2023
Society for Immunotherapy of Cancer (SITC) clinical practice guideline on immunotherapy for the treatment of melanoma, version 3.0
Pavlick A, Ariyan C, Buchbinder E, Davar D, Gibney G, Hamid O, Hieken T, Izar B, Johnson D, Kulkarni R, Luke J, Mitchell T, Mooradian M, Rubin K, Salama A, Shirai K, Taube J, Tawbi H, Tolley J, Valdueza C, Weiss S, Wong M, Sullivan R. Society for Immunotherapy of Cancer (SITC) clinical practice guideline on immunotherapy for the treatment of melanoma, version 3.0. Journal For ImmunoTherapy Of Cancer 2023, 11: e006947. PMID: 37852736, PMCID: PMC10603365, DOI: 10.1136/jitc-2023-006947.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsClinical practice guidelinesCutaneous melanomaTreatment of melanomaPractice guidelinesProlongs recurrence-free survivalCancer clinical practice guidelinesCell death protein 1Metastatic cutaneous melanomaBispecific T cell engager (BiTE) therapyChemotherapy-resistant diseaseRecurrence-free survivalDeath protein 1Long-term followManagement of patientsSpecial patient populationsImmunotherapy of cancerConsensus-based recommendationsPossibility of cureUnique toxicity profileQuality of lifeIntratumoral immunotherapyNeoadjuvant strategiesAdvanced diseaseBrain metastases
2020
Derangements in HUWE1/c-MYC pathway confer sensitivity to the BET bromodomain inhibitor GS-626510 in uterine cervical carcinoma
Bonazzoli E, Bellone S, Zammataro L, Gnutti B, Guglielmi A, Pelligra S, Nagarkatti N, Manara P, Tymon-Rosario J, Zeybek B, Altwerger G, Menderes G, Han C, Ratner E, Silasi DA, Huang GS, Andikyan V, Azodi M, Schwartz PE, Santin AD. Derangements in HUWE1/c-MYC pathway confer sensitivity to the BET bromodomain inhibitor GS-626510 in uterine cervical carcinoma. Gynecologic Oncology 2020, 158: 769-775. PMID: 32600791, PMCID: PMC8253557, DOI: 10.1016/j.ygyno.2020.06.484.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsCell Line, TumorFemaleHumansImidazolesIn Situ Hybridization, FluorescenceIsoxazolesMiceMiddle AgedProteinsProto-Oncogene Proteins c-mycSignal TransductionTumor Suppressor ProteinsUbiquitin-Protein LigasesUterine Cervical NeoplasmsXenograft Model Antitumor AssaysYoung AdultConceptsC-myc expressionC-Myc pathwayTwice-daily oral dosesC-MycWestern blotChemotherapy-resistant diseaseUterine cervical carcinomaPotential therapeutic targetEffective therapeutic agentDose-response decreaseCC xenograftsCell line growthOral dosesCervical carcinomaPrimary tumorDeletion/mutationClinical studiesTherapeutic targetTherapeutic agentsNormal tissuesBET inhibitorsVivo activityQRT-PCRCell proliferationGene deletion/mutationTransimmunization restores immune surveillance and prevents recurrence in a syngeneic mouse model of ovarian cancer
Alvero AB, Hanlon D, Pitruzzello M, Filler R, Robinson E, Sobolev O, Tedja R, Ventura A, Bosenberg M, Han P, Edelson RL, Mor G. Transimmunization restores immune surveillance and prevents recurrence in a syngeneic mouse model of ovarian cancer. OncoImmunology 2020, 9: 1758869. PMID: 32566387, PMCID: PMC7302442, DOI: 10.1080/2162402x.2020.1758869.Peer-Reviewed Original ResearchConceptsHigh-grade serous ovarian cancerSyngeneic mouse modelOvarian cancerRecurrent diseaseMouse modelRecurrent high-grade serous ovarian cancerEffective anti-tumor immune responseDendritic cell vaccination strategiesHuman cutaneous T cell lymphomaAnti-tumor immune responseMyeloid-derived suppressive cellsCutaneous T-cell lymphomaIntra-peritoneal tumorsWhole tumor antigenChemotherapy-resistant diseaseFirst-line standardT-cell lymphomaOvarian cancer accountsSerous ovarian cancerTumor-associated macrophagesImmunotherapeutic interventionsGynecologic malignanciesSuppressive cellsDisease coursePatient survival
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 abilityTumorsInhibition of BET Bromodomain Proteins with GS-5829 and GS-626510 in Uterine Serous Carcinoma, a Biologically Aggressive Variant of Endometrial Cancer
Bonazzoli E, Predolini F, Cocco E, Bellone S, Altwerger G, Menderes G, Zammataro L, Bianchi A, Pettinella F, Riccio F, Han C, Yadav G, Lopez S, Manzano A, Manara P, Buza N, Hui P, Wong S, Litkouhi B, Ratner E, Silasi DA, Huang GS, Azodi M, Schwartz PE, Schlessinger J, Santin AD. Inhibition of BET Bromodomain Proteins with GS-5829 and GS-626510 in Uterine Serous Carcinoma, a Biologically Aggressive Variant of Endometrial Cancer. Clinical Cancer Research 2018, 24: 4845-4853. PMID: 29941483, PMCID: PMC6168417, DOI: 10.1158/1078-0432.ccr-18-0864.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsAntineoplastic AgentsApoptosisAurora Kinase AAurora Kinase BAzepinesCell Line, TumorCell ProliferationCystadenocarcinoma, SerousDose-Response Relationship, DrugEndometrial NeoplasmsExome SequencingFemaleGene Expression Regulation, NeoplasticHumansMiceMiddle AgedPhosphorylationPrimary Cell CultureProteinsProto-Oncogene Proteins c-mycTriazolesUterine NeoplasmsXenograft Model Antitumor AssaysConceptsUterine serous carcinomaPrimary USC cell linesUSC cell linesC-myc expressionCell linesC-MycChemotherapy-resistant diseaseQRT-PCRHigh c-myc expressionDose-dependent decreaseDose-dependent increasePotential therapeutic targetEffective therapeutic agentMouse xenograft modelClin Cancer ResFresh frozen tumor tissueC-myc gene amplificationUSC xenograftsEndometrial cancerAggressive variantSerous carcinomaWhole-exome sequencing studiesClinical studiesConcentrations/dosesXenograft model
2017
Efficacy of neratinib in the treatment of HER2/neu-amplified epithelial ovarian carcinoma in vitro and in vivo
Menderes G, Bonazzoli E, Bellone S, Black JD, Lopez S, Pettinella F, Masserdotti A, Zammataro L, Litkouhi B, Ratner E, Silasi DA, Azodi M, Schwartz PE, Santin AD. Efficacy of neratinib in the treatment of HER2/neu-amplified epithelial ovarian carcinoma in vitro and in vivo. Medical Oncology 2017, 34: 91. PMID: 28397106, PMCID: PMC5896014, DOI: 10.1007/s12032-017-0956-8.Peer-Reviewed Original ResearchConceptsEpithelial ovarian carcinomaOvarian carcinoma xenograftsOvarian cancerOvarian carcinomaCarcinoma xenograftsPreclinical efficacyCell linesTumor cell linesHER2/neu expressionChemotherapy-resistant diseaseOvarian cancer cell linesAvailable treatment strategiesEfficacy of neratinibInhibits xenograft growthNovel therapeutic agentsPrimary tumor cell linesG0/G1 phaseCell cycle distributionCell signaling changesNeratinib treatmentCancer cell linesGynecologic malignanciesOverall survivalNeu expressionClinical trials
2014
Solitomab, an epithelial cell adhesion molecule/CD3 bispecific antibody (BiTE), is highly active against primary chemotherapy‐resistant ovarian cancer cell lines in vitro and fresh tumor cells ex vivo
English DP, Bellone S, Schwab CL, Roque DM, Lopez S, Bortolomai I, Cocco E, Bonazzoli E, Chatterjee S, Ratner E, Silasi D, Azodi M, Schwartz PE, Rutherford TJ, Santin AD. Solitomab, an epithelial cell adhesion molecule/CD3 bispecific antibody (BiTE), is highly active against primary chemotherapy‐resistant ovarian cancer cell lines in vitro and fresh tumor cells ex vivo. Cancer 2014, 121: 403-412. PMID: 25251053, PMCID: PMC4304922, DOI: 10.1002/cncr.29062.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntibodies, BispecificAntigens, NeoplasmCarcinoma, Ovarian EpithelialCD3 ComplexCell Adhesion MoleculesCell Line, TumorCytotoxicity, ImmunologicDrug Resistance, NeoplasmEpithelial Cell Adhesion MoleculeFemaleFlow CytometryHumansMiddle AgedNeoplasms, Glandular and EpithelialOvarian NeoplasmsT-LymphocytesConceptsOvarian cancer cell linesPeripheral blood lymphocytesTumor cellsCancer cell linesFlow cytometryBlood lymphocytesCell linesMalignant cellsChemotherapy-resistant cell linesChemotherapy-resistant ovarian cancerT cell-mediated killingT-cell activation markersCell-mediated cytotoxicity assayEpCAM expressionPrimary ovarian cancer cell linesFresh ovarian tumorsChemotherapy-resistant diseaseCD3 bispecific antibodyTumor-associated lymphocytesEpithelial ovarian carcinoma cell linesT cell cytotoxicityChromium release assaysFresh tumor cellsOvarian tumor cell linesOvarian tumor cells
2013
New Paradigms in Microtubule-Mediated Endocrine Signaling in Prostate Cancer
Mistry S, Oh W. New Paradigms in Microtubule-Mediated Endocrine Signaling in Prostate Cancer. Molecular Cancer Therapeutics 2013, 12: 555-566. PMID: 23635655, DOI: 10.1158/1535-7163.mct-12-0871.Peer-Reviewed Original ResearchConceptsProstate cancerMicrotubule-targeting agentsClinical management of prostate cancerManagement of prostate cancerTreatment of prostate cancerChemotherapy-resistant diseaseMetastatic prostate cancerProstate cancer therapyDesign mechanism-basedAnti-cancer therapyEndocrine signalsProstate carcinogenesisAdvanced diseasePredictive biomarkersAnti-microtubule agentsImproved survivalTherapeutic optionsProstateClinical managementClinical studiesClinical challengeCancer therapyReceptor signalingTherapyCancer
2011
High-grade, chemotherapy-resistant primary ovarian carcinoma cell lines overexpress human trophoblast cell-surface marker (Trop-2) and are highly sensitive to immunotherapy with hRS7, a humanized monoclonal anti-Trop-2 antibody
Varughese J, Cocco E, Bellone S, Bellone M, Todeschini P, Carrara L, Schwartz PE, Rutherford TJ, Pecorelli S, Santin AD. High-grade, chemotherapy-resistant primary ovarian carcinoma cell lines overexpress human trophoblast cell-surface marker (Trop-2) and are highly sensitive to immunotherapy with hRS7, a humanized monoclonal anti-Trop-2 antibody. Gynecologic Oncology 2011, 122: 171-177. PMID: 21453957, PMCID: PMC3104081, DOI: 10.1016/j.ygyno.2011.03.002.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, MonoclonalAntibody-Dependent Cell CytotoxicityAntigens, NeoplasmCell Adhesion MoleculesCell Line, TumorDrug Resistance, NeoplasmFemaleFlow CytometryHumansImmunoglobulin GImmunohistochemistryInterleukin-2Killer Cells, NaturalMiddle AgedMolecular Targeted TherapyOvarian NeoplasmsRNA, MessengerConceptsAntibody-dependent cellular cytotoxicityOvarian cancer cell linesTrop-2 expressionAnti-Trop-2 antibodyChemotherapy-resistant ovarian cancerPrimary ovarian cancer cell linesCancer cell linesOvarian carcinoma cell linesInterleukin-2Cell surface markersCarcinoma cell linesOvarian cancerCell linesTrop-2Therapeutic agentsChemotherapy-resistant diseaseNovel therapeutic agentsEffect of serumOvarian diseaseControl antibodyHRS7Real-time PCRCellular cytotoxicityCarcinoma specimensRelease assays
2007
Thirty-Gene Pharmacogenomic Test Correlates with Residual Cancer Burden after Preoperative Chemotherapy for Breast Cancer
Peintinger F, Anderson K, Mazouni C, Kuerer HM, Hatzis C, Lin F, Hortobagyi GN, Symmans WF, Pusztai L. Thirty-Gene Pharmacogenomic Test Correlates with Residual Cancer Burden after Preoperative Chemotherapy for Breast Cancer. Clinical Cancer Research 2007, 13: 4078-4082. PMID: 17634532, DOI: 10.1158/1078-0432.ccr-06-2600.Peer-Reviewed Original ResearchConceptsResidual cancer burdenRCB 0RCB scoreRCB-IIICancer burdenPharmacogenomic testsRCB-IIPreoperative chemotherapyRCB classBreast cancerChemotherapy-resistant diseaseLymph node featuresPathologic reviewPathologic responseResidual tumorStage IPatientsIII groupChemotherapyI groupGene expression profilingCategorical variablesMean scoreScoresCancerA pilot study of adjuvant bevacizumab after neoadjuvant chemotherapy for high-risk breast cancer
Mayer E, Miller K, Rugo H, Peppercorn J, Carey L, Ryabin N, Winer E, Burstein H. A pilot study of adjuvant bevacizumab after neoadjuvant chemotherapy for high-risk breast cancer. Journal Of Clinical Oncology 2007, 25: 561-561. DOI: 10.1200/jco.2007.25.18_suppl.561.Peer-Reviewed Original ResearchNeoadjuvant chemotherapyBreast cancerAdjuvant bevacizumabAntiangiogenic therapyAnthracycline-containing neoadjuvant chemotherapyHigh-risk breast cancerAdjuvant antiangiogenic therapyResidual invasive carcinomaSingle-agent bevacizumabCycles of therapyTreatment-related toxicityChemotherapy-resistant diseasePhase II trialResidual breast cancerRisk of recurrenceNovel antiangiogenic therapiesEligible patientsMild arthralgiaAgent bevacizumabBevacizumab monotherapyII trialPrimary endpointMedian ageOngoing trialsOral chemotherapyMicrotubule-Associated Protein-tau is a Bifunctional Predictor of Endocrine Sensitivity and Chemotherapy Resistance in Estrogen Receptor–Positive Breast Cancer
Andre F, Hatzis C, Anderson K, Sotiriou C, Mazouni C, Mejia J, Wang B, Hortobagyi GN, Symmans WF, Pusztai L. Microtubule-Associated Protein-tau is a Bifunctional Predictor of Endocrine Sensitivity and Chemotherapy Resistance in Estrogen Receptor–Positive Breast Cancer. Clinical Cancer Research 2007, 13: 2061-2067. PMID: 17404087, DOI: 10.1158/1078-0432.ccr-06-2078.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic Combined Chemotherapy ProtocolsBreast NeoplasmsDrug Resistance, NeoplasmEstrogen Receptor ModulatorsFemaleGene ExpressionGene Expression ProfilingHumansMiddle AgedNeoplasms, Hormone-DependentPrognosisReceptors, EstrogenRNA, MessengerTamoxifentau ProteinsConceptsTau mRNA expressionBreast cancerPredictive valueTau expressionMRNA expressionEndocrine therapyEstrogen receptor-positive breast cancerPositive primary breast cancerReceptor-positive breast cancerER-positive breast cancerBorderline nonsignificant associationLow tau expressionPure prognostic valueSystemic adjuvant therapyTaxane-containing chemotherapyChemotherapy-resistant diseasePathologic complete responseER-positive cancersPrimary breast cancerDifferent outcome groupsWilcoxon rank sum testRank sum testAdjuvant tamoxifenPreoperative paclitaxelAdjuvant therapy
2005
Treatment of Chemotherapy-Resistant Human Ovarian Cancer Xenografts in C.B-17/SCID Mice by Intraperitoneal Administration of Clostridium perfringens Enterotoxin
Santin AD, Cané S, Bellone S, Palmieri M, Siegel ER, Thomas M, Roman JJ, Burnett A, Cannon MJ, Pecorelli S. Treatment of Chemotherapy-Resistant Human Ovarian Cancer Xenografts in C.B-17/SCID Mice by Intraperitoneal Administration of Clostridium perfringens Enterotoxin. Cancer Research 2005, 65: 4334-4342. PMID: 15899825, DOI: 10.1158/0008-5472.can-04-3472.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsCarcinoma, PapillaryCell Line, TumorClaudin-3Claudin-4Cystadenocarcinoma, SerousDrug Resistance, NeoplasmEnterotoxinsFemaleHumansInjections, IntraperitonealMembrane ProteinsMiceMice, SCIDMiddle AgedOvarian NeoplasmsReceptors, Cell SurfaceUterine Cervical NeoplasmsXenograft Model Antitumor AssaysConceptsClaudin-4 genesRecurrent ovarian cancerPrimary ovarian tumorsOvarian cancerHuman ovarian cancerOvarian tumorsClaudin-3C.B-17/SCID micePrimary human ovarian cancersHuman ovarian cancer xenograftsCytotoxic Clostridium perfringensOvarian tumor burdenAdvanced stage diseaseChemotherapy-resistant diseaseLethal gynecologic malignancyOvarian cancer xenograftsRecurrent ovarian tumorsRelevant clinical modelInhibited tumor growthSCID mouse xenograftsDose-dependent cytotoxic effectTight junction proteinsHigh-affinity receptorQuantitative reverse transcription PCRClostridium perfringens enterotoxin
1997
Prostate carcinoma response to cytotoxic therapy: in vivo resistance.
Teicher BA, Kakeji Y, Ara G, Herbst RS, Northey D. Prostate carcinoma response to cytotoxic therapy: in vivo resistance. In Vivo 1997, 11: 453-61. PMID: 9509295.Peer-Reviewed Original ResearchConceptsPC-3 tumorsDU-145 tumorsTGF-beta mRNAPC-3 cellsDU-145 cellsLNCaP tumorsSingle dosesAndrogen-independent prostate cancerChemotherapy-resistant diseaseHuman prostate carcinoma cell linesConcentrations of melphalanIndependent prostate cancerProstate carcinoma cell linesProstate carcinoma xenograftsCytotoxic cancer therapyCell linesProstate cell linesVivo high levelsTime-dependent increaseChemotherapy administrationResistant diseaseCarcinoma cell linesCytotoxic therapyPlasma levelsCarcinoma response
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