History and exam
Key diagnostic factors
common
presence of risk factors
Key risk factors include increasing age, family history of ovarian cancer and/or breast cancer, having never used combined oral contraceptives, and BRCA 1 and BRCA2 mutations.
pelvic mass
Pelvic examination may detect a palpable adnexal mass (i.e., a mass in the ovaries, fallopian tubes, or surrounding connective tissue) or a fixed pelvic mass with nodularity along the recto-vaginal septum in patients with ovarian cancer. Omission of a pelvic examination at the first evaluation of ovarian cancer symptoms is associated with a delay in diagnosis.[74]
Referral to a gynaecological oncologist is recommended if a nodular or fixed pelvic mass is detected during a pelvic examination, or if a patient with an adnexal mass has additional physical examination findings that would suggest metastatic disease (e.g., ascites and pleural effusion).[81]
ascites
Findings consistent with ascites (e.g., fluid wave, shifting dullness) can often be detected in patients with advanced-stage disease.
Ascites is suspected by clinical symptoms, such as increasing abdominal girth, or ultrasound results.[98]
Referral to a gynaecological oncologist is recommended if there are physical examination findings that would suggest metastatic disease (e.g., ascites and pleural effusion).[81]
uncommon
pleural effusion
Findings consistent with a right-sided pleural effusion (e.g., diminished breath sounds or rales) can often be detected in patients with advanced-stage disease.
Patients are diagnosed with stage IVA ovarian cancer if they have pleural effusion that contains malignant cells.[99]
Referral to a gynaecological oncologist is recommended if there are physical examination findings that would suggest metastatic disease (e.g., ascites and pleural effusion).[81]
Other diagnostic factors
common
gastrointestinal symptoms
Often, the presenting symptoms of ovarian cancer are vague/non-specific and gastrointestinal-related (e.g., abdominal bloating, nausea and emesis, dyspepsia, early satiety, increased abdominal girth, abdominal cramping, diarrhoea, and constipation).[6][74]
In one study, approximately 95% of patients reported vague gastrointestinal symptoms before their diagnosis of ovarian cancer, and approximately 75% of patients had these symptoms for at least 3 months.[74]
urinary urgency or frequency
Urinary urgency or frequency is commonly reported in patients with ovarian cancer.[6]
symptom duration >3 months
In one study, approximately 95% of patients reported vague gastrointestinal symptoms before their diagnosis of ovarian cancer, and approximately 75% of patients had these symptoms for at least 3 months.[74]
abdominal distension
Can occur from the presence of a large ovarian mass, large-volume ascites, or an omental cake. On examination, there is dullness on percussion.
Referral to a gynaecological oncologist is recommended if there are physical examination findings that would suggest metastatic disease (e.g., ascites and pleural effusion).[81]
uncommon
pelvic/abdominal pain or pressure
Some patients with early-stage disease may present with pelvic/abdominal pain or pressure due to ovarian torsion.[2] Patients may also have acute onset of lower abdominal pain with associated nausea and emesis.
Risk factors
strong
genetic mutations associated with hereditary ovarian cancer
BRCA mutations account for most cases of hereditary ovarian cancer.[15] Ovarian cancer associated with BRCA mutations is usually high-grade and predominantly serous or endometrioid.[15] By age 70 to 80 years, women with an inherited BRCA1 mutation are estimated to have a 39% to 44% risk of ovarian cancer; those with an inherited BRCA2 mutation are estimated to have an 11% to 17% risk of ovarian cancer.[14][31][32]
Hereditary ovarian cancer risk is also associated with ATM, BRIP1, NBN, PALB2, STK11, RAD51C, and RAD51D mutations, and mutations related to Lynch syndrome (MSH2, MLH1, MSH6, PMS2, and EPCAM).[16][17] Estimates for risk of ovarian cancer vary (e.g., lifetime risk 3% to 5% for PALB2; 10% for RAD51C).[18]
For women with Lynch syndrome, MSH2, EPCAM, and MLH1 mutations are associated with higher risk than PMS2 and MSH6 mutations (e.g., risk by age 80 years 8% to 38% for MSH2/EPCAM; <1% to 13% for MSH6).[16]
Ovarian cancer associated with Lynch syndrome is generally diagnosed at a younger age than sporadic ovarian cancer.[33][34] Estimated mean age at diagnosis of 43-46 years has been reported for Lynch syndrome variants MLH1, MSH2, EPCAM, and MSH6; 51-59 years for Lynch syndrome variant PMS2.[16]
increasing age
family history of ovarian cancer, breast cancer, colorectal cancer, and/or endometrial cancer
In the US, the estimated lifetime risk of developing ovarian cancer is 1.1%.[8] Among women with one first-degree relative affected with ovarian cancer, the lifetime probability of developing ovarian cancer is 5%.[35] This increases to 7% with two affected first-degree relatives.[35]
A strong family history of breast cancer, especially pre-menopausal breast cancer, may be associated with mutations in BRCA1 or BRCA2.[36][37] Risk of ovarian cancer with a BRCA1 or BRCA2 mutation is estimated to be up to 44% and 17%, respectively, by age 70 to 80 years.[14][31][32]
ATM, PALB2, RAD51C, and RAD51D gene mutations are associated with hereditary breast and ovarian cancer syndrome.[18]
A strong family history of colorectal, endometrial, and/or ovarian cancer, especially if diagnosed at a young age (before age 50 years) or with a synchronous or metachronous Lynch syndrome-related cancer, may suggest Lynch syndrome.[16][20] Other Lynch syndrome-related cancers include gastric, small bowel, hepatobiliary, pancreatic, and urothelial cancers, and some types of breast cancer, brain tumours, and sebaceous skin tumours.[16][20]
never used combined oral contraceptives
Oral contraceptive use is associated with a decreased risk of developing ovarian cancer.[38][39][40]
Studies report that 5 years of oral contraceptive use results in a 50% decrease in ovarian cancer risk, which decreases further with longer duration of use.[38][39][40][41][42] This association does not appear to be altered by modifiable lifestyle characteristics, such as smoking, alcohol consumption, body mass index, or physical activity.[40]
Risk reduction appears to be associated with use of combined oral contraceptives only, and not progestogen-only oral contraceptives.[43]
weak
nulliparity
The odds of developing ovarian cancer decrease as parity increases.[44]
The protective mechanism conferred by pregnancy is related to the 'incessant ovulation' hypothesis of ovarian cancer. In this model, the trauma of ovulation is a putative factor in the development of ovarian cancer. Repeated hormonal stimulation of the ovarian epithelium and continued ovulation in the nulliparous state is thought to lead to malignant transformation.[45]
Breastfeeding has also been shown to be protective.[46] Breastfeeding and parity may have a synergistic effect on decreasing the risk of ovarian cancer.[47]
obesity
hormone therapy
Menopausal hormone therapy is associated with an increased risk of serous and endometrioid ovarian cancers.[51]
In one analysis, risk was increased with <5 years of use (relative risk 1.43, P <0.0001). In practical terms, however, this translated into 1 additional ovarian cancer per 1000 users and an estimated 1 death per 1700 users.[51]
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