A5045326986- DNA Repair Mechanisms
- BRCA gene mutations in cancer
- PARP inhibition in cancer therapy
- Biochemical Acid Research Studies
- Alcoholism and Thiamine Deficiency
- Monoclonal and Polyclonal Antibodies Research
- Peptidase Inhibition and Analysis
- Radiopharmaceutical Chemistry and Applications
- Metabolism and Genetic Disorders
- CRISPR and Genetic Engineering
Université de Montpellier
2022-2025
Inserm
2014-2025
Institut de Recherche en Cancérologie de Montpellier
2014-2025
Centre National de la Recherche Scientifique
2022-2023
BRCA1 deficiency is observed in approximately 25% of triple-negative breast cancer (TNBC). BRCA1, a key player homologous recombination (HR) repair, also involved stalled DNA replication fork protection and repair. Here, we investigated the sensitivity BRCA1-deficient TNBC models to frequently used chain terminator gemcitabine, which does not directly induce breaks. A large fraction cells was sensitive contrast their isogenic BRCA1-proficient counterparts. Gemcitabine treated accumulated...
Abstract Most high‐grade ovarian carcinomas (HGOCs) are sensitive to carboplatin (CBP)‐based chemotherapy but frequently recur within 24 months. Recurrent tumors remain CBP‐sensitive and acquire resistance only after several treatment rounds. Recurrences arise from a small number of residual tumor cells not amenable investigation in patients. We developed patient‐derived xenografts (PDXs) that allow the study these different stages recurrence acquisition resistance. generated PDX models...
About 15% of Triple-Negative-Breast-Cancer (TNBC) present silencing the BRCA1 promoter methylation and are assumed to be Homologous Recombination Deficient (HRD). BRCA1-methylated (BRCA1-Me) TNBC could, thus, eligible treatment based on PARP-inhibitors or Platinum salts. However, their actual HRD status is discussed, as these tumors suspected develop resistance after chemotherapy exposure. We interrogated sensitivity olaparib vs. carboplatin 8 Patient-Derived Xenografts (PDX) models. Four...
Abstract BRCA1, BRCA2 and RAD51, key players of homologous recombination (HR) repair, are also involved in stalled DNA replication fork protection repair. BRCA1-deficiency is encountered 25% Triple Negative Breast Cancer (TNBC). Here we investigated the sensitivity BRCA1 -deficient TNBC cell models to gemcitabine a frequently used poison that does not alter structure. We show BRCA1-deficient models, contrast their isogenic -proficient counterparts, superiorly sensitive gemcitabine,...