0000000000423794

AUTHOR

Pierre Olivier Frappart

0000-0002-8142-3878

showing 6 related works from this author

Pancreatic Ductal Adenocarcinoma (PDAC) Organoids: The Shining Light at the End of the Tunnel for Drug Response Prediction and Personalized Medicine.

2020

Simple Summary Pancreatic ductal adenocarcinoma (PDAC) causes massive medical problems because of late diagnosis and limited responsiveness to standard chemotherapeutic treatments. This makes PDAC one of the major causes of death by cancer. To address this problem, novel tools for early diagnosis and therapy are needed. The recent development of PDAC organoids, which represent micro-scale mini-tumors, offers promising new options for personalized drug-testing based on primary PDAC patient material. This overview article summarizes and discusses the current state-of-the-art in exploiting the organoid technology to improve clinical management of PDAC. Abstract Pancreatic ductal adenocarcinoma…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyPancreatic ductal adenocarcinomaendocrine system diseasesFOLFIRINOXdrug responseReviewchemotherapylcsh:RC254-28203 medical and health sciences0302 clinical medicineInternal medicinemedicineDrug responseSurvival rateorganoidsCause of death3D cell culturebusiness.industryCancerPDACpersonalized medicinelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseGemcitabinedigestive system diseases030104 developmental biologyOncology030220 oncology & carcinogenesisPersonalized medicinebusinessmedicine.drugCancers
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RINT1 Loss Impairs Retinogenesis Through TRP53-Mediated Apoptosis

2020

Genomic instability in the central nervous system (CNS) is associated with defective neurodevelopment and neurodegeneration. Congenital human syndromes that affect the CNS development originate from mutations in genes of the DNA damage response (DDR) pathways. RINT1 (Rad50-interacting protein 1) is a partner of RAD50, that participates in the cellular responses to DNA double-strand breaks (DSB). Recently, we showed that Rint1 regulates cell survival in the developing brain and its loss led to premature lethality associated with genomic stability. To bypass the lethality of Rint1 inactivation in the embryonic brain and better understand the roles of RINT1 in CNS development, we conditionally…

0301 basic medicineGenome instabilityDNA damagereplicative stressBiologyDNA damage responseRetinal ganglionganglion cellsCell and Developmental Biology03 medical and health sciences0302 clinical medicinemedicineoptic nerve hypoplasiaProgenitor celllcsh:QH301-705.5Original ResearchNeurogenesisNeurodegenerationneurodegenerationCell BiologyCell cyclemedicine.diseaseNeural stem cellCell biologyneurogenesis030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisvisual system developmentDevelopmental BiologyFrontiers in Cell and Developmental Biology
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ATRIP protects progenitor cells against DNA damage in vivo

2020

AbstractThe maintenance of genomic stability during the cell cycle of progenitor cells is essential for the faithful transmission of genetic information. Mutations in genes that ensure genome stability lead to human developmental syndromes. Mutations in Ataxia Telangiectasia and Rad3-related (ATR) or in ATR-interacting protein (ATRIP) lead to Seckel syndrome, which is characterized by developmental malformations and short life expectancy. While the roles of ATR in replicative stress response and chromosomal segregation are well established, it is unknown how ATRIP contributes to maintaining genomic stability in progenitor cells in vivo. Here, we generated the first mouse model to investigat…

CheckpointsProgrammed cell deathDNA damage[SDV]Life Sciences [q-bio]610 MedizinBiologyDNA replicationDNA damage responseArticle03 medical and health sciences0302 clinical medicine610 Medical sciencesmedicineProgenitor celllcsh:QH573-671GeneMitosisComputingMilieux_MISCELLANEOUSCell proliferation030304 developmental biology0303 health scienceslcsh:CytologyDisease modelCell cyclemedicine.diseaseCell biologyApoptosis030220 oncology & carcinogenesisAtaxia-telangiectasiaCell Death & Disease
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Telomerase and pluripotency factors jointly regulate stemness in pancreatic cancer stem cells

2021

© 2021 by the authors.

0301 basic medicineHomeobox protein NANOGCancer ResearchTelomerasePancreatic neoplasmsMedicinaBiologyStammzelleArticle03 medical and health sciences0302 clinical medicineSOX2Cancer stem cellPancreatic cancermedicineddc:610BauchspeicheldrüsenkrebsStemnessTelomeraseRC254-282Telomere lengthPancreas; CancerCancer stem cellsNeoplastic stem cellsCancer stem cells; Pancreatic cancer; Self-renewal; Stemness; Telomerase; Telomere lengthNeoplasms. Tumors. Oncology. Including cancer and carcinogensPancreatic cancermedicine.disease3. Good healthTelomere030104 developmental biologyOncologyKLF4030220 oncology & carcinogenesisCancer researchSelf-renewalStem cellDDC 610 / Medicine & health
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Progenitor death drives retinal dysplasia and neuronal degeneration in a mouse model of Atrip-Seckel syndrome

2020

ABSTRACT Seckel syndrome is a type of microcephalic primordial dwarfism (MPD) that is characterized by growth retardation and neurodevelopmental defects, including reports of retinopathy. Mutations in key mediators of the replication stress response, the mutually dependent partners ATR and ATRIP, are among the known causes of Seckel syndrome. However, it remains unclear how their deficiency disrupts the development and function of the central nervous system (CNS). Here, we investigated the cellular and molecular consequences of ATRIP deficiency in different cell populations of the developing murine neural retina. We discovered that conditional inactivation of Atrip in photoreceptor neurons …

lcsh:MedicineMedicine (miscellaneous)315BlindnessMicechemistry.chemical_compoundImmunology and Microbiology (miscellaneous)Cell DeathneurodevelopmentStem CellsNeurodegenerationapoptosisneurodegenerationSyndromeCell biologyDNA-Binding Proteinsdna damage responsemedicine.anatomical_structurePhotoreceptor Cells VertebrateResearch Articlelcsh:RB1-214NeurogenesisNeuroscience (miscellaneous)Embryonic DevelopmentBiologyRetinaGeneral Biochemistry Genetics and Molecular Biologylcsh:PathologymedicineAnimalsAbnormalities MultipleProgenitor cellVision OcularAdaptor Proteins Signal TransducingCell ProliferationProgenitorRetinalcsh:RRetinalEmbryo Mammalianmedicine.diseasephotoreceptorDisease Models AnimalSeckel syndromechemistryvisual system developmentNerve DegenerationRetinal dysplasiaRetinal DysplasiaTumor Suppressor Protein p53Primordial dwarfismDNA DamageDisease Models & Mechanisms
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PARP inhibitor resistance induces massive genome alterations responsible of the acquisition of multidrug resistance in DNA damage repair-deficient pa…

2020

Multiple drug resistancePancreatic cancerPARP inhibitorCancer researchmedicineBiologyDNA Damage Repairmedicine.diseaseGenomeDGVS Digital: BEST OF DGVS
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