Ovarian cancer is a cancer that forms in or in the ovary. It produces abnormal cells that have the ability to attack or spread to other parts of the body. When this process begins, there may be no or only unclear symptoms. The symptoms become more noticeable when the cancer develops. These symptoms may include bloating, pelvic pain, abdominal swelling, and loss of appetite, among others. Common areas where cancer can spread include stomach lining, lymph nodes, lungs, and liver.
The risk of ovarian cancer increases in women who have ovulated more during their lifetime. These include those who have never had a child, those who start ovulation at a younger age and those who reach menopause at older ages. Other risk factors include hormone therapy after menopause, fertility drugs, and obesity. Factors that reduce risk include hormonal birth control, tubal ligation, and breastfeeding. Approximately 10% of cases are associated with genetically inherited risk; women with mutations in the BRCA1 or BRCA2 genes have about 50% chance of getting the disease. The most common type of ovarian cancer, consisting of more than 95% of cases, is ovarian carcinoma. There are five major subtypes of ovarian carcinoma, where high-grade serous carcinomas are the most common. These tumors are believed to start in cells that cover the ovaries, although some may form in the fallopian tubes. Less common types of ovarian cancer include germ cell tumors and genital stromal tumor. The diagnosis of ovarian cancer is confirmed by tissue biopsy, usually raised during surgery.
Screening is not recommended in women who have an average risk, as evidence does not support a reduction in mortality and high levels of false-positive tests may lead to unnecessary surgery, which is accompanied by its own risk. Those at very high risk may have their ovaries removed as a precaution. If caught and treated in the early stages, ovarian cancer can often be cured. Treatment usually includes several combinations of surgery, radiation therapy, and chemotherapy. The results depend on the extent of the disease, subtype cancer present, and other medical conditions. The overall five-year survival rate in the United States is 45%. The results are worse in developing countries.
In 2012, new cases occur in 239,000 women. By 2015 it is present in 1.2 million women and resulted in 161,100 deaths worldwide. Among these women are the seventh most common cancer and the eight most common cause of death from cancer. The typical age of diagnosis is 63. Deaths from ovarian cancer are more common in North America and Europe than in Africa and Asia.
Video Ovarian cancer
Signs and symptoms
Initial symptoms
Early signs and symptoms of ovarian cancer may be absent or subtle. In most cases, symptoms appear for several months before being recognized and diagnosed. Symptoms can be misdiagnosed as irritable bowel syndrome. The early stages of ovarian cancer are less likely to cause pain. Symptoms may vary by subtype. The low malignant potential (LMP) tumor, also known as borderline tumor, does not cause elevated CA125 levels and can not be identified with ultrasound. The typical symptoms of LMP tumor may include abdominal distension or pelvic pain. Very large masses tend to be benign or borderline.
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 intercourse, loss of appetite, fatigue, diarrhea, indigestion, heartburn, constipation, nausea, feeling full, and possibly urinary symptoms (including frequent urination and urgent urination).
Symptoms later
The growing mass can cause pain if ovarian torsion develops. Symptoms can be caused by mass suppression of other abdominopelvic organs of metastasis. If these symptoms begin to occur more often or more severely than usual, especially after no significant history of these symptoms, ovarian cancer is considered. Metastasis can cause Mary Joseph's nodule. Rarely, teratomas can cause a growing teratoma syndrome or peritoneal gliomatosis. Some experience menometrorrhagia and abnormal vaginal bleeding after menopause in many cases. Other common symptoms include hirsutism, abdominal pain, virilization, and adnexal mass.
Children
In adolescents or children with ovarian tumors, symptoms may include severe abdominal pain, irritation of the peritoneum, or bleeding. The tumor symptoms of sex ropes produce hormones that can affect the development of secondary sex characteristics. Sex umbilical cord tumors in preschool children may be manifested by early puberty; abdominal pain and distension are also common. Adolescents with a sex umbilical cord tumor may develop amenorrhea. As the cancer becomes more advanced, it can cause fluid accumulation in the abdomen. If the malignancy has not been diagnosed at the time it causes ascites, it is usually diagnosed shortly thereafter. Further cancer can also cause stomach masses, lymph node mass, or pleural effusion.
Maps Ovarian cancer
Risk factors
Ovarian cancer is associated with the amount of time spent ovulating. Thus having no children is a risk factor for ovarian cancer, probably because ovulation is suppressed through pregnancy. During ovulation, cells are constantly stimulated to divide while the ovulation cycle continues. Therefore, people who have not been born to children at risk twice ovarian cancer than those who have. A longer ovulation period caused by early menstruation early and late menopause is also a risk factor. Both obesity and hormone replacement therapy also increase the risk.
The risk of developing ovarian cancer is less for women who have fewer menstrual cycles, no menstrual cycle, breastfeeding, oral contraceptives, have multiple pregnancies, and have an early pregnancy. The risk of developing ovarian cancer is reduced in women who have tubal ligation (colloquially known as having "bound tube"), both ovaries removed, or hysterectomy (surgery where the uterus, and sometimes cervix, is removed). Age is also a risk factor.
Hormones
The use of fertility drugs may contribute to the formation of limited ovarian tumors, but the relationship between the two is debatable and difficult to study. Fertility drugs may be associated with higher risk of tumor borders. Those who have been treated for infertility but remain nulliparous have a higher risk for epithelial ovarian cancer; However, those who were successfully treated for infertility and later delivery were not at higher risk. This may be due to the shedding of precancerous cells during pregnancy but the cause remains unclear. Risk factors may not be infertility itself, not treatment.
Hormonal conditions such as polycystic ovary syndrome and endometriosis are associated with ovarian cancer, but the relationship is not fully confirmed. Postmenopausal hormone replacement therapy (HRT) with estrogen may increase the risk of ovarian cancer. The association has not been confirmed in large-scale research, but important research including Millions of Women Studies has supported this relationship. Postmenopausal HRT with a combination of estrogen and progesterone may increase temporary risk if used for more than 5 years, but this risk returns to normal after discontinuation of therapy. Estrogen HRT with or without progestin increases the risk of endometrioid and serous tumors but decreases the risk of tumors of the musinosum. Higher estrogen doses increase this risk. Endometriosis is another risk factor for ovarian cancer, such as pain with menstruation. Endometriosis is associated with clear cell subtypes and endometrioids, low-grade serous tumors, stage I and II tumors, grade 1 tumors, and low mortality.
Before menopause, obesity can increase a person's risk of ovarian cancer, but this risk does not appear after menopause. This risk is also relevant for those who are both obese and never use HRT. A similar relationship with ovarian cancer appears in a higher person.
Genetics
Family history of ovarian cancer is a risk factor for ovarian cancer. People with nonpolyposis hereditary colon cancer (Lynch syndrome), and those with genetic abnormalities BRCA-1 and BRCA-2 are at increased risk.
The main genetic risk factor for ovarian cancer is a mutation in the DNA repair mismatch gene, which is present in 10% of ovarian cancer cases. Only one allele needs to be transferred to place someone at high risk. Genes can be inherited through maternal or paternal lines, but have variable penetration. Although mutations in these genes are usually associated with an increased risk of breast cancer, mutations also carry a large risk of ovarian cancer, an increased risk at age 40 and 50 years. The lowest risk quoted is 30% and the highest is 60%. Mutations in BRCA1 have a lifetime risk of developing ovarian cancer 15-45%. Mutations on BRCA2 are less risky than BRCA1 , with a 10% lifetime risk (lowest risk cited) up to 40% (highest risk cited). On average, BRCA-related cancers develop 15 years before their sporadic counterparts, because people who inherit mutations in one copy of their genes require only one mutation to initiate the carcinogenesis process, whereas people with two normal genes will need to get two mutations..
In the United States, five out of 100 women with first relative levels with ovarian cancer will eventually get their own ovarian cancer, placing them with affected family members at triples the risk of women with unaffected family members. Seven out of 100 women with two or more relatives with ovarian cancer will eventually get ovarian cancer. In general, 5-10% of cases of ovarian cancer have a genetic cause. BRCA mutations are associated with high quality serous nonmucinous ovarian cancer.
A strong family history of endometrial cancer, colon cancer, or other gastrointestinal cancers may suggest a syndrome known as non-collapsed hereditary colorectal cancer (also known as Lynch syndrome), which poses a higher risk of developing a number of cancers, including ovaries. cancer. Lynch syndrome is caused by mutations in the mismatch repair gene, including MSH2, MLH1, MLH6, PMS1 , and PMS2 . The risk of ovarian cancer for an individual with Lynch syndrome is between 10 and 12 percent. People of Icelandic descent, European Jewish descent/Ashkenazi Jewish descent, and Hungarian descent are at higher risk for epithelial ovarian cancer. The estrogen receptor beta gene (ESR2) appears to be a key pathogenesis and response to therapy. Other genes associated with ovarian cancer are BRIP1 , MSH6 , RAD51C and RAD51D . CDH1 , CHEK2 , PALB2 and RAD50 are also associated with ovarian cancer.
Some rare genetic disorders are associated with specific subtypes of ovarian cancer. Peutz-Jeghers syndrome, a rare genetic disorder, also affects people for umbilical cord tumors with annular tubules. Ollier's disease and Maffucci syndrome are associated with granulosa cell tumors in children and may also be associated with Sertoli-Leydig tumors. Benign fibroids are associated with nevoid basal cell carcinoma syndrome.
Environmental factors
Industrialized countries, with the exception of Japan, have high epithelial ovarian cancer rates, which may be caused by diet in those countries. Caucasians are at a 30-40% higher risk for ovarian cancer when compared with Blacks and Hispanics, probably due to socioeconomic factors; white women tend to have fewer children and different levels of gynecological operations that affect the risk of ovarian cancer.
The cohort study has found a correlation between milk consumption and ovarian cancer, but case-control studies do not show this correlation. There is mixed evidence of the effects of red meat and processed meats on ovarian cancer.
Temporary evidence suggests that powders, pesticides, and herbicides increase the risk of ovarian cancer. The American Cancer Society notes that until now, no research has been able to accurately link any chemicals in the environment, or in the human diet, directly to mutations that cause ovarian cancer.
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Alcohol consumption does not seem to be associated with ovarian cancer. Other factors that have been studied, such as smoking, low levels of vitamin D in the blood, presence of inclusion ovarian cysts, and infection with human papilloma virus (causing some cases of cervical cancer), have been shown to be risk factors for ovarian cancer. Carcinogenicity of talc perineum is controversial, as it may act as an irritant if it travels through the reproductive tract to the ovaries. Case-control studies have shown that the use of perineal talc increases the risk of ovarian cancer, but using talc more often does not create a greater risk. The use of talc elsewhere in the body is not associated with ovarian cancer. Seating regularly for prolonged periods is associated with higher mortality of epithelial ovarian cancers. The risk is not negated by regular exercise, even if it is lowered.
Increased age (up to 70s) is a risk factor for epithelial ovarian cancer because more mutations in cells can accumulate and eventually cause cancer. Those aged over 80 years have a slightly lower risk.
Tobacco smoking is associated with a higher risk of ovarian cancer of the musinosum; after quitting smoking, the risk eventually returns to normal. A high-fat animal diet may be associated with ovarian cancer, but the association is unclear. Diet seems to play a very small role, if any, in the risk of ovarian cancer. Higher levels of C-reactive protein are associated with a higher risk of ovarian cancer.
Protective factor
Ovulatory suppression, which in turn causes damage to the ovarian epithelium and, consequently, inflammation, is generally protective. This effect can be achieved by having children, using combined oral contraceptives, and breastfeeding, all of which are protective factors. A longer breastfeeding period correlates with a greater decrease in the risk of ovarian cancer. Every birth reduces the risk of ovarian cancer more, and this effect is seen up to five births. Combined oral contraceptives reduce the risk of ovarian cancer by up to 50%, and the protective effects of combined oral contraceptives can last 25-30 years after they are discontinued. Regular use of aspirin or acetaminophen (paracetamol) may be associated with lower risk of ovarian cancer; Other NSAIDs do not seem to have a similar protective effect.
Tubal ligation is protective because carcinogens can not reach the ovaries and fimbriae through the vagina, uterus, and fallopian tubes. Tubal ligation is also protective in women with BRCA1 mutations, but not BRCA2 mutations. Hysterectomy reduces risk, and the removal of both Fallopian tubes and ovaries (bilateral salpingo-oophorectomy) dramatically reduces the risk not only of ovarian cancer, but also of breast cancer. This is still a research topic, because the relationship between hysterectomy and lower risk of ovarian cancer is controversial. The reason why hysterectomy may be protective has not been explained by 2015.
Diets containing lots of low-fat carotene, fiber, and vitamins - in particular, diets with non-starch vegetables (eg broccoli and onions) - may be protective, although research is still ongoing in this area. Higher caffeine intake and consumption of more than two cups of tea a day have been associated with lower risk of ovarian cancer. Tobacco smoking is protective for sex umbilical cord tumors.
Pathophysiology
The form of ovarian cancer when errors in normal ovarian cell growth occur. Usually, when cells become old or damaged, they die, and new cells take their place. Cancer begins when new cells are formed unneeded, and old or damaged cells do not die as they should. The buildup of extra cells often forms a mass of tissue called growth or tumor. These abnormal cancer cells have many genetic disorders that cause them to grow excessively. When the ovaries release the egg, the egg follicle opens and becomes the corpus luteum. This structure needs to be improved by dividing the cells in the ovaries. Continuous ovulation for a long time means more ovarian repair by dividing the cells, which can obtain mutations in each division.
Overall, the most common gene mutations in ovarian cancer occur in NF1, BRCA1, BRCA2, and CDK12 . Type I ovarian cancer, which tends to be less aggressive, tends to have microsatellite instability in some genes, including oncogenes (especially BRAF and KRAS) and tumor suppressors (mostly PTEN ). The most common mutations in Type I cancer are cancer KRAS, BRAF, ERBB2, PTEN, PIK3CA, and ARID1A. Type II, a more aggressive type, has different mutated genes, including p53, BRCA1 , and BRCA2 . Low-grade cancers tend to have mutations in KRAS, whereas cancer of any rate developed from low malignant tumors tends to have a mutation in p53. Type I cancer tends to develop from precursor lesions, whereas Type II cancer can progress from serous tubal intraepithal carcinoma. Serous cancers with BRCA mutations also inevitably have p53 mutations, suggesting that removal of both functional genes is important for cancer progression.
In 50% of high-grade serous cancers, homologous recombination DNA repair was dysfunctional, as did the notch and FOXM1 signaling pathways. They also almost always have p53 mutations. In addition, mutations in high-grade serous carcinomas are difficult to characterize over high-level genomic instability. BRCA1 and BRCA2 are essential for the repair of homologous recombination DNA, and germline mutations in this gene are found in about 15% of people with ovarian cancer. The most common mutations in BRCA1 and BRCA2 are the frameshift mutation from the small Ashkenazi Jewish founding populations.
Nearly 100% of rare mucinous carcinomas have mutations in CRUDE and ERBB2 amplification (also known as Her2/neu ). Overall, 20% of ovarian cancers have mutations in Her2/neu .
Serous carcinomas can develop from serous tubal intraepithal carcinomas, rather than spontaneously developing from ovarian tissue. Other carcinomas develop from the cortical inclusion cyst, which is a group of epithelial ovarian cells in the stroma.
Diagnosis
Checkout
The diagnosis of ovarian cancer begins with a physical examination (including a pelvic exam), blood tests (for CA-125 and sometimes other markers), and transvaginal ultrasound. Sometimes rectovaginal examination is used to help plan the surgery. The diagnosis should be confirmed by surgery to examine the abdominal cavity, take a biopsy (tissue sample for microscopic analysis), and look for cancer cells in the stomach fluid. It helps to determine whether the ovarian mass is benign or malignant.
The early stages of ovarian cancer (I/II) are difficult to diagnose because most of the symptoms are nonspecific and therefore little use in diagnosis; As a result, it is rarely diagnosed until it spreads and progresses to the next stage (III/IV). In addition, the symptoms of ovarian cancer may seem similar to irritable bowel syndrome. In patients likely to become pregnant, BHCG levels can be measured during the diagnosis process. Serum alpha-fetoproteins, neuron-specific enolase, and lactate dehydrogenase can be measured in young girls and adolescents with suspected ovarian tumors because younger patients are more likely to have malignant germ cell tumors.
Physical examination, including pelvic examination, and pelvic ultrasound (transvaginal or other) are both important for diagnosis: Physical examination may reveal increased abdominal circumference and/or ascites (fluid in the abdominal cavity), while pelvic examination may reveal ovaries. or stomach masses. Adnexa 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 mass is caused by malignancy; However, there are other benign causes of adnexal masses, including ovarian follicle cysts, leiomyomas, endometriosis, ectopic pregnancy, hydrosalping, tubo ovarian abscess, ovarian torsion, dermoid cysts, cystadenoma (serosa or mucinosa), diverticular or appendiceal abscess, pelvic kidney, ureteral or bladder diverticulum, benign cystic mesothelioma of the peritoneum, peritoneal tuberculosis, or paraovarian cysts. A perceived ovary is also a sign of ovarian cancer in postmenopausal women. Other parts of the physical examination for suspected ovarian cancer may include breast examination and rectal examination. Palpation of supraclavicular, axillary, and inguinal lymph nodes may reveal lymphadenopathy, which may be indicative of metastasis. Another indicator may be the presence of pleural effusions, which may be noted in auscultation.
When ovarian malignancy is included in the list of diagnostic possibilities, a limited number of laboratory tests are demonstrated. A complete blood count and serum electrolyte test are usually obtained; when ovarian cancer is present, these tests often show high platelet counts (20-25% of people) and low blood sodium levels due to chemical signals secreted by the tumor. Positive tests for inhibin A and inhibin B may show granulosa cell tumors.
Blood tests for a marker molecule called CA-125 are useful in differential diagnosis and in the follow-up of the disease, but that alone has not proven to be an effective method for screening early stage ovarian cancer because of unacceptable lows. sensitivity and specificity. CA-125 levels in premenopausal men greater than 200 U/mL may indicate ovarian cancer, as does CA-125 increase above 35 U/mL in post-menopausal people. CA-125 levels are not accurate in early-stage ovarian cancer, because half of ovarian cancer patients of stage I have normal CA-125 levels. CA-125 may also increase 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 leiomyomas. HE4 is another candidate for ovarian cancer testing, although it has not been extensively tested. Other tumor markers for ovarian cancer include CA19-9, CA72-4, CA15-3, immunosuppressive acid proteins, haptoglobin-alpha, OVX1, mesothelin, lysophosphatidic acid, osteopontin, and fibroblast growth factor 23.
The use of a blood test panel can help in diagnosis. The OVA1 panel includes CA-125, beta-2 microglobulin, transferrin, apolipoprotein A1, and transthyretin. OVA1 above 5.0 in premenopausal and 4.4 in postmenopausal men indicates a high risk for cancer. A different set of laboratory tests are used to detect cord sex umbilical tumors. High levels of testosterone or dehydroepiandrosterone sulfate, combined with other symptoms and high levels of inhibin A and inhibin B may indicate SCST of any type.
Research is currently looking at ways to consider proteomic tumor markers in combination with other disease indicators (ie radiology and/or symptoms) to improve diagnostic accuracy. The challenge in such an approach is that the prevalence of different ovarian cancers means that testing with very high sensitivity and specificity will still produce some false-positive results, which in turn can cause problems such as performing surgical procedures in which cancer is not found intraoperatively. The genomic approach has not been developed for ovarian cancer.
CT scan is preferred to assess the extent of tumors in the abdominopelvic cavity, although magnetic resonance imaging may also be used. CT scans can also be useful for finding caking or differentiating fluid from solid tumors in the stomach, especially in low malignant potential tumors. However, it may not detect a smaller tumor. Occasionally, chest x-ray is used to detect metastasis in the chest or pleural effusion. Another test for metastatic disease, although rarely used, is barium enema, which may indicate whether the rectosigmoid colon is involved in the disease. Positron emission tomography, bone scan, and paracentesis are of limited use; in fact, paracentesis can cause metastases to form in place of needle insertion and may not yield useful results. However, paracentesis can be used in cases where there is no pelvic mass and ascites still present. A doctor who suspects ovarian cancer may also perform mammography or endometrial biopsy (in the case of abnormal bleeding) to assess the likelihood of malignancy of the breast and malignancy of the endometrium, respectively. Vaginal ultrasonography is often a first-line imaging study performed when adnexal masses are discovered. Some characteristics of the adnexa mass indicate ovarian malignancy; they are usually solid, irregular, multilocular, and/or large; and they usually have papillary features, central blood vessels, and/or irregular internal septations. However, SCST has no definitive characteristics in radiographic studies.
To definitively diagnose ovarian cancer, surgical procedures are required to examine the stomach. This can be an open procedure (laparotomy, incision through the abdominal wall) or keyhole surgery (laparoscopy). During this procedure, suspicious tissue is removed and transmitted for microscopic analysis. Typically, these include unilateral salpingo-oophorectomy, removal of one affected ovary and Fallopian tube. The fluid from the abdominal cavity can also be analyzed for cancer cells. If the cancer is found, this procedure can also be used to determine the extent of its spread (which is a form of tumor staging).
Risk score
A well-known method of estimating the risk of malignant ovarian cancer is the risk of malignant index (RMI), calculated on initial examination. More than 200 or 250 RMI scores are generally felt to show a high risk for ovarian cancer.
RMI is calculated as:
- RMI = ultrasound score x menopause score x level CA-125 in U/ml.
Two methods can be used to determine ultrasound scores and menopausal scores, with the resulting score referred to as RMI 1 and RMI 2, respectively, depending on what method is used.
Another method of measuring the risk of ovarian cancer is the Risk of Ovarian Cancer Algorithm (ROCA), observing the level over time and determining whether they are increasing fast enough to ensure transvaginal ultrasound. The risk of an Ovarian Malignancy algorithm uses CA-125 levels and HE4 levels to calculate the risk of ovarian cancer; may be more effective than RMI. The IOTA model can be used to estimate the probability that adnexal tumors are malignant. They include the LR2 risk model, Simple Rule Risk calculation (SRrisk) and Different Neoplasias Assessment in the Adnexa model (ADNEX) that can be used to assess the risk of malignancy in the adnexal mass, based on the characteristics and risk factors. The QCancer algorithm (Ovary) is used to predict the likelihood of ovarian cancer from risk factors.
Pathology
Ovarian cancer is classified according to the microscopic appearance of their structure (histology or histopathology). Histology dictates many aspects of clinical care, management, and prognosis. The gross pathology of ovarian cancer is very similar regardless of the histologic type: the tumor has a dense and cystic mass. According to SIER, the type of ovarian cancer in women aged 20 and over are:
Ovarian cancer is histologically and genetically divided into type I or type II. Type I cancer has a low histologic level, and includes endometrioid cell carcinoma, mucin, and clear cells. Type II cancers have higher histologic levels and include serous carcinoma and carcinosarcoma.
Epithelial carcinoma
Stromal-epithelial surface tumors, also known as ovarian epithelial carcinomas, are the most common type of ovarian cancer, representing about 90% of ovarian cancers. These include serous tumors, endometrioid tumors, and mucosal cystadenocarcinoma. Less common tumors are malignant Brenner tumors and ovarian transcellular cell carcinomas. Ovarian epithelial cancer develops from the epithelium, the layer of cells that cover the ovaries.
Serous carcinoma
Most people with epithelial ovarian carcinoma, about two-thirds, have serous carcinoma, although this proportion is estimated to be as high as 80%. Serous carcinoma is less aggressive than high-grade serous carcinoma, although it usually does not respond well to chemotherapy or hormonal treatment. Serous carcinoma is thought to begin in Fallopian tubes. Histologically, serous adenocarcinoma has a psammoma body. Low quality serous adenocarcinoma resembles Fallopian tube epithelium, whereas high-grade serum adenocarcinoma exhibits nuclear anaplasia and atypia.
50% of the time, bilateral serous carcinoma, and in 85% of cases, they have spread beyond the ovaries at the time of diagnosis. Most have a diameter of more than 15 cm.
Small cell carcinoma
Small cell carcinoma is rare and aggressive, with two major subtypes: hypercalcemic and pulmonary. This is usually fatal within 2 years after diagnosis. Hypercalcemia small cell hyper carcinoma greatly affects those in their 20s, causes high blood calcium levels, and affects one ovary. Ovarian small cell lung cancer usually affects both the ovaries of older women and looks like a carcinoma of lung cancer cells.
Primary peritoneal carcinoma
Primary peritoneal carcinoma develops from the peritoneum, the membrane covering the abdominal cavity that has the same embryonic origin as the ovaries. They are often discussed and classified with ovarian cancer when they affect the ovaries. They can develop even after the ovaries have been removed and may look similar to mesothelioma.
Clear cell carcinoma
Cell ovarian carcinoma clearly does not respond well to chemotherapy and may be associated with endometriosis. They represent about 5% of all endometrial cancers. Japanese women develop ovarian cancer cells clearly more often than other women groups.
Clear cell adenocarcinoma
Histopathologically clear cell adenocarcinoma is similar to other clear cell carcinomas, with clear cells and nail cells. They represent about 5-10% of epithelial ovarian cancers and are associated with endometriosis in the pelvic cavity. They are usually early stages and therefore can be cured via surgery, but sophisticated clear cell adenocarcinoma (about 20%) has a poor prognosis and is often resistant to platinum chemotherapy.
Endometrioid
Endometrioid adenocarcinoma forms about 15-20% of epithelial ovarian cancers. Because they are usually low levels, endometrioid adenocarcinoma has a good prognosis. These tumors often occur along with endometriosis or endometrial cancer.
Tumor mállerian malignant mixture (carcinosarcoma)
Tumor mÃÆ'¼llerian mixture makes up less than 1% ovarian cancer. They have epithelial and mesenchymal cells visible and tend to have a poor prognosis.
Mucinous
Tumor mukosa termasuk adenokarsinoma mucinous dan cystadenocarcinoma mucinous.
Mucinous adenocarcinoma
Mucosal adenocarcinoma is 5-10% of epithelial ovarian cancers. Histologically, they resemble intestinal or cervical adenocarcinomas, and are often completely metastases of the appendix or colon. Mucinous advanced adenocarcinoma has a poor prognosis, generally worse than serous tumors, and is often resistant to platinum chemotherapy, although rarely.
Pseudomyxoma peritonei
Pseudomyxoma peritonei refers to a collection of mucus or gelatin material packaged in the abdominopelvic cavity, which is rarely caused by an ovarian tumor of the primary musinosum. More generally, it is associated with ovarian cancer metastasis of bowel.
undifferentiated Epitelial
Undifferentiated cancer - in which cell type can not be determined - forms about 10% of epithelial ovarian cancers and has a relatively poor prognosis. When examined under a microscope, this tumor has very abnormal cells that are arranged in clumps or sheets. Usually there are clumps of serous cells that can be recognized in the tumor.
Malignant Brenner Tumor
Malignant Brenner tumors are rare. Histologically, they have solid fibrous stroma with transitional epithelial areas, and some squamous differentiation. To be classified as a malignant Brenner tumor, it should have a Brenner tumor focus and a transitional cell carcinoma. Transitional cell carcinoma components are usually less differentiated and resemble urinary tract cancer.
Transitional cell carcinoma
Transitional cell carcinoma represents less than 5% of ovarian cancers. Histologically, they look similar to bladder carcinoma. The prognosis is intermediate - better than most epithelial cancers but worse than the malignant Brenner tumor.
Stroma thongs strap gymnastic
Genital stromal tumors, including estrogen-producing granulosa cell tumors, thecoma benign, and Sertoli-Leydig virilizing cell tumor or arrhenoblastoma, account for 7% of ovarian cancers. They occur most often in women between 50 and 69 years, but can occur in women of all ages, including young girls. They are usually not aggressive and usually one-sided; Therefore they are usually treated with surgery only. Stromal tumor sex umbilical cord is a major hormone producing hormone tumor.
Some different cells of mesenchyme can cause sex-cord or stromal tumors. These include fibroblasts and endocrine cells. The symptoms of ovarian tumor of the sexes or stroma can be different from other types of ovarian cancer. Common signs and symptoms include ovarian torsion, bleeding from or rupture of the tumor, abdominal mass, and hormonal disorders. In children, precocious pseudopuberty can occur with granulosa cell tumors because they produce estrogen. This tumor causes menstrual abnormalities (excessive bleeding, rare menstruation, or no menstruation) or postmenopausal bleeding. Because these tumors produce estrogen, they can cause or occur in conjunction with endometrial cancer or breast cancer. Other sex-cord/stromal tumors come with different symptoms. Sertoli-Leydig cell tumors cause excessive virilization and hair growth due to the production of testosterone and androstenedione, which can also cause Cushing's syndrome in rare cases. Cord stromal tumors also occur that do not cause hormonal imbalances, including benign fibroma, which cause ascites and hydrothorax. With germ cell tumors, the sex-stromal ligament tumor is the most commonly diagnosed ovarian cancer in women under 20 years.
Granulosa cell tumor
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 teenage granulosa tumors, which develop before puberty or before age 30. Both develop in the ovarian follicle of the cell population that surrounds the germ cells.
Adult granulosa cell tumor
Adult granulosa cell tumors are characterized by slower onset (30 years, 50 average). This tumor produces high levels of estrogen, which causes its distinctive symptoms: menometrorrhagia; endometrial hyperplasia; soft, enlarged breasts; postmenopausal bleeding; and secondary amenorrhea. Tumor mass may cause other symptoms, including abdominal pain and distension, or symptoms similar to ectopic pregnancy if the tumor is bloody and ruptures.
Teenage granulosa cell tumor
Sertoli-Leydig cell tumor
Sertoli-Leydig tumors are most common in women before the age of 30, and especially common before puberty.
Sclerosing stromal tumors
Sclerosing stromal tumors usually occur in women before puberty or women before the age of 30.
Malignant cell tumor
Ovarian germ cell tumors develop from ovarian seed cells. Malignant cell tumors account for about 30% of ovarian tumors, but only 5% of ovarian cancers, because most germ cell tumors are teratomas and most are benign teratomas. Malignant teratomas tend to occur in older women, when one of the germ layers in the tumor develops into squamous cell carcinoma. Tumors of cells tend to occur in young women (20s-30s) and girls, forming 70% of ovarian cancers seen in this age group. Cell cell tumors can include dysgerminomas, teratomas, egg yolk sac tumors/endodermal sinus tumors, and choriocarcinoma, when they appear in the ovaries. Some germ cell tumors have a 12 isochromosome, in which one arm of chromosome 12 is removed and replaced with a duplicate of the other. 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. Overall, they metastasize more often than epithelial ovarian cancers. In addition, cancer markers used varied with tumor type: choriocarcinoma monitored with beta-HCG and endodermal sinus tumor with alpha-fetoprotein.
Tumors of germ cells are usually discovered when they become large, palpable masses. However, like genital umbilical cord tumors, they can cause torsional torque or bleeding and, in children, isosexual precocious puberty. They often metastasize to adjacent lymph nodes, especially para-aortic and pelvic lymph nodes. The most common symptom of germ cell tumor is subacute abdominal pain caused by tumor bleeding, necrosis, or ovarian capsule stretching. If the tumor ruptures, causing significant bleeding, or ovaries, can cause acute abdominal pain, which occurs in less than 10% of those with germ cell tumors. They can also secrete hormones that change the menstrual cycle. In 25% of germ cell tumors, cancer is found during routine examination and does not cause symptoms.
Diagnosing germ cell tumors may be difficult because normal menstrual cycles and puberty can cause pelvic pain and symptoms, and a young woman even believes that this symptom is pregnancy, and does not seek treatment due to the stigma of teenage pregnancy. Blood tests for alpha-fetoprotein, karyotype, human chorionic gonadotropin, and liver function are used to diagnose germ cell tumors and the potential of simultaneous gonadal dysgenesis. Germ cell tumors may initially be thought of as benign ovarian cysts.
Dysgerminoma
Dysgerminoma accounts for 35% of ovarian cancers in young women and is the most likely germ cell tumor to metastasize to lymph nodes; node metastasis occurs in 25-30% of cases. This tumor may have mutations in the KIT gene, a mutation known for its role in gastrointestinal stromal tumors. People with XY and ovarian karyotype (gonadal dysgenesis) or X, karyotype and ovary (Turner syndrome) who develop unilateral disgerminoma are at risk for gonadoblastoma in other ovaries, and in this case both ovaries are usually released when unilateral disgerminomas are found to avoid the risk of malignant tumors another. Gonadoblastoma in people with Swyer or Turner syndrome becomes malignant in about 40% of cases. However, in general, dysgerminoma is bilateral 10-20% of the time.
They are composed of cells that can not further differentiate and develop directly from germ cells or from gonadoblastoma. Dysgerminoma contains syncytiotrophoblasts in about 5% of cases, and therefore may cause elevated levels of hCG. In gross appearance, dysgerminoma is usually pink to brown, has several lobes, and is solid. Microscopically, they appear to be synonymous with seminoma and very close to the embryonic primordial germ cells, having large, polyhedral, and rounded clear cells. Uniform and round or square nuclei with prominent nucleoli and cytoplasm have high levels of glycogen. Inflammation is another prominent histological feature of dysgerminoma.
Choriocarcinoma
Choriocarcinoma may occur as a primary ovary tumor developing from germ cells, although it is usually a gestational disease that metastasizes to the ovaries. Primary ovarian choriocarcinoma has a poor prognosis and can occur without pregnancy. They produce high levels of hCG and can cause early puberty in children or menometrorrhagia (irregular and severe menstruation) after menarche.
The teratoma is immature (solid)
The immature or solid teratoma is the most common type of ovarian ovarian cell tumor, which accounts for 40-50% of cases. Teratomas are characterized by irregular tissue arising from the three layers of the embryo embryo: ectoderm, mesoderm, and endoderm; immature teratomas also have undifferentiated stem cells that make them more virulent than adult teratomas (dermoid cysts). Different tissues are seen in gross pathology and often include bone, cartilage, hair, mucus, or sebum, but this tissue is not visible from the outside, which appears to be a dense mass with lobes and cysts. Histologically, they have a large number of neuroectoderm arranged into sheets and tubules together with glia; the number of neural networks determines the histological level. Unmarried teratomas usually affect only one ovary (10% occur together with dermoid cysts) and usually metastasize throughout the peritoneum. They can also cause adult teratoma implants to grow throughout the stomach in a disease called growth teratoma syndrome; These are usually benign but will continue to grow during chemotherapy, and often require further surgery. Unlike mature teratomas, the immature teratoma forms much adhesion, making them less likely to cause ovarian torsion. There is no specific marker for undeveloped teratomas, but carcinoembryonic (CEA), CA-125, CA19-9, or AFP antigens can sometimes indicate undeveloped teratomas.
Stage I teratoma is the majority (75%) of cases and has the best prognosis, with 98% of patients surviving 5 years; if Stage I tumor is also level 1, it can be treated with a one-sided operation alone. Stage II although IV tumor forms a quarter of the remaining cases and has a worse prognosis, with 73-88% of patients surviving 5 years.
Adult teratoma (dermoid cyst)
Adult teratomas, or dermoid cysts, are rare tumors that comprise most of the benign tissues that develop after menopause. The tumor consists of irregular tissue with malignant tissue nodules, which can be of various types. The most common malignancies are squamous cell carcinoma, but adenocarcinoma, basal cell carcinoma, carcinoid tumor, neuroectodermal tumor, malignant melanoma, sarcoma, sebaceous tumor, and struma ovarii may also be part of dermoid cysts. They are treated with surgery and chemotherapy or platinum adjuvant radiation.
Egg yolk sac tumor/endodermal sinus tumor
The yolk sac tumor, formerly called endodermal sinus tumor, forms about 10-20% of malignant ovarian malignancy, and has the worst prognosis of all ovarian germ cell tumors. They occur before menarche (in one-third of cases) and after menarche (the remaining two-thirds of cases). Half of the people with egg yolk sac tumors are diagnosed at stage I. Usually, they are unilateral to metastasis, occurring in the peritoneal cavity and through the bloodstream to the lungs. Yellow pouch tumors grow quickly and easily recur, and are not easily treated after recurrence. Egg yolk sac tumor is highly treatable, with a 5% free survival rate of 93%, but stage II-IV tumors are less treatable, with a survival rate of 64-91%.
Their grimy appearance is dense, friable, and yellow, with necrotic and hemorrhagic areas. They also often contain cysts that may degenerate or rupture. Histologically, the yolk sac tumor is characterized by the presence of the Schiller-Duval body (which is pathognomonic for an egg yolk sac tumor) and reticular pattern. Tumors of yellow sacs generally emit alpha-fetoproteins and may be immunohistochemically stained by their presence; the level of alpha-fetoprotein in the blood is a useful recurrence marker.
Embryonal carcinoma
Embryonic carcinoma, a rare type of tumor usually found in mixed tumors, develops directly from germ cells but is not terminal differentiated; in rare cases can occur in the dysgenetic gonads. They can progress further to a variety of other neoplasms, including choriocarcinoma, egg yolk sac tumors, and teratomas. They occur in younger people, with median age at diagnosis 14, and exclusion of alpha-fetoprotein (in 75% of cases) and hCG.
Histologically, embryonal carcinomas appear similar to embryonic discs, consisting of epithelial, anaplastic cells in irregular sheets, with gland-like spaces and papillary structures.
Polyembryoma
Polyembryoma, the most immature form of teratoma and a very rare ovarian tumor, is histologically characterized by having multiple embryonic bodies with disc-like structures, egg yolk sacs, and amniotic sacs. The syncytiotrophoblast giant cells also occur in polyembryomas.
Squamous cell carcinoma
Primary ovarian squamous cell carcinoma is rare and has a poor prognosis when it goes. More specifically, ovarian squamous cell carcinoma is a cervical metastasis, an area of ​​differentiation in an endometrioid tumor, or derived from an adult teratoma.
Mixed tumor
Tumor mixture contains elements of more than one class of tumor histology above. To be classified as a mixed tumor, the minor type should form more than 10% of the tumor. Although mixed carcinoma can have a combination of cell types, the ovarian cancer of the mix is ​​usually serosa/endometrioid or clear cell/endometrioid. Mixed germ cell tumors make up about 25-30% of all gastric cell ovarian cancers, with a combination of dysgerminoma, an egg yolk sac tumor, and/or immature teratoma. The prognosis and treatment vary by type of component cell.
Secondary ovarian cancer
Ovarian cancer can also become secondary cancer, the result of metastasis from primary cancer elsewhere in the body. Approximately 7% of ovarian cancers are caused by metastasis, while the rest are primary cancers. Common primary cancers are breast cancer, colon cancer, appendix cancer, and stomach cancer (primary stomach cancer that metastasizes to the ovaries called Krukenberg tumors). Krumenberg's tumor has a pointy ring cell and a mucin cell. Endometrial cancer and lymphoma can also metastasize to the ovaries.
Bad malignant potential tumor
Low malignant potential ovarian tumors, also called borderline tumors, have some benign and some malignant features. LMP tumors make up about 10% -15% of all ovarian tumors. They develop earlier than epithelial ovarian cancer, around the age of 40-49 years. They usually do not have extensive invasions; 10% of LMP tumors have a stromal microinvasion area (& lt; 3mm, & lt; 5% tumor). LMP tumors have other abnormal features, including increased mitosis, changes in cell size or size of the nucleus, abnormal nuclei, cell stratification, and small projection of the cells (papillary projections). Serous and/or musinosum characteristics can be seen in histologic examination, and serous histology is a large majority of advanced LMP tumors. More than 80% of LMP tumors are Stage I; 15% are stages II and III and less than 5% are stage IV. LMP tumor implants are often non-invasive.
Staging
Ovarian cancer is staged using the FIGO staging system and uses information obtained after surgery, which may include total abdominal hysterectomy through laparotomy of the midline, removal of (usually) ovaries and Fallopian tubes (usually) omentum, peritoneal, retroperitoneal glandular lymph nodes (including pelvic and para-aortic lymph nodes), appendicitis of suspected musinosum tumors, and peritoneal biopsy for cytopathology. Approximately 30% of ovarian cancers that appear limited to the ovaries have metastasized microscopically, which is why stage I cancer should be completely staged. 22% of cancers considered stage I were observed to have lymphatic metastases. The AJCC stage is the same as the FIGO stage. The AJCC staging system describes primary tumor (T) levels, absence or presence of metastasis to adjacent lymph nodes (N), and absence or presence of distant metastases (M). The most common stage at diagnosis is stage IIIc, with more than 70% diagnosis.
FIGO
AJCC/TNM
The AJCC/TNM staging system shows where the tumor has progressed, spread to lymph nodes, and metastases.
The AJCC/TNM Stages can be correlated with the FIGO stages:
Grading
Class 1 tumors have well-differentiated cells (looks very similar to normal tissue) and are the ones with the best prognosis. Class 2 tumors are also called quite differentiated well and they consist of cells that resemble normal tissue. Class 3 tumors have the worst prognosis and their cells are abnormal, which are referred to as less differentiated.
Metastasis in ovarian cancer is very common in the stomach, and occurs through exfoliation, in which cancer cells rupture through the ovarian capsule and can move freely throughout the peritoneal cavity. Metastatic ovarian cancer usually grows on the surface of organs rather than inside; they are also common in omentum and peritoneal lining. Cancer cells can also travel through the lymphatic system and metastasize to the lymph nodes connected to the ovaries through the blood vessels; namely the lymph nodes along the infundibulopelvis ligaments, broad ligaments, and round ligaments. The most commonly affected groups include paraaortic, hypogastric, external iliac, obturator, and inguinal lymph nodes. Normally, ovarian cancer does not metastasize to the liver, lungs, brain, or kidneys unless it is a recurrent disease; this distinguishes ovarian cancer from various forms of other cancers.
Screening
There is no simple and reliable way to test ovarian cancer in women who have no signs or symptoms. Screening is not recommended in women who have an average risk, as evidence does not support a reduction in mortality and high levels of false-positive tests may lead to unnecessary surgery, which is accompanied by its own risk. The Pap test does not screen for ovarian cancer.
Ovarian cancer is usually only palpable at an advanced stage. Screening is not recommended using CA-125 measurements, HE4 levels, ultrasound, or adnexal palpation in women at an average risk. The risk of developing ovarian cancer in those with genetic factors can be reduced. Those with genetic predisposition may benefit from screening. This high risk group has benefited with early detection.
Ovarian cancer has a low prevalence, even in high-risk women groups from 50 to 60 (about one in 2000), and screening of women at an average risk is more likely to produce ambiguous results than detecting problems that require treatment.. Because ambiguous outcomes are more likely than detection of treatable problems, and because the usual response to ambiguous outcomes is invasive intervention, in women at average risk, the potential danger of having unchecked examinations outweighs the potential benefits. The purpose of screening is to diagnose ovarian cancer at an early stage, when it is more likely to be successfully treated.
Screening with transvaginal ultrasound, pelvic examination, and CA-125 levels can be used as a substitute for prevention surgery in women who have BRCA1 or BRCA2 mutations. This strategy has shown some success.
Prevention
People with a strong genetic risk for ovarian cancer may consider surgical removal of their ovaries as a precaution. This is often done after the completion of the fertile period. This reduces the likelihood of developing breast cancer (about 50%) and ovarian cancer (about 96%) in people at high risk. Women with BRCA gene mutations typically also have a Fallopian tube released at the same time (salpingo-oophorectomy), as they also have an increased risk of Fallopian tube cancer. However, these statistics may overestimate the risk reduction because of how they have been researched.
People with a significant family history for ovarian cancer are often referred to genetic counselors to see if they if testing for a BRCA mutation would be beneficial. Oral contraceptive use, absence of 'menstruation' during the menstrual cycle, and tubal binding reduce the risk. There may be associations developing ovarian cancer and ovarian stimulation during infertility treatments. Endometriosis has been associated with ovarian cancer. Human papillomavirus, smoking, and talc infections have not been identified as increasing the risk for developing ovarian cancer.
Management
Once it is determined that the ovaries, fallopian tubes, or primary peritoneal cancers are present, treatment is scheduled by gynecologic oncologists (doctors trained to treat cancer of the female reproductive system). Gynecologic oncologist doctors can perform surgery and give chemotherapy to women with ovarian cancer. Treatment plan developed.
Treatment usually involves surgery and chemotherapy, and occasionally radiotherapy, regardless of ovarian cancer subtype. Surgical treatment may be sufficient for malignant tumors that are well differentiated and confined to the ovaries. The addition of chemotherapy may be necessary for more aggressive tumors confined to the ovaries. For patients with advanced disease, a combination of surgical reduction with a combination of chemotherapy regimens is standard. Borderline tumors, even after spreading outside the ovaries, are well managed with surgery, and chemotherapy does not look useful. Surgery with a second look and maintenance chemotherapy has not been proven to benefit.
Surgery
Surgery has been the standard of care for several decades and may be required in obtaining specimens for diagnosis. Surgery depends on the extent of the nearest invasion of other tissues by cancer when diagnosed. This cancer rate is illustrated by determining it's stage, type of suspected, and cancerous rate. The gynecologic surgeon may remove one (unilateral oophorectomy) or both ovaries (bilateral oophorectomy). Fallopian tubes (salpingectomy), uterus (hysterectomy), and omentum (omentectomy) can also be removed. Normally, all these organs are discarded.
For low-stage, unilateral-stage IA cancers, only the ovaries involved (which should be uninterrupted) and Fallopian tubes will be eliminated. This can be done primarily in young people who want to maintain their fertility. However, the risk of microscopic metastasis exists and the staging must be completed. If any metastasis is found, a second operation to remove the remaining ovaries and uterus is required. Tranexamic acid may be administered prior to surgery to reduce the need for blood transfusions due to blood loss during surgery.
If a tumor in a premenopausal woman is determined to be a low malignant potential tumor during surgery, and it is clearly a 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 checked or removed. This is very important with tumor musinosum. In children or adolescents with ovarian cancer, surgeons usually try to maintain an ovary to allow for the completion of puberty, but if the cancer has spread, this is not always possible. Dysgerminoma in particular tends to affect both ovaries: 8-15% of dysgerminomas are present in both ovaries. People with low-grade tumors (well differentiated) are usually treated only with surgery, which is often curative. In general, germ cell tumors can be treated with unilateral surgery unless cancer is widespread or fertility is not a factor.
In advanced cancer, where complete removal is not an option, as many tumors may be removed in a procedure called debulking surgery. This surgery is not always successful, and is less successful in women with extensive metastases in peritoneal disease, stage IV, cancer in transverse liver, mesenterial, or diaphragmatic fissures, and large areas of ascites. The debulking operation is usually only done once. More complete debulking is associated with better outcomes: women with no evidence of macroscopic disease after debulking have a median survival of 39 months, compared with 17 months with incomplete surgery. By removing metastasis, many cells resistant to chemotherapy are removed, and the dead cell clumps are also removed. This allows chemotherapy to better reach the remaining cancer cells, which are more likely to grow rapidly and therefore chemosensitive.
Operation debulking Interval is another protocol used, where neoadjuvant chemotherapy is administered, debulking surgery is done, and chemotherapy is complete after debulking. Although no definitive studies have been completed, this proved to be approximately equivalent to primary debulking surgery in terms of survival, and showed a slightly lower morbidity.
There are several different surgical procedures that can be used to treat ovarian cancer. For stage I and II cancers, laparoscopic surgery (keyhole) may be used, but metastases can not be found. For advanced cancer, laparoscopy is not used, because the metastasis debulsing requires access to the entire peritoneal cavity. Depending on the extent of the cancer, the procedure may include bilateral salpingo-oophorectomy, biopsy across the peritoneum and abdominal lymphatic system, omentectomy, splenectomy, intestinal resection, peeling or resection, appendicitis, or even posterior pelvic exenteration.
To complete the ovarian cancer in full, lymphadenectomy may be included in the surgery, but significant survival benefits for this practice may not occur. This is very important in germ cell tumors because they often metastasize to nearby lymph nodes.
If ovarian cancer repeats, secondary surgery is sometimes a treatment option. It depends on how easily the tumor can be removed, how much fluid accumulates in the stomach, and overall health. This can be helpful in people who undergo their first surgery by s
Source of the article : Wikipedia
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