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
2002
Telomere dysfunction provokes regional amplification and deletion in cancer genomes
O'Hagan R, Chang S, Maser R, Mohan R, Artandi S, Chin L, DePinho R. Telomere dysfunction provokes regional amplification and deletion in cancer genomes. Cancer Cell 2002, 2: 149-155. PMID: 12204535, DOI: 10.1016/s1535-6108(02)00094-6.Peer-Reviewed Original ResearchConceptsTelomere dysfunctionAged humansMajor cancersPathogenic significanceDysfunctionEpithelial carcinogenesisArray comparative genomic hybridizationComparative genomic hybridizationCancer hotspotsGenomic profilesNonreciprocal translocationsTumorsMiceCarcinogenesisGenomic hybridizationChromosomal instability
2000
The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations
Ferguson D, Sekiguchi J, Chang S, Frank K, Gao Y, DePinho R, Alt F. The nonhomologous end-joining pathway of DNA repair is required for genomic stability and the suppression of translocations. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 6630-6633. PMID: 10823907, PMCID: PMC18682, DOI: 10.1073/pnas.110152897.Peer-Reviewed Original ResearchConceptsMouse embryonic fibroblastsEnd-joining pathwayGenomic stabilityNonreciprocal translocationsNonhomologous DNA end-joining pathwayExogenous DNA damaging agentsNonhomologous end-joining pathwayCell cycle checkpoint proteinsDNA-dependent proteinDramatic genomic instabilityDNA ligase IVAlternative repair pathwaysDNA damaging agentsMammalian genomesGenome instabilityLigase IVNonhomologous DNADNA repairGenomic instabilityRepair pathwaysChromosomal fragmentationEmbryonic fibroblastsCheckpoint proteinsDamaging agentsSuppression of translocation