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Telomere dysfunction and telomerase reactivation in the etiology and progression of liver cancer
Organization WASHINGTON UNIVERSITYLocation SAINT LOUIS, UNITED STATESPosted 13 Dec 2021Deadline 31 Dec 2025 ⚠️
NIHUS FederalResearch GrantFY2026AddressAntioncogene Protein p53Basal Transcription FactorBasal transcription factor genesBiochemicalCCN2CTGFCausalityCell BodyCell LineageCell modelCellsCellular RegulationCellular Tumor Antigen P53Cellular injuryCellular modelCicatrixComplexCopy Number PolymorphismDNA DamageDNA Damage RepairDNA InjuryDNA RepairDNA mutationDataDevelopmentDiseaseDisorderDistalDysfunctionEC 2.7.7.49ES cell differentiationESC differentiationElementsEtiologyEventFailureFibrosisFunctional disorderGeneral Transcription Factor GeneGeneral Transcription FactorsGenetic ChangeGenetic defectGenetic mutationGenome InstabilityGenomic InstabilityGoalsHepatic CancerHepatic CellsHepatic FailureHepatic Parenchymal CellHepatic Stellate CellHepatic TissueHepatocarcinomaHepatocellular CarcinomaHepatocellular cancerHepatocyteHepatomaHumanIGF-binding protein-related protein-2IGFBP-8IGFBP-rP2ImpairmentIn VitroInduced HepatocytesIto CellKO miceKnock-out MiceKnockout MiceKnowledgeLengthLinkLiverLiver CellsLiver Cells CarcinomaLiver FailureLiver FibrosisMalignant neoplasm of liverMethylationModelingModern ManMolecularMolecular Modeling Nucleic Acid BiochemistryMolecular Modeling Protein/Amino Acid BiochemistryMolecular ModelsMutationNull MouseOncoprotein p53P53PathogenesisPathway interactionsPatient outcomePatient-Centered OutcomesPatient-Focused OutcomesPatientsPhosphoprotein P53Phosphoprotein pp53PhysiologicPhysiologicalPhysiopathologyPositionPositioning AttributePrimary carcinoma of the liver cellsProcessPromoter RegionsPromotor RegionsProtein TP53ProtocolProtocols documentationRNA TranscriptaseRNA-Dependent DNA PolymeraseRNA-Directed DNA PolymeraseReverse TranscriptaseRevertaseRisk FactorsRoleScarsSignal PathwaySomatic MutationSystemTP53TP53 geneTRP53TelomeraseTelomere MaintenanceTelomere ShorteningTimeTranscription Factor Proto-OncogeneTranscription factor genesTumor Protein p53Tumor Protein p53 GeneUnscheduled DNA Synthesiscausationcell damagecell growth regulationcell injurycellular damageconnective tissue growth factorcopy number variantcopy number variationdamage to cellsdevelopmentaldifferentiation in embryonic stem cellsdisease causationembryonic precursor differentiationembryonic stem cell differentiationend stage liver diseaseend stage liver failurefibrotic liverfisp12 proteingenetic promoter elementgenetic promoter sequencegenome mutationhESChepatic body systemhepatic fibrosishepatic organ systemhepatocyte nuclear factorhuman ES cellhuman ESChuman derived pluripotent stem cellhuman embryonic stem cellhuman pluripotent stem celliHepsin vivoinjury to cellsinsulin-like growth factor binding protein 8liver cancerliver carcinomaliver functionliver malignancyloss of function mutationmalignant liver tumormolecular modelingmutantnovelp53 Antigenp53 Genesp53 Tumor Suppressorparacrinepathophysiologypathwaypatient oriented outcomespreventpreventingprogenitor biologyprogenitor cell biologypromoterpromoter sequencepromotorprotein p53responsesocial rolesomatic variantstellate cellstem and progenitor biologystem cell biologytargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttelomeretelomere attritiontelomere damagetelomeric damagetooltranscription factor
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PROJECT SUMMARY/ABSTRACT
Mutations in telomerase and telomere attrition are major risk factors for liver fibrosis and its progression
to hepatocellular carcinoma (HCC). However, due to a lack of adequate models and intrinsic difficulties in
studying human telomerase in physiologically relevant cells, the molecular mechanisms responsible for liver…
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