2024
KROCUS: A phase II study investigating the efficacy and safety of fulzerasib (GFH925) in combination with cetuximab in patients with previously untreated advanced KRAS G12C mutated NSCLC.
Gregorc V, González-Cao M, Salvagni S, Koumarianou A, Gil-Bazo I, Maio M, Viteri S, Majem M, Gutiérrez V, Bernabe Caro R, Sanmamed M, Zhu H, Shen H, Wang Y, Rosell R. KROCUS: A phase II study investigating the efficacy and safety of fulzerasib (GFH925) in combination with cetuximab in patients with previously untreated advanced KRAS G12C mutated NSCLC. Journal Of Clinical Oncology 2024, 42: lba8511-lba8511. DOI: 10.1200/jco.2024.42.17_suppl.lba8511.Peer-Reviewed Original ResearchTreatment-related adverse eventsDisease control ratePhase II studyEpidermal growth factor receptorKRAS G12C inhibitorsDose reduction/interruptionBrain metastasesII studySafety profileG12C inhibitorsBaseline PD-L1 expressionBaseline brain metastasesActivation of epidermal growth factor receptorPD-L1 expressionTreating NSCLC patientsAnti-EGFR antibodiesFront-line treatmentKRAS G12C mutationGrowth factor receptorNSCLC ptsNSCLC modelsTumor shrinkageFrontline therapyNSCLC patientsOpen-labelSummary of Research: Overall Survival with Osimertinib in Resected EGFR-Mutated NSCLC
Tsuboi M, Herbst R, John T, Kato T, Majem M, Grohé C, Wang J, Goldman J, Lu S, de Marinis F, Shepherd F, Lee K, Le N, Dechaphunkul A, Kowalski D, Bonanno L, Dómine M, Poole L, Bolanos A, Rukazenkov Y, Wu Y. Summary of Research: Overall Survival with Osimertinib in Resected EGFR-Mutated NSCLC. Targeted Oncology 2024, 19: 131-134. PMID: 38466534, PMCID: PMC10963460, DOI: 10.1007/s11523-024-01034-3.Peer-Reviewed Original ResearchNon-small cell lung cancerEGFR-mutant non-small cell lung cancerResected EGFR-mutant non-small cell lung cancerEpidermal growth factor receptorOverall survivalEGFR-mutantStage IB-IIIA non-small cell lung cancerPatients treated with osimertinibDisease-free survivalStage II-IIIAEffects of osimertinibCell lung cancerGrowth factor receptorCancer cell deathRisk of deathADAURA studyLength of time patientsOsimertinib groupTumor shrinkagePlacebo groupCancer-freeOsimertinibLung cancerFactor receptorCancer cells
2022
Phase 1/2 study of ARV-110, an androgen receptor (AR) PROTAC degrader, in metastatic castration-resistant prostate cancer (mCRPC).
Gao X, Burris H, Vuky J, Dreicer R, Sartor A, Sternberg C, Percent I, Hussain M, Kalebasty A, Shen J, Heath E, Abesada-Terk G, Gandhi S, McKean M, Lu H, Berghorn E, Gedrich R, Chirnomas S, Vogelzang N, Petrylak D. Phase 1/2 study of ARV-110, an androgen receptor (AR) PROTAC degrader, in metastatic castration-resistant prostate cancer (mCRPC). Journal Of Clinical Oncology 2022, 40: 17-17. DOI: 10.1200/jco.2022.40.6_suppl.017.Peer-Reviewed Original ResearchMetastatic castration-resistant prostate cancerNovel hormonal agentsProstate-specific antigenClinical activityBetter prostate-specific antigenOngoing phase 1/2 studyCastration-resistant prostate cancerBiomarker-defined subgroupsPhase 2 dosePhase 1/2 studyWild-type ARFourth subgroupPhase 1AR alterationsRECIST responseSpecific molecular profilePrior therapyAdverse eventsAR-V7Tumor shrinkageHormonal agentsTreatment optionsClinical historyDisease progressionProstate cancer
2020
A phase 1b expansion study of TAS‐102 with oxaliplatin for refractory metastatic colorectal cancer
Cecchini M, Kortmansky JS, Cui C, Wei W, Thumar JR, Uboha NV, Hafez N, Lacy J, Fischbach NA, Sabbath KD, Gomez CM, Sporn JR, Stein S, Hochster HS. A phase 1b expansion study of TAS‐102 with oxaliplatin for refractory metastatic colorectal cancer. Cancer 2020, 127: 1417-1424. PMID: 33351187, PMCID: PMC8085021, DOI: 10.1002/cncr.33379.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsColorectal NeoplasmsDrug Administration ScheduleDrug CombinationsDrug Resistance, NeoplasmFemaleFluorouracilHumansIrinotecanLeucovorinMaleMiddle AgedOrganoplatinum CompoundsOxaliplatinProgression-Free SurvivalPyrrolidinesResponse Evaluation Criteria in Solid TumorsThymineTrifluridineConceptsMetastatic colorectal cancerOverall response rateRefractory metastatic colorectal cancerProgression-free survivalTAS-102Colorectal cancerDay 1Primary endpointOverall survivalDose escalationDay 5Median progression-free survivalPhase 1b studyMedian overall survivalResponse Evaluation CriteriaTreat populationDose expansionPartial responseStandard dosesUnexpected side effectsStudy treatmentTumor shrinkageUnexpected toxicitiesSide effectsNovel antimetaboliteA phase I study of mRNA-2752, a lipid nanoparticle encapsulating mRNAs encoding human OX40L, IL-23, and IL-36γ, for intratumoral (iTu) injection alone and in combination with durvalumab.
Patel M, Bauer T, Jimeno A, Wang D, LoRusso P, Do K, Stemmer S, Maurice-Dror C, Geva R, Zacharek S, Laino A, Sun J, Frederick J, Zhou H, Randolph W, Cohen P, Meehan R, Sullivan R. A phase I study of mRNA-2752, a lipid nanoparticle encapsulating mRNAs encoding human OX40L, IL-23, and IL-36γ, for intratumoral (iTu) injection alone and in combination with durvalumab. Journal Of Clinical Oncology 2020, 38: 3092-3092. DOI: 10.1200/jco.2020.38.15_suppl.3092.Peer-Reviewed Original ResearchSolid tumor patientsPro-inflammatory cytokinesIL-23IL-36γTumor shrinkageTumor patientsPost-treatment tumor biopsiesSquamous cell bladder carcinomaTumor-associated immune cellsDose-escalation partAdvanced solid malignanciesGrade 3/4 toxicitiesCytokine IL-22PD-L1 expressionPD-L1 levelsPD-L1 immunohistochemistryTime of presentationAnalysis of tumorsUninjected lesionsFirst doseIL-22Elevated IFNIL-6Immunomodulatory effectsBladder carcinomaPotent BRD4 inhibitor suppresses cancer cell-macrophage interaction
Yin M, Guo Y, Hu R, Cai WL, Li Y, Pei S, Sun H, Peng C, Li J, Ye R, Yang Q, Wang N, Tao Y, Chen X, Yan Q. Potent BRD4 inhibitor suppresses cancer cell-macrophage interaction. Nature Communications 2020, 11: 1833. PMID: 32286255, PMCID: PMC7156724, DOI: 10.1038/s41467-020-15290-0.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAnimalsCell CommunicationCell Cycle ProteinsCell Line, TumorCell ProliferationDisease Models, AnimalDown-RegulationDrug DesignFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMacrophage Colony-Stimulating FactorMacrophagesMice, Inbred BALB CMice, NudeNeoplasmsPhosphorylationProto-Oncogene Proteins c-mycReceptors, Granulocyte-Macrophage Colony-Stimulating FactorSignal TransductionTranscription FactorsTreatment OutcomeConceptsTumor growthMajor clinical stagesBET inhibitorsProliferation of tumorsExtraterminal domain (BET) family proteinsTumor cell proliferationClinical stageTumor shrinkageSyngeneic modelPotent BRD4 inhibitorsSmall molecule inhibitorsSolid tumorsBRD4 inhibitionTumor cellsOral bioavailabilityCancer treatmentCell proliferationBRD4 inhibitorsMolecule inhibitorsMultiple mechanismsC-MycTumorsInhibitors
2019
B cell depletion or absence does not impede anti-tumor activity of PD-1 inhibitors
Damsky W, Jilaveanu L, Turner N, Perry C, Zito C, Tomayko M, Leventhal J, Herold K, Meffre E, Bosenberg M, Kluger HM. B cell depletion or absence does not impede anti-tumor activity of PD-1 inhibitors. Journal For ImmunoTherapy Of Cancer 2019, 7: 153. PMID: 31200747, PMCID: PMC6567557, DOI: 10.1186/s40425-019-0613-1.Peer-Reviewed Original ResearchConceptsPD-1 inhibitorsB cell contentB-cell depletionAnti-tumor activityB cellsMuMT miceCell depletionAnti-PD-1 inhibitorsAnti-PD-1 responseB-cell depleting drugsTumor-infiltrating B cellsImpaired B-cell functionT cell-dependent tumor rejectionPD-1 inhibitionMC38 colon cancerB cell functionAnti-tumor effectsB-cell malignanciesMurine cancer modelsCell contentOverall survivalTumor rejectionCD20 antibodyAutoimmune disordersTumor shrinkageA First-in-Human Study and Biomarker Analysis of NKTR-214, a Novel IL2Rβγ-Biased Cytokine, in Patients with Advanced or Metastatic Solid Tumors
Bentebibel SE, Hurwitz ME, Bernatchez C, Haymaker C, Hudgens CW, Kluger HM, Tetzlaff MT, Tagliaferri MA, Zalevsky J, Hoch U, Fanton C, Aung S, Hwu P, Curti BD, Tannir NM, Sznol M, Diab A. A First-in-Human Study and Biomarker Analysis of NKTR-214, a Novel IL2Rβγ-Biased Cytokine, in Patients with Advanced or Metastatic Solid Tumors. Cancer Discovery 2019, 9: 711-721. PMID: 30988166, DOI: 10.1158/2159-8290.cd-18-1495.Peer-Reviewed Original ResearchConceptsNKTR-214Tumor biopsiesDurable disease stabilizationImmuno-oncology agentsMulticenter phase IPathway-targeted agentsTreatment tumor biopsiesPhase II doseActivation of CD8Metastatic solid tumorsNatural killer cellsOutpatient regimenCheckpoint inhibitorsDisease stabilizationRegulatory cellsEffector phenotypeKiller cellsTreatment algorithmImmune activationTumor shrinkagePharmacodynamic markersImmune cellsClinical activityIL2 receptorHuman studies
2018
Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS
Kitajima S, Asahina H, Chen T, Guo S, Quiceno L, Cavanaugh J, Merlino A, Tange S, Terai H, Kim J, Wang X, Zhou S, Xu M, Wang S, Zhu Z, Thai T, Takahashi C, Wang Y, Neve R, Stinson S, Tamayo P, Watanabe H, Kirschmeier P, Wong K, Barbie D. Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS. Cancer Cell 2018, 34: 439-452.e6. PMID: 30205046, PMCID: PMC6422029, DOI: 10.1016/j.ccell.2018.08.009.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsAntineoplastic Agents, ImmunologicalCarcinoma, Non-Small-Cell LungCell Line, TumorDisease Models, AnimalDrug Resistance, NeoplasmHEK293 CellsHumansImmunity, InnateInsulin-Like Growth Factor ILung NeoplasmsMiceMice, TransgenicMitogen-Activated Protein Kinase KinasesPhosphoproteinsProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins p21(ras)Transcription FactorsYAP-Signaling ProteinsConceptsGenetically engineered mouse modelsMediators of acquired resistanceDownstream of KRASBET inhibitor JQ1Effective therapeutic strategyTumor shrinkageTargeted therapyIntermittent treatmentYAP1 signalingMouse modelPathway inhibitionBET inhibitionTherapeutic strategiesInhibitor JQ1YAP1 upregulationOncogenic KRASBET inhibitorsOvercome resistancePromoter acetylationIntrinsic resistancePotential translationKRASMEKInnateInhibition
2017
Whole exome sequencing (WES) of multiple spatially distinct biopsies from single metastatic lesions to evaluate tumour heterogeneity and identify actionable truncal mutations (ATMs) in patients (pts) with advanced solid malignancies using a radiologically-guided single-pass percutaneous technique.
Heong V, Wee B, Goh S, Tay D, Lee X, Soo R, Lim J, Sundar R, Chee C, Lee S, Ow S, Goh B, Yong W, Wong A, Gopinathan A, Lim D, Pang B, Feroz M, Soong R, Tan D. Whole exome sequencing (WES) of multiple spatially distinct biopsies from single metastatic lesions to evaluate tumour heterogeneity and identify actionable truncal mutations (ATMs) in patients (pts) with advanced solid malignancies using a radiologically-guided single-pass percutaneous technique. Journal Of Clinical Oncology 2017, 35: 2550-2550. DOI: 10.1200/jco.2017.35.15_suppl.2550.Peer-Reviewed Original ResearchTumor mutational burdenWhole-exome sequencingMetastatic lesionsNSCLC ptsHigh tumor mutational burdenEvaluate tumor heterogeneityCheckpoint inhibitorsStable diseaseTumor shrinkageTruncal mutationsCore biopsyMutational burdenSolid malignanciesComplication rateNon-synonymous variantsTumor heterogeneityIntratumoral heterogeneitySubclonal diversityGenomic profilingPercutaneous techniquesExome sequencingMutational heterogeneityAkt inhibitorMedian amountPoor quality DNA
2015
3D quantitative assessment of response to fractionated stereotactic radiotherapy and single-session stereotactic radiosurgery of vestibular schwannoma
Schneider T, Chapiro J, Lin M, Geschwind JF, Kleinberg L, Rigamonti D, Jusué-Torres I, Marciscano AE, Yousem DM. 3D quantitative assessment of response to fractionated stereotactic radiotherapy and single-session stereotactic radiosurgery of vestibular schwannoma. European Radiology 2015, 26: 849-857. PMID: 26139318, PMCID: PMC4698362, DOI: 10.1007/s00330-015-3895-9.Peer-Reviewed Original ResearchConceptsSingle-session stereotactic radiosurgeryTotal tumor volumeSignificant tumor shrinkageVestibular schwannomaTumor shrinkageStereotactic radiotherapyTumor volumeRadiation therapyStereotactic radiosurgeryT1-weighted contrast-enhanced MRISubsequent microsurgical resectionTumor-related symptomsSporadic vestibular schwannomaContrast-enhanced MRIFSRT groupRadiological progressionMicrosurgical resectionClinical outcomesSRS groupRetrospective analysisResponse assessmentPatientsVolumetric assessmentFSRTSchwannomaA retrospective analysis of RET translocation, gene copy number gain and expression in NSCLC patients treated with vandetanib in four randomized Phase III studies
Platt A, Morten J, Ji Q, Elvin P, Womack C, Su X, Donald E, Gray N, Read J, Bigley G, Blockley L, Cresswell C, Dale A, Davies A, Zhang T, Fan S, Fu H, Gladwin A, Harrod G, Stevens J, Williams V, Ye Q, Zheng L, de Boer R, Herbst RS, Lee JS, Vasselli J. A retrospective analysis of RET translocation, gene copy number gain and expression in NSCLC patients treated with vandetanib in four randomized Phase III studies. BMC Cancer 2015, 15: 171. PMID: 25881079, PMCID: PMC4412099, DOI: 10.1186/s12885-015-1146-8.Peer-Reviewed Original ResearchConceptsGene copy number gainCopy number gainsRET rearrangementsTumor samplesComparator armVandetanib treatmentNumber gainRandomized phase III studyPhase III clinical trialsCell lung cancer trialsObjective response ratePhase III studyLung cancer trialsRET protein expressionNSCLC subpopulationVandetanib armRadiologic evidenceIII studyNSCLC patientsObjective responseTumor shrinkageComparator drugsCancer trialsClinical trialsRetrospective analysis
2013
Retrospective evaluation of RET biomarker status and outcome to vandetanib in four phase III randomized NSCLC trials.
Platt A, Elvin P, Morten J, Ji Q, Donald E, Womack C, Su X, Zheng L, Gladwin A, Vasselli J, Lee J, De Boer R, Herbst R. Retrospective evaluation of RET biomarker status and outcome to vandetanib in four phase III randomized NSCLC trials. Journal Of Clinical Oncology 2013, 31: 8045-8045. DOI: 10.1200/jco.2013.31.15_suppl.8045.Peer-Reviewed Original ResearchRET fusionsNSCLC trialsTumor samplesRET fusion genesFusion-positive patientsGene copy number gainRET protein expressionRECIST responseRadiologic evidenceEvaluable dataTumor shrinkageNSCLC tumorsBiomarker statusIHC analysisCopy number gainsRET amplificationRetrospective evaluationPatientsPotential associationVandetanibRET expressionPrevalenceProtein expressionPhase IIIBiomarkersA study of MPDL3280A, an engineered PD-L1 antibody in patients with locally advanced or metastatic tumors.
Herbst R, Gordon M, Fine G, Sosman J, Soria J, Hamid O, Powderly J, Burris H, Mokatrin A, Kowanetz M, Leabman M, Anderson M, Chen D, Hodi F. A study of MPDL3280A, an engineered PD-L1 antibody in patients with locally advanced or metastatic tumors. Journal Of Clinical Oncology 2013, 31: 3000-3000. DOI: 10.1200/jco.2013.31.15_suppl.3000.Peer-Reviewed Original ResearchPD-L1RECIST responseSolid tumorsTumor-specific T cell immunityPD-L1 tumor statusDose-escalation cohortsTumor PD-L1PD-L1 antibodiesCancer immune evasionMetastatic solid tumorsT cell immunityPD ratePD-L1 bindingHuman monoclonal antibodyVariety of tumorsMultiple tumor typesProlonged SDsRECIST v1.1Expansion cohortDurable responsesMedian durationRadiographic progressionPD-1Negative tumorsTumor shrinkageClinical activity, safety, and biomarkers of MPDL3280A, an engineered PD-L1 antibody in patients with locally advanced or metastatic melanoma (mM).
Hamid O, Sosman J, Lawrence D, Sullivan R, Ibrahim N, Kluger H, Boasberg P, Flaherty K, Hwu P, Ballinger M, Mokatrin A, Kowanetz M, Chen D, Hodi F. Clinical activity, safety, and biomarkers of MPDL3280A, an engineered PD-L1 antibody in patients with locally advanced or metastatic melanoma (mM). Journal Of Clinical Oncology 2013, 31: 9010-9010. DOI: 10.1200/jco.2013.31.15_suppl.9010.Peer-Reviewed Original ResearchObjective response rateMM ptsPD-L1Tumor shrinkageAntitumor activityImmunotherapy-responsive diseasePD-L1 overexpressionTreatment-related deathsPD-L1 statusPD-L1 antibodiesHuman monoclonal antibodyInitial antitumor activityPt ageRECIST responseRECIST v1.1Median durationPrior surgeryPS 0Radiographic progressionSystemic therapyElevated ASTPD-1Dose escalationHistologic subtypeInitial treatment
2012
Phase I safety, pharmacokinetic, and pharmacodynamic study of the oral phosphatidylinositol-3-kinase and mTOR inhibitor BGT226 in patients with advanced solid tumors
Markman B, Tabernero J, Krop I, Shapiro G, Siu L, Chen L, Mita M, Cuero M, Stutvoet S, Birle D, Anak Ö, Hackl W, Baselga J. Phase I safety, pharmacokinetic, and pharmacodynamic study of the oral phosphatidylinositol-3-kinase and mTOR inhibitor BGT226 in patients with advanced solid tumors. Annals Of Oncology 2012, 23: 2399-2408. PMID: 22357447, DOI: 10.1093/annonc/mds011.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic AgentsBreast NeoplasmsColonic NeoplasmsDiarrheaFemaleFluorodeoxyglucose F18HumansImidazolesMaleMaximum Tolerated DoseMiddle AgedNauseaPhosphoinositide-3 Kinase InhibitorsProstatic NeoplasmsQuinolinesRadionuclide ImagingRadiopharmaceuticalsTOR Serine-Threonine KinasesTreatment OutcomeYoung AdultConceptsAdvanced solid tumorsPreliminary antitumor activityStable diseaseSystemic exposureAdaptive Bayesian logistic regression modelSolid tumorsPhase I dose-escalation studyI dose-escalation studyFluorodeoxyglucose positron emission tomographyStable metabolic diseaseVariable systemic exposureAntitumor activityDose-escalation studyLow systemic exposurePI3K pathway inhibitionDay three timesLogistic regression modelsAdverse eventsDose escalationFluorodeoxyglucose uptakeRapamycin inhibitorsTumor shrinkagePharmacodynamic studiesComputed tomographyMTOR inhibitors
2011
Preliminary Results of An Ongoing Phase I Trial of Oral Belinostat a Novel Histone Deacetylase Inhibitor in Patients with Lymphoid Malignancies,
Zain J, Foss F, Diefenbach C, Petrylak D, Narwal A, Neylon E, Knoblauch P, O'Connor O. Preliminary Results of An Ongoing Phase I Trial of Oral Belinostat a Novel Histone Deacetylase Inhibitor in Patients with Lymphoid Malignancies,. Blood 2011, 118: 3710. DOI: 10.1182/blood.v118.21.3710.3710.Peer-Reviewed Original ResearchHistone deacetylase inhibitorsTumor shrinkageSolid tumorsDeacetylase inhibitorsIntra-patient dose escalationOngoing phase I trialClass I/II histone deacetylase inhibitorEarly tumor shrinkageGrade 3 diarrheaMedian age 48Frequent adverse eventsNovel histone deacetylase inhibitorPhase I trialHighest dose levelMantle cell lymphomaAnorexia/Dose cohortsEvaluable diseaseQ3w scheduleStable diseaseAdverse eventsDaily doseDose escalationI trialNHL patients
2010
Carbonic anhydrase IX and pathological features as predictors of outcome in patients with metastatic clear‐cell renal cell carcinoma receiving vascular endothelial growth factor‐targeted therapy
Choueiri T, Regan M, Rosenberg J, Oh W, Clement J, Amato A, McDermott D, Cho D, Atkins M, Signoretti S. Carbonic anhydrase IX and pathological features as predictors of outcome in patients with metastatic clear‐cell renal cell carcinoma receiving vascular endothelial growth factor‐targeted therapy. BJU International 2010, 106: 772-778. PMID: 20230385, DOI: 10.1111/j.1464-410x.2010.09218.x.Peer-Reviewed Original ResearchMeSH KeywordsAgedAntigens, NeoplasmAntineoplastic AgentsBenzenesulfonatesCarbonic Anhydrase IXCarbonic AnhydrasesCarcinoma, Renal CellEpidemiologic MethodsFemaleHumansImmunohistochemistryIndolesKidney NeoplasmsMaleMiddle AgedNeoplasm ProteinsNiacinamidePhenylurea CompoundsPrognosisPyridinesPyrrolesSorafenibSunitinibTreatment OutcomeVascular Endothelial Growth Factor AConceptsMetastatic clear-cell renal cell carcinomaVEGF-targeted therapyCarbonic anhydrase IXClear-cell renal cell carcinomaClear-cell componentRenal cell carcinomaTumor shrinkageCell carcinomaClear-cellTreated with vascular endothelial growth factor (VEGF)-targeted therapyVascular endothelial growth factor (VEGF)-targeted therapyVascular endothelial growth factor-targeted therapyAssociated with greater tumor shrinkageCarbonic anhydrase IX expressionResponse to sorafenib treatmentSunitinib-treated patientsResponse to sunitinibSorafenib-treated patientsPredictors of outcomeSunitinib treatmentSorafenib treatmentPrimary endpointPredictive biomarkersPrognostic valueCAIX expression
2009
Final results of a phase I study of oral belinostat (PXD101) in patients with lymphoma
Zain J, Foss F, Kelly W, DeBono J, Petrylak D, Narwal A, Neylon E, Blumenschein G, Lassen U, O'Connor O. Final results of a phase I study of oral belinostat (PXD101) in patients with lymphoma. Journal Of Clinical Oncology 2009, 27: 8580-8580. DOI: 10.1200/jco.2009.27.15_suppl.8580.Peer-Reviewed Original ResearchNon-Hodgkin lymphomaHodgkin's diseaseDose escalationTumor shrinkageSolid tumorsIntra-patient dose escalationRefractory non-Hodgkin lymphomaPhase IAcceptable organ functionEarly tumor shrinkageMedian age 51Frequent adverse eventsPossible dose escalationMantle cell lymphomaHistone deacetylase inhibitorsEvaluable diseaseLeg DVTPrior regimensQ3w scheduleStable diseaseAdverse eventsDaily doseSafety profileCohort C.Preclinical activityPrognostic and predictive values of carbonic anhydrase IX (CAIX) and pathologic features in patients with metastatic clear cell renal cell carcinoma receiving targeted therapy
Choueiri T, Regan M, Oh W, Clement J, Amato A, McDermott D, Cho D, Atkins M, Signoretti S. Prognostic and predictive values of carbonic anhydrase IX (CAIX) and pathologic features in patients with metastatic clear cell renal cell carcinoma receiving targeted therapy. Journal Of Clinical Oncology 2009, 27: e16067-e16067. DOI: 10.1200/jco.2009.27.15_suppl.e16067.Peer-Reviewed Original ResearchMetastatic renal cell carcinomaVEGF-targeted therapyCarbonic anhydrase IXCarbonic anhydrase IX expressionRenal cell carcinomaTumor shrinkageCell carcinomaCAIX expressionHistological featuresAssociated with greater tumor shrinkageMetastatic clear cell renal cell carcinomaClear cell renal cell carcinomaResponse to sorafenib treatmentSunitinib-treated patientsResponse to sunitinibSorafenib-treated patientsTreated with immunotherapyCell renal cell carcinomaClear cell componentCell histologySorafenib treatmentPredictive biomarkersPrognostic valueTargeted therapyClinical benefit
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