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
2016
RNA-seq Identification of RACGAP1 as a Metastatic Driver in Uterine Carcinosarcoma
Mi S, Lin M, Brouwer-Visser J, Heim J, Smotkin D, Hebert T, Gunter MJ, Goldberg GL, Zheng D, Huang GS. RNA-seq Identification of RACGAP1 as a Metastatic Driver in Uterine Carcinosarcoma. Clinical Cancer Research 2016, 22: 4676-4686. PMID: 27121792, DOI: 10.1158/1078-0432.ccr-15-2116.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overCarcinosarcomaCase-Control StudiesCell MovementFemaleGene ExpressionGene Expression ProfilingGTPase-Activating ProteinsHigh-Throughput Nucleotide SequencingHumansInhibitor of Apoptosis ProteinsMiddle AgedNeoplasm MetastasisNeoplasm StagingSTAT3 Transcription FactorSurvivinTranscriptomeUterine NeoplasmsConceptsUterine carcinosarcomaTherapeutic targetCell line-derived xenograft modelSurvivin expressionRare aggressive malignancyPrimary surgical resectionHigh relapse rateNormal endometrial tissuesNovel therapeutic targetCarcinosarcoma cell lineEndometrial adenocarcinoma cellsFunctional assaysCell linesExtrauterine spreadPostmenopausal womenCancer Genome AtlasMedian survivalSurgical resectionExtrauterine metastasesRelapse rateBenign indicationsEndometrial tissueAggressive malignancyPoor responseTCGA cohort
2002
Liposomal Doxorubicin for Treatment of Metastatic Chemorefractory Vulvar Adenocarcinoma
Huang GS, Juretzka M, Ciaravino G, Kohler S, Teng NN. Liposomal Doxorubicin for Treatment of Metastatic Chemorefractory Vulvar Adenocarcinoma. Gynecologic Oncology 2002, 87: 313-318. PMID: 12468332, DOI: 10.1006/gyno.2002.6830.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAgedDoxorubicinDrug Resistance, NeoplasmFemaleHumansNeoplasm MetastasisPaget Disease, ExtramammaryVulvar NeoplasmsConceptsVulvar adenocarcinomaLiposomal doxorubicinPelvic lymph node dissectionGroin lymph nodesLymph node dissectionExtramammary Paget's diseaseYears of survivalWarrants further investigationBulky involvementGroin irradiationInitial therapyNode dissectionMultiagent chemotherapyRadical vulvectomyGynecologic malignanciesMetastatic diseaseLymph nodesInitial diagnosisMetastatic lesionsPaget's diseaseDramatic regressionRare entityDoxil treatmentEffective treatmentSubcutaneous lesions