Ovarian cancer

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Ovarian, fallopian-tube and primary peritoneal epithelial cancers share staging and treatment; high-grade serous carcinoma commonly originates from fimbrial tubal epithelium and presents after peritoneal dissemination. Risk rises after menopause and with greater lifetime ovulation, while pregnancy, breastfeeding and combined hormonal contraception reduce epithelial ovarian cancer risk. Germline or somatic BRCA1, BRCA2 and other repair defects increase high-grade serous risk and create sensitivity to platinum and PARP inhibition. Cells exfoliate into peritoneal fluid and implant on omentum, diaphragm, bowel serosa and pelvic surfaces, producing diffuse disease without deep organ invasion initially. Peritoneal inflammation, lymphatic obstruction and vascular permeability generate protein-rich fluid, distension and early satiety.

Recognition depends on the tempo, host context and anatomical pattern rather than one isolated result. Bloating, early satiety, pelvic or abdominal pain and urinary frequency occurring frequently and persistently are more concerning than occasional non-specific symptoms. Abdominal distension, shifting dullness, adnexal mass or rectovaginal nodularity indicates urgent suspected cancer referral. Weight loss, fatigue, altered bowel habit and reduced intake often accompany peritoneal disease. Investigation should answer immediate safety, diagnostic confirmation and extent in that order. Serum CA125 in primary care NICE advises ultrasound if CA125 is 35 units/mL or above; a normal result does not end assessment when symptoms persist or examination is abnormal. Pelvic and abdominal ultrasound Suspicious morphology or an examination mass requires urgent gynaecological cancer referral; benign ultrasound should trigger assessment for other causes and safety-netting. Contrast CT chest, abdomen and pelvis CT guides biopsy and operability but underestimates small peritoneal implants; expert surgical assessment remains necessary.

Management is determined by physiological urgency, disease extent, treatment intent and the person's priorities. The pathway moves through use ca125 and ultrasound without delay, then choose primary surgery or neoadjuvant therapy, then deliver platinum and maintenance coherently; each transition requires named multidisciplinary ownership. Follow-up must anticipate malignant bowel obstruction, pleural effusion, venous thromboembolism while measuring function and treatment toxicity.

Key points

Persistent frequent bloating, early satiety, pelvic pain or urinary urgency in an older woman warrants structured ovarian-cancer assessment.
A palpable pelvic mass or ascites requires urgent specialist referral; do not wait for CA125 before referring.
Without a mass, measure CA125 first and arrange pelvic and abdominal ultrasound when it is 35 units/mL or above.
Contrast CT stages suspected disease and estimates operability, but small peritoneal deposits can remain occult.
Obtain a core biopsy before neoadjuvant chemotherapy whenever safely feasible; CA125 and imaging are not histology.
Primary cytoreduction is preferred when complete macroscopic clearance is realistically achievable with acceptable morbidity.
Carboplatin–paclitaxel is the standard systemic backbone, followed by molecularly selected maintenance where indicated.
Offer germline testing at diagnosis and complete tumour BRCA or HRD testing early enough to guide maintenance treatment.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Age and ovulatory exposure

Risk rises after menopause and with greater lifetime ovulation, while pregnancy, breastfeeding and combined hormonal contraception reduce epithelial ovarian cancer risk.

Homologous-recombination deficiency

Germline or somatic BRCA1, BRCA2 and other repair defects increase high-grade serous risk and create sensitivity to platinum and PARP inhibition.

Lynch syndrome

Mismatch-repair pathogenic variants increase endometrioid and clear-cell ovarian cancers as part of a broader colorectal and endometrial cancer syndrome.

Endometriosis and tubal precursors

Endometriosis is associated with clear-cell and endometrioid cancer, while many high-grade serous cancers arise from distal fallopian-tube precursor epithelium.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Transcoelomic spread
Cells exfoliate into peritoneal fluid and implant on omentum, diaphragm, bowel serosa and pelvic surfaces, producing diffuse disease without deep organ invasion initially.
2
Ascites formation
Peritoneal inflammation, lymphatic obstruction and vascular permeability generate protein-rich fluid, distension and early satiety. In Ovarian cancer, this distinction materially changes mechanistic assessment.
3
Platinum sensitivity and resistance
DNA-repair-deficient tumours often respond deeply to platinum, while resistant clones emerge through repair restoration, drug efflux or altered replication stress.
4
Lymphatic and pleural spread
Pelvic and para-aortic nodes and transdiaphragmatic pleural involvement create advanced stage and respiratory symptoms. In Ovarian cancer, this distinction materially changes mechanistic assessment.
5
Bowel and ureteric compromise
Peritoneal implants and pelvic masses tether bowel or obstruct ureters, causing vomiting, hydronephrosis and renal dysfunction.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Persistent symptom cluster

Bloating, early satiety, pelvic or abdominal pain and urinary frequency occurring frequently and persistently are more concerning than occasional non-specific symptoms.

Ascites or pelvic mass

Abdominal distension, shifting dullness, adnexal mass or rectovaginal nodularity indicates urgent suspected cancer referral.

Constitutional and gastrointestinal change

Weight loss, fatigue, altered bowel habit and reduced intake often accompany peritoneal disease.

Pleural or thrombotic presentation

Breathlessness from pleural effusion or cancer-associated venous thrombosis may be the first clue to advanced disease.

Bowel obstructionRed flag

Colic, vomiting, distension and failure to pass stool or flatus requires emergency assessment for level, perforation and reversibility.

Inherited-risk pattern

Ovarian cancer at any age prompts germline assessment because family history alone misses many pathogenic variants.

Red flags requiring action

Persistent or frequent bloating, early satiety, pelvic or abdominal pain and urinary urgency occur especially in an older patient.
Ascites, a pelvic mass, nodularity or pleural effusion suggests advanced disease and needs urgent specialist assessment.
Vomiting, distension and obstipation suggests malignant bowel obstruction.
Sudden severe unilateral pelvic pain with nausea suggests torsion and requires emergency gynaecological review.
A first-degree family pattern of ovarian, early breast, pancreatic, prostate or Lynch-associated cancers raises inherited risk.
Rapid breathlessness, unilateral leg swelling or pleuritic pain suggests effusion or venous thromboembolism.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serum CA125 in primary careFirst step
Why
Triage persistent compatible symptoms in women without an obvious pelvic mass or ascites.
Interpretation and limitations
NICE advises ultrasound if CA125 is 35 units/mL or above; a normal result does not end assessment when symptoms persist or examination is abnormal.
02
Pelvic and abdominal ultrasound
Why
Characterise ovaries, morphology, vascularity, ascites and pelvic disease after symptoms or raised CA125.
Interpretation and limitations
Suspicious morphology or an examination mass requires urgent gynaecological cancer referral; benign ultrasound should trigger assessment for other causes and safety-netting.
03
Contrast CT chest, abdomen and pelvis
Why
Stage peritoneal, nodal, pleural and visceral disease and judge likelihood of complete cytoreduction.
Interpretation and limitations
CT guides biopsy and operability but underestimates small peritoneal implants; expert surgical assessment remains necessary.
04
Image-guided core biopsy
Why
Confirm histological type before neoadjuvant or systemic treatment when primary surgery is not the first step.
Interpretation and limitations
Core an omental, peritoneal, nodal or other safe deposit; cytology alone may be accepted only when core is unsafe and the clinical context is compelling.
05
Surgical staging pathology
Why
Establish histology, stage, tumour response and residual disease during primary cytoreduction.
Interpretation and limitations
Use comprehensive RCPath reporting, including tubes and SEE-FIM assessment where applicable; residual disease after surgery is a major prognostic variable.
06
Germline BRCA and broader panel
Why
Identify inherited risk and inform PARP maintenance and family prevention.
Interpretation and limitations
Offer at diagnosis through the mainstreamed pathway; negative family history does not remove eligibility.
07
Tumour HRD and molecular testing
Why
Identify somatic BRCA or homologous-recombination deficiency and less common subtype-specific targets.
Interpretation and limitations
Use validated tumour tissue early enough for maintenance decisions and interpret HRD as a predictive continuum rather than a diagnosis.
08
Risk of malignancy index
Why
Combine ultrasound, menopausal status and CA125 to support referral triage for an adnexal mass.
Interpretation and limitations
A score supports but does not override malignant morphology, ascites, symptoms or specialist judgement, and it is not used to monitor treated cancer.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Benign ovarian cyst

Simple morphology and low-risk context may support surveillance, but persistence, growth, solid components or postmenopausal status changes management.

Endometrioma

Typical homogeneous low-level echoes and endometriosis symptoms suggest benign disease, while mural nodules or postmenopausal change require expert review.

Uterine fibroid

A pedunculated fibroid can mimic an adnexal mass; ultrasound and MRI establish uterine origin. In Ovarian cancer, this distinction materially changes diagnostic assessment.

Gastrointestinal cancer

Krukenberg metastases and primary colorectal, gastric or appendiceal peritoneal cancer can resemble ovarian primary and require site-directed pathology.

Heart, liver or renal ascites

Systemic fluid disease can elevate CA125 through mesothelial irritation, so marker and ascites alone do not establish ovarian cancer.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01SymptomsUse CA125 and ultrasound without delayFirst stepA patient, especially aged 50 or over, reports persistent bloating, early satiety, pelvic pain or urinary frequency.

1Examine abdomen and pelvis; a mass or ascites warrants urgent referral rather than waiting for a marker.
2In primary care without an obvious mass, measure CA125 and arrange pelvic and abdominal ultrasound when it is 35 units/mL or above.
3AlternativeRefer suspicious ultrasound urgently; if tests are normal but symptoms persist, investigate alternative gastrointestinal, urinary and gynaecological causes and safety-net.

02StageChoose primary surgery or neoadjuvant therapyImaging suggests ovarian, tubal or primary peritoneal cancer.

1Obtain CT chest, abdomen and pelvis, performance, nutrition and surgical assessment focused on achieving complete macroscopic cytoreduction.
2Offer primary cytoreductive surgery when complete or near-complete removal is feasible with acceptable morbidity.
3When primary surgery is unlikely to achieve benefit or fitness is limited, obtain core tissue before neoadjuvant carboplatin–paclitaxel and plan interval surgery after response review.

03SystemicDeliver platinum and maintenance coherentlyEpithelial ovarian cancer is confirmed after surgery or core biopsy.

1Use carboplatin–paclitaxel for most high-grade epithelial cancers, adjusting for stage, histological subtype, frailty, neuropathy and renal function.
2Add bevacizumab in an eligible commissioned setting after reviewing bowel, wound, blood pressure, proteinuria and bleeding risk.
3Use germline and tumour BRCA or HRD results plus response to select PARP-inhibitor maintenance under current NICE guidance.

04RelapseBase recurrence treatment on biology and goalsSymptoms, CA125 trend or imaging suggests recurrent disease after primary therapy.

1Confirm clinically meaningful progression and define distribution, treatment-free interval, previous toxicity, BRCA or HRD status and performance.
2Use platinum-based combinations for platinum-sensitive relapse and non-platinum, targeted or trial options for resistant disease according to current pathways.
3Consider secondary cytoreduction only in carefully selected patients and integrate bowel, ascites, pleural, pain, thrombosis and palliative support early.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Provides first-line adjuvant, neoadjuvant and selected recurrent platinum-sensitive treatment.

Carboplatin with paclitaxel

A standard epithelial ovarian regimen gives paclitaxel 175 mg/m² IV followed by carboplatin targeted at AUC 5–6 IV on day 1 every 21 days, usually for 6 cycles with protocolled adjustments.

Calculate carboplatin from reliable GFR, use hypersensitivity precautions and antiemesis, and monitor counts, neuropathy, renal and liver function, infection and paclitaxel reactions before each cycle.

Provides maintenance PARP inhibition after platinum response in eligible BRCA-mutated or HRD-associated ovarian cancer settings.

Olaparib

Use 300 mg orally twice daily continuously as tablets, with interruption and reduction to 250 mg then 200 mg twice daily for toxicity according to the licensed indication and maintenance duration.

Confirm the exact molecular and treatment indication, monitor blood count monthly early and then regularly, and investigate persistent cytopenia for myelodysplasia; review nausea, fatigue, renal function and interactions.

Suppresses VEGF-driven angiogenesis and can prolong disease control in selected advanced or recurrent ovarian cancer.

Bevacizumab

A common ovarian-cancer schedule is 15 mg/kg IV every 3 weeks with carboplatin–paclitaxel, then continued alone for the protocol-defined total duration in an eligible commissioned setting.

Review bowel involvement and perforation risk, recent surgery and wound healing, hypertension, proteinuria, bleeding, thrombosis and fistula; pause around major operations according to product guidance.

Reduces the high postoperative venous-thromboembolism risk alongside mechanical measures and mobilisation.

Enoxaparin after major ovarian cancer surgery

A common prophylactic regimen is 40 mg subcutaneously once daily, started at the locally authorised postoperative time and considered for extension to 28 days after major abdominal or pelvic cancer surgery.

Adjust for renal function and body weight, monitor bleeding and platelets, and coordinate with neuraxial procedures; this dose does not treat established thrombosis.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Malignant bowel obstruction

Diffuse peritoneal disease causes single or multiple transition points, vomiting, aspiration, dehydration and difficult surgical decisions.

Pleural effusion

Transdiaphragmatic or pleural spread causes dyspnoea and may require drainage, pleurodesis or catheter alongside systemic treatment.

Venous thromboembolism

High thrombotic risk is amplified by surgery, immobility and systemic therapy and may be the presenting event.

Ureteric obstruction

Pelvic disease can cause hydronephrosis, infection and renal loss, requiring stent or nephrostomy to preserve function and treatment options.

Treatment-related neuropathy and marrow toxicity

Paclitaxel and platinum can cause sensory neuropathy, cytopenia, hypersensitivity, renal or hearing effects that influence later treatment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During first-line therapy, review symptoms, examination, CA125 when initially informative and interval CT at decision points rather than after every dose.
Check full blood count, renal and liver function, neuropathy, infection and hypersensitivity before each platinum–taxane cycle.
During PARP maintenance, monitor blood count, fatigue, nausea and persistent cytopenia with prompt marrow investigation when indicated.
After bevacizumab, follow blood pressure, urine protein, bleeding, wound healing, bowel pain and fistula or perforation symptoms.
After treatment, use symptom-triggered review and agreed follow-up; a CA125 rise alone requires shared discussion because early treatment of marker-only relapse does not automatically improve survival.
Ensure germline results, family referral and risk-reducing advice are completed and not lost after the immediate cancer treatment decision.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Symptoms are a pattern

Frequent persistent bloating and early satiety differ from occasional fluctuation and deserve testing even without a palpable mass.

A mass bypasses CA125 triage

Ascites or a pelvic mass needs urgent specialist referral; a reassuring marker must not postpone it.

Tissue precedes neoadjuvant treatment

When chemotherapy comes before surgery, obtain a core diagnosis so metastatic gastrointestinal cancer or another histology is not treated as ovarian cancer.

Complete cytoreduction matters

The aim of surgery is no visible residual disease when achievable safely, not simply removing both ovaries.

Genetics is treatment

BRCA and HRD information affects maintenance choices and simultaneously creates prevention opportunities for relatives.

11Common pitfallsFrequent interpretation and management errors.

01
Using CA125 as a screening test in asymptomatic average-risk women.
02
Reassuring a patient with a mass or ascites because CA125 is normal.
03
Starting neoadjuvant chemotherapy without adequate tissue when biopsy is feasible.
04
Undertaking low-volume non-specialist debulking that compromises complete cytoreduction.
05
Starting bevacizumab despite uncontrolled hypertension, unhealed surgery or high perforation risk.
06
Failing to offer germline testing because family history is negative.