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
2011
A KRAS variant is a biomarker of poor outcome, platinum chemotherapy resistance and a potential target for therapy in ovarian cancer
Ratner ES, Keane FK, Lindner R, Tassi RA, Paranjape T, Glasgow M, Nallur S, Deng Y, Lu L, Steele L, Sand S, Muller RU, Bignotti E, Bellone S, Boeke M, Yao X, Pecorelli S, Ravaggi A, Katsaros D, Zelterman D, Cristea MC, Yu H, Rutherford TJ, Weitzel JN, Neuhausen SL, Schwartz PE, Slack FJ, Santin AD, Weidhaas JB. A KRAS variant is a biomarker of poor outcome, platinum chemotherapy resistance and a potential target for therapy in ovarian cancer. Oncogene 2011, 31: 4559-4566. PMID: 22139083, PMCID: PMC3342446, DOI: 10.1038/onc.2011.539.Peer-Reviewed Original ResearchMeSH Keywords3' Untranslated RegionsAgedAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorBRCA1 ProteinBRCA2 ProteinCarboplatinCell Line, TumorCell SurvivalDrug Resistance, NeoplasmFemaleGenotypeHumansKaplan-Meier EstimateMiddle AgedMultivariate AnalysisMutationNeoplasms, Glandular and EpithelialOvarian NeoplasmsPaclitaxelPolymorphism, Single NucleotidePrognosisProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Ras ProteinsRNA InterferenceTreatment OutcomeConceptsEpithelial ovarian cancerEOC patientsKRAS-variantOvarian cancerPoor outcomeCancer riskTumor biologyPlatinum resistanceComplete clinical dataBiomarkers of outcomeDirect targetingEOC cell growthKnown BRCA mutationsFuture treatment approachesSubset of tumorsPlatinum chemotherapy resistanceCell linesNeoadjuvant chemotherapyBRCA mutationsClinical dataTreatment approachesChemotherapy resistanceKRAS oncogeneMultivariate analysisPatients