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YU238259 Is a Novel Inhibitor of Homology-Dependent DNA Repair That Exhibits Synthetic Lethality and Radiosensitization in Repair-Deficient Tumors.
Stachelek, Gregory C; Peterson-Roth, Elizabeth; Liu, Yanfeng; Fernandez, Rafael J; Pike, Luke R G; Qian, Jack M; Abriola, Laura; Hoyer, Denton; Hungerford, William; Merkel, Janie; Glazer, Peter M.
Afiliación
  • Stachelek GC; Department of Therapeutic Radiology, Yale School of Medicine, New Haven, Connecticut. Department of Genetics, Yale School of Medicine, New Haven, Connecticut.
  • Peterson-Roth E; Department of Therapeutic Radiology, Yale School of Medicine, New Haven, Connecticut.
  • Liu Y; Department of Therapeutic Radiology, Yale School of Medicine, New Haven, Connecticut.
  • Fernandez RJ; Department of Therapeutic Radiology, Yale School of Medicine, New Haven, Connecticut.
  • Pike LR; Department of Therapeutic Radiology, Yale School of Medicine, New Haven, Connecticut.
  • Qian JM; Department of Therapeutic Radiology, Yale School of Medicine, New Haven, Connecticut.
  • Abriola L; Yale Center for Molecular Discovery, West Haven, Connecticut.
  • Hoyer D; Yale Center for Molecular Discovery, West Haven, Connecticut.
  • Hungerford W; Yale Center for Molecular Discovery, West Haven, Connecticut.
  • Merkel J; Yale Center for Molecular Discovery, West Haven, Connecticut.
  • Glazer PM; Department of Therapeutic Radiology, Yale School of Medicine, New Haven, Connecticut. Department of Genetics, Yale School of Medicine, New Haven, Connecticut. peter.glazer@yale.edu.
Mol Cancer Res ; 13(10): 1389-97, 2015 Oct.
Article en En | MEDLINE | ID: mdl-26116172
UNLABELLED: Radiotherapy and DNA-damaging chemotherapy are frequently utilized in the treatment of solid tumors. Innate or acquired resistance to these therapies remains a major clinical challenge in oncology. The development of small molecules that sensitize cancers to established therapies represents an attractive approach to extending survival and quality of life in patients. Here, we demonstrate that YU238259, a member of a novel class of DNA double-strand break repair inhibitors, exhibits potent synthetic lethality in the setting of DNA damage response and DNA repair defects. YU238259 specifically inhibits homology-dependent DNA repair, but not non-homologous end-joining, in cell-based GFP reporter assays. Treatment with YU238259 is not only synergistic with ionizing radiation, etoposide, and PARP inhibition, but this synergism is heightened by BRCA2 deficiency. Further, growth of BRCA2-deficient human tumor xenografts in nude mice is significantly delayed by YU238259 treatment even in the absence of concomitant DNA-damaging therapy. The cytotoxicity of these small molecules in repair-deficient cells results from an accumulation of unresolved DNA double-strand breaks. These findings suggest that YU238259 or related small molecules may have clinical benefit to patients with advanced BRCA2-negative tumors, either as a monotherapy or as an adjuvant to radiotherapy and certain chemotherapies. IMPLICATIONS: We have identified a novel series of compounds that demonstrate synthetic lethality in DNA repair-deficient cell and animal models and have strong potential for clinical translation.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fármacos Sensibilizantes a Radiaciones / Sulfonamidas / Benzamidas / Reparación del ADN / Neoplasias Tipo de estudio: Prognostic_studies Aspecto: Patient_preference Límite: Animals / Humans Idioma: En Revista: Mol Cancer Res Asunto de la revista: BIOLOGIA MOLECULAR / NEOPLASIAS Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fármacos Sensibilizantes a Radiaciones / Sulfonamidas / Benzamidas / Reparación del ADN / Neoplasias Tipo de estudio: Prognostic_studies Aspecto: Patient_preference Límite: Animals / Humans Idioma: En Revista: Mol Cancer Res Asunto de la revista: BIOLOGIA MOLECULAR / NEOPLASIAS Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos