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Genomic Determinants of Homologous Recombination Deficiency across Human Cancers.
Qing, Tao; Wang, Xinfeng; Jun, Tomi; Ding, Li; Pusztai, Lajos; Huang, Kuan-Lin.
Afiliación
  • Qing T; Breast Medical Oncology, School of Medicine, Yale University, New Haven, CT 06511, USA.
  • Wang X; Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
  • Jun T; Division of Hematology and Medical Oncology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Ding L; Department of Medicine, McDonnell Genome Institute, Washington University in St. Louis, St. Louis, MO 63110, USA.
  • Pusztai L; Department of Genetics, Siteman Cancer Center, Washington University in St. Louis, St. Louis, MO 63110, USA.
  • Huang KL; Breast Medical Oncology, School of Medicine, Yale University, New Haven, CT 06511, USA.
Cancers (Basel) ; 13(18)2021 09 12.
Article en En | MEDLINE | ID: mdl-34572800
Germline BRCA1/2 mutations associated with HRD are clinical biomarkers for sensitivity to poly-ADP ribose polymerase inhibitors (PARPi) treatment in breast, ovarian, pancreatic, and prostate cancers. However, it remains unclear whether other mutations may also lead to HRD and PARPi sensitivity across a broader range of cancer types. Our goal was to determine the germline or somatic alterations associated with the HRD phenotype that might therefore confer PARPi sensitivity. Using germline and somatic genomic data from over 9000 tumors representing 32 cancer types, we examined associations between HRD scores and pathogenic germline variants, somatic driver mutations, and copy number deletions in 30 candidate genes involved in homologous recombination. We identified several germline and somatic mutations (e.g., BRCA1/2, PALB2, ATM, and ATR mutations) associated with HRD phenotype in ovarian, breast, pancreatic, stomach, bladder, and lung cancer. The co-occurrence of germline BRCA1 variants and somatic TP53 mutations was significantly associated with increasing HRD in breast cancer. Notably, we also identified multiple somatic copy number deletions associated with HRD. Our study suggests that multiple cancer types include tumor subsets that show HRD phenotype and should be considered in the future clinical studies of PARPi and synthetic lethality strategies exploiting HRD, which can be caused by a large number of genomic alterations.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Cancers (Basel) Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Cancers (Basel) Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza