A5024591696- DNA Repair Mechanisms
- Cancer-related Molecular Pathways
- Cancer therapeutics and mechanisms
- interferon and immune responses
- Cancer, Hypoxia, and Metabolism
- Mitochondrial Function and Pathology
- Bioactive Compounds and Antitumor Agents
- Ubiquitin and proteasome pathways
- Carcinogens and Genotoxicity Assessment
- Herpesvirus Infections and Treatments
- RNA regulation and disease
- Systemic Lupus Erythematosus Research
- PARP inhibition in cancer therapy
- Animal Virus Infections Studies
- Cytomegalovirus and herpesvirus research
- RNA Research and Splicing
- Microtubule and mitosis dynamics
- CRISPR and Genetic Engineering
- Cancer Genomics and Diagnostics
- Metal-Catalyzed Oxygenation Mechanisms
- HIV Research and Treatment
Centre National de la Recherche Scientifique
2017-2025
Institut de Génétique Humaine
2017-2025
Université de Montpellier
2017-2024
La Ligue Contre le Cancer
2024
Although many patients with colorectal cancer initially respond to the chemotherapeutic agent oxaliplatin, acquired resistance this treatment remains a major challenge long-term management of disease. To identify molecular targets oxaliplatin in cancer, we performed an shRNA-based loss-of-function genetic screen using kinome library. We found that silencing ataxia-telangiectasia mutated and RAD3-related (ATR), serine/threonine protein kinase involved response DNA stress, restored sensitivity...
Cancer cells display high levels of oncogene-induced replication stress (RS) and rely on DNA damage checkpoint for viability. This feature is exploited by cancer therapies to either increase RS unbearable or inhibit kinases involved in the response. Thus far, treatments that combine these two strategies have shown promise but also severe adverse effects. To identify novel, better-tolerated anticancer combinations, we screened a collection plant extracts found natural compounds from plant,...
CDC7-DBF4 kinase (DDK) initiates DNA replication in eukaryotes by activating the replicative MCM helicase. DDK has diverse and apparently conflicting roles checkpoint response various organisms, but underlying mechanisms are far from settled. We show that human promotes limited resection of newly synthesized at stalled forks or sites damage to initiate signaling. is also required for efficient fork restart G2/M cell cycle arrest. exhibits genetic interactions with ssDNA exonuclease EXO1...
Abstract Cancer cells display high levels of oncogene-induced replication stress (RS) and rely on DNA damage checkpoint for viability. This feature is exploited by cancer therapies to either increase RS unbearable or inhibit kinases involved in the response (DDR). Thus far, treatments that combine these two strategies have shown promise but also severe adverse effects. To identify novel, better-tolerated anticancer combinations, we screened a collection plant extracts found natural compounds...
<title>Abstract</title> Cancer cells display high levels of oncogene-induced replication stress (RS) and rely on DNA damage checkpoint for viability. This feature is exploited by cancer therapies to either increase RS unbearable or inhibit kinases involved in the response (DDR). Thus far, treatments that combine these two strategies have shown promise but also severe adverse effects. To identify novel, better-tolerated anticancer combinations, we screened a collection plant extracts found...
Cancer cells display high levels of oncogene-induced replication stress (RS) and rely on DNA damage checkpoint for viability. This feature is exploited by cancer therapies to either increase RS unbearable or inhibit kinases involved in the response (DDR). Thus far, treatments that combine these two strategies have shown promise but also severe adverse effects. To identify novel, better-tolerated anticancer combinations, we screened a collection plant extracts found natural compounds from...
Cancer cells display high levels of oncogene-induced replication stress (RS) and rely on DNA damage checkpoint for viability. This feature is exploited by cancer therapies to either increase RS unbearable or inhibit kinases involved in the response. Thus far, treatments that combine these two strategies have shown promise but also severe adverse effects. To identify novel, better-tolerated anticancer combinations, we screened a collection plant extracts found natural compounds from plant,...
<div>Abstract<p>Although many patients with colorectal cancer initially respond to the chemotherapeutic agent oxaliplatin, acquired resistance this treatment remains a major challenge long-term management of disease. To identify molecular targets oxaliplatin in cancer, we performed an shRNA-based loss-of-function genetic screen using kinome library. We found that silencing ataxia-telangiectasia mutated and RAD3-related (ATR), serine/threonine protein kinase involved response DNA...
<p>Suppression of ATR expression sensitizes HCT116-R1 cells to oxaliplatin.</p>
<div>Abstract<p>Although many patients with colorectal cancer initially respond to the chemotherapeutic agent oxaliplatin, acquired resistance this treatment remains a major challenge long-term management of disease. To identify molecular targets oxaliplatin in cancer, we performed an shRNA-based loss-of-function genetic screen using kinome library. We found that silencing ataxia-telangiectasia mutated and RAD3-related (ATR), serine/threonine protein kinase involved response DNA...
<p>Effect of ATR inhibition combined with oxaliplatin treatment on the and ATM pathways.</p>
<p>Oxaliplatin combined with the ATR inhibitor VE-822 induces immune death signalling</p>
<p>Effect of ATR inhibition combined with oxaliplatin treatment on the and ATM pathways.</p>
<p>Oxaliplatin combined with the ATR inhibitor VE-822 induces immune death signalling</p>
<p>Suppression of ATR expression sensitizes HCT116-R1 cells to oxaliplatin.</p>
Abstract CDC7-DBF4 kinase (DDK) is required to initiate DNA replication in eukaryotes by activating the replicative MCM helicase. DDK has also been reported have diverse and sometimes conflicting roles checkpoint response various organisms but underlying mechanisms are far from settled. Here we show that human promotes limited resection of newly synthesized at stalled forks or sites damage signaling. for efficient fork restart G2/M cell cycle arrest. exhibits genetic interactions with ssDNA...
Abstract Despite the recent advances achieved in treatment of colon cancer, tumor resistance is a frequent cause chemotherapy failure. The aim this project thus to identify new targets involved oxaliplatin using phenotypic high-throughput screening. We established oxaliplatin-resistant cellular clones from carcinoma cell line HCT-116. Using clone displaying mild resistance, HCT116-R1 (i.e., with an IC50 10-fold higher than parental line), we performed genetic screening based on short hairpin...