2011
Essential roles for Pot1b in HSC self-renewal and survival
Wang Y, Shen MF, Chang S. Essential roles for Pot1b in HSC self-renewal and survival. Blood 2011, 118: 6068-6077. PMID: 21948176, PMCID: PMC3234665, DOI: 10.1182/blood-2011-06-361527.Peer-Reviewed Original ResearchAgingAnemia, AplasticAnimalsApoptosisBone Marrow CellsBone Marrow DiseasesBone Marrow Failure DisordersCell DifferentiationCell SurvivalCells, CulturedChromosomes, MammalianDNA DamageDNA-Binding ProteinsFemaleHematopoietic Stem CellsHemoglobinuria, ParoxysmalMaleMiceMice, Inbred ICRMice, Mutant StrainsMice, SCIDTelomereTumor Suppressor Protein p53
2005
Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice
Hingorani SR, Wang L, Multani AS, Combs C, Deramaudt TB, Hruban RH, Rustgi AK, Chang S, Tuveson DA. Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice. Cancer Cell 2005, 7: 469-483. PMID: 15894267, DOI: 10.1016/j.ccr.2005.04.023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCadherinsCarcinoma, Pancreatic DuctalCentrosomeChromosomal InstabilityChromosome AberrationsCytogenetic AnalysisDisease ProgressionGene ExpressionGene Expression RegulationGene RearrangementGenes, Tumor SuppressorHomeodomain ProteinsIntegrasesMiceMice, Inbred C57BLMice, Inbred StrainsMice, Mutant StrainsMice, TransgenicMutation, MissenseNeoplasm MetastasisOncogene Proteins v-erbBProto-Oncogene Proteins p21(ras)Ras ProteinsSurvival AnalysisTelomereTrans-ActivatorsTranslocation, GeneticTumor Suppressor Protein p53ConceptsPancreatic ductal adenocarcinomaTumor suppressor gene pathwaysDistinct genetic pathwaysGenetic requirementsGenetic pathwaysGenomic instabilityGene pathwaysChromosomal instabilityEndogenous expressionHuman diseasesNonreciprocal translocationsDuctal adenocarcinomaMetastatic pancreatic ductal adenocarcinomaHuman carcinomasDisease pathogenesisMouse pancreasDifferent biological behaviorPathwayMetastatic carcinomaPrimary carcinomaTreatment strategiesCarcinomaBiological behaviorDevelopment of detectionTranslocation
2004
Essential role of limiting telomeres in the pathogenesis of Werner syndrome
Chang S, Multani AS, Cabrera NG, Naylor ML, Laud P, Lombard D, Pathak S, Guarente L, DePinho RA. Essential role of limiting telomeres in the pathogenesis of Werner syndrome. Nature Genetics 2004, 36: 877-882. PMID: 15235603, DOI: 10.1038/ng1389.Peer-Reviewed Original ResearchConceptsWerner syndromeCultured cellsComplex cellular phenotypesElevated genomic instabilityDNA damage fociPremature aging syndromesWRN deficiencyReplicative senescenceCellular phenotypesGenomic instabilityAging syndromesGenetic dataMutational inactivationPremature senescenceChromosomal instabilityTelomerase expressionHair grayingPremature agingDisease phenotypeEssential roleWRNMice nullSenescenceAutosomal recessive diseaseType II diabetes
2003
Chromosome stability, in the absence of apoptosis, is critical for suppression of tumorigenesis in Trp53 mutant mice
Liu G, Parant J, Lang G, Chau P, Chavez-Reyes A, El-Naggar A, Multani A, Chang S, Lozano G. Chromosome stability, in the absence of apoptosis, is critical for suppression of tumorigenesis in Trp53 mutant mice. Nature Genetics 2003, 36: 63-68. PMID: 14702042, DOI: 10.1038/ng1282.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell CycleChromosomal InstabilityGenes, p53LymphomaMiceMice, Mutant StrainsPloidiesConceptsTrp53-null miceCell cycle arrestEarly onsetCycle arrestPartial cell cycle arrestMonths of ageTrp53 mutant miceSpontaneous tumorsSpontaneous tumorigenesisRare mutant formMutant miceThymic lymphomasMiceHuman tumorsSuppression of tumorigenesisTumorsAbsence of apoptosisP53 proteinP53-dependent apoptosisInduces ApoptosisLymphomaApoptosisTumorigenesisTumor suppressorP53-induced apoptosis