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Roles of CUX1 proteins in DNA damage responses and the resistance of cancer cells to radiotherapy and chemotherapy
Dr. Nepveu’s laboratory studies the regulation of transcription in mammalian cells and, in particular, the roles of transcription factors in DNA damage responses. We combine a vast array of molecular biology and functional genomic approaches together with tissue culture and mouse models to investigate how alterations in DNA repair and DNA damage responses contribute to the initiation and progression of cancer. We study how defects in DNA repair can contribute to tumor initiation and how certain cancer cells become dependent on specific DNA repair pathways. It is generally accepted that defects in DNA repair, whether transient or permanent, contribute to tumor development and progression. Yet, to replicate their DNA and proliferate, cancer cells need DNA repair mechanisms, perhaps even more so than normal cells. Moreover, efficient DNA repair mechanisms can enable cancer cells to resist radiotherapy and chemotherapy. We are entering a new era of cancer research in which patients will be stratified for appropriate therapy on the basis of their DNA repair status, rather than on the tissue of origin, and where combination treatments will include DNA repair inhibitors. The goal of our work is to use the acquired knowledge to exacerbate the sensitivity of cancer cells to radiotherapy and specific chemotherapeutic treatments.
Roles of CUX1 proteins in DNA damage responses and the resistance of cancer cells to radiotherapy and chemotherapy
Dr. Nepveu’s laboratory studies the regulation of transcription in mammalian cells and, in particular, the roles of transcription factors in DNA damage responses. We combine a vast array of molecular biology and functional genomic approaches together with tissue culture and mouse models to investigate how alterations in DNA repair and DNA damage responses contribute to the initiation and progression of cancer. We study how defects in DNA repair can contribute to tumor initiation and how certain cancer cells become dependent on specific DNA repair pathways. It is generally accepted that defects in DNA repair, whether transient or permanent, contribute to tumor development and progression. Yet, to replicate their DNA and proliferate, cancer cells need DNA repair mechanisms, perhaps even more so than normal cells. Moreover, efficient DNA repair mechanisms can enable cancer cells to resist radiotherapy and chemotherapy. We are entering a new era of cancer research in which patients will be stratified for appropriate therapy on the basis of their DNA repair status, rather than on the tissue of origin, and where combination treatments will include DNA repair inhibitors. The goal of our work is to use the acquired knowledge to exacerbate the sensitivity of cancer cells to radiotherapy and specific chemotherapeutic treatments.
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Elise Vickridge,Camila C. F. Faraco, Fanny Lo, Hedyeh Rahimian, Zi Yang Liu, Payman S. Tehrani,Billel Djerir,Zubaidah M. Ramdzan,Lam Leduy,Alexandre Marechal,Anne-Claude Gingras,Alain Nepveu
NUCLEIC ACIDS RESEARCHno. 1 (2024): 223-242
crossref(2023)
NAR CANCERno. 1 (2023)
Journal of Radiation and Cancer Researchno. 2 (2018): 67-78
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