Overview of epithelial carcinoma of the ovary, fallopian tube, and peritoneum

INTRODUCTION — Ovarian cancer is the second most common gynecologic malignancy in resource-rich countries and the third most common gynecologic malignancy in resource-limited countries (cervical cancer is the most common) [1]. The majority of ovarian malignancies (95 percent) are epithelial; the remainder arise from other ovarian cell types (germ cell tumors, sex cord-stromal tumors (figure 1)).

High-grade serous carcinoma, the most common histologic subtype of epithelial ovarian carcinoma, is regarded as closely related to fallopian tube and peritoneal serous carcinoma, based upon similarities in histology and clinical behavior. Some experts have proposed that these carcinomas all originate in the fallopian tubes. Based upon their common features, these carcinomas will be discussed as one clinical entity and referred to as epithelial ovarian carcinoma (EOC) in this topic review. Distinctions between these conditions will also be addressed.

An overview of EOC is presented here. Related topics are discussed in detail separately, including:

●Histopathology (see "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Histopathology")

●Epidemiology and risk factors (see "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Incidence and risk factors")

●Screening for ovarian cancer (see "Screening for ovarian cancer")

●Clinical features and diagnosis (see "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Clinical features and diagnosis" and "Early detection of epithelial ovarian cancer: Role of symptom recognition")

●Staging and surgical treatment (see "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Surgical staging")

●Patient selection for neoadjuvant therapy (see "Patient selection and approach to neoadjuvant chemotherapy for newly diagnosed advanced ovarian cancer")

●Adjuvant therapy (see "Adjuvant therapy of early-stage (stage I and II) epithelial ovarian, fallopian tube, or peritoneal cancer" and "First-line chemotherapy for advanced (stage III or IV) epithelial ovarian, fallopian tube, and peritoneal cancer")

●Special considerations for breast cancer susceptibility gene (BRCA)-associated ovarian cancer (see "Management of ovarian cancer associated with BRCA and other genetic mutations", section on 'Newly diagnosed BRCA-associated ovarian cancers')

●Posttreatment surveillance and survivorship issues (see "Approach to survivors of epithelial ovarian, fallopian tube, or peritoneal carcinoma")

●Relapsed disease (see "Medical treatment for relapsed epithelial ovarian, fallopian tube, or peritoneal cancer: Platinum-sensitive disease" and "Medical treatment for relapsed epithelial ovarian, fallopian tube, or peritoneal cancer: Platinum-resistant disease")

HISTOPATHOLOGY AND PATHOGENESIS — The majority of primary ovarian malignancies (95 percent) are epithelial; the remainder are germ cell or sex cord-stromal tumors (figure 1) [2]. Subtypes of epithelial ovarian cancer include high-grade serous, low-grade serous, endometrioid, clear cell, and mucinous; serous is the most common subtype (75 percent of epithelial carcinomas) [2-4]. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Histopathology".)

Serous, clear cell, and endometrioid ovarian carcinomas often appear to arise from tissues not normally present in the ovary, such as the fallopian tube, müllerian inclusion cysts, endometriosis, and endosalpingiosis. The connection between endometriosis and development of endometrioid and clear cell ovarian carcinomas is reviewed separately. (See "Endometriosis in adults: Pathogenesis, epidemiology, and clinical impact", section on 'Ovarian cancer risk'.)

The origin of mucinous carcinoma is not known. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Histopathology", section on 'Mucinous carcinoma'.)

Ovarian sex cord-stromal tumors arise from the dividing cells that would typically give rise to specialized gonadal stroma surrounding the oocytes, including granulosa cells, theca cells, Sertoli cells, Leydig cells, and fibroblasts. (See "Sex cord-stromal tumors of the ovary: Epidemiology, clinical features, and diagnosis in adults", section on 'Pathogenesis'.)

Ovarian germ cell tumors are histologically diverse but have a common origin in the primitive germ cell. (See "Ovarian germ cell tumors: Pathology, epidemiology, clinical manifestations, and diagnosis".)

EPIDEMIOLOGY AND RISK FACTORS — Ovarian cancer is the second most common gynecologic malignancy in resource-rich countries and the third most common gynecologic malignancy in resource-limited countries (cervical cancer is the most common) [1]. Ovarian cancer is the second most common gynecologic malignancy and the most common cause of gynecologic cancer death in the United States.

The average age at diagnosis of ovarian cancer in the United States is 63 years old [5]. The age at diagnosis of ovarian cancer is younger among patients with a hereditary ovarian cancer syndrome. The lifetime risk of developing ovarian cancer is 1.3 percent. A detailed discussion of the epidemiology of EOC can be found separately. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Incidence and risk factors", section on 'Incidence'.)

An increased risk of EOC is associated with: increasing age, infertility, endometriosis, polycystic ovarian syndrome, and cigarette smoking (for mucinous carcinomas (table 1)). Factors that are associated with a decreased risk include: previous pregnancy, history of breastfeeding, oral contraceptives, use of an intrauterine device, and tubal ligation.

Several ovarian cancer susceptibility genes have been identified, primarily BRCA1, BRCA2, as well as other genes in the homologous recombination pathway as well as mismatch repair genes associated with Lynch syndrome (hereditary nonpolyposis colorectal cancer). A personal or family history of breast cancer had been thought of as a risk factor for ovarian cancer; however, BRCA gene mutations appear to account for a significant amount of this increased risk. This is discussed in more detail below. (See 'Testing for hereditary cancer syndromes' below.)

A detailed discussion of the risk factors for EOC can be found separately. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Incidence and risk factors", section on 'Probable risk factors'.)

CLINICAL PRESENTATION — The clinical presentation of EOC may be either subacute or acute. The majority of patients have stage III disease (disease that has spread throughout the peritoneal cavity and/or that involves lymph nodes) at diagnosis [6]. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Clinical features and diagnosis" and "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Incidence and risk factors", section on 'Incidence'.)

Most commonly, EOC presents in a subacute fashion (eg, pelvic or abdominal pain, bloating, gastrointestinal symptoms) in patients with either early or advanced disease (table 2). These conditions are usually evaluated in an outpatient setting. Alternatively, an adnexal mass may be discovered incidentally at the time of imaging performed for another indication. Symptoms of EOC are discussed in detail separately. (See "Early detection of epithelial ovarian cancer: Role of symptom recognition".)

Patients who present in an acute fashion are typically those with advanced disease who present with a condition that requires urgent care and evaluation (eg, pleural effusion, bowel obstruction).

DIAGNOSIS — EOC is a histologic diagnosis, based upon pathology evaluation of tissue following surgical removal of an ovary or fallopian tube or biopsies of the peritoneum. Less frequently, the diagnosis is based upon tissue or fluid obtained via image-guided biopsy, paracentesis, or thoracentesis.

The evaluation and diagnosis of EOC is discussed in detail separately. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Clinical features and diagnosis".)

TESTING FOR HEREDITARY CANCER SYNDROMES — All patients with a diagnosis of ovarian, fallopian tube, or peritoneal cancer should have a genetic risk evaluation, irrespective of their family history [7]. Patients with epithelial carcinoma of the ovary should be offered testing for BRCA1 or BRCA2 mutations as well as other familial cancer syndromes (eg, Lynch syndrome). Patients with clear cell, endometrioid, or mucinous ovarian cancer should be offered testing for DNA mismatch repair deficiency.

The presence of a familial cancer syndrome may impact treatment or posttreatment care. Surgical planning/counseling may be impacted as well. For example, patients with BRCA mutations have higher response rates to certain treatments, such as poly(ADP-ribose) polymerase (PARP) inhibitors [7], and patients with Lynch syndrome are at an increased risk of having a synchronous primary cancer (eg, endometrial, colon) at the time of surgical staging. These concepts are discussed in more detail elsewhere. (See "Genetic testing and management of individuals at risk of hereditary breast and ovarian cancer syndromes" and "Lynch syndrome (hereditary nonpolyposis colorectal cancer): Clinical manifestations and diagnosis" and "Management of ovarian cancer associated with BRCA and other genetic mutations".)

While genetic testing is recommended for all patients with EOC, not all patients have testing performed. In a retrospective study including over 8500 patients with EOC, biomarker testing was performed in only 55 percent of patients, but with higher rates (66 percent) during the last year of the study period (2020) [8]. Medicaid insurance, lack of insurance coverage, poor performance status (ie, Eastern Cooperative Oncology Group [ECOG] status ≥2), and nonserous histologies were associated with lower rates of biomarker testing.

STAGING AND TREATMENT — Surgical staging and cytoreduction followed by adjuvant chemotherapy is the management approach used for most patients with EOC. It is thought that optimal cytoreductive surgery increases the likelihood that chemotherapy will result in long-term disease-free survival.

Deciding on neoadjuvant treatment versus primary debulking surgery — For most patients, EOC is treated surgically and followed by adjuvant platinum- and taxane-based chemotherapy. However, neoadjuvant chemotherapy (NACT) prior to definitive surgery is an alternative option in selected patients (eg, stage IV disease, extensive extraperitoneal metastasis, poor performance status) with biopsy-proven müllerian malignancy (algorithm 1). Patient selection and rationale for a neoadjuvant approach is discussed elsewhere. (See "Patient selection and approach to neoadjuvant chemotherapy for newly diagnosed advanced ovarian cancer".)

Staging and surgical treatment — EOC is surgically and pathologically staged according to the 2017 eighth edition American Joint Committee on Cancer (AJCC) and the joint 2017 International Federation of Gynecology and Obstetrics (FIGO)/Tumor, Node, Metastasis (TNM) classification system (table 3).

Total extrafascial hysterectomy and bilateral salpingo-oophorectomy with pelvic and paraaortic lymph node dissection is the standard staging procedure for EOC [9]. Cytology is performed of pelvic washings and the surface of the diaphragm; omentectomy is also performed. Cytoreduction (surgical "debulking"), which may include bowel or partial hepatic resection, is performed when metastases are evident. Staging is typically performed via laparotomy or laparoscopy, which may be robotically assisted.

Staging, cytoreductive operations, and other surgical treatment of EOC, as well as anesthesia for such procedures, are discussed in detail separately. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Surgical staging" and "Anesthesia for cytoreductive surgery with heated intraperitoneal chemotherapy".)

●Special considerations for those undergoing neoadjuvant treatment

•Although some patients in whom neoadjuvant therapy is being considered may undergo a biopsy for diagnosis, diagnostic laparoscopy may also be used to determine appropriateness for primary debulking surgery (versus neoadjuvant therapy). (See "Patient selection and approach to neoadjuvant chemotherapy for newly diagnosed advanced ovarian cancer", section on 'Role of diagnostic laparoscopy'.)

•For patients undergoing NACT, an interval surgery may be performed after three to four cycles of chemotherapy, at which time hysterectomy and bilateral salpingo-oophorectomy should be performed, along with resection of residual bulky disease. (See "Patient selection and approach to neoadjuvant chemotherapy for newly diagnosed advanced ovarian cancer", section on 'Treatment evaluation and subsequent approach'.)

Chemotherapy — Most patients with early-stage EOC should receive adjuvant chemotherapy, specifically those with stage IC or II disease, clear cell histology (any grade), or high tumor grade (table 3). Those with advanced disease (stage III or IV) should also receive adjuvant therapy if they underwent primary surgical cytoreduction. However, patients who are unlikely to become optimally cytoreduced (ie, <10 mm of residual disease at the end of surgery) or who are not good candidates for surgery due to medical comorbidities at the time of diagnosis may be considered for NACT instead. (See "Patient selection and approach to neoadjuvant chemotherapy for newly diagnosed advanced ovarian cancer".)

The preferred chemotherapy regimen is a platinum-based combination (which may be used in the adjuvant or neoadjuvant setting). However, treatment options differ based on extent of disease at staging.

For patients with early-stage disease, we prefer carboplatin and paclitaxel administered every three weeks for six cycles. However, it is reasonable to individualize the number of cycles based upon patient risk factors and the tolerance of therapy. In this case, we prefer a minimum of three cycles be administered. (See "Adjuvant therapy of early-stage (stage I and II) epithelial ovarian, fallopian tube, or peritoneal cancer".)

For patients with advanced EOC, the options depend on the surgical outcomes. (See "First-line chemotherapy for advanced (stage III or IV) epithelial ovarian, fallopian tube, and peritoneal cancer".)

●For patients with optimally cytoreduced EOC (ie, <1 cm residual disease at the completion of surgery), options include either intraperitoneal (IP) carboplatin or cisplatin, intravenous (IV) paclitaxel, and IP paclitaxel chemotherapy or IV therapy alone with carboplatin and paclitaxel, administered for a total of six cycles. In some patients, bevacizumab is included in this regimen. (See "First-line chemotherapy for advanced (stage III or IV) epithelial ovarian, fallopian tube, and peritoneal cancer", section on 'Incorporation of angiogenesis inhibitors'.)

●For patients with suboptimally cytoreduced EOC (ie, ≥1 cm residual disease), we administer a platinum-based doublet such as carboplatin plus paclitaxel IV for six cycles. These patients are not candidates for IP therapy.

●For those patients whose disease is in remission after their primary chemotherapy, maintenance therapy with poly(ADP-ribose) polymerase (PARP) inhibitors is offered. (See "First-line chemotherapy for advanced (stage III or IV) epithelial ovarian, fallopian tube, and peritoneal cancer", section on 'Approach'.)

●Special considerations for those with BRCA-associated ovarian cancer are found elsewhere. (See "Management of ovarian cancer associated with BRCA and other genetic mutations", section on 'Newly diagnosed BRCA-associated ovarian cancers'.)

PROGNOSIS — Approximately 80 percent of patients with early-stage disease are recurrence-free at five years. However, the majority of patients with advanced-stage ovarian cancer will relapse. Among those with relapsed disease, mortality is high. The five-year survival rates by stage for epithelial ovarian and fallopian tube carcinomas are shown in the table (table 4).

In an analysis of almost 1900 stage III ovarian cancer patients treated with primary surgery and six cycles of platinum/paclitaxel, the major prognostic factors associated with improved outcome were younger age, low volume of residual disease, good performance status, and serous histology [10]. Others have reported that patients with residual tumor burden less than 1 cm in diameter without debulking did better than those who required debulking to achieve this residual tumor burden. Among patients who achieve optimal debulking, those with less advanced disease at initial surgery did better than those with more advanced disease [11,12]. The importance of debulking is discussed elsewhere. (See "Cancer of the ovary, fallopian tube, and peritoneum: Surgical cytoreduction".)

Younger patients are more likely to have a favorable prognosis because they are more likely to have tumors of less aggressive histology and lower grade, and better baseline performance status [13,14]. In a database study of over 5000 patients, 294 of whom were <40 years, those who were <40 years had a median overall survival of 75 months, versus 46 months among those ≥40 years [13].

The volume of residual disease is the only major prognostic factor that the surgeon can address. As such, resectability is, in part, influenced by the experience, judgment, and effort of the surgeon [15].

The biologic characteristics of ovarian cancer may help predict the patient's prognosis and response to medical and surgical therapies. As an example, preliminary studies into these characteristics have found an association with relapse or survival with the decline in cancer antigen 125 after surgery and cancer cell expression of nuclear maspin expression [16,17]. In addition, a 2013 meta-analysis found that high expression of the progesterone receptor (PR) was associated with improvement in overall survival (hazard ratio [HR] 0.88, 95% CI 0.82-0.95). However, while elevated levels of human epidermal growth factor receptor 2 (HER2) predicted worse survival (HR 1.41, 95% CI 1.05-1.89) [18], expression of estrogen receptors was not significantly associated with outcomes.

Retrospective studies have suggested that patients upstaged to stage IIIC based on nodal involvement alone may have a better prognosis than IIIC patients with gross intraabdominal disease larger than 2 cm, even if optimally cytoreduced [19,20]. These results require confirmation.

Patients with BRCA gene mutations, particularly BRCA2, appear to have a somewhat better prognosis than noncarriers. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Incidence and risk factors", section on 'BRCA variants'.)

POSTTREATMENT SURVEILLANCE — Following all first-line treatment for EOC, monitoring should include routine history and physical, assessment of cancer antigen 125 (CA 125; or other tumor markers if they were elevated on initial presentation), and other testing if clinically indicated (eg, imaging or laboratory assessments) [21]. The specific schedule of posttreatment surveillance evaluations is discussed elsewhere. (See "Approach to survivors of epithelial ovarian, fallopian tube, or peritoneal carcinoma", section on 'Post-treatment surveillance'.)

CA 125 surveillance — Following patients longitudinally by CA 125 may help identify patients for surgical treatment at recurrence and thereby increase the likelihood of an optimal cytoreduction. However, there is no clear impact of serial CA 125 measurements on overall survival. (See "Approach to survivors of epithelial ovarian, fallopian tube, or peritoneal carcinoma", section on 'Role of CA 125 surveillance'.)

No role for routine imaging — Standard imaging techniques, including ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET), have limited sensitivity to detect recurrent EOC [22]. There are some data to support the use of PET/CT to detect early recurrent disease, but we do not perform surveillance imaging studies in asymptomatic patients given lack of evidence for a survival benefit. This is discussed in more detail elsewhere. (See "Approach to survivors of epithelial ovarian, fallopian tube, or peritoneal carcinoma", section on 'No role for routine imaging'.)

RELAPSED DISEASE — Despite initial therapy, the majority of patients with advanced-stage ovarian cancer will relapse and require additional treatment. The likelihood for recurrence depends on many factors, including distribution of disease at initial presentation, success of initial surgical cytoreduction (ie, the presence of any residual disease), the rapidity of cancer antigen 125 resolution, and treatment response after primary therapy. However, a predictive marker for recurrence has not been prospectively verified.

Some patients may be appropriate candidates for secondary cytoreduction. (See "Cancer of the ovary, fallopian tube, and peritoneum: Surgical options for recurrent cancer", section on 'Candidates' and "Cancer of the ovary, fallopian tube, and peritoneum: Surgical options for recurrent cancer", section on 'Outcome of cytoreduction'.)

Additionally, the approach to systemic treatment depends upon the amount of time that has elapsed between the completion of platinum-based treatment and the detection of relapse, known as the platinum-free interval (PFI). This is because the PFI correlates with progression-free survival (PFS), overall survival (OS), and response to subsequent treatment (both with platinum and nonplatinum agents as well as cytoreduction).

●Patients with a PFI of six months or longer are considered to have chemotherapy-sensitive disease (often also termed "platinum-sensitive"). (See "Medical treatment for relapsed epithelial ovarian, fallopian tube, or peritoneal cancer: Platinum-sensitive disease".)

●Patients with a PFI of less than six months are considered to have chemotherapy-resistant disease (often also termed "platinum-resistant"). Of this group, those patients who progress while on platinum-based therapy are often referred to as having "platinum-refractory" disease. The management of these patients is discussed separately. (See "Medical treatment for relapsed epithelial ovarian, fallopian tube, or peritoneal cancer: Platinum-resistant disease".)

ISSUES IN SURVIVORS

Fertility preservation — Fertility preservation options are limited for patients with EOC, since most cases are diagnosed at an advanced stage and hysterectomy and bilateral salpingo-oophorectomy is part of staging and surgical treatment. Fertility-preserving surgery (ie, unilateral salpingo-oophorectomy) is typically reserved for patients with stage IA EOC or those with borderline ovarian tumors who desire future childbearing. (See "Epithelial carcinoma of the ovary, fallopian tube, and peritoneum: Surgical staging", section on 'Staging in patients who desire fertility preservation'.)

Other posttreatment issues — Issues pertaining to survivorship for patients previously treated for EOC are not as well studied as they are for many other cancers. This may be in part due to an overall poor prognosis and small population of affected individuals. A detailed discussion of issues in EOC survivors, including medical and psychosocial effects (eg, gastrointestinal toxicity, neurologic effects, menopause management, and sexual dysfunction), can be found separately. (See "Approach to survivors of epithelial ovarian, fallopian tube, or peritoneal carcinoma".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Ovarian, fallopian tube, and peritoneal cancer".)

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Ovarian cancer is the second most common gynecologic malignancy and the most common cause of gynecologic cancer death in the United States. The average age at diagnosis of ovarian cancer in the United States is 63 years old. The age at diagnosis of ovarian cancer is younger among patients with a hereditary ovarian cancer syndrome (breast cancer susceptibility [BRCA] gene mutations or Lynch syndrome). The lifetime risk of developing ovarian cancer is approximately 1 percent. (See 'Epidemiology and risk factors' above.)

●Histopathology – The majority of primary ovarian malignancies (95 percent) are derived from epithelial cells; the remainder arise from other ovarian cell types (germ cell tumors, sex cord-stromal tumors (figure 1)). Serous carcinoma, the most common histologic subtype of epithelial ovarian carcinoma (EOC), is similar in histology and clinical behavior to fallopian tube and peritoneal carcinomas. It has been proposed that ovarian and peritoneal carcinomas originate in the fallopian tubes. (See 'Histopathology and pathogenesis' above.)

●Risk factors

•Risk factors for EOC include increasing age, infertility, and endometriosis (table 1). Patients with ovarian cancer susceptibility genes (eg, BRCA gene mutations and Lynch syndrome) are at the highest risk of ovarian cancer.

•Factors that are associated with a decreased risk include previous pregnancy, history of breastfeeding, use of oral contraceptives or an intrauterine device, and tubal ligation. (See 'Epidemiology and risk factors' above.)

●Clinical presentation – The clinical presentation may be either subacute or acute. Most commonly, the presentation is subacute (eg, pelvic or abdominal pain, bloating) or an adnexal mass is discovered incidentally (table 2). An acute presentation may occur in patients with advanced disease and includes pleural effusion or bowel obstruction. (See 'Clinical presentation' above.)

●Diagnosis – EOC is a histologic diagnosis. Pathology evaluation is performed following surgical removal of an ovary or fallopian tube or biopsies of the peritoneum. (See 'Diagnosis' above.)

●Genetic testing – All patients with a diagnosis of ovarian, fallopian tube, or peritoneal cancer should be referred for genetic counseling and testing, irrespective of their family history. The presence of a familial cancer syndrome (eg, BRCA1 or BRCA2, Lynch syndrome) may have treatment implications. (See 'Testing for hereditary cancer syndromes' above.)

●Treatment

•Most patients with EOC undergo surgical staging, which is staged according to the joint 2017 International Federation of Gynecology and Obstetrics (FIGO)/Tumor, Node, Metastasis (TNM) classification system (table 3). Total hysterectomy and bilateral salpingo-oophorectomy with pelvic and paraaortic lymph node dissection is the standard staging procedure. Cytoreduction, including bowel or partial hepatic resection, is also performed when metastases are evident. (See 'Staging and surgical treatment' above.)

•Most patients with EOC also require adjuvant chemotherapy treatment, specifically those with stage IC or II disease; those with stage III or IV disease who are candidates for primary surgical cytoreduction; and those with clear cell histology (any grade) or high tumor grade (table 3). (See 'Chemotherapy' above.)

•Patients who are unlikely to become optimally cytoreduced (ie, <10 mm of residual disease at the end of surgery) or who are not good candidates for surgery due to medical comorbidities at the time of diagnosis may be considered for neoadjuvant chemotherapy (NACT) instead; a biopsy is typically performed before NACT to confirm a müllerian malignancy. (See 'Deciding on neoadjuvant treatment versus primary debulking surgery' above and "Patient selection and approach to neoadjuvant chemotherapy for newly diagnosed advanced ovarian cancer".)

●Prognosis – Major prognostic factors associated with improved outcomes among patients with resected EOC include younger age, low volume of residual disease, good performance status, and serous histology (table 4). (See 'Prognosis' above.)

●Posttreatment surveillance – Posttreatment surveillance includes routine history and physical, assessment of cancer antigen 125 or other tumor markers if they were elevated on initial presentation, and other testing if clinically indicated (eg, imaging or laboratory assessments). The specific schedule of posttreatment surveillance evaluations is discussed elsewhere. (See 'Posttreatment surveillance' above and "Approach to survivors of epithelial ovarian, fallopian tube, or peritoneal carcinoma", section on 'Post-treatment surveillance'.)

●Relapsed disease – Despite initial therapy, the majority of patients with advanced-stage ovarian cancer will relapse and require additional treatment. The approach to treatment depends upon the amount of time that has elapsed between the completion of platinum-based treatment and the detection of relapse, known as the platinum-free interval (PFI). (See 'Relapsed disease' above.)