0000000000528790

AUTHOR

Arnaud Coquelle

showing 2 related works from this author

Patients with colorectal tumors with microsatellite instability and large deletions in HSP110 T17 have improved response to 5-fluorouracil–based chem…

2014

Background & Aims Patients with colorectal tumors with microsatellite instability (MSI) have better prognoses than patients with tumors without MSI, but have a poor response to 5-fluorouracil–based chemotherapy. A dominant-negative form of heat shock protein (HSP)110 (HSP110DE9) expressed by cancer cells with MSI, via exon skipping caused by somatic deletions in the T 17 intron repeat, sensitizes the cells to 5-fluorouracil and oxaliplatin. We investigated whether HSP110 T 17 could be used to identify patients with colorectal cancer who would benefit from adjuvant chemotherapy with 5-fluorouracil and oxaliplatin. Methods We characterized the interaction between HSP110 and HSP110DE9 using su…

MaleModels MolecularOrganoplatinum CompoundsColorectal cancermedicine.medical_treatment[SDV]Life Sciences [q-bio]Leucovorin0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsHSP110 Heat-Shock ProteinsComputingMilieux_MISCELLANEOUSColectomySequence Deletion0303 health sciencesGastroenterologyPrimary tumor3. Good healthOxaliplatinTreatment OutcomeFluorouracilChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleMicrosatellite InstabilityFluorouracilColorectal Neoplasmsmedicine.drugBlotting WesternAntineoplastic AgentsBiology03 medical and health sciencesCell Line TumormedicineBiomarkers TumorHumans030304 developmental biologyAgedRetrospective StudiesChemotherapyHepatologyBase SequenceMicrosatellite instabilityCancerSurface Plasmon Resonancemedicine.diseaseMolecular biologySurvival AnalysisIntronsOxaliplatinCancer cellCancer researchFollow-Up StudiesGastroenterology
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Dicer prevents genome instability in response to replication stress

2019

Dicer, an endoribonuclease best-known for its role in microRNA biogenesis and RNA interference pathway, has been shown to play a role in the DNA damage response and repair of double-stranded DNA breaks (DSBs) in mammalian cells. However, it remains unknown whether Dicer is also important to preserve genome integrity upon replication stress. To address this question, we focused our study on common fragile sites (CFSs), which are susceptible to breakage after replication stress. We show that inhibition of the Dicer pathway leads to an increase in CFS expression upon induction of replication stress and to an accumulation of 53BP1 nuclear bodies, indicating transmission of replication-associate…

0301 basic medicineGenome instabilityreplication stressDNA damageChromosomal fragile siteBiologygenomic instabilitycommon fragile siteCell biologySettore BIO/18 - Genetica03 medical and health sciences030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisFANCD2biology.proteinDicer PathwayMitosiscommon fragile sitesDroshaResearch PaperDicerDicerOncotarget
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