2017
Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer
Genovese G, Carugo A, Tepper J, Robinson F, Li L, Svelto M, Nezi L, Corti D, Minelli R, Pettazzoni P, Gutschner T, Wu C, Seth S, Akdemir K, Leo E, Amin S, Molin M, Ying H, Kwong L, Colla S, Takahashi K, Ghosh P, Giuliani V, Muller F, Dey P, Jiang S, Garvey J, Liu C, Zhang J, Heffernan T, Toniatti C, Fleming J, Goggins M, Wood L, Sgambato A, Agaimy A, Maitra A, Roberts C, Wang H, Viale A, DePinho R, Draetta G, Chin L. Synthetic vulnerabilities of mesenchymal subpopulations in pancreatic cancer. Nature 2017, 542: 362-366. PMID: 28178232, PMCID: PMC7609022, DOI: 10.1038/nature21064.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinoma, Pancreatic DuctalDeoxycytidineEndoplasmic Reticulum StressFemaleGemcitabineGenes, mycGenes, rasHumansMaleMAP Kinase Kinase 4MAP Kinase Signaling SystemMesodermMiceMosaicismOncogene Protein p55(v-myc)Pancreatic NeoplasmsProteolysisProto-Oncogene Proteins p21(ras)SMARCB1 ProteinTranscriptome
2013
Transcription factor-pathway coexpression analysis reveals cooperation between SP1 and ESR1 on dysregulating cell cycle arrest in non-hyperdiploid multiple myeloma
Wang X, Yan Z, Fulciniti M, Li Y, Gkotzamanidou M, Amin S, Shah P, Zhang Y, Munshi N, Li C. Transcription factor-pathway coexpression analysis reveals cooperation between SP1 and ESR1 on dysregulating cell cycle arrest in non-hyperdiploid multiple myeloma. Leukemia 2013, 28: 894-903. PMID: 23925045, PMCID: PMC4155324, DOI: 10.1038/leu.2013.233.Peer-Reviewed Original ResearchConceptsCell cycle arrestCycle arrestCoexpression analysisCell cycle arrest genesHyperdiploid MMCell cycle arrest pathwaysNon-hyperdiploid multiple myelomaDistinct chromosomal alterationsMyeloma subtypeMultiple myelomaTranscription factorsArrest pathwaysSp1Low coexpressionProper regulationHuman cancersDifferent survival outcomesChromosomal alterationsPlasma B cellsCoexpressionCell linesNovel hypothesisSurvival outcomesMyeloma proliferationClinical utility