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Epithelial ovarian cancer is separated by histological subtype, and high-grade serous carcinoma dominates both in frequency and in how the molecular discussion is framed. DNA repair capability, specifically homologous recombination, is the organising molecular idea. Germline testing is discussed for all patients with the relevant histology rather than being triggered by family history.
Also called Epithelial ovarian cancer, High-grade serous carcinoma, Fallopian tube and primary peritoneal cancer.
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High-grade serous ovarian cancer is the disease where homologous recombination status is most central, and where the germline question is raised for essentially everyone rather than only for those with a family history.
Epithelial ovarian cancer is separated by histological subtype, and high-grade serous carcinoma dominates both in frequency and in how the molecular discussion is framed. DNA repair capability, specifically homologous recombination, is the organising molecular idea. Germline testing is discussed for all patients with the relevant histology rather than being triggered by family history.
01Before any molecular question
Usually established first: histological subtype and grade, stage, and whether surgery has achieved complete cytoreduction. Ovarian cancer, fallopian tube cancer and primary peritoneal cancer are frequently grouped together because they behave similarly.
Usually already established
02
The divisions below are not labels. Each one changes what the treatment discussion is actually about.
High-grade serous
The most common subtype, characterised by near-universal TP53 alteration and frequent homologous recombination deficiency. The subtype in which the molecular discussion is most developed.
Low-grade serous
Biologically distinct, slower growing, with MAPK pathway alterations such as KRAS, NRAS and BRAF more prominent.
Clear cell and endometrioid
Distinct biology again, with ARID1A and PI3K pathway alterations discussed, and an association with endometriosis.
Mucinous
Uncommon, and behaves more like a gastrointestinal cancer in several respects, including which markers are discussed.
03What is discussed
BRCA1 and BRCA2 are central, both as inherited and as tumour-only findings. Beyond them, homologous recombination deficiency describes a broader functional state that can arise from other genes in the same pathway or be measured as a genomic scar signature. TP53 alteration is near-universal in high-grade serous disease and is diagnostic rather than actionable. In low-grade serous disease, KRAS, NRAS and BRAF dominate. ARID1A and PI3K pathway alterations appear in clear cell and endometrioid subtypes. Mismatch repair deficiency is uncommon but assessed, particularly in non-serous subtypes.
BRCA1 and BRCA2
Central to both the germline and the tumour discussion. The distinction between the two matters for relatives.
HRD
Homologous recombination deficiency. A functional state, measured by a scar signature rather than by one gene.
TP53
Near-universal in high-grade serous disease. Supports the diagnosis rather than opening a treatment.
KRAS, NRAS, BRAF
More relevant in low-grade serous disease than in high-grade.
ARID1A
Associated with clear cell and endometrioid subtypes.
MMR / MSI
Uncommon in serous disease, more relevant in endometrioid and clear cell subtypes.
This is not an exhaustive list, and which markers are relevant depends on the individual case. Not every marker listed is assessed in every patient.
04What is tested, and from what
Two questions are usually asked in parallel: is there an inherited alteration, and does the tumour show homologous recombination deficiency? They are answered by different tests, on different samples, and the germline answer has implications for relatives that the tumour answer does not. Timing matters because the results are relevant to decisions made after initial treatment rather than months later.
Germline testing is discussed for all patients with epithelial ovarian cancer regardless of family history, because the prior probability is high enough that family history is an unreliable filter. A germline BRCA1 or BRCA2 finding has direct implications for the patient and opens a cascade testing pathway for relatives, who may be able to act on the information before any cancer develops. Lynch syndrome genes are also relevant, particularly in non-serous subtypes.
Cancer genetics and hereditary riskPlasma testing is less established here than in lung or breast cancer, in part because tissue is usually available from surgery. Serial ctDNA is under study for detecting recurrence earlier than CA-125 and imaging, and the same question applies as elsewhere: what would be done differently with an earlier signal.
More on ctDNA monitoring05The timing question
Testing that arrives after the decision it was meant to inform has already been made is a common and avoidable problem. This is the sequence in which molecular information tends to become relevant.
06Take these to your team
When a decision is being made
Questions worth raising with a treating team.
At progression, recurrence or resistance
The molecular picture at diagnosis is not always the molecular picture later.
07What shapes eligibility
Homologous recombination status, prior treatment sequence, and the interval since last treatment are the criteria that most commonly determine eligibility. Histological subtype is also frequently specified, and low-grade serous disease has its own distinct trial landscape.
| Term | What it means |
|---|---|
| High-grade serous | The most common subtype of epithelial ovarian cancer, and the one most of the molecular literature refers to. |
| Homologous recombination | A high-fidelity DNA repair mechanism. When it fails, cells become dependent on other, more error-prone routes. |
| HRD score | A measurement of the genomic damage left behind by failed repair, used as a functional readout rather than a single gene test. |
| Cascade testing | Offering testing to relatives once an inherited alteration is found in the family. |
| Cytoreduction | Surgery aimed at removing as much visible disease as possible. |
These are the services most often relevant to this cancer. Which of them applies is a clinical question, not an automatic one.
This entry is educational. It describes what is commonly discussed in this cancer, not what should happen for any individual. Which of it applies depends on the specific diagnosis, stage, prior treatment and the person themselves. Nothing here is a recommendation, and no list of biomarkers here is exhaustive. Decisions belong with a treating team who know the whole case.
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