporosis]]. After surgery, hormone replacement therapy can be considered, especially in younger women. This therapy can consist of a combination of estrogen and progesterone, or estrogen alone. Estrogen alone is safe after hysterectomy; when the uterus is still present, unopposed estrogen dramatically raises the risk of [[endometrial cancer]].<ref name=Jayson/> Estrogen therapy after surgery does not change survival rates.<ref name=":7" /> People having ovarian cancer surgery are typically hospitalized afterwards for 3–4 days and spend around a month recovering at home.<ref>{{Cite web|title = Surgery for ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/surgery-for-ovarian-cancer|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150518161131/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/surgery-for-ovarian-cancer|archivedate = 2015-05-18}}</ref> Surgery outcomes are best at hospitals that do a large number of ovarian cancer surgeries.<ref name="Hoffman35" />
 
It is unclear if [[laparoscopy]] or [[laparotomy]] is better or worse for FIGO stage I ovarian cancer.<ref>{{cite journal | vauthors = Falcetta FS, Lawrie TA, Medeiros LR, da Rosa MI, Edelweiss MI, Stein AT, Zelmanowicz A, Moraes AB, Zanini RR, Rosa DD | display-authors = 6 | title = Laparoscopy versus laparotomy for FIGO stage I ovarian cancer | journal = The Cochrane Database of Systematic Reviews | volume = 10 | pages = CD005344 | date = October 2016 | pmid = 27737492 | pmc = 6464147 | doi = 10.1002/14651858.CD005344.pub4 }}</ref> There is also no apparent difference between total abdominal hysterectomy and supracervical hysterectomy for advanced cancers. Approximately 2.8% of people having a first surgery for advanced ovarian cancer die within two weeks of the surgery (2.8% [[perioperative mortality]] rate).<ref name=":7" /> More aggressive surgeries are associated with better outcomes in advanced (stage III or IV) ovarian cancer.<ref name="Hoffman35" />
 
=== Քիմիոթերապիա ===
[[Chemotherapy]] has been a general [[standard of care]] for ovarian cancer for decades, although with variable protocols. Chemotherapy is used after surgery to treat any residual disease, if appropriate. In some cases, there may be reason to perform chemotherapy first, followed by surgery. This is called "neoadjuvant chemotherapy", and is common when a tumor cannot be completely removed or optimally debulked via surgery. Though it has not been shown to increase survival, it can reduce the risk of complications after surgery. If a unilateral salpingo-oophorectomy or other surgery is performed, additional chemotherapy, called "adjuvant chemotherapy", can be given.<ref name=Jayson/><ref name=":7" /> Adjuvant chemotherapy is used in stage 1 cancer typically if the tumor is of a high histologic grade (grade 3) or the highest substage (stage 1c), provided the cancer has been optimally staged during surgery.<ref name=":7" /><ref name=":2" /> [[Bevacizumab]] may be used as an adjuvant chemotherapy if the tumor is not completely removed during surgery or if the cancer is stage IV; it can extend progression-free survival but has not been shown to extend overall survival.<ref name=":7" /> Chemotherapy is curative in approximately 20% of advanced ovarian cancers;<ref name="Hoffman35" /> it is more often curative with malignant germ cell tumors than epithelial tumors.<ref name=":8" /> Adjuvant chemotherapy has been found to improve survival and reduce the risk of ovarian cancer recurring compared to no adjuvant therapy in women with early stage epithelial ovarian cancer.<ref>{{cite journal | vauthors = Lawrie TA, Winter-Roach BA, Heus P, Kitchener HC | title = Adjuvant (post-surgery) chemotherapy for early stage epithelial ovarian cancer | journal = The Cochrane Database of Systematic Reviews | issue = 12 | pages = CD004706 | date = December 2015 | pmid = 26676202 | pmc = 6457737 | doi = 10.1002/14651858.cd004706.pub5 }}</ref>
 
Chemotherapy in ovarian cancer typically consists of [[platins]], a group of [[platinum]]-based drugs, combined with non-platins. Common therapies can include [[paclitaxel]], [[cisplatin]], [[topotecan]], doxorubicin, [[epirubicin]], and [[gemcitabine]]. [[Carboplatin]] is typically given in combination with either [[paclitaxel]] or [[docetaxel]]; the typical combination is carboplatin with paclitaxel.<ref name=Jayson/><ref name=":7" /> Carboplatin is superior to cisplatin in that it is less toxic and has fewer side effects, generally allowing for an improved quality of life in comparison, though both are similarly effective.<ref name=":7" /> Three-drug regimens have not been found to be more effective,<ref name="Jayson" /> and platins alone or nonplatins alone are less effective than platins and nonplatins in combination.<ref name=":7" /> Chemotherapy can be given [[chemotherapy#Delivery|intravenously]] or [[intraperitoneal chemotherapy|in the peritoneal cavity]].<ref name=Harrisons/> Though intraperitoneal chemotherapy is associated with longer progression-free survival and overall survival, it also causes more adverse side effects than intravenous chemotherapy.<ref name=":7" /> It is mainly used when the cancer has been optimally debulked. Intraperitoneal chemotherapy can be highly effective because ovarian cancer mainly spreads inside the peritoneal cavity, and higher doses of the drugs can reach the tumors this way.<ref name="Hoffman35" />
 
Chemotherapy can cause [[anemia]]; intravenous iron has been found to be more effective than oral [[iron supplement]]s in reducing the need for [[blood transfusion]]s.<ref name=":7" /> Typical cycles of treatment involve one treatment every 3 weeks, repeated for 6 weeks or more.<ref name=":3">{{Cite web|title = Drugs used for ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/drugs-used-for-ovarian-cancer|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = dead|archiveurl = https://web.archive.org/web/20150518091158/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/drugs-used-for-ovarian-cancer|archivedate = 2015-05-18}}</ref> Fewer than 6 weeks (cycles) of treatment is less effective than 6 weeks or more.<ref name=":7" /> Germ-cell malignancies are treated differently than other ovarian cancers&nbsp;— a regimen of [[bleomycin]], [[etoposide]], and cisplatin (BEP) is used with 5 days of chemotherapy administered every 3 weeks for 3 to 4 cycles.<ref name="Harrisons" /><ref name=":8" /> Chemotherapy for germ cell tumors has not been shown to cause [[Amenorrhoea|amenorrhea]], infertility, [[Congenital disorder|birth defects]], or [[miscarriage]].<ref name=":8" /> [[Maintenance chemotherapy]] has not been shown to be effective.<ref name=":7" />
 
In people with ''BRCA'' mutations, platinum chemotherapy is more effective.<ref name=Jayson/> Germ-cell tumors and malignant sex-cord/stromal tumors are treated with chemotherapy, though dysgerminomas and sex-cord tumors are not typically very responsive.<ref name=Harrisons/><ref name=Current/>
 
====Platinum-sensitive or platinum-resistant==== <!-- initial target for platinum-resistant ovarian cancer -->
If ovarian cancer recurs, it is considered partially platinum-sensitive or platinum-resistant, based on the time since the last recurrence treated with platins: partially platinum-sensitive cancers recurred 6–12 months after last treatment, and platinum-resistant cancers have an interval of less than 6 months. Second-line chemotherapy can be given after the cancer becomes symptomatic, because no difference in survival is seen between treating asymptomatic (elevated CA-125) and symptomatic recurrences.{{Medical citation needed|date=November 2017}}
 
For platinum-sensitive tumors, platins are the drugs of choice for second-line chemotherapy, in combination with other cytotoxic agents. Regimens include carboplatin combined with [[doxorubicin#Liposomal formulations|pegylated liposomal doxorubicin]], [[gemcitabine]], or [[paclitaxel]].<ref name="Harrisons" /> Carboplatin-doublet therapy can be combined with paclitaxel for increased efficacy in some cases. Another potential adjuvant therapy for platinum-sensitive recurrences is [[olaparib]], which may improve [[progression-free survival]] but has not been shown to improve [[overall survival]].<ref name=":7" /> ([[Olaparib]], a [[PARP inhibitor]], was approved by the [[US FDA]] for use in BRCA-associated ovarian cancer that had previously been treated with chemotherapy.<ref>{{cite web |url = https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm427554.htm?sf34855004=1 |title = FDA approves Lynparza to treat advanced ovarian cancer: First LDT companion diagnostic test also approved to identify appropriate patients |first = Stephanie |last = Yao |date = 19 December 2014 |publisher = U.S. Food and Drug Administration |url-status = live |archiveurl = https://web.archive.org/web/20150914092851/https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm427554.htm?sf34855004=1 |archivedate = 14 September 2015 }}</ref><ref name=":60">{{Cite web|title = Innovative treatment for gynaecological cancers approved for Cancer Drugs Fund|url = https://www.nice.org.uk/news/article/innovative-treatment-for-gynaecological-cancers-approved-for-cancer-drugs-fund|accessdate = 2019-08-14|url-status = live}}</ref>) For recurrent germ cell tumors, an additional 4 cycles of BEP chemotherapy is the first-line treatment for those tho have been treated with surgery or platins.
 
If the tumor is determined to be platinum-resistant, [[vincristine]], [[dactinomycin]], and [[cyclophosphamide]] (VAC) or some combination of paclitaxel, gemcitabine, and [[oxaliplatin]] may be used as a second-line therapy.<ref name=":8" />
 
For platinum-resistant tumors, there are no high-efficacy chemotherapy options. Single-drug regimens (doxorubicin or [[topotecan]]) do not have high response rates,<ref name="Jayson" /> but single-drug regimens of topotecan, pegylated liposomal doxorubicin, or gemcitabine are used in some cases.<ref name="Harrisons" /><ref name=":7" /> Topotecan cannot be used in people with an intestinal blockage. Paclitaxel used alone is another possible regimen, or it may be combined with liposomal doxorubicin, gemcitabine, cisplatin, topotecan, [[etoposide]], or [[cyclophosphamide]].<ref name=":3" /> ( See also Palliative care below.)
 
=== Ճառագայթային բուժում ===
Dysgerminomas are most effectively treated with radiation,<ref name=Current/> though this can cause infertility and is being phased out in favor of chemotherapy.<ref name=Harrisons/> Radiation therapy does not improve survival in people with well-differentiated tumors.<ref name="Harrisons" />
 
In stage 1c and 2 cancers, radiation therapy is used after surgery if there is the possibility of residual disease in the pelvis but the abdomen is cancer-free. Radiotherapy can also be used in palliative care of advanced cancers. A typical course of radiotherapy for ovarian cancer is 5 days a week for 3–4 weeks. Common side effects of radiotherapy include diarrhea, constipation, and frequent urination.<ref name=":4">{{Cite web|title = Radiotherapy for ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/radiotherapy-for-ovarian-cancer|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150518160124/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/radiotherapy-for-ovarian-cancer|archivedate = 2015-05-18}}</ref>
 
=== Հորմոնալ բուժում ===
Despite the fact that 60% of ovarian tumors have [[estrogen receptor]]s, ovarian cancer is only rarely responsive to hormonal treatments. Estrogen alone does not have an effect on the cancer, and [[tamoxifen]] and [[letrozole]] are rarely effective.<ref name=Jayson/> "Some women with borderline malignancy ovarian cancer and stromal ovarian cancer may receive hormonal therapy."<ref name = CanadianCS2017/>
 
=== Իմունոթերապիա ===
Immunotherapy is a topic of current research in ovarian cancer. In some cases, the antibody drug [[bevacizumab]], though still a topic of active research, is used to treat advanced cancer along with chemotherapy.<ref name=":2" /> It has been approved for this use in the European Union.<ref name=":6" />
 
=== Շարունակական հսկողություն ===
Specific follow-up depends on, for example, the type and stage of ovarian cancer, the treatment, and the presence of any symptoms. Usually, a check-up appointment is made about every 2 to 3 months initially, followed by twice per year for up to 5 years.<ref>{{cite web |url = http://www.cancerresearchuk.org/cancer-help/type/ovarian-cancer/treatment/follow-up-for-ovarian-cancer |title = Follow up for ovarian cancer |publisher = Cancer Research UK |url-status = live |archiveurl = https://web.archive.org/web/20140829010226/http://www.cancerresearchuk.org/cancer-help/type/ovarian-cancer/treatment/follow-up-for-ovarian-cancer |archivedate = 2014-08-29 |date = 2017-08-30 }}</ref> For epithelial ovarian cancers, the most common test upon follow-up is CA-125 level. However, treatment based only on elevated CA-125 levels and not any symptoms can increase side effects without any prolongation of life, so the implication of the outcome of a CA-125 test can be discussed before taking it.<ref name=ACSfollowup>[http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-after-follow-up Follow-up care] {{webarchive|url=https://web.archive.org/web/20131225025103/http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-after-follow-up |date=2013-12-25 }} from [[American Cancer Society]]. Last Medical Review: 03/21/2013. Last Revised: 02/06/2014</ref> The recommendation as of 2014 is recurrent cancer may be present if the CA-125 level is twice normal.<ref name=Jayson/> Treating a recurrence detected by CA-125 does not improve survival.<ref name=":7" />
 
For women with [[germ-cell tumor]]s, follow-up tests generally include [[alpha-fetoprotein]] (AFP) and/or [[human chorionic gonadotropin]]. For women with [[stromal cancer]]s, tests for hormones like estrogen, testosterone, and [[inhibin]] are sometimes helpful.<ref name=ACSfollowup/> Inhibin can also be useful for monitoring the progress of sex-cord tumors, along with [[mullerian inhibiting substance]]. AFP can also be used to monitor Sertoli-Leydig tumors.<ref name=Harrisons/> In dysgerminomas, [[lactate dehydrogenase]] and its two [[isozyme]]s ([[LDH-1]] and [[LDH-2]]) are used to test for recurrence.<ref name=":8" />
 
Women with ovarian cancer may not need routine surveillance imaging to monitor the cancer unless new symptoms appear or [[tumor markers]] begin rising.<ref name="SGOfive">{{Citation |author1 = Society of Gynecologic Oncology |author1-link = Society of Gynecologic Oncology |date = February 2014 |title = Five Things Physicians and Patients Should Question |publisher = Society of Gynecologic Oncology |work = [[Choosing Wisely]]: an initiative of the [[ABIM Foundation]] |url = http://www.choosingwisely.org/doctor-patient-lists/society-of-gynecologic-oncology/ |accessdate = 19 February 2013 |url-status = live |archiveurl = https://web.archive.org/web/20131201052931/http://www.choosingwisely.org/doctor-patient-lists/society-of-gynecologic-oncology/ |archivedate = 1 December 2013 }}, which cites
* {{cite journal | vauthors = Bhosale P, Peungjesada S, Wei W, Levenback CF, Schmeler K, Rohren E, Macapinlac HA, Iyer RB | title = Clinical Utility of Positron Emission Tomography/Computed Tomography in the Evaluation of Suspected Recurrent Ovarian Cancer in the Setting of Normal CA-125 Levels | journal = International Journal of Gynecological Cancer | volume = 20 | issue = 6 | pages = 936–944 | date = August 2010 | pmid = 20683399 | doi = 10.1111/IGC.0b013e3181e82a7f }}</ref> Imaging without these indications is discouraged because it is unlikely to detect a recurrence, improve survival, and because it has its own costs and side effects.<ref name="SGOfive"/> However, CT imaging can be used if desired, though this is not common.<ref name=Jayson/> If a tumor is easily imaged, imaging may be used to monitor the progress of treatment.<ref>{{Cite web|title = Chemotherapy for ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/chemotherapy-for-ovarian-cancer|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150518091204/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/chemotherapy-for-ovarian-cancer|archivedate = 2015-05-18}}</ref>
 
=== Ամոքիչ բուժում ===
[[Palliative care]] focuses on relieving symptoms and increasing or maintaining quality of life. This type of treatment's purpose is not to cure the cancer but to make the woman more comfortable while living with cancer that can not be cured. It has been recommended as part of the treatment plan for any person with advanced ovarian cancer or patients with significant symptoms.<ref>{{cite web|title=ASCO Provisional Clinical Opinion: The Integration of Palliative Care into Standard Oncology Care |url=http://www.asco.org/quality-guidelines/asco-provisional-clinical-opinion-integration-palliative-care-standard-oncology |publisher=ASCO |accessdate=20 August 2014 |url-status=dead |archiveurl=https://web.archive.org/web/20140821114944/http://www.asco.org/quality-guidelines/asco-provisional-clinical-opinion-integration-palliative-care-standard-oncology |archivedate=21 August 2014 }}</ref> In platinum-refractory and platinum-resistant cases, other palliative chemotherapy is the main treatment.<ref name="Hoffman35" /><ref name = CanadianCS2017/>
 
Palliative care can entail treatment of symptoms and complications of the cancer, including pain, nausea, constipation, ascites, [[bowel obstruction]], [[edema]], [[pleural effusion]], and [[mucositis]]. Especially if the cancer advances and becomes incurable, treatment of symptoms becomes one of the main goals of therapy. Palliative care can also entail helping with decision-making such as if or when [[hospice care]] is appropriate, and the preferred place for the patient at end of life care.<ref name=":7" />
 
Bowel obstruction can be treated with [[palliative surgery]] ([[colostomy]], [[ileostomy]], or internal bypass) or medicine, but surgery has been shown to increase survival time.<ref name="Jayson" /><ref name=":7" /> Palliative surgery may result in [[short bowel syndrome]], [[enterocutaneous fistula]], or re-obstruction; or may not be possible due to the extent of obstruction.<ref name="Hoffman35" /> Other treatments of complications can include [[total parenteral nutrition]], a [[low-residue diet]], palliative [[gastrostomy]], and adequate pain control.<ref name="Jayson" /> Bowel obstruction can also be treated with [[octreotide]] when palliative surgery is not an option. Cancer can also block the [[ureters]], which can be relieved by a [[nephrostomy]] or a [[ureteric stent]]. Ascites can be relieved by repeated [[paracentesis]] or placement of a [[Drain (surgery)|drain]] to increase comfort.<ref name=":5">{{Cite web|title = Treating advanced ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/treating-advanced-ovarian-cancer|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150519050942/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/treating-advanced-ovarian-cancer|archivedate = 2015-05-19}}</ref> Pleural effusions can be treated in a similar manner, with repeated [[thoracentesis]], [[pleurodesis]], or placement of a drain.<ref name="Hoffman35" />
 
Radiation therapy can be used as part of the palliative care of advanced ovarian cancer, since it can help to shrink tumors that are causing symptoms.<ref name=CanadianCS2017>{{cite web|url=http://www.cancer.ca/en/cancer-information/cancer-type/ovarian/treatment/?region=on|title=Treatment of ovarian cancer|publisher=Canadian Cancer Society|accessdate=17 June 2017|url-status=live|archiveurl=https://web.archive.org/web/20161026174509/http://www.cancer.ca/en/cancer-information/cancer-type/ovarian/treatment/?region=on|archivedate=26 October 2016}}</ref> Palliative radiotherapy typically lasts for only a few treatments, a much shorter course of therapy than non-palliative radiotherapy.<ref name=":4" /> It is also used for palliation of chemotherapy-resistant germ cell tumors.<ref name=":8" />
 
=== Հոգեսոցիալական խնամք ===
Ovarian cancer has a significant effect on [[quality of life]], psychological health and well-being. Interventions are available to help with the needs and social support. Many ovarian cancer survivors report a good quality of life and [[optimism]]. Others reported a "spiritual change" that helped them find [[Meaning of life|meaning]] during their experience. Others have described their loss of faith after their diagnosis with ovarian cancer. Those who have gone through treatment sometimes experience [[social isolation]] but benefit from having relationships with other survivors. [[Frustration]] and [[Guilt (emotion)|guilt]] have been described by some who have expressed their inability to care for their family.<ref name=":9" />
 
[[Self-esteem]] and [[body image]] changes can occur due to [[hair loss]], removal of ovaries and other reproductive structures, and [[scar]]s. There is some improvement after hair grows in. Sexual issues can develop. The removal of ovaries results in surgically-induced [[menopause]] that can result in [[Dyspareunia|painful intercourse]], vaginal dryness, loss of [[Hypoactive sexual desire disorder|sexual desire]] and being tired. Though prognosis is better for younger survivors, the impact on sexuality can still be substantial.<ref name=":9" />
 
[[Anxiety]], [[Depression (mood)|depression]] and [[Distress in cancer caregiving|distress]] is present in those surviving ovarian cancer at higher rates than in the general population.<ref name=":9" /><ref>{{cite journal | vauthors = Watts S, Prescott P, Mason J, McLeod N, Lewith G | title = Depression and anxiety in ovarian cancer: a systematic review and meta-analysis of prevalence rates | journal = BMJ Open | volume = 5 | issue = 11 | pages = e007618 | date = November 2015 | pmid = 26621509 | pmc = 4679843 | doi = 10.1136/bmjopen-2015-007618 }}</ref> The same psychosocial problems can develop in family members. Emotional effects can include a [[Death anxiety (psychology)|fear of death]], [[sadness]], memory problems and difficulty in concentrating. When optimism was adopted by those at the beginning of their treatment, they were less likely to develop distress. Those who have fear of the cancer recurring may have difficulty in expressing [[joy]] even when disease-free. The more treatments that a woman undergoes, the more likely the loss of [[hope]] is expressed. Women often can cope and reduce negative psychosocial effects by a number of strategies. Activities such as traveling, spending additional time with family and friends, ignoring [[statistics]], journaling and increasing involvement in [[Spirituality|spirituall]]<nowiki/>y-based events are adaptive.<ref name=":9" />
 
== Կանխատեսում ==
[[File:Relative survival of ovarian cancer by stage.png|thumb|upright=1.3|Relative [[five-year survival]] of invasive epithelial ovarian cancer by stage<ref name =ACS/>]]
Ovarian cancer usually has a relatively poor [[prognosis]]. It is disproportionately deadly because it lacks any clear early detection or screening test, meaning most cases are not diagnosed until they have reached advanced stages.<ref name="SGOfive"/><ref name=Jayson/>
 
Ovarian cancer metastasizes early in its development, often before it has been diagnosed. High-grade tumors metastasize more readily than low-grade tumors. Typically, tumor cells begin to metastasize by growing in the peritoneal cavity.<ref name=Harrisons/> More than 60% of women presenting with ovarian cancer have stage-III or stage-IV cancer, when it has already spread beyond the ovaries. Ovarian cancers shed cells into the naturally occurring fluid within the abdominal cavity. These cells can then implant on other abdominal (peritoneal) structures, including the uterus, [[urinary bladder]], [[bowel]], [[mesentery|lining of the bowel wall]], and [[Greater omentum|omentum]], forming new tumor growths before cancer is even suspected.
 
The five-year survival rate for all stages of ovarian cancer is 46%; the one-year survival rate is 72% and the ten-year survival rate is 35%.<ref>{{Cite web|title = Statistics and outlook for ovarian cancer|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/statistics-and-outlook-for-ovarian-cancer|website = www.cancerresearchuk.org|accessdate = 2015-05-16|url-status = live|archiveurl = https://web.archive.org/web/20150518192429/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/statistics-and-outlook-for-ovarian-cancer|archivedate = 2015-05-18}}</ref> For cases where a diagnosis is made early in the disease, when the cancer is still confined to the primary site, the five-year survival rate is 92.7%.<ref name="SEER">Survival rates based on SEER incidence and NCHS mortality statistics, as cited by the National Cancer Institute in [http://seer.cancer.gov/statfacts/html/ovary.html SEER Stat Fact Sheets&nbsp;— Cancer of the Ovary] {{webarchive|url=https://web.archive.org/web/20140706145616/http://seer.cancer.gov/statfacts/html/ovary.html |date=2014-07-06 }}</ref> About 70% of women with advanced disease respond to initial treatment, most of whom attain complete remission, but half of these women experience a recurrence 1–4 years after treatment.<ref name=Harrisons/> [[Brain metastasis]] is more common in stage III/IV cancer but can still occur in cancers staged at I/II. People with brain metastases survive a median of 8.2 months, though surgery, chemotherapy, and [[Whole brain radiotherapy|whole brain radiation therapy]] can improve survival.<ref name=":7" />
 
Ovarian cancer survival varies significantly with subtype. Dysgerminomas have a very favorable prognosis. In early stages, they have a five-year survival rate of 96.9%.<ref name=Current/> Around two-thirds of dysgerminomas are diagnosed at stage I.<ref name=":8" /> Stage-III dysgerminomas have a five-year survival of 61%; when treated with BEP chemotherapy after incomplete surgical removal, dysgerminomas have a 95% two-year survival rate. Sex-cord-stromal malignancies also have a favorable prognosis; because they are slow-growing, even those with metastatic disease can survive a decade or more.<ref name=Harrisons/> Low malignant potential tumors usually only have a bad prognosis when there are invasive tumor implants found in the peritoneal cavity.<ref name=Hoffman35/>
 
Complications of ovarian cancer can include spread of the cancer to other organs, progressive function loss of various organs, ascites, and intestinal obstructions, which can be fatal. Intestinal obstructions in multiple sites are the most common proximate cause of death.<ref name=Jayson/> Intestinal obstruction in ovarian cancer can either be a true obstruction, where tumor blocks the [[intestinal lumen]], or a pseudo-obstruction, when tumor prevents normal [[peristalsis]].<ref>{{cite book |last1 = Gucalp |first1 = Rasim |last2 = Dutcher |first2 = Janice | name-list-format = vanc |chapter = Oncologic Emergencies |veditors = Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J |title = Harrison's Principles of Internal Medicine |publisher = McGraw-Hill |year = 2012 |edition = 18th |isbn = 978-0-07-174889-6|title-link = Harrison's Principles of Internal Medicine }}</ref> Continuous accumulation of ascites can be treated by placing a drain that can be self-drained.<ref name=Jayson/>
 
=== Կանխատեսման գործոններ ===
There are a number of [[prognostic factor]]s in ovarian cancer. Positive prognostic factors - those indicating better chances of survival - include no residual disease after surgery (stage III/IV), complete macroscopic resection (stage IV), BRCA2 mutations, young age (under 45 years), nonserous type, low histologic grade, early stage, co-occurrence with endometrial cancer, and low CA-125 levels. There is conflicting evidence for BRCA1 as a prognostic factor. Conversely, negative prognostic factors - those that indicate a worse chance of survival - include rupture of the ovarian capsule during surgery, older age (over 45 years), mucinous type, stage IV, high histologic grade, clear cell type, upper abdominal involvement, high CA-125 levels, the presence of tumor cells in the blood, and elevated [[Cyclooxygenase 2|cyclooxygenase-2]].<ref name=":7" />
 
Expression of various mRNAs can also be prognostic for ovarian cancer. High levels of [[Drosha]] and [[Dicer]] are associated with improved survival, whereas high levels of [[let-7b]], [[HIF1A]], [[EPH receptor A1|EphA1]], and [[Poly ADP ribose polymerase|poly(ADP-ribose) polymerase]] are associated with worse survival. Cancers that are positive for [[WT1]] carry a worse prognosis; estrogen-receptor positive cancers have a better prognosis.<ref name=":7" />
 
=== Ապրելիության ցուցանիշներ ===
Overall five-year survival rates for all types of ovarian cancer are presented below by stage and histologic grade:<ref name=Harrisons/>
{| class="wikitable" align="left" style="text-align: center; margin-right: 10px;"
! Փուլ
! Ապրելիություն
|-
| I
| 90–95%
|-
| II
| 70–80%
|-
| III
| 20–50%
|-
| IV
| 1–5%
|}
 
{| class="wikitable" align="left" style="text-align: center;"
! Հյուսվածաբանական աստիճան
! Ապրելիություն
|-
| Low grade
| 88%
|-
| Intermediate grade
| 58%
|-
| High grade
| 27%
|}
 
{{clear}}
 
The survival rates given below are for the different types of ovarian cancer, according to [[American Cancer Society]].<ref name=ACS>{{cite web|title=Survival rates for ovarian cancer, by stage|url=http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-survival-rates|website=American Cancer Society|accessdate=29 October 2014|url-status=live|archiveurl=https://web.archive.org/web/20141029204610/http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-survival-rates|archivedate=29 October 2014}}</ref> They come from the [[National Cancer Institute]], SEER, and are based on patients diagnosed from 2004 to 2010.
 
{| class="wikitable" align="left" style="text-align: center; margin-right: 10px;"
! colspan="2" | Invasive epithelial ovarian cancer
|-
! Stage
! Relative five-year<br/>survival rate
|-
| I
| 90%
|-
| IA
| 94%
|-
| IB
| 92%
|-
| IC
| 85%
|-
| II
| 70%
|-
| IIA
| 78%
|-
| IIB
| 73%
|-
| III
| 39%
|-
| IIIA
| 59%
|-
| IIIB
| 52%
|-
| IIIC
| 39%
|-
| IV
| 17%
|}
 
{| class="wikitable" align="left" style="text-align: center; margin-right: 10px;"
! colspan="2" | Ovarian stromal tumors
|-
! Stage
! Relative five-year<br/>survival rate
|-
| I
| 95%
|-
| II
| 78%
|-
| III
| 65%
|-
| IV
| 35%
|}
 
{| class="wikitable" align="left" style="text-align: center; margin-right: 10px;"
! colspan="2" | Germ cell tumors of the ovary
|-
! Stage
! Relative five-year<br/>Survival Rate
|-
| I
| 98%
|-
| II
| 94%
|-
| III
| 87%
|-
| IV
| 69%
|}
 
{| class="wikitable" align="left" style="text-align: center; margin-right: 10px;"
! colspan="2" | Fallopian tube carcinoma
|-
! Stage
! Relative five-year<br/>survival rate
|-
| I
| 87%
|-
| II
| 86%
|-
| III
| 52%
|-
| IV
| 40%
|}
 
{| class="wikitable" align="left" style="text-align: center; margin-right: 10px;"
! colspan="2" | Low malignant potential tumors<ref name=Hoffman35/>
|-
! Stage
! Relative five-year<br/>survival rate
|-
| I
| 99%
|-
| II
| 98%
|-
| III
| 96%
|-
| IV
| 77%
|}
 
{{clear}}
 
=== Recurrence rates ===
Ovarian cancer frequently recurs after treatment. Overall, in a 5-year period, 20% of stage I and II cancers recur. Most recurrences are in the abdomen.<ref name="Hoffman35" /> If a recurrence occurs in advanced disease, it typically occurs within 18 months of initial treatment (18 months [[progression-free survival]]). Recurrences can be treated, but the disease-free interval tends to shorten and chemoresistance increases with each recurrence.<ref name=Jayson/> When a dysgerminoma recurs, it is most likely to recur within a year of diagnosis, and other malignant germ cell tumors recur within 2 years 90% of the time. Germ cell tumors other than dysgerminomas have a poor prognosis when they relapse, with a 10% long-term survival rate.<ref name=":8"/> Low malignant potential tumors rarely relapse, even when fertility-sparing surgery is the treatment of choice. 15% of LMP tumors relapse after unilateral surgery in the previously unaffected ovary, and they are typically easily treated with surgery. More advanced tumors may take up to 20 years to relapse, if they relapse at all, and are only treated with surgery unless the tumor has changed its histological characteristics or grown very quickly. In these cases, and when there is significant ascites, chemotherapy may also be used. Relapse is usually indicated by rising CA-125 levels and then progresses to symptomatic relapse within 2–6 months.<ref name=Hoffman35/> Recurrent sex cord-stromal tumors are typically unresponsive to treatment but not aggressive.<ref name=":8"/>
 
It is the most deadly gynecologic cancer.<ref name="Hoffman35">{{cite book |chapter = Epithelial Ovarian Cancer |pages = 853–878 |title = Williams Gynecology |edition = 2nd |publisher = McGraw Hill Medical |first1 = Barbara L. |last1 = Hoffman |first2 = John O. |last2 = Schorge |first3 = Joseph I. |last3 = Schaffer |first4 = Lisa M. |last4 = Halvorson |first5 = Karen D. |last5 = Bradshaw |first6 = F. Gary |last6 = Cunningham | name-list-format = vanc |isbn = 978-0-07-171672-7 |year = 2012 |ref={{harvid|Williams Gynecology|2012}}}}</ref>
 
==Epidemiology==
[[File:Ovary cancer world map - Death - WHO2004.svg|thumb|upright=1.3|[[Age adjustment|Age-standardized]] death from ovarian cancer per 100,000&nbsp;inhabitants in 2004<ref>{{cite web |url=http://www.who.int/entity/healthinfo/global_burden_disease/gbddeathdalycountryestimates_female_2004.xls?ua=1 |title=WHO Disease and injury country estimates |year=2009 |work=World Health Organization |accessdate=June 15, 2017 }} The statistics are from 2004. This weblink opens up with an automatic Excel file download</ref>{{refbegin|2}}
{{legend|#b3b3b3|no data}}
{{legend|#ffff65|less than 0.6}}
{{legend|#fff200|0.6–1.2}}
{{legend|#ffdc00|1.2–1.8}}
{{legend|#ffc600|1.8–2.4}}
{{legend|#ffb000|2.4–3}}
{{legend|#ff9a00|3–3.6}}
{{legend|#ff8400|3.6–4.2}}
{{legend|#ff6e00|4.2–4.8}}
{{legend|#ff5800|4.8–5.4}}
{{legend|#ff4200|5.4–6}}
{{legend|#ff2c00|6–7}}
{{legend|#cb0000|more than 7}}
{{refend}}]]
 
In 2014, the number of new cases that occurred in developed countries was about 9.4 per 100,000, compared to 5.0 per 100,000 in developing countries.<ref name="Jayson" /> Globally, about 160,000 people died from ovarian cancer in 2010. This was an increase from 113,000 in 1990.<ref name=Loz_2012>{{cite journal | vauthors = Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, etal | title = Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010 | journal = Lancet | volume = 380 | issue = 9859 | pages = 2095–128 | date = December 2012 | pmid = 23245604 | doi = 10.1016/S0140-6736(12)61728-0 | hdl = 10536/DRO/DU:30050819 }}</ref> The number of new cases per year in Europe is approximately 5–15 per 100,000 women.<ref name=":7" /> In Europe, [[Lithuania]], [[Latvia]], [[Ireland]], [[Slovakia]], and the [[Czech Republic]] have the highest incidences of ovarian cancer, whereas [[Portugal]] and [[Cyprus]] have the lowest incidences.<ref name=":7" /> In 2008, the five-year survival rate was 44%. This has increased since 1977 when the survival rate was 36%.<ref name=":9">{{cite journal | vauthors = Roland KB, Rodriguez JL, Patterson JR, Trivers KF | title = A literature review of the social and psychological needs of ovarian cancer survivors | journal = Psycho-Oncology | volume = 22 | issue = 11 | pages = 2408–18 | date = November 2013 | pmid = 23760742 | doi = 10.1002/pon.3322 }}</ref>
 
===United States===
[[File:Ovarian cancer by age group.png|thumb|left|upright=1.3|Ovarian cancer cases diagnosed by age group in the US<ref name="SEER"/>]]
 
In 2010, in the United States, an estimated 21,880 new cases were diagnosed and 13,850 women died of ovarian cancer. Around 1,800 of the new diagnoses were sex-cord or stromal tumors.<ref name="Harrisons" />
 
In 2014, over 220,000 diagnoses of epithelial ovarian cancer were made yearly.<ref name="Jayson" /> The overall lifetime risk in the US is around 1.6%<ref name="Harrisons">{{cite book |last = Seiden |first = Michael V. |chapter = Gynecologic Malignancies |veditors = Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J |title = Harrison's Principles of Internal Medicine |publisher = McGraw-Hill |year = 2012 |edition = 18th |isbn = 978-0-07-174889-6|title-link = Harrison's Principles of Internal Medicine }}</ref><ref name=":7" /> In the US, ovarian cancer affects 1.3–1.4% and is the cause of death of about 1% of women.<ref name="Hoffman35" /><ref name="merck">{{cite web |title=Ovarian Cancer |date=September 2013 |work=The Merck Manual for Health Care Professionals |url=http://www.merckmanuals.com/professional/gynecology_and_obstetrics/gynecologic_tumors/ovarian_cancer.htm |first1 = Pedro T. |last1 = Ramirez |first2 = David M. |last2 = Gershenson | name-list-format = vanc }}{{open access}}</ref> In the United States, it is also the fifth-most common cancer in women but the fourth-most common cause of cancer death.<ref name=":7" /> This decrease made it the ninth-most common cancer in women.<ref name="Hoffman35" />
 
The risks from developing specific types of ovarian cancer varies. Germ cell tumors and sex cord-stromal tumors are less common than epithelial tumors. The number of new cases a year in the US is 0.4 per 100,000 women and 0.2 per 100,000 women, respectively. In young people, sex-cord stromal tumors and germ cell tumors total 1% of overall ovarian cancer.<ref name=":8" /> Ovarian cancer represents approximately 4% of cancers diagnosed in women.<ref name=":7" />
 
===United Kingdom===
It is the 5th most common cancer in UK women.<ref name=":7" /><ref name="CRUKRisks">{{cite web |url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/about/ovarian-cancer-risks-and-causes |title = Ovarian cancer risks and causes |publisher = Cancer Research UK |accessdate = 29 January 2015 |date = 15 January 2014 |url-status = live |archiveurl = https://web.archive.org/web/20150221095418/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/about/ovarian-cancer-risks-and-causes |archivedate = 21 February 2015 }}</ref> In the UK, the incidence rate over the whole population is 21.6 per 100,000.
 
In the United Kingdom as of 2014, approximately 7,000–7,100 yearly diagnoses with 4,200 deaths.<ref name="Jayson" /><ref name="CRUKRisks" /> The risk in the UK is similar, at 1.7%. [[Ashkenazi Jew]]ish women carry mutated ''BRCA'' alleles five times more often than the rest of the population, giving them a higher risk developing ovarian cancer.<ref name="Jayson" /> It is the fifth-leading cause of cancer-related deaths in the US in 2008 and estimated to be 15,000.<ref name="Harrisons" /><ref name="merck" /> Ovarian cancer is the fifth-most common cancer in women in the UK (around 7,100 women were diagnosed with the disease in 2011), and it is the fifth-most common cause of cancer death in women (around 4,300 women died in 2012).<ref>{{cite web|title=Ovarian cancer statistics|url=http://www.cancerresearchuk.org/cancer-info/cancerstats/types/ovary/|website=Cancer Research UK|accessdate=28 October 2014|url-status=live|archiveurl=https://web.archive.org/web/20141006122756/http://www.cancerresearchuk.org/cancer-info/cancerstats/types/ovary/|archivedate=6 October 2014}}</ref>
 
===Ethnicity===
 
Black women have twice the risk for sex cord-stromal tumors compared to non-Black women.<ref name=":8" />
 
===Older women===
In the US, the incidence rate in women over 50 is approximately 33 per 100,000.<ref>{{Cite book|title = Ovarian Cancer|last = Hennessy|first = Bryan T.|publisher = McGraw-Hill|year = 2011|last2 = Suh|first2 = Grace K.|last3 = Markman|first3 = Maurie | name-list-format = vanc |work = The MD Anderson Manual of Medical Oncology| veditors = Kantarjian HM, Wolff RA, Koller CA |url = http://accessmedicine.mhmedical.com/content.aspx?bookid=379&Sectionid=39902056|isbn = 978-0-07-170106-8|edition = 2e|url-status = live|archiveurl = https://web.archive.org/web/20170910175639/http://accessmedicine.mhmedical.com/content.aspx?bookid=379&Sectionid=39902056|archivedate = 2017-09-10}}</ref> The rate of ovarian cancer between 1993 and 2008 decreased in women of the 40–49 age cohort and in the 50–64 age cohort.<ref name="Jayson" /> Ovarian cancer is most commonly diagnosed after menopause,<ref name="CRUKRisks" /> between the ages of 60 and 64. Ninety percent of ovarian cancer occurs in women over the age of 45 and 80% in women over 50.<ref name=":7" /> Older women are more likely to present with advanced ovarian cancer.<ref name="Gib2016"/>
 
== In pregnancy ==
Malignant germ cell tumors are the type of ovarian cancer most likely to occur during [[pregnancy]]. They are typically diagnosed when an adnexal mass is found on examination (in 1–2% of all pregnancies), a tumor is seen on ultrasound, or the parent's level of alpha-fetoprotein is elevated. Dermoid cysts and dysgerminomas are the most common germ cell tumors during pregnancy. Germ cell tumors diagnosed during pregnancy are unlikely to have metastasized and can be treated by surgery and, in some cases, chemotherapy, which carries the risk of birth defects. Yolk sac tumors and immature teratomas grow particularly quickly and are usually treated with chemotherapy even during pregnancy; however, dysgerminomas that have been optimally debulked may be treated after childbirth.<ref name=":8" />
 
== Other animals ==
Ovarian tumors have been reported in [[equine]] [[mare]]s. Reported tumor types include teratoma,<ref name="pmid15065985">{{cite journal | vauthors = Catone G, Marino G, Mancuso R, Zanghì A | title = Clinicopathological features of an equine ovarian teratoma | journal = Reprod. Domest. Anim. | volume = 39 | issue = 2 | pages = 65–9 | date = April 2004 | pmid = 15065985 | doi = 10.1111/j.1439-0531.2003.00476.x }}</ref><ref name="pmid16363331">{{cite journal | vauthors = Lefebvre R, Theoret C, Doré M, Girard C, Laverty S, Vaillancourt D | title = Ovarian teratoma and endometritis in a mare | journal = Can. Vet. J. | volume = 46 | issue = 11 | pages = 1029–33 | date = November 2005 | pmid = 16363331 | pmc = 1259148 }}</ref> [[cystadenocarcinoma]],<ref name="pmid15957389">{{cite journal | vauthors = Son YS, Lee CS, Jeong WI, Hong IH, Park SJ, Kim TH, Cho EM, Park TI, Jeong KS | title = Cystadenocarcinoma in the ovary of a Thoroughbred mare | journal = Aust. Vet. J. | volume = 83 | issue = 5 | pages = 283–4 | date = May 2005 | pmid = 15957389 | doi = 10.1111/j.1751-0813.2005.tb12740.x }}</ref> and particularly [[granulosa cell tumor]].<ref name="pmid17542368">{{cite journal | vauthors = Frederico LM, Gerard MP, Pinto CR, Gradil CM | title = Bilateral occurrence of granulosa-theca cell tumors in an Arabian mare | journal = Can. Vet. J. | volume = 48 | issue = 5 | pages = 502–5 | date = May 2007 | pmid = 17542368 | pmc = 1852596 }}</ref><ref name=pmid12867740>{{cite journal | vauthors = Hoque S, Derar RI, Osawa T, Taya K, Watanabe G, Miyake Y | title = Spontaneous repair of the atrophic contralateral ovary without ovariectomy in the case of a granulosa theca cell tumor (GTCT) affected mare | journal = J. Vet. Med. Sci. | volume = 65 | issue = 6 | pages = 749–51 | date = June 2003 | pmid = 12867740 | doi = 10.1292/jvms.65.749 }}</ref><ref name=pmid9364230>{{cite journal | vauthors = Sedrish SA, McClure JR, Pinto C, Oliver J, Burba DJ | title = Ovarian torsion associated with granulosa-theca cell tumor in a mare | journal = J. Am. Vet. Med. Assoc. | volume = 211 | issue = 9 | pages = 1152–4 | date = November 1997 | pmid = 9364230 }}</ref><ref name=pmid3507181>{{cite journal | vauthors = Moll HD, Slone DE, Juzwiak JS, Garrett PD | title = Diagonal paramedian approach for removal of ovarian tumors in the mare | journal = Vet Surg | volume = 16 | issue = 6 | pages = 456–8 | year = 1987 | pmid = 3507181 | doi = 10.1111/j.1532-950X.1987.tb00987.x | url = http://www3.interscience.wiley.com/journal/119849124/abstract | archive-url = https://archive.today/20121010165817/http://www3.interscience.wiley.com/journal/119849124/abstract | url-status = dead | archive-date = 2012-10-10 }}</ref><ref name=pmid2835223>{{cite journal | vauthors = Doran R, Allen D, Gordon B | title = Use of stapling instruments to aid in the removal of ovarian tumours in mares | journal = Equine Vet. J. | volume = 20 | issue = 1 | pages = 37–40 | date = January 1988 | pmid = 2835223 | doi = 10.1111/j.2042-3306.1988.tb01450.x }}</ref>
 
== Հետազոտություններ ==
===Սկրինինգ===
Screening by hysteroscopy to obtain cell samples obtained for histological examination is being developed. This is similar to the current pap smear that is used to detect cervical cancer.<ref name="GizzoNoventa2016">{{cite journal | vauthors = Gizzo S, Noventa M, Quaranta M, Vitagliano A, Saccardi C, Litta P, Antona D | title = A novel hysteroscopic approach for ovarian cancer screening/early diagnosis | journal = Oncology Letters | volume = 13 | issue = 2 | pages = 549–553 | date = February 2017 | pmid = 28356928 | pmc = 5351187 | doi = 10.3892/ol.2016.5493 }} subscription required</ref> The UK Collaborative Trial of Ovarian Cancer Screening is testing a screening technique that combines CA-125 blood tests with transvaginal ultrasound.<ref name=Jayson/> Other studies suggest that this screening procedure may be effective.<ref name=":6">{{Cite web|title = Ovarian cancer research|url = http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/whats-new-in-ovarian-cancer-research|website = www.cancerresearchuk.org|access-date = 2015-05-16|url-status = live|archive-url = https://web.archive.org/web/20150509015810/http://www.cancerresearchuk.org/about-cancer/type/ovarian-cancer/treatment/whats-new-in-ovarian-cancer-research|archive-date = 2015-05-09}}</ref> Although results published in 2015 were not conclusive, there was some evidence that screening may save lives in the long-term.<ref>{{cite journal | vauthors = Jacobs IJ, Menon U, Ryan A, Gentry-Maharaj A, Burnell M, Kalsi JK, Amso NN, Apostolidou S, Benjamin E, Cruickshank D, Crump DN, Davies SK, Dawnay A, Dobbs S, Fletcher G, Ford J, Godfrey K, Gunu R, Habib M, Hallett R, Herod J, Jenkins H, Karpinskyj C, Leeson S, Lewis SJ, Liston WR, Lopes A, Mould T, Murdoch J, Oram D, Rabideau DJ, Reynolds K, Scott I, Seif MW, Sharma A, Singh N, Taylor J, Warburton F, Widschwendter M, Williamson K, Woolas R, Fallowfield L, McGuire AJ, Campbell S, Parmar M, Skates SJ | display-authors = 6 | title = Ovarian cancer screening and mortality in the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a randomised controlled trial | journal = Lancet | volume = 387 | issue = 10022 | pages = 945–956 | date = March 2016 | pmid = 26707054 | pmc = 4779792 | doi = 10.1016/S0140-6736(15)01224-6 }}</ref> As a result, the trial has been extended and will publish definitive results at the end of 2019. One major problem with screening is no clear progression of the disease from stage I (noninvasive) to stage III (invasive) is seen, and it may not be possible to find cancers before they reach stage III. Another problem is that screening methods tend to find too many suspicious lesions, most of which are not cancer, but malignancy can only be assessed with surgery.<ref name=Jayson/> The ROCA method combined with transvaginal ultrasonography is being researched in high-risk women to determine if it is a viable screening method. It is also being investigated in normal-risk women as it has shown promise in the wider population.<ref name=Hoffman35/> Studies are also in progress to determine if screening helps detect cancer earlier in people with BRCA mutations.<ref name=":6" />
 
===Prognosis research===
Research into various [[prognostic factor]]s for ovarian cancer is also going on. Recent research shows that [[thrombocytosis]] predicts lower survival and higher stage cancer.<ref name=Jayson/> Ongoing research is also investigating the benefits of surgery for recurrent ovarian cancer.<ref name=":6" />
 
===Իմունոթերապիա===
While an active area of research, as of 2018 there is no goodevidence that [[immunotherapy]] is effective for ovarian cancer.<ref name="pmid30199097">{{cite journal | vauthors = Paijens ST, Leffers N, Daemen T, Helfrich W, Boezen HM, Cohlen BJ, Melief CJ, de Bruyn M, Nijman HW | title = Antigen-specific active immunotherapy for ovarian cancer | journal = Cochrane Database Syst Rev | volume = 9 | issue = | pages = CD007287 | date = September 2018 | pmid = 30199097 | pmc = 6513204 | doi = 10.1002/14651858.CD007287.pub4 }}</ref> However, trials of the antibody and [[VEGF]] inhibitor [[bevacizumab]], which can slow the [[angiogenesis|growth of new blood vessels]] in the cancer, have shown promising results, especially in combination with [[pazopanib]], which also slows the process of blood vessel growth. Bevacizumab has been particularly effective in preliminary studies on stage-III and -IV cancer<ref name=Jayson/> and has been cited as having at least a 15% response rate.<ref name=Harrisons/> It is being investigated particularly in mucinous ovarian cancers.<ref name=":6" />
 
===Ֆարմակոլոգիա===
[[mTOR inhibitor]]s were a highly investigated potential treatment in the 2000s and 2010s, but the side effects of these drugs (particularly [[hyperglycemia]] and [[hyperlipidemia]]) were not well tolerated and the survival benefit not confirmed. PI3 kinase inhibitors have been of interest, but they tend to be highly toxic and cause [[diarrhea]]. Another investigated drug is [[selumetinib]], a [[MAPK]] inhibitor. It improved survival, but did not correlate with any mutations found in tumors.<ref name=Jayson/>
 
Bevacizumab can also be combined with platinum chemotherapy, a combination that has had positive preliminary results in PFS, but equivocal results regarding overall survival. One disadvantage to these treatments is the side effect profile, which includes [[hypertension|high blood pressure]] and [[proteinuria]]. The drug can also exacerbate bowel disease, leading to [[fistula]]e or [[bowel perforation]]. [[Vintafolide]], which consists of an [[antifolate]] conjugated with [[vinblastine]], is also in clinical trials; it may prove beneficial because [[folate receptor]]s are overexpressed in many ovarian cancers.<ref name=Jayson/> Another potential immunotherapy is [[trastuzumab]], which is active against tumors positive for Her2/neu mutations.<ref name=Harrisons/> Other angiogenesis inhibitors are also being investigated as potential ovarian cancer treatments. [[Combretastatin]] and [[pazopanib]] are being researched in combination for recurrent ovarian cancer. [[Trebananib]] and [[tasquinimod]] are other angiogenesis inhibitors being investigated. The [[monoclonal antibody]] [[farletuzumab]] is being researched as an adjuvant to traditional chemotherapy. Another type of immunotherapy involves [[vaccines]], including [[TroVax]].<ref name=":6" />
 
An alternative to BEP chemotherapy, a regimen of 3 cycles of [[carboplatin]] and [[etoposide]], is a current topic of research for germ cell malignancies.<ref name=":8" />
 
[[Intraperitoneal chemotherapy]] has also been under investigation during the 2000s and 2010s for its potential to deliver higher doses of cytotoxic agent to tumors. Preliminary trials with cisplatin and paclitaxel have shown it is not well tolerated, but does improve survival, and more tolerable regimens are being researched.<ref name=Jayson/> Cisplatin and paclitaxel are both being researched as intraperitoneal chemotherapy agents. A specific chemotherapy regimen for rare clear-cell cancers is also under investigation: [[irinotecan]] combined with cisplatin.<ref name=":6" />
 
[[PARP inhibitor]]s have also shown promise in early trials, particularly in people with ''BRCA'' gene mutations, since the BRCA protein interacts with the PARP pathway. It is also being studied in recurrent ovarian cancer in general, where preliminary studies have shown longer PFS. Specifically, [[olaparib]] has shown greater survival compared to doxorubicin, though this treatment is still being investigated. It is not clear yet which [[biomarker]]s are predictive of responsiveness to PARP inhibitors.<ref name=Jayson/> [[Rucaparib]] is another PARP inhibitor being researched in BRCA-positive and BRCA-negative recurrent advanced ovarian cancer. [[Niraparib]] is a PARP inhibitor being tested in BRCA-positive recurrent ovarian cancer.<ref name=":6" />
 
[[Tyrosine kinase inhibitors]] are another investigational drug class that may have applications in ovarian cancer. Angiogenesis inhibitors in the [[receptor tyrosine kinase]] inhibitor group, including [[pazopanib]], [[cediranib]], and [[nintedanib]], have also been shown to increase progression free survival (PFS), but their benefit for overall survival has not been investigated as of 2015.<ref name="Jayson" /> Preliminary research showed that cediranib combined with platins in recurrent ovarian cancer increased the time to second recurrence by 3–4 months and increased survival by 3 months.<ref name=":6" /> [[MK-1775]] is a tyrosine kinase inhibitor that is being used in combination with paclitaxel and carboplatin in platinum-sensitive cancers with p53 mutations. [[Nintedanib]] is being researched as a potential therapy in combination with cyclophosphamide for people with recurrences.<ref name=":6" />
 
[[Histone deacetylase inhibitor|Histone deacetylase inhibitors]] (HDACi) are another area of research.
 
===Հորմոն և ճառագայթում ===
Hormone therapies are a topic of current research in ovarian cancer, particularly, the value of certain medications used to treat breast cancer. These include [[tamoxifen]], [[letrozole]], and [[anastrozole]]. Preliminary studies have showed a benefit for tamoxifen in a small number of people with advanced ovarian cancer. Letrozole may help to slow or stop growth of [[estrogen receptor]] positive ovarian cancer. Anastrozole is being investigated in postmenopausal people with estrogen receptor-positive cancer.<ref name=":6" />
 
Research into mitigating side effects of ovarian cancer treatment is also ongoing. [[Radiation fibrosis]], the formation of scar tissue in an area treated with radiation, may be relieved with [[Hyperbaric medicine|hyperbaric oxygen therapy]], but research has not been completed in this area. Treatment of ovarian cancer may also cause people to experience psychiatric difficulties, including [[Depression (mood)|depression]]. Research is ongoing to determine how counseling and psychotherapy can help people who have ovarian cancer during treatment.<ref name=":6" />
 
===Բորբոքում===
 
There are some indications that pelvic inflammatory disease may be associated with ovarian cancer, especially in non-western countries. It may be due to the inflammatory process present with pelvic inflammatory disease.<ref name="IngerslevHogdall2017">{{cite journal | vauthors = Ingerslev K, Hogdall E, Schnack TH, Skovrider-Ruminski W, Hogdall C, Blaakaer J | title = The potential role of infectious agents and pelvic inflammatory disease in ovarian carcinogenesis | journal = Infectious Agents and Cancer | volume = 12 | issue = 1 | pages = 25 | year = 2017 | pmid = 28529540 | pmc = 5437405 | doi = 10.1186/s13027-017-0134-9 }}</ref>
 
===Կլինիկական հետազոտություններ===
[[Clinical trial]]s are monitored and funded by US governmental organizations to test treatment options to see if they are safe and effective. These include NIH Clinical Research Trials and You ([[National Institutes of Health]]),<ref>{{cite web|url=https://www.nih.gov/health-information/nih-clinical-research-trials-you|title=NIH Clinical Research Trials and You|accessdate=17 June 2017|url-status=live|archiveurl=https://web.archive.org/web/20170608133010/https://www.nih.gov/health-information/nih-clinical-research-trials-you|archivedate=8 June 2017}}</ref> Learn About Clinical Trials ([[National Cancer Institute]]),<ref>{{cite web|url=https://www.cancer.gov/about-cancer/treatment/clinical-trials|title=Clinical Trials Information for Patients and Caregivers|website=National Cancer Institute|accessdate=17 June 2017|url-status=live|archiveurl=https://web.archive.org/web/20170616213104/https://www.cancer.gov/about-cancer/treatment/clinical-trials|archivedate=16 June 2017}}</ref> Search for Clinical Trials (National Cancer Institute),<ref>{{cite web|url=https://www.cancer.gov/about-cancer/treatment/clinical-trials/search/|title=Find NCI-Supported Clinical Trials|website=National Cancer Institute|accessdate=17 June 2017|url-status=live|archiveurl=https://web.archive.org/web/20170701064612/https://www.cancer.gov/about-cancer/treatment/clinical-trials/search|archivedate=1 July 2017|date=2016-06-23}}</ref> ClinicalTrials.gov (National Institutes of Health).<ref>{{cite web|url=https://www.clinicaltrials.gov/|title=Home&nbsp;— ClinicalTrials.gov|website=www.clinicaltrials.gov|accessdate=17 June 2017|url-status=live|archiveurl=https://web.archive.org/web/20170616200907/https://www.clinicaltrials.gov/|archivedate=16 June 2017}}</ref><ref name = CDCfeb2017/> Clinical trials are also conducted in Canada.<ref>{{cite web|url=http://www.canadiancancertrials.ca/|title=Home - Canadian Cancer Trials|website=www.canadiancancertrials.ca|accessdate=17 June 2017|url-status=live|archiveurl=https://web.archive.org/web/20170626081519/http://canadiancancertrials.ca/|archivedate=26 June 2017}}</ref>
 
== Ծանոթագրություններ ==
{{Reflist}}
 
== Further reading ==
{{refbegin}}
* {{cite journal | vauthors = Cannistra SA | title = Cancer of the ovary | journal = N. Engl. J. Med. | volume = 351 | issue = 24 | pages = 2519–29 | date = December 2004 | pmid = 15590954 | doi = 10.1056/NEJMra041842}}
* {{cite book |vauthors=Petrucelli N, Daly MB, Feldman GL |title=BRCA1 and BRCA2 Hereditary Breast/Ovarian Cancer |year=2013 |id=NBK1247 |pmid=20301425 |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK1247/|chapter=BRCA1- and BRCA2-Associated Hereditary Breast and Ovarian Cancer |publisher=University of Washington, Seattle }}
{{refend}}
 
== External links ==
* {{cite web|title=Ovarian, Fallopian Tube, and Primary Peritoneal Cancer - Patient Version|url=https://www.cancer.gov/types/ovarian/hp|publisher=National Cancer Institute|accessdate=30 March 2017}}
* [http://www.mountsinai.org/patient-care/service-areas/obgyn-and-reproductive-services/areas-of-care/gynecologic-oncology/ovarian-cancer/infographic/ovariancancerinfo What is Ovarian Cancer Infographic, information on ovarian cancer] - [[Mount Sinai Hospital, New York]]
 
{{Medical resources
| ICD10 = {{ICD10|C|56||c|51}}
| ICD9 = {{ICD9|183}}, {{ICD9|220}}
| ICDO = varied
| OMIM =
| MedlinePlus = 000889
| eMedicineSubj = med
| eMedicineTopic = 1698
| DiseasesDB = 9418
| MeshID = D010051
}}
 
{{Genital neoplasia}}
{{Authority control}}
 
{{DEFAULTSORT:Ovarian Cancer}}
[[Category:Ovarian cancer| ]]
[[Category:Gynaecological cancer]]
[[Category:Gynaecology]]
[[Category:Oncology]]
[[Category:RTT]]
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