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HRD-positive means the tumour's genome carries the scars of failed double-strand break repair (or a BRCA mutation), measured as a genomic instability score. In ovarian cancer it selects niraparib, and olaparib with bevacizumab, as first-line maintenance.
The Myriad myChoice CDx combines tumour BRCA1/2 status with a genomic instability score built from loss of heterozygosity, telomeric allelic imbalance and large-scale state transitions; the assay calls HRD-positive at a GIS of 42 or more (the PRIMA and PAOLA-1 trials' cut-off) or any deleterious BRCA mutation. Niraparib's US label defines HRD-positive status as 'a deleterious or suspected deleterious BRCA mutation, and/or genomic instability' and the olaparib plus bevacizumab first-line maintenance indication is for HRD-positive advanced ovarian cancer. Because the scar accumulates over time, HRD status is read on tumour tissue and does not capture reversion, which is why HRD-positive tumours can still be PARP-resistant.
In plain words · DNA repair genes. Inheriting a broken copy raises breast and ovarian cancer risk, but tumours that lose them become uniquely vulnerable to PARP inhibitors and platinum.
HRD-positive on a myChoice report (a BRCA mutation or a genomic instability score of 42 or more) means your ovarian cancer is likely to respond to PARP inhibitors: niraparib alone, or olaparib with bevacizumab, are on label as maintenance after first chemotherapy. An HRD-negative result does not rule out niraparib, whose first-line label covers all comers, but the expected benefit is smaller.
Written only from the label or guideline text cited on this page. Not medical advice; your own report and the reading your team gives it come first.
HRD-positive: a deleterious or suspected deleterious tumour BRCA1/2 mutation, or a genomic instability score at or above the assay's cut-off (42 on the myChoice CDx), computed from loss of heterozygosity, telomeric allelic imbalance and large-scale state transitions.
“Deleterious or suspected deleterious germline or somatic mutations in BRCA1 and BRCA2 genes and/or positive Genomic Instability Score”
FDA: List of FDA-Authorized Companion Diagnostic Devices| Threshold | Drug | Cancer | Regulator | Source |
|---|---|---|---|---|
| HRD-positive (BRCA mutation and/or genomic instability) | Niraparib | Ovarian cancer | FDA | label |
| HRD-positive | Olaparib | Ovarian cancer | FDA | label |
| Device | Maker | Indication and sample | Drug | PMA / 510(k) |
|---|---|---|---|---|
| Myriad myChoice CDx | Myriad Genetic Laboratories | Ovarian Cancer - Tissue | Olaparib | P190014/S003 (05/08/2020) |
| Myriad myChoice CDx | Myriad Genetic Laboratories | Ovarian Cancer - Tissue | Niraparib | P190014/S011 (03/10/2026) |
Matched on the name and aliases of the readout in the title, setting and summary of each trial; a match is a mention, not proof the readout was an entry criterion.
It defines who a homologous recombination result should send to platinum: core-gene and biallelic carriers, germline or somatic, rather than any repair-gene variant.
It is the best population-based estimate of how much TNBC is homologous recombination deficient, shows that most of it is not germline BRCA, and argues that whole-genome sequencing at diagnosis could stratify trials and pick out the low group that needs something other than DNA-damaging chemotherapy.
One pairing page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
The survival evidence behind platinum in early triple-negative disease, and the first large demonstration that most triple-negative tumours are DNA-repair deficient whether or not BRCA is mutated, which is why HRD scores have not become a platinum selection test.
Signatures find repair-deficient tumours that gene panels miss, and they mark the minority in which checkpoint drugs have a rationale.
One technology page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
This paper set the HRD score threshold the myChoice assay still uses and showed that genomic scars extend platinum sensitivity beyond BRCA carriers in early TNBC, though the TNT trial later found the same score did not predict carboplatin benefit in advanced disease.
The genomic case for platinum in BRCA-type pancreatic cancer, four years before POLO built a maintenance strategy on top of it.
Shares Triple-negative breast cancer (TNBC), Pancreatic ductal adenocarcinoma, Prostate cancer and the tags biomarker, genome-wide.
Shares Platinum-sensitive / platinum-resistant, Tumour (somatic or germline) BRCA1/2 mutation and HRR gene alterations, Homologous recombination repair gene mutation in prostate cancer, High-grade serous ovarian cancer.
Shares Early triple-negative breast cancer, Triple-negative breast cancer (TNBC), Pancreatic ductal adenocarcinoma and the tags biomarker, genome-wide.
Shares HRDetect is a predictor of BRCA1 and BRCA2 deficiency based on mutational signatures, Homologous recombination deficiency (HRD) score predicts response to platinum-containing neoadjuvant chemotherapy in patients with triple-negative breast cancer, myChoice CDx, High-grade serous ovarian cancer.
Shares HRDetect is a predictor of BRCA1 and BRCA2 deficiency based on mutational signatures, Homologous recombination deficiency (HRD) score predicts response to platinum-containing neoadjuvant chemotherapy in patients with triple-negative breast cancer, Whole-genome sequencing of triple-negative breast cancers in a population-based clinical study, myChoice CDx.
Shares Tumour (somatic or germline) BRCA1/2 mutation and HRR gene alterations, Homologous recombination repair gene mutation in prostate cancer, BRCA1 / BRCA2 (HRD), Prostate cancer and the tag biomarker.
Shares Association of distinct mutational signatures with correlates of increased immune activity in pancreatic ductal adenocarcinoma, Whole-genome sequencing of triple-negative breast cancers in a population-based clinical study, Genomic methods identify homologous recombination deficiency in pancreas adenocarcinoma and optimize treatment selection, Whole genomes redefine the mutational landscape of pancreatic cancer.
Shares BRCA or PALB2-mutant pancreatic ductal adenocarcinoma, Olaparib, BRCA1 / BRCA2 (HRD), Pancreatic ductal adenocarcinoma and the tag brca.