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Ovarian Cancer

  • Author: Andrew E Green, MD; Chief Editor: from Memorial Sloan-Kettering - Yukio Sonoda, MD  more...
 
Updated: Aug 24, 2016
 

Practice Essentials

Ovarian cancer is the most common cause of cancer death from gynecologic tumors in the United States. Malignant ovarian lesions include primary lesions arising from normal structures within the ovary and secondary lesions from cancers arising elsewhere in the body. Primary lesions include epithelial ovarian carcinoma (70% of all ovarian malignancies). Current research suggests that the majority of these originate from the fallopian tubes.  

Stromal tumors of the ovary include germ-cell tumors, sex-cord stromal tumors, and other more rare types. Metastases to the ovaries are relatively frequent; common sources are tumors in the endometrium, breast, colon, stomach, and cervix. See the image below.

An enlarged ovary with a papillary serous carcinom An enlarged ovary with a papillary serous carcinoma on the surface.

Signs and symptoms

Early ovarian cancer causes minimal, nonspecific, or no symptoms. The patient may feel an abdominal mass. Most cases are diagnosed in an advanced stage.

Epithelial ovarian cancer presents with a wide variety of vague and nonspecific symptoms, including the following:

  • Bloating; abdominal distention or discomfort
  • Pressure effects on the bladder and rectum
  • Constipation
  • Vaginal bleeding
  • Indigestion and acid reflux
  • Shortness of breath
  • Tiredness
  • Weight loss
  • Early satiety

Symptoms independently associated with the presence of ovarian cancer include pelvic and abdominal pain, increased abdominal size and bloating, and difficulty eating or feeling full.[1] Symptoms associated with later-stage disease include gastrointestinal symptoms such as nausea and vomiting, constipation, and diarrhea.[2] Presentation with swelling of a leg due to venous thrombosis is not uncommon. Paraneoplastic syndromes due to tumor-mediated factors lead to various presentations.

See Clinical Presentation for more detail.

Diagnosis

Physical findings are uncommon in patients with early disease. Patients with more advanced disease may present with ovarian or pelvic mass, ascites, pleural effusion, or abdominal mass or bowel obstruction.

The presence of advanced ovarian cancer is often suspected on clinical grounds, but it can be confirmed only pathologically by removal of the ovaries or, when the disease is advanced, by sampling tissue or ascitic fluid.

Screening

The US Preventive Services Task Force (USPSTF) recommends against screening (with serum CA125 level or transvaginal ultrasonography) for ovarian cancer in the general population.[3] The National Cancer Institute (NCI) recommends that high-risk women seek advice from their physicians and consider having annual ultrasonographic examinations and annual CA125 testing, as well as consider oophorectomy or participation in a clinical trial.

Laboratory testing

No tumor marker (eg, CA125, beta-human chorionic gonadotropin, alpha-fetoprotein, lactate dehydrogenase) is completely specific; therefore, use diagnostic immunohistochemistry testing in conjunction with morphologic and clinical findings. Also, obtain a urinalysis to exclude other possible causes of abdominal/pelvic pain, such as urinary tract infections or kidney stones.

Imaging studies

Routine imaging is not required in all patients in whom ovarian cancer is highly suggested. In cases in which the diagnosis is uncertain, consider the following imaging studies:

  • Pelvic ultrasonography [4, 5] : Warranted
  • Pelvic and abdominal computed tomography (CT) scanning [4, 5] : Warranted
  • Pelvic and abdominal magnetic resonance imaging: Increases specificity of imaging when sonography findings are indeterminate [6]
  • Chest radiography: Routine imaging to exclude lung metastases
  • Mammography: Part of preoperative workup for women older than 40 years who have not had one in the preceding 6-12 months; estrogen-producing tumors may increase the risk of breast malignancies, and breast cancers can metastasize to the ovaries and are often bilateral

In patients with diffuse carcinomatosis and GI symptoms, a GI tract workup may be indicated, including one of the following imaging studies:

  • Upper and/or lower endoscopy
  • Barium enema
  • Upper GI series

Procedures

Fine-needle aspiration (FNA) or percutaneous biopsy of an adnexal mass is not routinely recommended, as it may delay diagnosis and treatment of ovarian cancer. Instead, if a clinical suggestion of ovarian cancer is present, the patient should undergo laparoscopic evaluation or  laparotomy, based on the presentation,  for diagnosis and staging. An FNA or diagnostic paracentesis should be performed in patients with diffuse carcinomatosis or ascites without an obvious ovarian mass.

See Workup for more detail.

Management

Standard treatment for women with ovarian cancer involves aggressive debulking surgery and chemotherapy. The aim of cytoreductive surgery is to confirm the diagnosis, define the extent of disease, and resect all visible tumor.  Neoadjuvant chemotherapy is increasingly used. 

Surgery

The type of procedure depends on whether or not disease is visible outside the ovaries. When no disease is visible outside the ovaries, or no lesion greater than 2 cm is present outside of the pelvis, the patient requires formal surgical staging, including peritoneal cytology, multiple peritoneal biopsies, omentectomy, pelvic and para-aortic lymph node sampling, and biopsies of the diaphragmatic peritoneum.

If disease greater than 2 cm is noted then aggressive surgical debulking, with the intent to remove all visible diseaes should be undertaken. If the surgeon determines that optimal debulking is not possible, then neoadjuvant chemotherapy should be considered. For patients with stage IV disease, surgery should be individualized on the basis of presentation.

Surgical procedures that may be performed in women with ovarian cancer are as follows:

  • Surgical staging
  • Cytoreductive surgery
  • Interval debulking
  • Laparoscopic surgery
  • Secondary surgery

Chemotherapy

Postoperative chemotherapy is indicated in all patients with ovarian cancer, except those who have surgical-pathologic stage I disease with low-risk characteristics. Standard postoperative chemotherapy for ovarian cancer is combination therapy with a platinum compound and a taxane (eg, carboplatin and paclitaxel). Additional agents for recurrent disease include the following:

  • Liposomal doxorubicin
  • Etoposide
  • Topotecan
  • Gemcitabine
  • Vinorelbine
  • Ifosfamide
  • Fluorouracil
  • Melphalan
  • Altretamine
  • Bevacizumab
  • Olaparib

Adjunctive medications include the following:

  • Cytoprotective agents (eg, mesna)
  • Antiemetics (eg, ondansetron, granisetron, palonosetron, dexamethasone)

See Treatment and Medication for more detail.

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Background

Malignant lesions of the ovaries include primary lesions arising from normal structures within the ovary and secondary lesions from cancers arising elsewhere in the body. Primary lesions include epithelial ovarian carcinoma (70% of all ovarian malignancies), germ-cell tumors, sex-cord stromal tumors, and other more rare types. Metastases to the ovaries are relatively frequent, with the most common being from the endometrium, breast, colon, stomach, and cervix.

Although many histologic types of ovarian tumors have been described, more than 90% of ovarian malignancies are epithelial tumors. Many of these actually originate in the fallopian tubes. (See Pathophysiology.)

The precise cause of ovarian cancer is unknown. However, several risk and contributing factors (including both reproductive and genetic factors) have been identified. (See Etiology.)

Ovarian cancer is the most common cause of cancer death from gynecologic tumors in the United States. Around the world, more than 200,000 women are estimated to develop ovarian cancer every year and about 100,000 die from the disease. The lifetime risk of a woman developing epithelial ovarian cancer is 1 in 70. (See Epidemiology.)

Early disease causes minimal, nonspecific, or no symptoms. Therefore, most cases are diagnosed in an advanced stage. Prognosis in ovarian cancer is closely related to the stage at diagnosis; thus, overall, prognosis for these patients remains poor. (See Presentation and Prognosis.)

Standard treatment involves aggressive debulking surgery followed by chemotherapy. The incorporation of neoadjuvant chemotherapy has recently increased, with multiple studies indicating that in some situations it offers an improvement in morbidity and possibly survival.(See Treatment and Medication.)

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Pathophysiology

Historically, most theories of the pathophysiology of ovarian cancer included the concept that it begins with the dedifferentiation of the cells overlying the ovary. During ovulation, these cells can be incorporated into the ovary, where they then proliferate. However, new evidence indicates that the majority of these tumors actually originate in the fimbria of the fallopian tube. Detailed pathologic studies have pushed much of the thinking about the origin of these tumors in this direction.[7]  

Ovarian cancer typically spreads to the peritoneal surfaces and omentum. Spread can occur by local extension, lymphatic invasion, intraperitoneal implantation, hematogenous dissemination, or transdiaphragmatic passage. Intraperitoneal dissemination is the most common and recognized characteristic of ovarian cancer. Malignant cells can implant anywhere in the peritoneal cavity but are more likely to implant in sites of stasis along the peritoneal fluid circulation.

These mechanisms of dissemination represent the rationale to conduct surgical staging, debulking surgery, and intraperitoneal administration of chemotherapy. In contrast, hematogenous spread is clinically unusual early on in the disease process, although it is not infrequent in patients with advanced disease.

Epithelial tumors represent the most common histology (90%) of ovarian tumors. Other histologies include the following:

  • Sex-cord stromal tumors
  • Germ cell tumors
  • Primary peritoneal carcinoma
  • Metastatic tumors of the ovary

Epithelial ovarian cancer

Epithelial ovarian cancer is thought to arise from epithelium covering the fimbria of the fallopian tubes, or the ovaries, both of which are derived from the coelomic epithelium in fetal development. This coelomic epithelium is also involved in formation of the müllerian ducts, from which the fallopian tubes, uterus, cervix, and upper vagina develop.

Four main histologic subtypes, which are similar to carcinoma, arise in the epithelial lining of the cervix, uterus, and fallopian tube, as follows:

  • Serous (from fallopian tube)
  • Endometrioid (endometrium)
  • Mucinous (cervix)
  • Clear cell (mesonephros)

Some variation is observed in the patterns of spread and disease distribution within the various histologic subtypes.

Epithelial tumors are found as partially cystic lesions with solid components. The surface may be smooth or covered in papillary projections (see the image below), and the cysts contain fluid ranging from straw-colored to opaque brown or hemorrhagic.

An enlarged ovary with a papillary serous carcinom An enlarged ovary with a papillary serous carcinoma on the surface.

Epithelial ovarian cancer most often spreads initially within the peritoneal cavity (see the image below). Metastatic disease often is found on the peritoneal surfaces, particularly on the undersurface of the diaphragms, the paracolic gutters, the bladder, and the cul-de-sac. Other common sites are as follows:

  • Surface of the liver
  • Mesentery and serosa of the large and small bowel
  • Omentum
  • Uterus
  • Para-aortic and pelvic lymph nodes
Metastases from epithelial ovarian carcinoma invol Metastases from epithelial ovarian carcinoma involving the omentum.

Outside the peritoneal cavity, epithelial ovarian cancer may spread to the pleural cavity, lungs, and groin lymph nodes. The presence of pleural effusion does not necessarily indicate disease in the chest, and malignancy can be diagnosed only cytologically. Mucinous tumors tend to form large dominant masses, while papillary serous tumors have a more diffuse distribution and are more commonly bilateral. Endometrioid and clear-cell variants more commonly exhibit local invasion, retroperitoneal disease, and hepatic metastases.

Increasing evidence suggests that a high proportion of high-grade serous carcinoma originates from distal fallopian tube epithelium or the tuboperitoneal junction rather than the ovarian surface epithelium. Serous intraepithelial or early invasive carcinoma has been found in up to 10% of fallopian tubes from BRCA mutation carriers who had undergone prophylactic bilateral salpingo-oophorectomies. Clinical, molecular, and genetic studies, as well as in vitro and animal models, have also supported a tubal origin for high-grade serous ovarian carcinoma.[7, 8]

Those findings have prompted the suggestion that prevention of ovarian cancer in selected women at high risk could be better accomplished with salpingectomy. A study comparing standard risk-reducing salpingo-oophorectomy with the combination of early risk-reducing salpingectomy and delayed oophorectomy in BRCA carriers is currently recruiting participants.[9]

Tumors of low malignant potential

Tumors of low malignant potential (LMP), or borderline tumors, are a distinct variety of epithelial ovarian cancer that behave in a much less aggressive fashion and have a very favorable prognosis. These tumors cause great anxiety to patients, and the concept of LMP sometimes is difficult to explain. They comprise approximately 20% of malignant ovarian tumors. The mean age of diagnosis is younger than for invasive epithelial ovarian cancer, at approximately 48 years, and no large peak of incidence is observed.

These tumors are staged identically to epithelial ovarian cancer, using the FIGO (Fédération Internationale de Gynécologie et d'Obstétrique; International Federation of Obstetrics and Gynecology) system. In contrast to epithelial ovarian cancer, however, most LMP tumors are stage I at presentation, with a distribution as follows:

  • Stage IA: 51%
  • Stage IB: 6%
  • Stage IC: 18%
  • Stages II-III: 15%
  • Stage IV: 2%

LMP tumors can cause a range of symptoms similar to epithelial ovarian cancer, including increasing abdominal girth, an abdominal mass, abdominal pain, abnormal uterine bleeding, urinary symptoms, and gastrointestinal symptoms. They may be asymptomatic and found on routine physical examination or ultrasound scan.

For more information, see Borderline Ovarian Cancer.

Malignant germ cell tumors

Malignant germ cell tumors (GCTs), which include dysgerminoma, endodermal sinus tumor, malignant teratoma, embryonal carcinoma, and choriocarcinoma, are thought to derive from primitive germ cells in the embryonic gonad. GCT of the ovary is much rarer than GCT of the testis in males, and much of the development of the management approach has been based on experience with male GCT.

Common characteristics of these tumors include rapid growth, a predilection for lymphatic spread, frequent mixtures of tumor types, and a predominantly unilateral pattern of ovarian involvement (except for dysgerminoma). GCT is much more common in young women but occasionally occurs in infants and older women.

Many GCTs produce tumor markers that can be measured in the blood and then used to monitor response to treatment and for follow-up care. Endodermal sinus tumors secrete alpha-fetoprotein and choriocarcinoma, and dysgerminomas occasionally secrete beta human chorionic gonadotropin (bHCG). Dysgerminoma may secrete lactate dehydrogenase and placental alkaline phosphatase.

No factors have been established related to etiology, apart from an increased incidence associated with dysgenetic gonads.

Although these tumors may be asymptomatic and present as a palpable mass, many patients present with abdominal pain. The mass may lead to acute pain due to torsion, rupture, or hemorrhage, or, patients may have abdominal distension, vaginal bleeding, or fever.

Most are stage I and confined to the ovary at the time of diagnosis.

Dysgerminoma

This is the most common malignant GCT and represents 3-5% of all ovarian malignancies. Ninety percent occur in people younger than 30 years, and 75% occur in the second and third decades, with a median age of 22 years.

Dysgerminomas are bilateral in 10-35% of cases. Five percent occur in phenotypic females with abnormal gonads. They may have a 46XY karyotype with pure gonadal dysgenesis or androgen insensitivity syndrome, or, they may have a 45X, 46XY karyotype with mixed gonadal dysgenesis. Dysgerminomas may be large and usually are solid, with a smooth external surface and a fleshy pink-tan color inside. The majority are confined to the ovary at diagnosis, but approximately 25% of otherwise stage I dysgerminomas have lymph node metastasis.

For more information, see Ovarian Dysgerminomas.

Cystic teratoma

Teratomas are germ cell tumors commonly composed of multiple cell types derived from one or more of the 3 germ layers. Inconsistent nomenclature often confuses discussions of various subtypes of teratomas. The word is derived from the Greek teras, meaning monster, which Virchow coined in the first edition of his book on tumors published in 1863.[10] Teratomas range from benign, well-differentiated (mature) cystic lesions to those that are solid and malignant (immature). Additionally, teratomas may be monodermal and highly specialized. Rarely, within some mature teratomas certain elements (most commonly squamous components) undergo malignant transformation.

In 1831, Leblanc coined the term dermoid cyst in the veterinary literature when he removed a lesion that resembled skin at the base of a horse's skull, which he called a “kyste dermoid.”[11] Both dermoid and teratoma, terms now more than a century old, remain in general use and often are used interchangeably with various preferences among subspecialties. The earliest implications were that dermoids comprised elements similar to skin and its appendages, whereas teratomas had no such limits. Dermoids now are recognized as often being trigeminal and containing practically any type of tissue.

For those who continue to make a distinction, dermoids are tumors that maintain rather orderly arrangements, with well-differentiated ectodermal and mesodermal tissues surrounding endodermal components. Teratomas, specifically solid teratomas, are essentially devoid of organization; thus, the presence of some degree of organization, a high degree of cellular differentiation, and cystic structure differentiates dermoids from teratomas (see the images below).[10]

Mature cystic teratoma of the ovary exhibiting mul Mature cystic teratoma of the ovary exhibiting multiple tissue types.
Mature cystic teratoma of the ovary with hair, seb Mature cystic teratoma of the ovary with hair, sebaceous material, and thyroid tissue.

For more information, see Teratoma, Cystic.

Immature teratoma

This is the second most common GCT. It occurs mostly in females aged 10-20 years but may occur after menopause. The tumor spreads most commonly to peritoneal surfaces.

Other germ cell tumors

Endodermal sinus tumor occurs at a mean age of 18 years, and one third occur before puberty. Embryonal carcinoma and choriocarcinoma are extremely rare.

Sex-cord stromal tumors

These include tumors arising from the sex cords; granulosa cells; Sertoli cells; and the specialized stroma of the genital ridge, theca, and Leydig cells. They comprise fewer than 5% of all ovarian tumors.

Although granulosa cell tumors are malignant and Sertoli-Leydig cell tumors less so, they behave in a much less malignant fashion than epithelial ovarian cancers. Benign tumors in the group include thecoma and fibroma. Granulosa cell tumors and pure Sertoli cell tumors commonly secrete estrogen, while Leydig cell tumors and combined Sertoli-Leydig tumors often secrete androgens.

Granulosa cell tumor

This is the most common malignant sex-cord stromal tumor. Ninety percent of granulosa cell tumors are stage I at the time of diagnosis. This tumor account for approximately 2% of all ovarian tumors and can be divided into adult (95%) and juvenile (5%) types based on histologic findings. Juvenile granulosa cell tumor is a variant of granulosa cell tumor that is rarely malignant. It most often presents in young girls with isosexual precocious puberty. The tumor is usually unilateral and confined to the ovary and can be managed with surgery alone.

Granulosa cell tumor can occur at any age, with a mean age of the early 50s. Because of the secretion of estrogen, the presenting features depend on the patient's age. Prepubertal girls typically present with precocious sexual development, women of reproductive age have heavy or irregular periods, and postmenopausal women may have postmenopausal bleeding. At all ages, the tumor may present with acute abdominal pain due to rupture or hemorrhage.

The tumors vary in size and may be solid or partially cystic (see the image below).

Granulosa cell tumor excised from a woman aged 44 Granulosa cell tumor excised from a woman aged 44 years. Note the yellowish tumor that has eroded through, onto the surface of the ovary.

The cut surface may be gray-white or yellow, depending on lipid content. Necrosis and hemorrhage often are present, with cystic compartments filled with fluid or clotted blood (see the image below).

This photo shows a granulosa cell tumor, with the This photo shows a granulosa cell tumor, with the cut surface showing classic features of a hemorrhagic cyst and yellowish solid component.

The microscopic features are granulosa cells in a wide variety of patterns, and characteristic Call-Exner bodies may be present.

For more information, see Granulosa-Theca Cell Tumors.

Sertoli-Leydig cell tumor

These tumors are rare. They are a form of low-grade malignancy that typically produces androgens and rarely estrogens.

Other rare tumors

Small-cell carcinoma is a rare type of carcinoma that occurs in females aged 2-46 years. It often is associated with hypercalcemia.

The most common form of sarcoma in the ovary is the mixed mesodermal sarcoma or carcinosarcoma.

Metastatic tumors of the ovary arise from direct extension and spread within the bloodstream or lymphatic system or within the peritoneal cavity. Sites of origin include the endometrium; cervix; and nongynecologic sites such as breast, colon, and stomach. The classic Krukenberg tumor refers to bilateral enlargement of the ovaries from metastases from a signet-ring carcinoma of the stomach.

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Etiology

The precise cause of ovarian cancer is unknown, but several risk and contributing factors have been identified.

Hippisley-Cox and Coupland developed an algorithm to determine risk of ovarian cancer in women with and without symptoms.[12] In their cohort study, 10% of women with the highest predicted risk had 63% of all ovarian cancers diagnosed over the next 2 years.

Reproductive factors

Parity is an important risk factor. The risk of epithelial ovarian cancer is increased in women who have not had children and possibly those with early menarche or late menopause. Women who have been pregnant have a 50% decreased risk for developing ovarian cancer compared with nulliparous women. Multiple pregnancies offer an increasingly protective effect. Oral contraceptive use decreases the risk of ovarian cancer significantly.

These factors support the idea that risk for ovarian cancer is related to ovulation. Two theories regarding this relationship have been proposed. The incessant ovulation theory suggests that repeated ovarian epithelial trauma caused by follicular rupture and subsequent epithelial repair results in genetic alterations within the surface epithelium. The gonadotropin theory proposes that persistent stimulation of the ovaries by gonadotropins, coupled with local effects of endogenous hormones, increases surface epithelial proliferation and subsequent mitotic activity.

Thus, the probability of ovarian cancer may be related to the number of ovulatory cycles, and conditions that suppress the ovulatory cycle may play a protective role. Ovulation suppression has been shown to decrease cancer incidence. Although treatment with agents that induce ovulation in women with infertility has been suggested to increase the incidence of epithelial ovarian cancer, this is unproven.

Genetic factors

Family history plays an important role in the risk of developing ovarian cancer. The lifetime risk for developing ovarian cancer is 1.6% in the general population. This compares with a 4-5% risk when 1 first-degree family member is affected, rising to 7% when 2 relatives are affected. From 5-10% of cases of ovarian cancer occur in an individual with a family history of the disease. Only a small percentage of these patients have an inherited genetic abnormality, and the risk of this occurrence increases with the strength of the family history. Hereditary epithelial ovarian cancer occurs at a younger age (approximately 10 years younger) than nonhereditary epithelial ovarian cancer, but the prognosis may be somewhat better.

Integrated genomic analyses by the Cancer Genome Atlas Research Network have revealed high-grade serous ovarian cancer is characterized by TP53 mutations in almost all tumors. The findings also include the low prevalence but statistically recurrent somatic mutations in 9 further genes, including NF1, BRCA1, BRCA2, RB1, and CDK12, along with 113 significant focal DNA copy number aberrations and promoter methylation events involving 168 genes. Pathway analyses revealed defective homologous recombination in about half of all tumors, and that NOTCH and FOXM1 signaling are involved in serous ovarian cancer pathophysiology.[13]

Evidence from the Cancer Genome Atlas Network showed that serous ovarian tumors and breast basal-like tumors shared a number of molecular characteristics, such as the types and frequencies of genomic mutations, suggesting that ovarian and breast cancer may have a related etiology and potentially similar responsiveness to some of the same therapies.[14]

At least two syndromes of hereditary ovarian cancer are clearly identified, involving either (1) disorders of the genes associated with breast cancer, BRCA1 and BRCA2, or (2) more rarely, genes within the Lynch II syndrome complex. Breast/ovarian cancer syndrome is associated with early onset of breast or ovarian cancer. Inheritance follows an autosomal dominant transmission. It can be inherited from either parent.

Most cases are related to the BRCA1 gene mutation. BRCA1 is a tumor suppressor gene that inhibits cell growth when functioning properly; the inheritance of mutant alleles of BRCA1 leads to a considerable increase in risk for developing ovarian cancer.

Approximately 1 person in 4000 in the general population carries a mutation of BRCA1. Some populations have a much higher rate of BRCA1 and BRCA2 mutations, especially Ashkenazi Jews. In families with 2 first-degree relatives (mother, sister, or daughter) with premenopausal epithelial ovarian cancer, the likelihood of a female relative having an affected BRCA1 or BRCA2 gene is as high as 40%. The probability is much lower when the disease occurs in relatives postmenopausally.

Individuals with a BRCA1 gene mutation have a 50-85% lifetime risk of developing breast cancer and a 15-45% risk of developing epithelial ovarian cancer. Those with a BRCA2 gene mutation have a 50-85% lifetime risk of developing breast cancer and a 10-20% risk of developing epithelial ovarian cancer. Families with BRCA2 mutations are at risk for developing cancer of the prostate, larynx, pancreas, and male breast.

Germline mutations in the BRCA1 and BRCA2 genes are associated with increased risks of breast and ovarian cancers; however, in an investigation of a common genetic variation at the 9p22.2 locus, a decreased risk of ovarian cancer was noted in carriers of a BRCA1 or BRCA2 mutation.[15]

Families with Lynch II syndrome or hereditary nonpolyposis colorectal cancer are characterized by a high risk for developing colorectal, endometrial, stomach, small bowel, breast, pancreas, and ovarian cancers. This syndrome is caused by mutations in the mismatch repair genes. Mutations have been demonstrated in mismatch repair genes MSH2, MLH1, PMS1, and PMS2.

Women with a history of breast cancer have an increased risk of epithelial ovarian cancer.

In a study by Rafner et al, whole-genome sequencing identified a rare mutation in BRIP1, which behaves like a classical tumor suppressor gene in ovarian cancer.[16] This allele was also associated with breast cancer.

Previous hormone therapy

A nationwide prospective cohort study over 10 years that included all Danish women aged 50-79 years concluded that risk for ovarian cancer is increased with hormone therapy, regardless of duration of use, formulation, estrogen dose, regimen, progestin type, and administration route.[17] Nearly 1 million women without hormone-sensitive cancer or bilateral oophorectomy were followed. In an average of 8 years of follow-up, 3068 ovarian cancers were detected, of which 2681 were epithelial cancers.

Current users of hormones had incidence rate ratios for all ovarian cancers of 1.38 (95% confidence interval [CI], 11.26-1.51) compared with women who never took hormone therapy. Risk declined as years since last hormone use increased. Incidence rates in current and never users of hormones were 0.52 and 0.40 per 1000 years, respectively. This translates to approximately one extra ovarian cancer for approximately 8300 women taking hormone therapy each year.

Other factors

The use of talcum powder on the vulva and perineum may be associated with increased risk of epithelial ovarian cancer.[18] High lactose consumption has been associated with increased risk of ovarian cancer, but evidence linking lactose and specific dairy products with ovarian cancer remains contradictory.[19, 20]

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Epidemiology

In the United States, the incidence of ovarian cancer is 12.1 per 100,000 women per year, based on 2008-2012 cases.[21] The incidence of ovarian cancer has been slowly decreasing since the mid-1980s; it decreased by 0.9% per year from 2007 to 2011.[22] Ovarian cancer is more common in whites than in African Americans (12.8 versus 9.8 cases per 100,000 women per year, respectively).[21]

Epithelial ovarian cancer can occur in girls as young as 15 years, but the mean age at diagnosis is 63 years, and most cases are diagnosed in women 55-64 years of age. In the United States, the estimated lifetime risk is 1.3%.[21]

The American Cancer Society estimates that 22,280 new cases of ovarian cancer will be diagnosed in 2016 and 14,240 women will die from the disease.[22] Although ovarian cancer is the 17th most common cancer in women, it is the fifth most common cause of cancer death in woman, accounting for 5% of cancer deaths—more than any other gynecologic cancer.[22, 21] From 2007 to 2011, the death rate from ovarian cancer decreased by 2.0% per year in white women and was stable in black women.[22]

International statistics

Internationally, the incidence ranges from 3.1 cases per 100,000 women in Japan to 21 cases per 100,000 women in Sweden. Around the world, more than 200,000 women are estimated to develop ovarian cancer every year and about 100,000 die from the disease.

Epithelial ovarian cancer occurs most commonly in white women in the industrialized countries of northern and western Europe and North America and least commonly in India and Asia. Asian women have low risk unless they relocate to North America or Europe. Scandinavian and Norwegian women have the highest risk.

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Prognosis

Although the 5-year survival rate for ovarian cancer has improved significantly in the past 30 years, the prognosis for ovarian cancer remains poor overall, with a 46% 5-year survival rate. The prognosis of ovarian cancer is closely related to the stage at diagnosis,[23, 24] as determined according to the staging system developed by the International Federation of Gynecology and Obstetrics (FIGO). (See Staging.) Approximately 20%, 5%, 58%, and 17% of women present with stage I, II, III, and IV, respectively.

The 5-year survival rates (rounded to the nearest whole number) for epithelial ovarian carcinoma by FIGO stage are as follows:

  • Stage IA - 87%
  • Stage IB - 71%
  • Stage IC - 79%
  • Stage IIA - 67%
  • Stage IIB - 55%
  • Stage IIC - 57%
  • Stage IIIA - 41%
  • Stage IIIB - 25%
  • Stage IIIC - 23%
  • Stage IV - 11%
  • Overall survival rate – 46%

Bakhru et al found poorer survival among patients with ovarian cancer and diabetes. Although the underlying reason for this association is unknown, further studies are needed.[25]

Among women with high-grade serous ovarian cancer, BRCA2 mutation but not BRCA1 deficiency was associated with improved survival, improved chemotherapy response, and genome instability compared with BRCA wild-type.[26]

A study by Bolton et al found improved 5-year overall survival among carriers of BRCA1 or BRCA2, with BRCA1 having the best prognosis.[27]

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Prognosis of Tumors of Low Malignant Potential

Overall survival rate at 5 years according to FIGO is shown below. Others have reported better survival rates with 5-year, 10-year, 15-year, and 20-year survival for patients with serous LMP as 97%, 95%, 92%, and 89%, respectively.

Five-year-survival rate for LMP tumors by FIGO stage (survival percentages rounded to nearest whole number) are as follows:

  • Stage IA - 93%
  • Stage IB - 90%
  • Stage IC - 91%
  • Stage IIA - 88%
  • Stage IIB - 86%
  • Stage IIC - 100%
  • Stage IIIA - 29%
  • Stage IIIB - 75%
  • Stage IIIC - 62%
  • Stage IV - 30%
  • Overall survival rate - 86%
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Patient Education

For patient education resources, see the Cancer Center and the Women's Health Center. Also, see the patient education articles Ovarian Cancer and Ovarian Cysts.

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Contributor Information and Disclosures
Author

Andrew E Green, MD Consulting Staff, Northeast Georgia Medical Center

Andrew E Green, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, Society of Gynecologic Oncology, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Coauthor(s)

Agustin A Garcia, MD Associate Professor of Medicine, University of Southern California Keck School of Medicine

Agustin A Garcia, MD is a member of the following medical societies: European Society for Medical Oncology, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Samina Ahmed, MD Fellow, Division of Oncology, Department of Medicine, University of Southern California, Keck School of Medicine

Samina Ahmed, MD is a member of the following medical societies: American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Chief Editor

from Memorial Sloan-Kettering - Yukio Sonoda, MD Associate Professor, Weill Cornell Medical College; Associate Attending Surgeon, Gynecology Service, Department of Surgery, Memorial Hospital for Cancer and Allied Diseases; Associate Member, Memorial Sloan-Kettering Cancer Center

from Memorial Sloan-Kettering - Yukio Sonoda, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Surgeons, American Medical Association, Society of Gynecologic Oncology, Society of Laparoendoscopic Surgeons, AAGL, American Society of Clinical Oncology, International Gynecologic Cancer Society, Japanese Medical Society of America, Korean American Medical Assocation

Disclosure: Nothing to disclose.

Acknowledgements

Robert P Edwards, MD Professor, Department of Obstetrics, Gynecology, and Reproductive Science, University of Pittsburgh; Vice-Chair, Clinical Affairs, Director, Ovarian Cancer Center of Excellence, Magee-Womens Hospital of University of Pittsburgh

Robert P Edwards, MD is a member of the following medical societies: American Association for Cancer Research, American College of Obstetricians and Gynecologists, American College of Surgeons, American Medical Association, and Society for Gynecologic Investigation

Disclosure: Nothing to disclose.

C William Helm, MB, BCh, MA, FRCS(Edin), FRCS Professor, Division of Gynecologic Oncology, Saint Louis University School of Medicine

C William Helm, MB, BCh, MA, FRCS(Edin), FRCS is a member of the following medical societies: American College of Obstetricians and Gynecologists, European Society of Gynaecologic Oncology, and International Gynecologic Cancer Society

Disclosure: ThermaSolutions, Inc Grant/research funds Research Registry of patients treated with hyperthemic intraperitoneal chemotherapy; Sanofi-Aventis, Inc Grant/research funds Support for and investigator initiated research study of HIPEC for consolidation in ovarian cancer; ThermaSolutions, Inc Honoraria Speaking and teaching; UpToDate Royalty Online Text Book Chapters; Genzyme, Inc Honoraria Speaking and teaching

Warner K Huh, MD Professor, Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Senior Scientist, Comprehensive Cancer Center, University of Alabama School of Medicine

Warner K Huh, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Surgeons, American Society of Clinical Oncology, Massachusetts Medical Society, and Society of Gynecologist Oncologists

Disclosure: MERCK Consulting fee Consulting; ROCHE PHARMA/DIAGNOSTICS Consulting fee Consulting; INTUITIVE SURGICAL Proctor Fee Consulting; Qiagen Consulting fee Consulting

Karen Loeb Lifford, MD Director of General Gynecology, Associate Program Director, Department of Obstetrics and Gynecology, Instructor, Brigham and Women's Hospital, Harvard Medical School

Karen Loeb Lifford, MD is a member of the following medical societies: Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Michel E Rivlin, MD Professor, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine

Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Goff BA, Mandel LS, Drescher CW, Urban N, Gough S, Schurman KM, et al. Development of an ovarian cancer symptom index: possibilities for earlier detection. Cancer. 2007 Jan 15. 109(2):221-7. [Medline].

  2. Ryerson AB, Eheman C, Burton J, McCall N, Blackman D, Subramanian S, et al. Symptoms, diagnoses, and time to key diagnostic procedures among older U.S. women with ovarian cancer. Obstet Gynecol. 2007 May. 109(5):1053-61. [Medline].

  3. [Guideline] Moyer VA. Screening for ovarian cancer: U.S. Preventive Services Task Force reaffirmation recommendation statement. Ann Intern Med. 2012 Dec 18. 157(12):900-4. [Medline]. [Full Text].

  4. Fleischer A. Ovarian cancer. Fleischer AC, Javitt MC, Jeffrey RB Jr, et al. Clinical Gynecologic Imaging. Philadelphia, Pa: Lippincott Williams & Wilkins; 1996. 107.

  5. Yazbek J, Raju SK, Ben-Nagi J, Holland TK, Hillaby K, Jurkovic D. Effect of quality of gynaecological ultrasonography on management of patients with suspected ovarian cancer: a randomised controlled trial. Lancet Oncol. 2008 Feb. 9(2):124-31. [Medline].

  6. Iyer VR, Lee SI. MRI, CT, and PET/CT for ovarian cancer detection and adnexal lesion characterization. AJR Am J Roentgenol. 2010 Feb. 194(2):311-21. [Medline].

  7. Reade CJ, McVey RM, Tone AA, Finlayson SJ, McAlpine JN, Fung-Kee-Fung M, et al. The fallopian tube as the origin of high grade serous ovarian cancer: review of a paradigm shift. J Obstet Gynaecol Can. 2014 Feb. 36 (2):133-40. [Medline].

  8. Gharwan H, Bunch KP, Annunziata CM. The role of reproductive hormones in epithelial ovarian carcinogenesis. Endocr Relat Cancer. 2015 Dec. 22 (6):R339-63. [Medline].

  9. Harmsen MG, Arts-de Jong M, Hoogerbrugge N, Maas AH, Prins JB, Bulten J, et al. Early salpingectomy (TUbectomy) with delayed oophorectomy to improve quality of life as alternative for risk-reducing salpingo-oophorectomy in BRCA1/2 mutation carriers (TUBA study): a prospective non-randomised multicentre study. BMC Cancer. 2015 Aug 19. 15:593. [Medline].

  10. Pantoja E, Noy MA, Axtmayer RW, Colon FE, Pelegrina I. Ovarian dermoids and their complications. Comprehensive historical review. Obstet Gynecol Surv. 1975 Jan. 30(1):1-20. [Medline].

  11. Comerci JT Jr, Licciardi F, Bergh PA, Gregori C, Breen JL. Mature cystic teratoma: a clinicopathologic evaluation of 517 cases and review of the literature. Obstet Gynecol. 1994 Jul. 84(1):22-8. [Medline].

  12. Hippisley-Cox J, Coupland C. Identifying women with suspected ovarian cancer in primary care: derivation and validation of algorithm. BMJ. 2011 Jan 4. 344:d8009. [Medline]. [Full Text].

  13. Integrated genomic analyses of ovarian carcinoma. Nature. 2011 Jun 29. 474(7353):609-15. [Medline].

  14. Koboldt DC, Fulton RS, McLellan MD, Schmidt H, Kalicki-Veizer J, McMichael JF, et al. Comprehensive molecular portraits of human breast tumours. Nature. 2012 Sep 23. [Medline].

  15. Ramus SJ, Kartsonaki C, Gayther SA, Pharoah PD, Sinilnikova OM, Beesley J, et al. Genetic Variation at 9p22.2 and Ovarian Cancer Risk for BRCA1 and BRCA2 Mutation Carriers. J Natl Cancer Inst. 2011 Jan 19. 103(2):105-116. [Medline].

  16. Rafnar T, Gudbjartsson DF, Sulem P, et al. Mutations in BRIP1 confer high risk of ovarian cancer. Nat Genet. 2011 Oct 2. 43(11):1104-7. [Medline].

  17. Mørch LS, Løkkegaard E, Andreasen AH, Krüger-Kjaer S, Lidegaard O. Hormone therapy and ovarian cancer. JAMA. 2009 Jul 15. 302(3):298-305. [Medline].

  18. Cramer DW, Vitonis AF, Terry KL, Welch WR, Titus LJ. The Association Between Talc Use and Ovarian Cancer: A Retrospective Case-Control Study in Two US States. Epidemiology. 2016 May. 27 (3):334-46. [Medline].

  19. Genkinger JM, Hunter DJ, Spiegelman D, Anderson KE, Arslan A, et al. Dairy products and ovarian cancer: a pooled analysis of 12 cohort studies. Cancer Epidemiol Biomarkers Prev. 2006 Feb. 15 (2):364-72. [Medline].

  20. Liu J, Tang W, Sang L, Dai X, Wei D, Luo Y, et al. Milk, yogurt, and lactose intake and ovarian cancer risk: a meta-analysis. Nutr Cancer. 2015. 67 (1):68-72. [Medline].

  21. Surveillance, Epidemiology, and End Results Program. SEER Stat Fact Sheets: Ovary Cancer. National Cancer Institute. Available at http://seer.cancer.gov/statfacts/html/ovary.html. Accessed: March 21, 2016.

  22. American Cancer Society. Cancer Facts & Figures 2016. American Cancer Society. Available at http://www.cancer.org/acs/groups/content/@research/documents/document/acspc-047079.pdf. Accessed: March 21, 2016.

  23. Chan JK, Teoh D, Hu JM, Shin JY, Osann K, Kapp DS. Do clear cell ovarian carcinomas have poorer prognosis compared to other epithelial cell types? A study of 1411 clear cell ovarian cancers. Gynecol Oncol. 2008 Jun. 109(3):370-6. [Medline].

  24. Woodward ER, Sleightholme HV, Considine AM, Williamson S, McHugo JM, Cruger DG. Annual surveillance by CA125 and transvaginal ultrasound for ovarian cancer in both high-risk and population risk women is ineffective. BJOG. 2007 Dec. 114(12):1500-9. [Medline].

  25. Bakhru A, Buckanovich RJ, Griggs JJ. The impact of diabetes on survival in women with ovarian cancer. Gynecol Oncol. 2011 Apr. 121(1):106-11. [Medline].

  26. Yang D, Khan S, Sun Y, et al. Association of BRCA1 and BRCA2 mutations with survival, chemotherapy sensitivity, and gene mutator phenotype in patients with ovarian cancer. JAMA. 2011 Oct 12. 306(14):1557-65. [Medline].

  27. Bolton KL, Chenevix-Trench G, Goh C, et al. Association between BRCA1 and BRCA2 mutations and survival in women with invasive epithelial ovarian cancer. JAMA. 2012 Jan 25. 307(4):382-90. [Medline].

  28. Goff BA, Mandel LS, Melancon CH, Muntz HG. Frequency of symptoms of ovarian cancer in women presenting to primary care clinics. JAMA. 2004 Jun 9. 291(22):2705-12. [Medline]. [Full Text].

  29. [Guideline] American College of Obstetricians and Gynecologists. ACOG Practice Bulletin. Management of adnexal masses. Obstet Gynecol. 2007 Jul. 110 (1):201-14. [Medline].

  30. Suh-Burgmann E, Kinney W. Potential harms outweigh benefits of indefinite monitoring of stable adnexal masses. Am J Obstet Gynecol. 2015 Dec. 213 (6):816.e1-4. [Medline].

  31. Suh-Burgmann E, Kinney W. The Value of Ultrasound Monitoring of Adnexal Masses for Early Detection of Ovarian Cancer. Front Oncol. 2016. 6:25. [Medline]. [Full Text].

  32. Anthoulakis C, Nikoloudis N. Pelvic MRI as the "gold standard" in the subsequent evaluation of ultrasound-indeterminate adnexal lesions: a systematic review. Gynecol Oncol. 2014 Mar. 132 (3):661-8. [Medline].

  33. Coleman RL, Herzog TJ, Chan DW, Munroe DG, Pappas TC, Smith A, et al. Validation of a Second-generation Multivariate Index Assay for Malignancy Risk of Adnexal Masses. Am J Obstet Gynecol. 2016 Mar 9. [Medline].

  34. [Guideline] Wright AA, Bohlke K, Armstrong DK, Bookman MA, Cliby WA, Coleman RL, et al. Neoadjuvant Chemotherapy for Newly Diagnosed, Advanced Ovarian Cancer: Society of Gynecologic Oncology and American Society of Clinical Oncology Clinical Practice Guideline. J Clin Oncol. 2016 Aug 8. [Medline]. [Full Text].

  35. [Guideline] National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology, Ovarian Cancer Including Fallopian Tube Cancer and Primary Peritoneal Cancer. Available at http://www.nccn.org/professionals/physician_gls/pdf/ovarian.pdf. Version 1.2016; Accessed: August 15, 2016.

  36. Tanaka YO, Okada S, Yagi T, Satoh T, Oki A, Tsunoda H, et al. MRI of endometriotic cysts in association with ovarian carcinoma. AJR Am J Roentgenol. 2010 Feb. 194(2):355-61. [Medline].

  37. Stany MP, Maxwell GL, Rose GS. Clinical decision making using ovarian cancer risk assessment. AJR Am J Roentgenol. 2010 Feb. 194(2):337-42. [Medline].

  38. Buys SS, Partridge E, Black A, Johnson CC, Lamerato L, Isaacs C, et al. Effect of screening on ovarian cancer mortality: the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Randomized Controlled Trial. JAMA. 2011 Jun 8. 305(22):2295-303. [Medline].

  39. Lachance JA, Choudhri AF, Sarti M, et al. A nomogram for estimating the probability of ovarian cancer. Gynecol Oncol. 2011 Apr. 121(1):2-7. [Medline].

  40. van Nagell JR Jr, Miller RW, DeSimone CP, et al. Long-term survival of women with epithelial ovarian cancer detected by ultrasonographic screening. Obstet Gynecol. 2011 Dec. 118(6):1212-21. [Medline].

  41. Hirai M, Hirai Y, Tsuchida T, et al. Stage IA Ovarian Cancers: Comparison of Sonographic Findings and Histopathologic Types Between Patients With Normal and Elevated Serum Cancer Antigen 125 Levels. J Ultrasound Med. 2011 Jul. 30(7):943-52. [Medline].

  42. Buys SS, Partridge E, Black A, et al. Effect of screening on ovarian cancer mortality: the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Randomized Controlled Trial. JAMA. 2011 Jun 8. 305(22):2295-303. [Medline].

  43. No JH, Jeon YT, Park IA, et al. Activation of mTOR signaling pathway associated with adverse prognostic factors of epithelial ovarian cancer. Gynecol Oncol. 2011 Apr. 121(1):8-12. [Medline].

  44. Tapia V, Gabler F, Munoz M, et al. Tyrosine kinase A receptor (trkA): a potential marker in epithelial ovarian cancer. Gynecol Oncol. 2011 Apr. 121(1):13-23. [Medline].

  45. Lin HW, Tu YY, Lin SY, et al. Risk of ovarian cancer in women with pelvic inflammatory disease: a population-based study. Lancet Oncol. 2011 Sep. 12(9):900-4. [Medline].

  46. Zeppernick F, Meinhold-Heerlein I. The new FIGO staging system for ovarian, fallopian tube, and primary peritoneal cancer. Arch Gynecol Obstet. 2014 Nov. 290 (5):839-42. [Medline].

  47. Lin L, Liu C, Tan H, et al. Anaesthetic technique may affect prognosis for ovarian serous adenocarcinoma: a retrospective analysis. Br J Anaesth. 2011 Jun. 106(6):814-22. [Medline].

  48. van der Burg ME, van Lent M, Buyse M, et al. The effect of debulking surgery after induction chemotherapy on the prognosis in advanced epithelial ovarian cancer. Gynecological Cancer Cooperative Group of the European Organization for Research and Treatment of Cancer. N Engl J Med. 1995 Mar 9. 332(10):629-34. [Medline].

  49. Rose PG, Nerenstone S, Brady MF, Clarke-Pearson D, Olt G, Rubin SC. Secondary surgical cytoreduction for advanced ovarian carcinoma. N Engl J Med. 2004 Dec 9. 351(24):2489-97. [Medline].

  50. Tangjitgamol S, Manusirivithaya S, Laopaiboon M, Lumbiganon P. Interval debulking surgery for advanced epithelial ovarian cancer. Cochrane Database Syst Rev. 2009 Jan 21. CD006014. [Medline].

  51. Park JY, Eom JM, Kim DY, Kim JH, Kim YM, Kim YT, et al. Secondary cytoreductive surgery in the management of platinum-sensitive recurrent epithelial ovarian cancer. J Surg Oncol. 2010 Jan 15. [Medline].

  52. Fruscio R, Garbi A, Parma G, Lissoni AA, Garavaglia D, Bonazzi CM, et al. Randomized Phase III Clinical Trial Evaluating Weekly Cisplatin for Advanced Epithelial Ovarian Cancer. J Natl Cancer Inst. 2011 Jan 7. [Medline].

  53. Katsumata N, Yasuda M, Takahashi F, Isonishi S, Jobo T, Aoki D, et al. Dose-dense paclitaxel once a week in combination with carboplatin every 3 weeks for advanced ovarian cancer: a phase 3, open-label, randomised controlled trial. Lancet. 2009 Oct 17. 374(9698):1331-8. [Medline].

  54. Katsumata N, Yasuda M, Isonishi S, et al, for the Japanese Gynecologic Oncology Group. Long-term results of dose-dense paclitaxel and carboplatin versus conventional paclitaxel and carboplatin for treatment of advanced epithelial ovarian, fallopian tube, or primary peritoneal cancer (JGOG 3016): a randomised, controlled, open-label trial. Lancet Oncol. 2013 Sep. 14(10):1020-6. [Medline].

  55. Morgan MA, Sill MW, Fujiwara K, et al. A phase I study with an expanded cohort to assess the feasibility of intraperitoneal carboplatin and intravenous paclitaxel in untreated ovarian, fallopian tube, and primary peritoneal carcinoma: A Gynecologic Oncology Group study. Gynecol Oncol. 2011 May 1. 121(2):264-8. [Medline]. [Full Text].

  56. Kurtz JE, Kaminsky MC, Floquet A, et al. Ovarian cancer in elderly patients: carboplatin and pegylated liposomal doxorubicin versus carboplatin and paclitaxel in late relapse: a Gynecologic Cancer Intergroup (GCIG) CALYPSO sub-study. Ann Oncol. 2011 Nov. 22(11):2417-23. [Medline].

  57. Winter-Roach BA, Kitchener HC, Dickinson HO. Adjuvant (post-surgery) chemotherapy for early stage epithelial ovarian cancer. Cochrane Database Syst Rev. 2009 Jan 21. CD004706. [Medline].

  58. Nelson R. Pazopanib improves PFS in advanced ovarian cancer. Medscape Medical News. June 1, 2013. Available at http://www.medscape.com/viewarticle/805168. Accessed: June 17, 2013.

  59. Du Bois A, Floquet A, Kim JW, et al. Randomized, double-blind, phase III trial of pazopanib versus placebo in women who have not progressed after first-line chemotherapy for advanced epithelial ovarian, fallopian tube, or primary peritoneal cancer (AEOC): results of an international Intergroup trial (AGO-OVAR16). Presented at the 49th Annual Meeting of the American Society of Clinical Oncology; June 1, 2013; Chicago, IL. Abstract LBA5503.

  60. Tewari D, Java JJ, Salani R, Armstrong DK, Markman M, Herzog T, et al. Long-term survival advantage and prognostic factors associated with intraperitoneal chemotherapy treatment in advanced ovarian cancer: a gynecologic oncology group study. J Clin Oncol. 2015 May 1. 33(13):1460-6. [Medline]. [Full Text].

  61. Armstrong DK, Bundy B, Wenzel L, Huang HQ, Baergen R, Lele S. Intraperitoneal cisplatin and paclitaxel in ovarian cancer. N Engl J Med. 2006 Jan 5. 354(1):34-43. [Medline].

  62. Hess LM, Benham-Hutchins M, Herzog TJ, Hsu CH, Malone DC, Skrepnek GH. A meta-analysis of the efficacy of intraperitoneal cisplatin for the front-line treatment of ovarian cancer. Int J Gynecol Cancer. 2007 May-Jun. 17(3):561-70. [Medline].

  63. Elit L, Oliver TK, Covens A, Kwon J, Fung MF, Hirte HW. Intraperitoneal chemotherapy in the first-line treatment of women with stage III epithelial ovarian cancer: a systematic review with metaanalyses. Cancer. 2007 Feb 15. 109(4):692-702. [Medline].

  64. NCI Clinical Announcement on Intraperitoneal Chemotherapy in Ovarian Cancer. National Cancer Institute. Available at http://ctep.cancer.gov/highlights/docs/clin_annc_010506.pdf.

  65. Jaaback K, Johnson N, Lawrie TA. Intraperitoneal chemotherapy for the initial management of primary epithelial ovarian cancer. Cochrane Database Syst Rev. 2011 Nov 9. 11:CD005340. [Medline].

  66. Tanner EJ, Black DR, Zivanovic O, et al. Patterns of first recurrence following adjuvant intraperitoneal chemotherapy for stage IIIC ovarian cancer. Gynecol Oncol. 2012 Jan. 124(1):59-62. [Medline].

  67. Joly F, Ray-Coquard I, Fabbro M, et al. Decreased hypersensitivity reactions with carboplatin-pegylated liposomal doxorubicin compared to carboplatin-paclitaxel combination: analysis from the GCIG CALYPSO relapsing ovarian cancer trial. Gynecol Oncol. 2011 Aug. 122(2):226-32. [Medline].

  68. Pignata S, Scambia G, Ferrandina G, et al. Carboplatin Plus Paclitaxel Versus Carboplatin Plus Pegylated Liposomal Doxorubicin As First-Line Treatment for Patients With Ovarian Cancer: The MITO-2 Randomized Phase III Trial. J Clin Oncol. 2011 Sep 20. 29(27):3628-35. [Medline].

  69. Vergote I, Tropé CG, Amant F, Kristensen GB, Ehlen T, Johnson N, et al. Neoadjuvant chemotherapy or primary surgery in stage IIIC or IV ovarian cancer. N Engl J Med. 2010 Sep 2. 363(10):943-53. [Medline].

  70. Markman M, Liu PY, Moon J, Monk BJ, Copeland L, Wilczynski S, et al. Impact on survival of 12 versus 3 monthly cycles of paclitaxel (175 mg/m2) administered to patients with advanced ovarian cancer who attained a complete response to primary platinum-paclitaxel: follow-up of a Southwest Oncology Group and Gynecologic Oncology Group phase 3 trial. Gynecol Oncol. 2009 Aug. 114(2):195-8. [Medline]. [Full Text].

  71. Parmar MK, Ledermann JA, Colombo N, du Bois A, Delaloye JF, Kristensen GB. Paclitaxel plus platinum-based chemotherapy versus conventional platinum-based chemotherapy in women with relapsed ovarian cancer: the ICON4/AGO-OVAR-2.2 trial. Lancet. 2003 Jun 21. 361(9375):2099-106. [Medline].

  72. Pfisterer J, Plante M, Vergote I, du Bois A, Hirte H, Lacave AJ. Gemcitabine plus carboplatin compared with carboplatin in patients with platinum-sensitive recurrent ovarian cancer: an intergroup trial of the AGO-OVAR, the NCIC CTG, and the EORTC GCG. J Clin Oncol. 2006 Oct 10. 24(29):4699-707. [Medline].

  73. du Bois A, Herrstedt J, Hardy-Bessard AC, Müller HH, Harter P, Kristensen G, et al. Phase III trial of carboplatin plus paclitaxel with or without gemcitabine in first-line treatment of epithelial ovarian cancer. J Clin Oncol. 2010 Sep 20. 28(27):4162-9. [Medline].

  74. Hess LM, Rong N, Monahan PO, Gupta P, Thomaskutty C, Matei D. Continued chemotherapy after complete response to primary therapy among women with advanced ovarian cancer: A meta-analysis. Cancer. 2010 Nov 15. 116(22):5251-60. [Medline].

  75. Sehouli J, Stengel D, Harter P, Kurzeder C, Belau A, Bogenrieder T, et al. Topotecan Weekly Versus Conventional 5-Day Schedule in Patients With Platinum-Resistant Ovarian Cancer: A Randomized Multicenter Phase II Trial of the North-Eastern German Society of Gynecological Oncology Ovarian Cancer Study Group. J Clin Oncol. 2010 Nov 29. [Medline].

  76. Haldar K, Gaitskell K, Bryant A, et al. Epidermal growth factor receptor blockers for the treatment of ovarian cancer. Cochrane Database Syst Rev. 2011 Oct 5. CD007927. [Medline].

  77. Bevacizumab solution in combination with Paclitaxel. U.S. Food and Drug Administration. Available at http://www.fda.gov/Drugs/InformationOnDrugs/ApprovedDrugs/ucm423159.htm. Accessed: November 25, 2014.

  78. Pujade-Lauraine E, Hilpert F, Weber B, Reuss A, Poveda A, Kristensen G, et al. Bevacizumab combined with chemotherapy for platinum-resistant recurrent ovarian cancer: The AURELIA open-label randomized phase III trial. J Clin Oncol. 2014 May 1. 32(13):1302-8. [Medline].

  79. Aghajanian C, Blank SV, Goff BA, Judson PL, Teneriello MG, Husain A, et al. OCEANS: a randomized, double-blind, placebo-controlled phase III trial of chemotherapy with or without bevacizumab in patients with platinum-sensitive recurrent epithelial ovarian, primary peritoneal, or fallopian tube cancer. J Clin Oncol. 2012 Jun 10. 30 (17):2039-45. [Medline].

  80. Aghajanian C, Goff B, Nycum LR, Wang YV, Husain A, Blank SV. Final overall survival and safety analysis of OCEANS, a phase 3 trial of chemotherapy with or without bevacizumab in patients with platinum-sensitive recurrent ovarian cancer. Gynecol Oncol. 2015 Oct. 139 (1):10-6. [Medline].

  81. Rebbeck TR, Lynch HT, Neuhausen SL, Narod SA, Van't Veer L, Garber JE. Prophylactic oophorectomy in carriers of BRCA1 or BRCA2 mutations. N Engl J Med. 2002 May 23. 346(21):1616-22. [Medline].

  82. Stone RL, Nick AM, McNeish IA, et al. Paraneoplastic thrombocytosis in ovarian cancer. N Engl J Med. 2012 Feb 16. 366(7):610-8. [Medline].

  83. Ledermann J, Harter P, Gourley C, Friedlander M, Vergote I, Rustin G, et al. Olaparib maintenance therapy in platinum-sensitive relapsed ovarian cancer. N Engl J Med. 2012 Apr 12. 366(15):1382-92. [Medline].

  84. Kaufman B, Shapira-Frommer R, Schmutzler RK, Audeh MW, Friedlander M, Balmaña J, et al. Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation. J Clin Oncol. 2015 Jan 20. 33(3):244-50. [Medline]. [Full Text].

  85. Kaye SB, Lubinski J, Matulonis U, Ang JE, Gourley C, Karlan BY, et al. Phase II, open-label, randomized, multicenter study comparing the efficacy and safety of olaparib, a poly (ADP-ribose) polymerase inhibitor, and pegylated liposomal doxorubicin in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer. J Clin Oncol. 2012 Feb 1. 30(4):372-9. [Medline]. [Full Text].

  86. Rungruang B, Miller A, Richard SD, et al. Should stage IIIC ovarian cancer be further stratified by intraperitoneal vs. retroperitoneal only disease?: a Gynecologic Oncology Group study. Gynecol Oncol. 2012 Jan. 124(1):53-8. [Medline].

  87. Daponte A, Kostopoulou E, Kollia P, Papamichali R, Vanakara P, Hadjichristodoulou C, et al. L1 (CAM) (CD171) in ovarian serous neoplasms. Eur J Gynaecol Oncol. 2008. 29(1):26-30. [Medline].

  88. [Guideline] American College of Obstetricians and Gynecologists. Elective and risk-reducing salpingo-oophorectomy. National Guideline Clearinghouse. Available at http://guideline.gov/content.aspx?id=12190. Accessed: May 11, 2015.

  89. Finch AP, Lubinski J, Møller P, Singer CF, Karlan B, Senter L, et al. Impact of Oophorectomy on Cancer Incidence and Mortality in Women With a BRCA1 or BRCA2 Mutation. J Clin Oncol. 2014 Feb 24. [Medline].

  90. Zhang S, Royer R, Li S, et al. Frequencies of BRCA1 and BRCA2 mutations among 1,342 unselected patients with invasive ovarian cancer. Gynecol Oncol. 2011 May 1. 121(2):353-7. [Medline].

  91. Burke W, Daly M, Garber J, Botkin J, Kahn MJ, Lynch P, et al. Recommendations for follow-up care of individuals with an inherited predisposition to cancer. II. BRCA1 and BRCA2. Cancer Genetics Studies Consortium. JAMA. 1997 Mar 26. 277 (12):997-1003. [Medline].

  92. [Guideline] American College of Obstetricians and Gynecologists Committee on Gynecologic Practice. Committee Opinion No. 477: the role of the obstetrician-gynecologist in the early detection of epithelial ovarian cancer. Obstet Gynecol. 2011 Mar. 117 (3):742-6. [Medline]. [Full Text].

  93. [Guideline] Moyer VA, U.S. Preventive Services Task Force. Risk assessment, genetic counseling, and genetic testing for BRCA-related cancer in women: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2014 Feb 18. 160 (4):271-81. [Medline]. [Full Text].

  94. [Guideline] National Comprehensive Cancer Network. Genetic/Familial High-Risk Assessment: Breast and Ovarian. NCCN. Available at http://www.nccn.org/professionals/physician_gls/pdf/genetics_screening.pdf. Accessed: August 20, 2016.

  95. [Guideline] Robson ME, Storm CD, Weitzel J, Wollins DS, Offit K, American Society of Clinical Oncology. American Society of Clinical Oncology policy statement update: genetic and genomic testing for cancer susceptibility. J Clin Oncol. 2010 Feb 10. 28 (5):893-901. [Medline]. [Full Text].

  96. [Guideline] Balmaña J, Díez O, Rubio IT, Cardoso F, ESMO Guidelines Working Group. BRCA in breast cancer: ESMO Clinical Practice Guidelines. Ann Oncol. 2011 Sep. 22 Suppl 6:vi31-4. [Medline]. [Full Text].

  97. [Guideline] American College of Obstetricians and Gynecologists, ACOG Committee on Practice Bulletins--Gynecology, ACOG Committee on Genetics, Society of Gynecologic Oncologists. ACOG Practice Bulletin No. 103: Hereditary breast and ovarian cancer syndrome. Obstet Gynecol. 2009 Apr. 113 (4):957-66. [Medline].

  98. [Guideline] Society of Gynecologic Oncology. SGO Clinical Practice Statement: Genetic Testing for Ovarian Cancer. SGO. Available at https://www.sgo.org/clinical-practice/guidelines/genetic-testing-for-ovarian-cancer. October 2014; Accessed: August 20, 2016.

  99. [Guideline] Society of Gynecologic Oncology. SGO Clinical Practice Statement: Salpingectomy for Ovarian Cancer Prevention. SGO. Available at https://www.sgo.org/clinical-practice/guidelines/sgo-clinical-practice-statement-salpingectomy-for-ovarian-cancer-prevention. November 2013; Accessed: August 20, 2016.

  100. Prat J, FIGO Committee on Gynecologic Oncology. Staging classification for cancer of the ovary, fallopian tube, and peritoneum. Int J Gynaecol Obstet. 2014 Jan. 124 (1):1-5. [Medline].

  101. Ovary and primary peritoneal carcinoma. Edge SB, Byrd DR, Compton CC, Fritz AG, Greene FL, Trotti A, eds. AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer-Verlag; 2010. 419-428.

  102. [Guideline] Salani R, Backes FJ, Fung MF, Holschneider CH, Parker LP, Bristow RE, et al. Posttreatment surveillance and diagnosis of recurrence in women with gynecologic malignancies: Society of Gynecologic Oncologists recommendations. Am J Obstet Gynecol. 2011 Jun. 204 (6):466-78. [Medline]. [Full Text].

  103. Hetland TE, Hellesylt E, Florenes VA, et al. Class III ß-tubulin expression in advanced-stage serous ovarian carcinoma effusions is associated with poor survival and primary chemoresistance. Hum Pathol. 2011 Jul. 42(7):1019-26. [Medline].

 
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An enlarged ovary with a papillary serous carcinoma on the surface.
Metastases from epithelial ovarian carcinoma involving the omentum.
Inside of a large, smooth-surfaced tumor replacing the ovary. Final histologic studies indicated the tumor was a mucinous carcinoma of low malignant potential. Note the multiple cysts with thick septa between. This tumor was extensively sectioned and was a mucinous carcinoma of low malignant potential.
Granulosa cell tumor excised from a woman aged 44 years. Note the yellowish tumor that has eroded through, onto the surface of the ovary.
This photo shows a granulosa cell tumor, with the cut surface showing classic features of a hemorrhagic cyst and yellowish solid component.
Mature cystic teratoma of the ovary exhibiting multiple tissue types.
Mature cystic teratoma of the ovary with hair, sebaceous material, and thyroid tissue.
Dr. Oliver Zivanovic, MD, PhD, discusses the role of hyperthermic intraperitoneal chemotherapy in ovarian cancer. Courtesy of Memorial Sloan-Kettering Cancer Center.
Dr. Oliver Zivanovic, MD, PhD, demonstrates hyperthermic intraperitoneal chemotherapy for ovarian cancer. Courtesy of Memorial Sloan-Kettering Cancer Center.
 
 
 
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