2018
Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors
Li C, Bonazzoli E, Bellone S, Choi J, Dong W, Menderes G, Altwerger G, Han C, Manzano A, Bianchi A, Pettinella F, Manara P, Lopez S, Yadav G, Riccio F, Zammataro L, Zeybek B, Yang-Hartwich Y, Buza N, Hui P, Wong S, Ravaggi A, Bignotti E, Romani C, Todeschini P, Zanotti L, Zizioli V, Odicino F, Pecorelli S, Ardighieri L, Silasi DA, Litkouhi B, Ratner E, Azodi M, Huang GS, Schwartz PE, Lifton RP, Schlessinger J, Santin AD. Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors. Proceedings Of The National Academy Of Sciences Of The United States Of America 2018, 116: 619-624. PMID: 30584090, PMCID: PMC6329978, DOI: 10.1073/pnas.1814027116.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsAzepinesBRCA1 ProteinBRCA2 ProteinCell Line, TumorClass I Phosphatidylinositol 3-KinasesFemaleHumansMiceMutationNeoplasm MetastasisNeoplasm Recurrence, LocalOvarian NeoplasmsProteinsProto-Oncogene Proteins c-mycTriazolesTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsOvarian cancerWhole-exome sequencingC-myc amplificationRecurrent tumorsPrimary tumorBET inhibitorsChemotherapy-resistant diseaseRecurrent ovarian cancerLethal gynecologic malignancyBilateral ovarian cancerChemotherapy-resistant tumorsPrimary metastatic tumorsMutational landscapeSomatic mutationsFresh-frozen tumorsGynecologic malignanciesMetastatic tumorsPrimary cell linesC-MYC gainPIK3CA amplificationTranscoelomic metastasisTherapeutic targetPatientsMetastatic abilityTumors
2015
Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds
Amin ARMR, Karpowicz PA, Carey TE, Arbiser J, Nahta R, Chen ZG, Dong JT, Kucuk O, Khan GN, Huang GS, Mi S, Lee HY, Reichrath J, Honoki K, Georgakilas AG, Amedei A, Amin A, Helferich B, Boosani CS, Ciriolo MR, Chen S, Mohammed SI, Azmi AS, Keith WN, Bhakta D, Halicka D, Niccolai E, Fujii H, Aquilano K, Ashraf SS, Nowsheen S, Yang X, Bilsland A, Shin DM. Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds. Seminars In Cancer Biology 2015, 35: s55-s77. PMID: 25749195, PMCID: PMC4561219, DOI: 10.1016/j.semcancer.2015.02.005.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsCarcinogenesisCell ProliferationDNA-Binding ProteinsGrowth Differentiation Factor 15Hippo Signaling PathwayHumansKruppel-Like Transcription FactorsMolecular Targeted TherapyNeoplasmsNuclear ProteinsProtein Serine-Threonine KinasesPTEN PhosphohydrolaseRetinoblastoma ProteinSignal TransductionSomatomedinsTranscription FactorsTumor Suppressor Protein p53ConceptsInsulin-like growth factorGrowth signalingCancer cellsGrowth differentiation factor 15Cell growthSuppression of genesActivation of genesDifferentiation factor 15AT-rich interactive domain 1ASignaling processesRetinoblastoma proteinFactor 15Tensin homologRb pathwayClinical settingSignalingGrowth factorAdverse effectsDomain 1AMolecular targetsPotential targetPathwayHippoGenesImportant pathway