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Ovarian cancer

Ovarian cancer is a cancerous tumor of an ovary. It may originate from the ovary itself or more commonly from communicating nearby structures such as fallopian tubes or the inner lining of the abdomen. The ovary is made up of three different cell types including epithelial cells, germ cells, and stromal cells. When these cells become abnormal, they can divide and form tumors. These cells can also invade or metastasize (spread) to other parts of the body. When this process begins, there may be no or only vague symptoms. Symptoms become more noticeable as the cancer progresses. These symptoms may include bloating, vaginal bleeding, pelvic pain, abdominal swelling, constipation, and loss of appetite, among others. Common areas to which the cancer may spread include the lining of the abdomen, lymph nodes, lungs, and liver.

Signs and symptoms
Early symptoms Early signs and symptoms of ovarian cancer may be absent or subtle. In most cases, symptoms exist for several months before being recognized and diagnosed. Symptoms can often be misdiagnosed as irritable bowel syndrome. The early stages of ovarian cancer tend to be painless which makes it difficult to detect it early on. Symptoms can vary based on the subtype. Because of the anatomic location of the ovaries deep in the pelvis, most masses are large and advanced at the time of diagnosis. The growing mass may cause pain if ovarian torsion develops. 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. Metastases may cause a Sister Mary Joseph nodule. Rarely, teratomas can cause growing teratoma syndrome or peritoneal gliomatosis. Some experience menometrorrhagia and abnormal vaginal bleeding after menopause in most cases. Other common symptoms include hirsutism, abdominal pain, virilization, and an adnexal mass. Children In adolescents or children with ovarian tumors, symptoms can include severe abdominal pain, irritation of the peritoneum, or bleeding. Sex cord stromal tumors produce hormones that can lead to the premature development of secondary sex characteristics. Sex cord-stromal tumors in prepubertal children may be manifested by signs of 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 an accumulation of fluid in the abdomen and lead to distension. If the malignancy has not been diagnosed by the time it causes ascites, it is typically diagnosed shortly thereafter. Advanced cancers can also cause abdominal masses, lymph node masses, or pleural effusion. == Risk factors ==
Risk factors
Many known risk factors may increase a woman's risk of developing ovarian cancer. The risk of developing ovarian cancer is related to the amount of time a woman spends ovulating. Since ovulation is suppressed during pregnancy, not having children also increases the risk of ovarian cancer. 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. 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 women. In general, 5–10% of ovarian cancer cases have a genetic cause. Other genes that have been associated with ovarian cancer are BRIP1, MSH6, RAD51C and RAD51D. CDH1, CHEK2, PALB2 and RAD50 have also been associated with ovarian cancer. Several rare genetic disorders are associated with specific subtypes of ovarian cancer. Peutz–Jeghers syndrome, a rare genetic disorder, also predisposes women to sex cord tumour with annular tubules. The American Cancer Society recommends a healthy eating pattern that includes plenty of fruits, vegetables, whole grains, and a diet that avoids or limits red and processed meats and processed sugar. High consumption of total, saturated, and trans-fats increases ovarian cancer risk. A 2021 umbrella review found that coffee, egg, and fat intake significantly increases the risk of ovarian cancer. There is mixed evidence from studies on ovarian cancer risk and consumption of dairy products. Environmental factors Industrialized nations, except Japan, have high rates of epithelial ovarian cancer, which may be due to diet in those countries. White women are at a 30–40% higher risk for ovarian cancer when compared to Black women and Hispanic women, likely due to socioeconomic factors; white women tend to have fewer children and different rates of gynecologic surgeries that affect risk for ovarian cancer. 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. Other Other factors that have been investigated, such as smoking, low levels of vitamin D in the blood, 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. 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. or acetaminophen (paracetamol) may be associated with a lower risk of ovarian cancer; other NSAIDs do not seem to have a similar protective effect. A 2021 review found that green leafy vegetables, allium vegetables, fiber, flavanoids and green tea intake can significantly reduce ovarian cancer risk. == Pathophysiology ==
Pathophysiology
Ovarian cancer forms when errors in normal ovarian cell growth occur. Usually, when cells grow old or get damaged, they die, and new cells take their place. Cancer starts when new cells form unnecessarily, and old or damaged cells do not die as they should. The buildup of extra cells often forms a mass of tissue called an ovarian tumor or growth. These abnormal cancer cells have many genetic abnormalities that cause them to grow excessively. When an ovary releases an egg, the egg follicle bursts open and becomes the corpus luteum. This structure needs to be repaired by dividing the cells in the ovary. Continuous ovulation for a long time means more repair of the ovary by dividing cells, which can acquire mutations in each division. Overall, the most common gene mutations in ovarian cancer occur in 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 and KRAS) and tumor suppressors (most notably PTEN). The most common mutations in Type I cancers are KRAS, BRAF, ERBB2, PTEN, PIK3CA, and ARID1A. Type II cancers, the more aggressive type, have different genes mutated, including p53, BRCA1, and BRCA2. 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. Type I cancers tend to develop from precursor lesions, whereas Type II cancers can develop from a serous tubal intraepithelial carcinoma. Serous cancers that have BRCA mutations also inevitably have p53 mutations, indicating that the removal of both functional genes is important for cancer to develop. In 50% of high-grade serous cancers, homologous recombination DNA repair is dysfunctional, as are the 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 mutations in these genes are found in about 15% of women with ovarian cancer. The most common mutations in BRCA1 and BRCA2 are the frameshift mutations that originated in a small founding population of Ashkenazi Jews. Almost 100% of rare mucinous carcinomas have mutations in KRAS and amplifications of ERBB2 (also known as Her2/neu). Overall, 20% of ovarian cancers have mutations in Her2/neu. 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. == Diagnosis ==
Diagnosis
Examination 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. Sometimes a rectovaginal examination is used to help plan a surgery. Additionally, symptoms of ovarian cancer may appear similar to irritable bowel syndrome. In women 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 women with ovarian cancer are more likely to have malignant germ cell tumors. HE4 is another candidate for ovarian cancer testing. 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. The OVA1 panel includes CA-125, beta-2 microglobulin, transferrin, apolipoprotein A1, and transthyretin. OVA1 above 5.0 in premenopausal women and 4.4 in postmenopausal women indicates a high risk for cancer. Risk scoring A widely recognized method of estimating the risk of malignant ovarian cancer is the risk of malignancy index (RMI), calculated based on an initial workup. An RMI score of over 200 or 250 is generally felt to indicate high risk for ovarian cancer. They include the 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 the risk of malignancy in an adnexal mass, based on its characteristics and risk factors. The QCancer (Ovary) algorithm is used to predict the likelihood of ovarian cancer from risk factors. 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. It is the most common cause of gynecologic cancer death. Annually worldwide, 230,000 women will be diagnosed and 150,000 will die. It has a 46% 5 year survival rate after diagnosis because of the advanced stage of the disease at the time of diagnosis. High grade serous carcinoma accounts for 75% of all epithelial ovarian cancer. STIC is characterised by • Abnormal p53 staining • Ki67 proliferation index in excess of 10% • Positive WT1 (to exclude metastases) This rare malignancy most commonly affects young women under the age of 40 years old with a range between 14 months and 58 years. The tumor secretes Parathyroid hormone related protein which acts similarly to PTH and binds PTH receptors in the bone and kidney causing hypercalcemia. The hypercalcemic subtype is very aggressive and has an overall survival rate of 16% with a recurrence rate of 65% in patients who receive treatment. They can develop even after the ovaries have been removed and may appear similar to mesothelioma. The highest incidence of clear-cell carcinoma of the ovary have been observed among young Asian women, especially those of Korean, Taiwanese, and Japanese background. The median age of diagnosis is around 53 years. Several different cells from the mesenchyme can give rise to sex-cord or stromal tumors. These include fibroblasts and endocrine cells. The symptoms of a sex-cord or stromal ovarian tumor can differ from those of 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, isosexual precocious pseudopuberty may occur with granulosa cell tumors since they produce estrogen. These tumors cause abnormalities in menstruation (excessive bleeding, infrequent menstruation, or 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 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. 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. Common primary cancers are breast cancer, colon cancer, appendiceal cancer, and stomach cancer (primary gastric cancers that metastasize to the ovary are called Krukenberg tumors). Borderline tumors Ovarian borderline tumors, sometimes called low malignant potential (LMP) ovarian tumors, have some benign and some malignant features. The most common stage at diagnosis is stage IIIc, with over 70% of diagnoses. Metastasis in ovarian cancer is very common in the abdomen and occurs via exfoliation, where cancer cells burst through the ovarian capsule and can 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 infundibulopelvic ligament, the broad ligament, and the round ligament. The most commonly affected groups include the paraaortic, hypogastric, external iliac, obturator, and inguinal lymph nodes. Usually, ovarian cancer does not metastasize to the liver, lung, brain, or kidneys unless it is a recurrent disease; this differentiates ovarian cancer from many other forms of cancer. == Prevention ==
Prevention
Women with high 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 women 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. the Ovarian Cancer Research Alliance and the Society of Gynecologic Oncology now recommend that women who are not planning on having additional children and who are undergoing surgical procedures such as tubal ligation (having one's "tubes tied") undergo opportunistic salpingectomy — i.e. simultaneously having their fallopian tubes removed. OVCARE — BC Cancer's multi-institutional and multidisciplinary ovarian research group — began recommending salpingectomy at the time of hysterectomy and in place of tubal ligation in 2010. Women with a significant family history of ovarian cancer are often referred to a genetic counselor to see if testing for BRCA mutations would be beneficial. There may be an association between 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. == Screening ==
Screening
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. The Pap test does not screen for ovarian cancer. Screening is not recommended using CA-125 measurements, HE4 levels, ultrasound, or adnexal palpation in women who are at average risk. Currently, there is no national screening programme in the UK for ovarian cancer. CA125 and transvaginal ultrasound can be utilised, but there is minimal evidence to suggest this decreases mortality. More recently, the Risk of Ovarian Cancer Algorithm (ROMA) has been shown to detect earlier cancers using CA125 and age, but again does not provide a robust measure to decrease mortality at present. Ovarian cancer has low prevalence, even in the high-risk group of women from ages 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 that 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. There have been some screening trials that have used age, family history of ovarian cancer, and mutation status to identify target populations for screening. == Management ==
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. Treatment usually involves surgery and chemotherapy, and sometimes radiotherapy, regardless of the subtype of ovarian cancer. Surgical treatment may be sufficient for well-differentiated malignant tumors confined to the ovary. The 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. Since 1980, platinum-based drugs have had an important role in treating ovarian cancer. Borderline tumors, even following spread outside of the ovary, are managed well with surgery, and chemotherapy is not seen as useful. Second-look surgery and maintenance chemotherapy have not been shown to provide benefit. For low-grade, unilateral stage-IA cancers, only the involved ovary (which must be unruptured) and the 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. 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 transverse fissure of the liver, mesentery, or diaphragm, and large areas of ascites. Debulking surgery is typically done once. Computed tomography (abdominal CT) is often used to assess if primary debulking surgery is possible, but low certainty evidence also suggests fluorodeoxyglucose‐18 (FDG) PET/CT and MRI may be useful as an addition for assessing macroscopic incomplete debulking. 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. Several different surgical procedures can be employed to treat ovarian cancer. For stage I and II cancer, laparoscopic (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 stripping or resection, appendectomy, or even a posterior pelvic exenteration. or LGSOC. This is particularly important in germ cell tumors because they frequently metastasize to nearby lymph nodes. It also can be helpful in people who had their first surgery done by a generalist and in epithelial ovarian cancer. The major side effect of 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. Surgery outcomes are best at hospitals that do a large number of ovarian cancer surgeries. 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). Chemotherapy in ovarian cancer typically consists of platins, a group of platinum-based drugs, combined with non-platins. Platinum-based drugs have been used since 1980. 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. Platinum combinations can offer improved survival over single platinum. In people with relapsed ovarian cancer, evidence suggests topotecan has a similar effect on overall survival as paclitaxel and topotecan plus thalidomide, whilst it is superior to treosulfan and not as effective as pegylated liposomal doxorubicin in platinum-sensitive people. Chemotherapy can be given intravenously or in the peritoneal cavity. Typical cycles of treatment involve one treatment every 3 weeks, repeated for 6 weeks or more. Fewer than 6 weeks (cycles) of treatment is less effective than 6 weeks or more.) For recurrent germ cell tumors, an additional 4 cycles of BEP chemotherapy is the first-line treatment for those who have been treated with surgery or platins. Tumors that have a high expression of a protein called ALDH1A1 are found to be resistant to chemotherapy and this resistance can be overcome by blocking ALDH1A1. 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. Novocure sponsored a phase-2 trial proving the efficacy of tumor treating fields in recurrent platinum-resistant ovarian carcinoma, in conjunction with weekly paclitaxel chemotherapy. Radiotherapy late effects (and occurrence rates) include osteonecrosis (8-20%), bladder ulceration (2.5%) and irreversible lumbosacral plexopathy. Hormonal therapy Despite the fact that 60% of ovarian tumors have estrogen receptors, ovarian cancer is only rarely responsive to hormonal treatments. A Cochrane review found a lack of evidence about the effects of tamoxifen in people with relapsed ovarian cancer. Estrogen alone does not have an effect on the cancer, and tamoxifen and letrozole are rarely effective. For epithelial ovarian cancers, the most common test upon follow-up is the CA-125 level. However, treatment based only on elevated CA-125 levels and not any symptoms can increase side effects without prolonging life, so the implications of the outcome of a CA-125 test can be discussed before taking it. The recommendation as of 2014 is that recurrent cancer may be present if the CA-125 level is twice normal. 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. Palliative care 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. In platinum-refractory and platinum-resistant cases, other palliative chemotherapy is the main treatment. Pleural effusions can be treated in a similar manner, with repeated thoracentesis, pleurodesis, or placement of a drain. Palliative radiotherapy typically lasts for only a few treatments, a much shorter course of therapy than non-palliative radiotherapy. The same psychosocial problems can develop in family members. Emotional effects can include a fear of death, sadness, memory problems, and difficulty concentrating. When optimism was adopted by those at the beginning of their treatment, they were less likely to develop distress. Those who have a 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 through several strategies. Activities such as traveling, spending additional time with family and friends, ignoring statistics, journaling, and increasing involvement in spiritually-based events are adaptive. == Prognosis ==
Prognosis
of invasive epithelial ovarian cancer by stage 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%. 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. Continuous accumulation of ascites can be treated by placing a drain that can be self-drained. They come from the National Cancer Institute, SEER, and are based on patients diagnosed from 2004 to 2010. Recurrence rates Ovarian cancer frequently recurs after treatment. Overall, in 5 years, 20% of stage I and II cancers recur. Most recurrences are in the abdomen. ==Epidemiology==
Epidemiology
death from ovarian cancer per 100,000 inhabitants in 2004 s (including non-cancerous tumors) by incidence and risk of ovarian cancer. Globally, in 2018, the incidence of ovarian cancer was 6.6 per 100,000 and mortality was 3.9. Globally, about 160,000 people died from ovarian cancer in 2010. This was an increase from 113,000 in 1990. The number of new cases per year in Europe is approximately 5–15 per 100,000 women. United States In 2022, in the United States, an estimated 19,880 new cases were diagnosed, and 12,810 women died of ovarian cancer. The 5-year relative survival rate is 49.7%. Around 57% of cases have metastasized at the time of diagnosis. In the United States, it is also the fifth-most common cancer in women but the fourth-most common cause of cancer death. The incidence rate over the whole UK population is 21.6 per 100,000. As of 2014, the UK saw approximately 7,000–7,100 yearly diagnoses with 4,200 deaths. Early symptoms are often mistaken for common conditions such as cystitis or irritable bowel syndrome, and about 40 per cent of UK women wrongly believe that cervical screening detects ovarian cancer, an increase from 30 per cent in 2016. 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. Ovarian cancer is most commonly diagnosed after menopause, 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. Older women are more likely to present with advanced ovarian cancer. == In pregnancy ==
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 parents' 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. == Other animals ==
Other animals
Ovarian tumors have been reported in equine mares. Reported tumor types include teratoma, cystadenocarcinoma, and particularly granulosa cell tumor. == Research ==
Research
Screening Screening by hysteroscopy to obtain cell samples obtained for histological examination is being developed. This is similar to the current Pap smear, which is used to detect cervical cancer. The UK Collaborative Trial of Ovarian Cancer Screening is testing a screening technique that combines CA-125 blood tests with transvaginal ultrasound. Although results published in 2015 were not conclusive, there was some evidence that screening may save lives in the long-term. 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. However, trials of the antibody and VEGF inhibitor bevacizumab, which can slow the 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 Clinical trials Clinical trials 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), Learn About Clinical Trials (National Cancer Institute), Search for Clinical Trials (National Cancer Institute), ClinicalTrials.gov (National Institutes of Health). ==See also==
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