ArticleThe oncologist2025
Genomic landscape and homologous recombination repair deficiency signature in stage I-III and de novo stage IV primary breast cancers.
Article in The oncologist, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Genomic landscape and therapeutic implications of Anaplastic Lymphoma Kinase fusion-positive colorectal cancer.The oncologist · 2026Article
- Homologous Recombination Deficiency in Ovarian and Breast Cancers: Biomarkers, Diagnosis, and Treatment.Current issues in molecular biology · 2025Review
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9 authors.
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Abstract
purposeWe compared genomic alterations and a homologous recombination deficiency (HRD) signature (HRDsig) in primary tumors from stage I-III to those in de novo stage IV breast cancers and from stage I-III cancers with early (<2 years after diagnosis) versus late (>2 years) recurrence.
methodsDe-identified genomic and clinical data of primary breast cancers (stage I-III N = 910, stage IV N = 783) from the United States, the nationwide clinico-genomic database of Flatiron Health and Foundation Medicine were analyzed. Genomic results included the mutation status of 324 cancer-related genes and HRDsig, a DNA scar-based measure of HRD.
resultsNo significant differences were observed in the frequencies of genomic alterations across disease stages, or between stage I-III cancers with early versus late relapse. Overall, the most prevalent biomarkers were PIK3CA mutation and HRDsig positivity. HRDsig positivity was observed in 82% of germline or somatic g/sBRCA1/2 or germline PALB2 (gPALB2) mutated cancers, 13.1% in cancers with other HR-repair (HRR) gene alterations (ATM, BARD1, BRIP1, CDK12, CHEK1, CHEK2, FANCL, somatic PALB2 (sPALB2), RAD51B, RAD51C, RAD51D and RAD54L), and also in 16.5% of HRR wild-type cancers. HRDsig positivity was observed across receptor subtypes and was the highest in TNBC (30%), followed by ER+/HER2- cancers (17%), then HER2 + cancers (8.7%).
conclusionsEarly-stage (I-III) and de novo stage IV breast cancers shared a similar prevalence of targetable genomic alterations and overall genomic landscape. HRDsig identified approximately 16% of breast cancers without g/sBRCA/gPALB2 alteration that might potentially benefit from PARP inhibitors or platinum-based treatments and should be tested in future clinical studies.
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