ArticleMolecular therapy. Nucleic acids2021
A transcriptional signature detects homologous recombination deficiency in pancreatic cancer at the individual level.
Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 20 citations in OpenAlex.
- Multiomics analysis of homologous recombination deficiency across cancer types.Biomolecules & biomedicine · 2024Article
- The coexistence of a BRCA2 germline and a DICER1 somatic variant in two first-degree cousins suggests their potential synergic effect.Scientific reports · 2024Article
- Review
- Unravelling homologous recombination repair deficiency and therapeutic opportunities in soft tissue and bone sarcoma.EMBO molecular medicine · 2023Article
- Article
- Validation of genomic and transcriptomic models of homologous recombination deficiency in a real-world pan-cancer cohort.BMC cancer · 2022Article
- A Risk Model Developed Based on Homologous Recombination Deficiency Predicts Overall Survival in Patients With Lower Grade Glioma.Frontiers in genetics · 2022Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
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Abstract
Pancreatic cancer (PC) with homologous recombination deficiency (HRD) has been reported to benefit from poly ADP-ribose polymerase (PARP) inhibitors. However, accurate identification of HRD status for PC patients from the transcriptional level is still a great challenge. Here, based on a relative expression ordering (REO)-based algorithm, we developed an HRD signature including 24 gene pairs (24-GPS) using PC transcriptional profiles from The Cancer Genome Atlas (TCGA). HRD samples classified by 24-GPS showed worse overall survival (p = 4.4E-3 for TCGA; p = 1.2E-3 for International Cancer Genome Consortium-Australia cohort; p = 6.4E-2 for GSE17891; p = 7.5E-2 for GSE57495) and higher HRD scores than non-HRD samples (p = 1.4E-4). HRD samples showed highly unstable genomic characteristics and also displayed HRD-related alterations at the epigenomic and proteomic levels. Moreover, HRD cell lines identified by 24-GPS tended to be sensitive to PARP inhibitors (p = 6.6E-2 for olaparib; p = 2.6E-3 for niraparib). Compared with the non-HRD group, the HRD group presented lower immune scores and CD4/CD8 T cell infiltration proportion. Interestingly, PC tumor cells with co-inhibition of PARP-related genes and
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