Ovarian cancer and adnexal masses

• Ovarian cancer is a group of diseases rather than one: high-grade serous carcinoma, the commonest, starts in the fallopian tube fimbria and spreads across the peritoneum; endometrioid, clear cell, mucinous, low-grade serous and non-epithelial tumours have different biology. ^[1]
• More than half of women present late because symptoms are vague and slowly progressive: persistent bloating, early satiety, pelvic or abdominal pain and urinary urgency or frequency.
• There is no effective population screening. Recognition rests on a structured symptom history, pelvic examination, transvaginal ultrasound, CA125 and a risk score such as the Risk of Malignancy Index.
• Complete surgical cytoreduction followed by platinum-based chemotherapy is the backbone. Maintenance with PARP inhibitors, alone or with bevacizumab, benefits BRCA-mutated or HRD tumours.
• Germ cell and sex cord-stromal tumours mostly affect younger women; they are highly curable with fertility-sparing surgery and platinum-based chemotherapy.

By the end of this page you should be able to:

1. Describe the epithelial, germ cell and sex cord-stromal ovarian tumours and their characteristic markers.
2. List risk and protective factors, including BRCA-related lifetime risk and the ages advised for risk-reducing surgery.
3. Work through the presentation, examination and investigation of an adnexal mass, including CA125 age-banded thresholds and the Risk of Malignancy Index.
4. Apply the FIGO staging system and plan staging or cytoreductive surgery.
5. Select chemotherapy for early, advanced and recurrent disease, and choose maintenance appropriately.
6. Recognise complications, prognosis and prevention, and adapt care in pregnancy, children and older adults.

An adnexal mass is any mass in the region of the ovary, fallopian tube or adjacent tissues. Ovarian cancer means a malignant neoplasm of the ovary, fallopian tube or peritoneum; these sites share the FIGO staging system because they have similar routes of spread and the primary site is often impossible to identify.

Epithelial tumours account for the great majority of ovarian cancers. The main histological types are serous, mucinous, endometrioid, clear cell and Brenner tumours. Serous carcinomas are the commonest and split into low-grade and high-grade. More than 90% of fallopian tube carcinomas are high-grade serous, and the majority are thought to arise at the fimbrial end of the tube via a TP53-mutated serous tubal intraepithelial carcinoma (STIC). ^[1]

• High-grade serous carcinoma: almost universal TP53 mutation, rapid peritoneal spread, usually advanced at diagnosis.
• Low-grade serous carcinoma: KRAS or BRAF mutations in about half, more indolent, chemotherapy-resistant.
• Endometrioid and clear cell carcinoma: often arise in endometriosis, tend to present at earlier stage.
• Mucinous carcinoma: expansile (confluent, non-destructive) or infiltrative (stromal invasion) subtypes. A raised CEA or CA19-9 and a low CA125 to CEA ratio point toward a gastrointestinal primary.
• Borderline (low malignant potential) tumours: not frankly invasive, affect younger women, about 75% are stage I at diagnosis, with a 10-year survival of approximately 95%. ^[1]

Germ cell tumours arise from primitive germ cells and are the commonest ovarian tumours in women in their second and third decades. They are highly chemosensitive, and even metastatic disease is usually curable.

Dysgerminoma is the ovarian equivalent of testicular seminoma.

These arise from ovarian stroma and sex cords. Granulosa cell tumours account for about 70% of sex cord-stromal tumours and 3 to 5% of all ovarian neoplasms, and are usually hormone-secreting. ^[1]

• Adult granulosa cell tumour: peak in the first postmenopausal decade, oestrogen-producing, postmenopausal bleeding, marker inhibin B (or AMH).
• Juvenile granulosa cell tumour: sexual precocity, young women.
• Sertoli-Leydig cell tumour: androgen-producing, virilisation.
• Fibroma and thecoma: usually benign solid tumours; large fibromas may cause Meigs syndrome (ascites plus pleural effusion).

These tumours are indolent and recur late; stage at diagnosis is the most important prognostic factor.

Malignant ovarian tumours occur at all ages, but the subtype changes with age.

• In the USA in 2023 there were nearly 19,710 new cases and an estimated 13,270 deaths ^[1].
• Ovarian cancer makes up about 23% of gynaecological cancers but 47% of deaths from female genital tract malignancies, and remains the fifth leading cause of cancer death in women ^[1].
• The lifetime risk of being diagnosed with ovarian cancer is 1.3%, and the risk of dying from it is about 0.9% ^[1].
• The incidence of epithelial tumours is 9 to 17 per 100,000, with the highest rates in high-income countries; incidence rises with age and peaks at 60 to 64 years ^[1].
• In low- and middle-income countries the median age at diagnosis is about a decade earlier, and outcomes are worse at every stage, driven by access to diagnosis and treatment rather than biology ^[1].

• Nulliparity, which roughly doubles the risk ^[1].
• Early menarche and late menopause ^[1].
• Age, especially over 50 years.
• Family history or an inherited predisposition (below).
• Lynch syndrome type II, linked to endometrioid or clear cell ovarian cancers that are usually stage I ^[1].

Hereditary factors are involved in about 20% of ovarian, tubal and peritoneal cancers ^[1].

• At least 15% of women with high-grade non-mucinous ovarian cancers carry a germline BRCA1 or BRCA2 mutation, and 44% of carriers have no family history of breast or ovarian cancer ^[1]. All women with high-grade non-mucinous invasive ovarian cancer should be offered genetic counselling and testing, whatever their age or family history ^[1].
• Germline BRCA1 raises the lifetime risk of ovarian, tubal and peritoneal cancer to 39 to 44%; BRCA2 to 10 to 20% ^[1]. BRCA1-associated cancers present earlier, with a median age in the mid-40s ^[1].
• Other moderate-risk genes include BRIP1, RAD51C, RAD51D, PALB2 and the mismatch repair genes of Lynch syndrome; multigene panel testing is recommended ^[1].
• Risk-reducing bilateral salpingo-oophorectomy (RR-BSO) is advised after counselling and completion of childbearing: at 35 to 40 years for BRCA1 carriers, and 40 to 45 years for BRCA2 carriers ^[1]. Surgery reduces ovarian cancer-specific mortality, but a peritoneal cancer can still occur rarely, more often if STIC lesions are present ^[1].
• Opportunistic salpingectomy at the time of hysterectomy for benign disease is recommended by some guidelines for women not at genetic risk, to lower the later high-grade serous cancer risk ^[1].

• Oral contraceptive use ^[1].
• An early first pregnancy ^[1].
• Opportunistic salpingectomy ^[1].
• RR-BSO in BRCA carriers (above).

The modern view is that most high-grade serous carcinomas do not begin in the ovarian surface epithelium, but in the distal fallopian tube. A TP53 mutation signature progresses to a STIC in the fimbria, which then exfoliates onto the ovary and peritoneum, producing the familiar pattern of widespread abdominal disease with ascites ^[1].

Other epithelial types are slower, precursor-driven tumours: endometriosis gives rise to endometrioid and clear cell carcinoma; mucinous adenomas progress through borderline to mucinous carcinoma with stromal invasion; atypical proliferative serous tumours precede low-grade serous carcinoma, which carries MAP kinase pathway mutations rather than TP53 mutations.

Dissemination is mainly transcoelomic. Tumour cells shed into the peritoneal cavity implant on the omentum, peritoneum, bowel serosa and diaphragm, causing malignant ascites, and later a pleural effusion. Lymphatic spread reaches pelvic and para-aortic nodes. Haematogenous spread is relatively late, explaining hepatic parenchymal and other distant metastases.

Because early disease is silent and micro-metastases appear early, about two-thirds of epithelial cancers are stage III or IV at diagnosis ^[1]. Clear cell, mucinous and endometrioid cancers more often stay at early stage, whereas high-grade serous cancer is usually advanced ^[1].

Symptoms are insidious and are often present for only a few weeks; the duration does not reliably separate early from advanced disease ^[1].

Characteristic symptoms of epithelial ovarian cancer, especially when occurring more than 12 times per month, are ^[2]:

• persistent abdominal distension (bloating)
• feeling full early, or loss of appetite
• pelvic or abdominal pain
• increased urinary urgency or frequency

Later or non-specific symptoms include weight loss, fatigue, change in bowel habit, dyspepsia and abnormal vaginal bleeding, the last being uncommon ^[1]. Advanced disease brings ascites with abdominal distension, breathlessness from raised intra-abdominal pressure or pleural effusion. A gastric, colonic or breast primary that has metastasised to the ovaries (Krukenberg tumour) can mimic primary ovarian cancer.

A CA125 to CEA ratio greater than 25 to 1 favours an ovarian primary, but does not completely exclude a gastrointestinal one ^[1]. When imaging or a high CA125 raises suspicion of malignancy in a young woman, hCG and AFP are mandatory to exclude a germ cell tumour ^[1].

General, breast, pelvic and rectal examination is performed. Look for ascites, a fixed pelvic or abdominal mass, pleural effusion, cachexia, lymphadenopathy and a breast lump. Palpable ovaries in a postmenopausal woman are always abnormal.

1. Pregnancy test (urine, then quantitative serum hCG if needed) for every woman of reproductive age ^[1].
2. Transvaginal ultrasound, describing size, locularity, solid areas, septations, papillary projections, wall, vascularity, bilaterality, ascites and metastases.
3. Serum CA125, interpreted with age and menopausal status. CA125 is raised in most epithelial ovarian cancers but also in benign conditions, so it is not diagnostic alone ^[1].
4. Risk of Malignancy Index (RMI), ROMA or OVERA where available ^[1].
5. Further imaging: CT of the abdomen and pelvis delineates intra-abdominal extent and is the standard staging scan; MRI helps when ultrasound is uncertain; chest imaging screens for pleural effusion. Gastroscopy or colon assessment is indicated when CEA or CA19-9 is raised. Mammography is considered given the age profile.
6. Subtype markers (table above): AFP and beta-hCG in younger women; inhibin B or AMH when a granulosa cell tumour is suspected.

NICE NG12 (updated 15 April 2026) sets age-banded CA125 thresholds for primary care in people aged 40 years or over with persistent symptoms suggesting ovarian cancer ^[2].

In people under 40, CA125 is not used in isolation; instead an urgent direct-access ultrasound of the abdomen and pelvis is considered ^[2]. Persistent symptoms that should raise the question are bloating, early satiety or loss of appetite, pelvic or abdominal pain, increased urinary urgency or frequency, particularly more than 12 times per month, with weight loss, fatigue or change in bowel habit as further prompts ^[2]. Ascites or a pelvic or abdominal mass (not obviously fibroids) warrants direct referral ^[2]. If the ultrasound suggests ovarian cancer, suspected cancer pathway referral is made ^[2].

RMI I is the NICE-recommended pre-surgical score for a pelvic mass. It multiplies ultrasound score, menopausal status and serum CA125 ^[3].

RMI = U × M × CA125 (IU/ml)

• U (ultrasound score): one point each for multilocular cysts, solid areas, metastases, ascites or bilateral lesions. U = 0 for score 0; U = 1 for score 1; U = 3 for score 2 to 5.
• M (menopausal status): 1 = premenopausal; 3 = postmenopausal (no period for more than one year, or a woman over 50 who has had a hysterectomy).
• CA125: the measured value.

A cut-off of 200 or more is usually taken as indicating high risk of malignancy and triggers referral to a gynaecological oncologist ^[3].

• Refer on a suspected cancer pathway if examination identifies ascites or a pelvic or abdominal mass not obviously fibroids ^[2].
• In women aged 39 or under with persistent symptoms, do not use CA125 alone; consider urgent direct-access ultrasound ^[2].
• In women aged 50 or over with symptoms suggestive of irritable bowel syndrome that have appeared for the first time, test for ovarian cancer, because IBS rarely presents for the first time at that age ^[2].

There is no single biomarker that diagnoses ovarian cancer. The diagnosis is established by histology, usually obtained at surgery. Most patients have raised CA125, an adnexal mass and peritoneal disease, but cancer is only proven on tissue.

Ovarian, fallopian tube and peritoneal cancers share the FIGO staging classification, revised in 2014 and restated in the 2025 FIGO update. A laparotomy with full surgical exploration determines the stage.

Chest radiographs screen for pleural effusion. Serum CA125 does not contribute to stage. Where possible the primary site (ovary, tube or peritoneum) should be designated.

These recommendations draw on the FIGO/Berek 2025 update, the ESGO/ESMO consensus literature and the ESMO practice guidelines with their 2026 express update ^[1][4]. Care of women with suspected or proven ovarian cancer should sit with a gynaecological oncology team.

A thorough surgical staging laparotomy underpins management; minimally invasive staging is increasingly accepted ^[1]. When there is no visible metastasis the following should be performed:

• careful evaluation of all peritoneal surfaces
• retrieval of ascites, or peritoneal washings if no ascites is present
• infracolic omentectomy
• selective pelvic and para-aortic lymphadenectomy, at least ipsilateral if disease is unilateral
• biopsy or resection of any suspicious lesion
• random peritoneal biopsies, including the subdiaphragmatic surfaces, paracolic recesses and pelvic sidewalls
• total abdominal hysterectomy and bilateral salpingo-oophorectomy in most cases
• appendectomy if the tumour is mucinous and the appendix looks abnormal

The ovaries and tubes are examined thoroughly; the SEE-FIM protocol is used for the distal tube, particularly in BRCA carriers. Fertility-sparing surgery is supported for stage I epithelial cancers of suitable histology, for borderline and sex cord-stromal tumours, and at all stages of germ cell tumours ^[1].

At least two-thirds of women present with stage III or IV disease. The strongest prognostic factor is the volume of residual disease after surgery; complete (no macroscopic) resection gives the best survival ^[1]. Patients fit for surgery undergo primary debulking (hysterectomy, salpingo-oophorectomy, omentectomy, maximal cytoreduction). Removal of clinically negative lymph nodes during cytoreduction does not improve progression-free or overall survival and is not undertaken, on the basis of the LION trial ^[1].

For women with stage IIIC or IV disease who are not fit for upfront surgery, or whose disease is unlikely to be optimally cytoreduced, neoadjuvant chemotherapy for three to four cycles with histological confirmation is given, followed by interval debulking surgery and further chemotherapy (EORTC and CHORUS trials show equivalent survival with less morbidity) ^[1].

Early-stage disease. Stage IA and IB grade 1 to 2 epithelial cancers need no adjuvant chemotherapy. Higher-grade tumours, high-grade serous tumours and stage IC disease receive adjuvant platinum-based chemotherapy, although the absolute survival benefit is uncertain in thoroughly staged IA or IB cases ^[1]. All stage II disease requires adjuvant chemotherapy. Stage I tumours usually receive three to six cycles ^[1]. Stage I clear cell and stage I mucinous (expansile type) cancers are areas of ongoing uncertainty ^[1].

Advanced disease. Six cycles of platinum-based combination chemotherapy is the standard, with carboplatin and a taxane. Standard intravenous regimens from the reviewed literature are ^[1]:

Docetaxel is an option for patients who react to paclitaxel or develop early neuropathy; carboplatin with pegylated liposomal doxorubicin is another alternative. Single-agent carboplatin alone gives worse progression-free survival than combination regimens in vulnerable elderly patients and should not be the default. Intraperitoneal chemotherapy is debated; it is applicable only after optimal debulking with less than 1 cm residual disease and only in experienced centres. Maintenance bevacizumab may be considered: 15 mg/kg added to carboplatin and paclitaxel in stages with macroscopic residual or stage IV disease gave progression-free survival benefits without an overall survival benefit in GOG 218 and an intravenous bevacizumab dose of 7.5 mg/kg, followed by maintenance, in ICON7 ^[1].

Hyperthermic intraperitoneal chemotherapy at interval debulking is controversial: the OVHIPEC trial showed benefit, but ESGO does not recommend it at secondary cytoreduction, while NCCN guidelines acknowledge it as an option.

Maintenance therapy. Almost 80% of women with advanced disease relapse. There is no benefit from maintenance cytotoxic chemotherapy. Maintenance PARP inhibitors improve progression-free survival in patients with no evidence of disease, complete or partial response to first-line platinum ^[1][4].

• BRCA1/2-mutated disease: olaparib for 2 years; olaparib plus bevacizumab for 15 months; rucaparib for 2 years; or niraparib for 3 years. ^[4]
• BRCA1/2 wild-type but HRD-positive tumours: rucaparib for 2 years; niraparib for 3 years; or olaparib plus bevacizumab for 15 months.
• HRD-negative tumours: bevacizumab for 15 months, or rucaparib or niraparib, can be recommended, depending on disease distribution, response and patient preference. ^[4]

Rucaparib has been added by the 2026 ESMO express update as a first-line maintenance option, with progression-free survival benefits in HRD-positive, intention-to-treat and HRD-negative populations ^[4]. Olaparib showed a hazard ratio for progression of about 0.3 in SOLO1 with 2 years of maintenance after platinum plus partial or complete response ^[1]. Long-term follow-up has not shown an overall survival benefit in all populations.

Recurrent disease. With one exception, recurrent disease is not curable; the aim is to control symptoms and maintain quality of life. Patients whose relapse occurs more than 6 months after last platinum therapy (platinum-sensitive or platinum-eligible) receive platinum-based doublet therapy. Options include carboplatin plus paclitaxel, or carboplatin with pegylated liposomal doxorubicin or gemcitabine, with or without bevacizumab ^[1]. Relapse within 6 months (platinum-resistant or platinum non-eligible) uses non-platinum regimens such as weekly paclitaxel, pegylated liposomal doxorubicin, topotecan or gemcitabine, with bevacizumab where appropriate. Mirvetuximab soravtansine is recommended for recurrent high-grade serous cancer with a platinum-free interval under 6 months and high folate receptor alpha expression, after one to three prior lines ^[4]. Maintenance with PARP inhibitors is also an option after response in platinum-sensitive recurrence.

Secondary cytoreduction benefits carefully selected patients (single or limited recurrence, long treatment-free interval, complete resection possible) ^[1]. No second-look laparotomy or adjuvant chemotherapy after first-line treatment is of proven benefit in stable disease.

Low-grade serous cancers are relatively indolent, present at a younger age, and respond poorly to chemotherapy. Surgical management is the same as for high-grade disease (with fertility-sparing options in younger women). Endocrine therapy (aromatase inhibitors) is widely used for recurrent or metastatic disease, and bevacizumab is active. Trametinib improved progression-free survival over chemotherapy from 7.2 to 13 months in recurrent disease ^[1].

These usually present at stage I. Surgery is the mainstay; chemotherapy has not been shown to help. For stage I disease in women wishing fertility, unilateral salpingo-oophorectomy can be considered, with inspection of the contralateral ovary. Recurrence is common but late; secondary cytoreduction is preferred.

Surgery. Conservative, fertility-sparing surgery by laparotomy with careful examination and limited cytoreduction is standard in all stages, because these tumours are highly chemosensitive and usually affect young women. The uterus and contralateral ovary are preserved; wedge biopsy of a normal ovary is avoided; partial oophorectomy on one side is considered if both ovaries are involved. For advanced disease, three to four cycles of neoadjuvant BEP may be used with fertility preservation. Stage IA grade 1 to 2 immature teratoma and stage IA dysgerminoma can be observed after surgery. ^[1]

Chemotherapy (dysgerminoma). Etoposide 100 mg/m2 intravenously daily for 5 days every 3 weeks for 3 cycles, cisplatin 20 mg/m2 intravenously daily for 5 days every 3 weeks for 3 cycles, and bleomycin 30 international units intravenously or intramuscularly on days 1, 8 and 15 for 12 weeks; bleomycin may be omitted (4 cycles of EP are used instead). With bulky residual disease, 3 to 4 courses of BEP or EP are used. ^[1]

Chemotherapy (non-dysgerminoma). Etoposide 100 mg/m2 daily for 5 days, cisplatin 20 mg/m2 daily for 5 days and bleomycin 30 IU on days 1, 8 and 15 over 12 weeks: three cycles for good-prognosis disease, four cycles for intermediate or poor-risk disease. After chemotherapy, residual masses containing mature teratoma elements should be resected (growing teratoma syndrome). ^[1]

Follow-up. Monthly in year one, then 2-monthly, 3-monthly, 4-monthly and then every 6 months in years 5 to 10, with CA125, AFP or beta-hCG as appropriate and imaging when indicated. ^[1]

Surgical staging with cytoreduction is the mainstay, with conservative surgery in young women. Adjuvant chemotherapy does not add proven benefit in stage I disease. For advanced or recurrent disease, platinum-based chemotherapy (BEP, or carboplatin and paclitaxel) has response rates of 63 to 80%. BEP is used as four cycles (bleomycin 20 units/m2 intravenously on day 1, etoposide 75 mg/m2 on days 1 to 5, cisplatin 20 mg/m2 on days 1 to 5, every 3 weeks); carboplatin (AUC 6) plus paclitaxel (175 mg/m2) every 3 weeks for 6 cycles is an alternative with apparently similar response and less toxicity. Bevacizumab (around 16% response rate as single agent), letrozole, anastrozole and other hormonal therapies are used for recurrence. Surveillance relies on inhibin B and AMH, with pelvic ultrasound every 6 months after fertility-sparing surgery. Breast cancer screening should be remembered, because adult granulosa cell tumours carry increased risk ^[1].

• Malignant ascites and pleural effusion; bowel obstruction from peritoneal carcinomatosis.
• Thromboembolism and infection in advanced disease.
• Chemotherapy toxicity: myelosuppression (anaemia, neutropenia, thrombocytopenia), neuropathy, nephrotoxicity, ototoxicity, nausea, fatigue; bleomycin pulmonary toxicity (especially over 40 years).
• Surgical morbidity from cytoreductive and bowel resection.
• Fertility loss after non-conservative surgery; premature menopause.

Prognosis is governed primarily by stage, histological type and grade, and completeness of cytoreduction ^[1]. Patients whose disease is confined to the ovary or fallopian tube at diagnosis do very well, whereas about two-thirds present as stage III or IV. Most relapses of advanced high-grade serous cancer occur within approximately 16 months of completing treatment. High-risk stage I subgroups (clear cell, mucinous infiltrative) and granulosa cell tumours (which recur late) follow their own patterns. Overall survival in stage IV disease with complete cytoreduction and modern treatment is far better than in the era of the EORTC and CHORUS trials, but no specific percentage for each stage is given here, because published figures vary by cohort and era.

There is no effective general population screening that reduces mortality from ovarian, tubal or peritoneal cancer. Trials of CA125 and/or transvaginal ultrasound in average-risk and high-risk women have not had acceptable sensitivity and specificity. The US Preventive Services Task Force recommends against screening asymptomatic women with pelvic ultrasound or serum tumour markers. Risk-reducing salpingo-oophorectomy remains the treatment of choice for high-risk women ^[1].

• Genetic counselling and testing for all women with high-grade non-mucinous invasive ovarian cancer, and cascade testing for relatives ^[1].
• BRCA carriers: RR-BSO at the recommended ages (above), followed by surveillance for peritoneal disease.
• Opportunistic (incidental) bilateral salpingectomy at the time of hysterectomy for women wishing to keep their ovaries ^[1].
• Oral contraceptive use and parity reduce risk ^[1].
• Symptom awareness and prompt referral for persistent symptoms ^[2].

Ovarian masses in pregnancy are usually benign, but physiological cysts must be distinguished from neoplasms. When surgery is needed, the second trimester is preferred; fertility and fetal considerations shape the approach, and germ cell tumours in particular are treated with fertility-preserving surgery and chemotherapy that can often be deferred until after viability. Management is individualised by a multidisciplinary team.

Germ cell tumours are by far the commonest ovarian malignancy in the second and third decades, and juvenile granulosa cell tumours also occur in childhood. These tumours are highly curable and are treated with conservative surgery, often avoiding chemotherapy in the lowest stages. Chemotherapy can be used safely; fertility is usually preserved. Any ovarian mass in a prepubertal child needs prompt assessment.

Older women more often present with advanced disease and have more comorbidity. Primary debulking may be unsafe; neoadjuvant chemotherapy reduces perioperative morbidity and mortality with equivalent cancer outcomes. In very frail patients (EWOC-1), carboplatin and paclitaxel in combination produced better progression-free and overall survival than carboplatin alone, although treatment must be individualised. Single-agent carboplatin is reserved for those unable to tolerate combinations. ^[1]

Transvaginal ultrasound and symptom awareness are the practical tools. CA125 may be unavailable; RMI cannot be calculated easily. Referral pathways should be agreed locally. Germ cell and granulosa cell tumours are curable even with modest resources, because fertility-sparing surgery and BEP are widely available. The removal of a tubal primary is feasible with basic gynaecological surgery.

• Ovarian cancer is an umbrella: high-grade serous disease usually originates in the fallopian tube fimbria and disseminates transcoelomically.
• Most women present with advanced disease; persistent bloating, early satiety, pain, and urinary frequency are the red-flag symptoms.
• There is no effective screening for the average-risk population. Manage risk by genetics, RR-BSO at the recommended ages, salpingectomy and symptom awareness.
• CA125 is not diagnostic; use age-banded thresholds in women aged 40 or over, and RMI (cut-off 200 or more) to triage masses.
• Complete cytoreduction plus six cycles of carboplatin and a taxane is the cornerstone of treatment.
• PARP inhibitors improve progression-free survival in BRCA-mutated or HRD tumours, with or without bevacizumab.
• Germ cell and sex cord-stromal tumours mostly affect young women, have characteristic markers, are usually curable and allow fertility-preserving treatment.
• Granulosa cell tumours recur late and are surveilled with inhibin B and AMH.

Adnexal mass and ovarian cancer assessment overlaps with abnormal uterine bleeding, contraception and intrauterine systems, polycystic ovary syndrome, endometriosis, menopause, breast cancer, colonic cancer, iron deficiency anaemia and genetic counselling for BRCA. These topic links are listed as plain text until the corresponding MedGrasp pages are verified.