2011
The RAG2 C terminus suppresses genomic instability and lymphomagenesis
Deriano L, Chaumeil J, Coussens M, Multani A, Chou Y, Alekseyenko AV, Chang S, Skok JA, Roth DB. The RAG2 C terminus suppresses genomic instability and lymphomagenesis. Nature 2011, 471: 119-123. PMID: 21368836, PMCID: PMC3174233, DOI: 10.1038/nature09755.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsChromosome DeletionChromosomes, MammalianDisease ProgressionDNA-Binding ProteinsGene Rearrangement, T-LymphocyteGenes, Immunoglobulin Heavy ChainGenes, p53Genomic InstabilityIn Situ Hybridization, FluorescenceKaplan-Meier EstimateLymphomaMiceProtein Serine-Threonine KinasesReceptors, Antigen, T-CellRecombination, GeneticThymus GlandTranslocation, GeneticTumor Suppressor ProteinsConceptsRAG2 C terminusGenomic instabilityC-terminusTCRα/δDNA double-strand breaksT-cell receptor lociDouble-strand breaksGenomic stabilityComplex chromosomal translocationReceptor locusChromosomal translocationsSimilar defectsLymphomagenesisThymic lymphomasTerminusLociRecombinaseTailRAG2TranslocationDeletionRecombinationRoleLymphoid malignanciesMice
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
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
Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice
Artandi S, Chang S, Lee S, Alson S, Gottlieb G, Chin L, DePinho R. Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice. Nature 2000, 406: 641-645. PMID: 10949306, DOI: 10.1038/35020592.Peer-Reviewed Original ResearchConceptsEpithelial cancersSoft tissue sarcomasTelomere lengthP53 mutant miceTumor suppressor gene mutationsSuppressor gene mutationsNon-reciprocal translocationsTissue sarcomasTelomere dysfunctionAged humansMutant miceCytogenetic featuresCancerMiceHuman carcinomasGene mutationsEpithelial renewalTelomerase expressionCritical reductionCarcinomaDysfunctionHigh rateReverse transcriptaseEukaryotic chromosomesNucleoprotein complexes