2023
Phase II window study of olaparib alone or with cisplatin or durvalumab in operable Head and Neck Cancer
Moutafi M, Koliou G, Papaxoinis G, Economopoulou P, Kotsantis I, Gkotzamanidou M, Anastasiou M, Pectasides D, Kyrodimos E, Delides A, Giotakis E, Papadimitriou N, Panayiotides I, Perisanidis C, Fernandez A, Xirou V, Poulios C, Gagari E, Yaghoobi V, Gavrielatou N, Shafi S, Aung T, Kougioumtzopoulou A, Kouloulias V, Palialexis K, Gkolfinopoulos S, Strati A, Lianidou E, Fountzilas G, Rimm D, Foukas P, Psyrri A. Phase II window study of olaparib alone or with cisplatin or durvalumab in operable Head and Neck Cancer. Cancer Research Communications 2023, 3: 1514-1523. PMID: 37575280, PMCID: PMC10414130, DOI: 10.1158/2767-9764.crc-23-0051.Peer-Reviewed Original ResearchConceptsObjective response rateTumor microenvironmentPD-L1Operable headResponse rateDeath ligand 1 (PD-L1) levelsPathologic complete response ratePhase II window studyNeck squamous cell carcinomaPD-L1 CPSComplete response rateSerious adverse eventsPercentage of patientsInhibitor-based treatmentSquamous cell carcinomaEffective antitumor responseImmunosuppressive tumor microenvironmentInflammatory tumor microenvironmentTumor cell proliferationColony-stimulating factor 1 receptor (CSF1R) genePrimary endpointSecondary endpointsAdverse eventsOpportunity trialAntitumor responseUterine leiomyosarcomas harboring MAP2K4 gene amplification are sensitive in vivo to PLX8725, a novel MAP2K4 inhibitor
McNamara B, Harold J, Manavella D, Bellone S, Mutlu L, Hartwich T, Zipponi M, Yang-Hartwich Y, Demirkiran C, Verzosa M, Yang K, Choi J, Dong W, Buza N, Hui P, Altwerger G, Huang G, Andikyan V, Clark M, Ratner E, Azodi M, Schwartz P, Burton E, Inagaki H, Albers A, Zhang C, Bollag G, Schlessinger J, Santin A. Uterine leiomyosarcomas harboring MAP2K4 gene amplification are sensitive in vivo to PLX8725, a novel MAP2K4 inhibitor. Gynecologic Oncology 2023, 172: 65-71. PMID: 36958197, PMCID: PMC10192120, DOI: 10.1016/j.ygyno.2023.03.009.Peer-Reviewed Original ResearchConceptsUterine leiomyosarcomaPDX modelsGain of functionMedian overall survivalPhase I trialOral gavage dailyVivo activityTumor growth inhibitionTumor volume differencesTumor cell proliferationOverall survivalTolerable toxicityI trialOral treatmentTreatment cohortsGavage dailyAggressive tumorsSCID miceULMS patientsPK studiesTumor samplesWestern blotCell proliferationControl vehicleLeiomyosarcoma
2022
Neurospora crassa is a potential source of anti-cancer agents against breast cancer
Han R, Yang H, Ling C, Lu L. Neurospora crassa is a potential source of anti-cancer agents against breast cancer. Breast Cancer 2022, 29: 1032-1041. PMID: 35881300, DOI: 10.1007/s12282-022-01383-9.Peer-Reviewed Original ResearchConceptsBreast cancerT-47DBreast cancer stem cellsBreast cancer cell linesBreast cancer invasivenessCancer stem cell-related genesStem cell-related genesTumor cell proliferationCancer stem cellsMouse model resultsAnti-tumor agentsCell-related genesAnti-cancer agentsCancer cell linesTumor growthCancer invasivenessCancer stemCell proliferationMCF-10ACell linesCancerInhibition rateStem cellsSpheroid formationCASP3 activity
2021
Association of Immunophenotype With Pathologic Complete Response to Neoadjuvant Chemotherapy for Triple-Negative Breast Cancer
Filho OM, Stover DG, Asad S, Ansell PJ, Watson M, Loibl S, Geyer CE, Bae J, Collier K, Cherian M, O’Shaughnessy J, Untch M, Rugo HS, Huober JB, Golshan M, Sikov WM, von Minckwitz G, Rastogi P, Maag D, Wolmark N, Denkert C, Symmans WF. Association of Immunophenotype With Pathologic Complete Response to Neoadjuvant Chemotherapy for Triple-Negative Breast Cancer. JAMA Oncology 2021, 7: 603-608. PMID: 33599688, PMCID: PMC7893540, DOI: 10.1001/jamaoncol.2020.7310.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerPathologic complete responseNeoadjuvant chemotherapyGene expression-based molecular subtypesComplete responseMolecular subtypesBreast cancerClinical trialsSecondary analysisStage IIEnd pointAddition of carboplatinClinical stage IIDe-escalate therapyHigh pCR ratePrespecified end pointPrespecified secondary analysisSecondary end pointsStandard neoadjuvant chemotherapySimilar baseline characteristicsSubset of patientsT cell infiltrationRandomized clinical trialsTumor cell proliferationWhole transcriptome RNA sequencing
2020
Electronic cigarettes promotes the lung colonization of human breast cancer in NOD-SCID-Gamma mice.
Huynh D, Huang J, Le LTT, Liu D, Liu C, Pham K, Wang H. Electronic cigarettes promotes the lung colonization of human breast cancer in NOD-SCID-Gamma mice. International Journal Of Clinical And Experimental Pathology 2020, 13: 2075-2081. PMID: 32922603, PMCID: PMC7476960.Peer-Reviewed Original ResearchE-cigsNOD-SCIDGamma miceTumor cellsCig vapour extractElectronic cigarette smokingHuman breast cancer cell line MDA-MB-231Breast cancer cell line MDA-MB-231Cancer cell line MDA-MB-231Human breast cancer cellsCell line MDA-MB-231E-cig exposureHuman breast cancerMetastasis-promoting effectsTail vein injectionBreast cancer cellsTumor cell proliferationMDA-MB-231Tumor cell apoptosisCig exposureCigarette smokingLung metastasesTumor loadTumor mortalityBreast cancerPotent 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-MycTumorsInhibitorsMicroRNA‑34a expression affects breast cancer invasion in vitro and patient survival via downregulation of E2F1 and E2F3 expression.
Han R, Zhao J, Lu L. MicroRNA‑34a expression affects breast cancer invasion in vitro and patient survival via downregulation of E2F1 and E2F3 expression. Oncology Reports 2020, 43: 2062-2072. PMID: 32186770, DOI: 10.3892/or.2020.7549.Peer-Reviewed Original ResearchConceptsBreast cancerNormal breast tissueMDA-MB-231 cellsPatient survivalT-47DKaplan-Meier survival curvesBreast tissueCancer-associated mortalityLonger survival timeCommon cancer typesExpression levelsReverse transcription-quantitative PCRPotential therapeutic toolBreast cancer invasionMicroRNA-34a expressionTranscription-quantitative PCRTumor cell proliferationOverall survivalUnderlying molecular mechanismsCaspase-3 activityDownregulation of E2F1Clinical managementExpression of E2F1Survival timeClinical relevance
2019
Prohibitin promotes de-differentiation and is a potential therapeutic target in neuroblastoma
MacArthur I, Bei Y, Garcia H, Ortiz M, Toedling J, Klironomos F, Rolff J, Eggert A, Schulte J, Kentsis A, Henssen A. Prohibitin promotes de-differentiation and is a potential therapeutic target in neuroblastoma. JCI Insight 2019, 5 PMID: 30998507, PMCID: PMC6542629, DOI: 10.1172/jci.insight.127130.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell Cycle CheckpointsCell DedifferentiationCell DifferentiationCell Line, TumorCell ProliferationChild, PreschoolChromosomes, Human, Pair 17HumansMAP Kinase Signaling SystemMiceNeuroblastomaProhibitinsProtein Kinase InhibitorsPyridonesPyrimidinonesRepressor ProteinsRNA-SeqRNA, MessengerSequence Analysis, RNAWhole Genome SequencingXenograft Model Antitumor AssaysConceptsLong arm of chromosome 17Neuroblastoma cellsSlow cell cycle progressionExpression of prohibitinImpaired ERK1/2 activationGene expression programsWhole genomeHigh-risk neuroblastomaChromosome 17Long armDe-differentiationPromote tumor cell proliferationTumor cell proliferationRNA sequencingAssociated with suppressionEctopic expressionProhibitinProliferation of neuroblastoma cellsCytogenetic hallmarkProhibitin expressionExpression programsAssociated with lossNeuronal developmentERK1/2 activationNeuroblastoma outcomeSyntaphilin Is a Novel Biphasic Biomarker of Aggressive Prostate Cancer and a Metastasis Predictor
Hwang MJ, Bryant KG, Seo JH, Liu Q, Humphrey PA, Melnick MAC, Altieri DC, Robert ME. Syntaphilin Is a Novel Biphasic Biomarker of Aggressive Prostate Cancer and a Metastasis Predictor. American Journal Of Pathology 2019, 189: 1180-1189. PMID: 31079810, PMCID: PMC6560381, DOI: 10.1016/j.ajpath.2019.02.009.Peer-Reviewed Original ResearchConceptsProstate cancerTumor bulkInvasive frontHigh Gleason grade prostate cancerLocalized prostate cancerGrade prostate cancerAggressive prostate cancerCell proliferationKi-67 labelingTumor cell proliferationMetastasis predictorMetastatic diseaseDistant metastasisGleason gradeAccessible biomarkersProstate tumorsMetastatic potentialNovel markerCancerBiphasic patternProliferative rateHigh expressionOxidative metabolismReduced levelsTumors
2018
Inhibition of mTORC1 by lncRNA H19 via disrupting 4E-BP1/Raptor interaction in pituitary tumours
Wu ZR, Yan L, Liu YT, Cao L, Guo YH, Zhang Y, Yao H, Cai L, Shang HB, Rui WW, Yang G, Zhang XB, Tang H, Wang Y, Huang JY, Wei YX, Zhao WG, Su B, Wu ZB. Inhibition of mTORC1 by lncRNA H19 via disrupting 4E-BP1/Raptor interaction in pituitary tumours. Nature Communications 2018, 9: 4624. PMID: 30397197, PMCID: PMC6218470, DOI: 10.1038/s41467-018-06853-3.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsCabergolineCarcinogenesisCarrier ProteinsCell Cycle ProteinsCell Line, TumorCell ProliferationDisease ProgressionDown-RegulationFemaleHEK293 CellsHeterograftsHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MicePhosphoproteinsPhosphorylationPituitary NeoplasmsRibosomal Protein S6 Kinases, 70-kDaRNA, Long NoncodingUp-RegulationConceptsPituitary tumorsTumor growthTumor progressionLong noncoding RNA H19Potential therapeutic targetTumor growth regulationHuman pituitary tumorsFunction of H19Pituitary tumor cell proliferationTumor cell proliferationPrimary pituitary adenomaCabergoline treatmentPituitary adenomasTherapeutic targetInhibition of mTORC1RNA H19LncRNA H19H19 expressionAberrant expressionTumorsCell proliferationProgressionH19Growth regulationAdenomasN 6 -methyladenine DNA Modification in Glioblastoma
Xie Q, Wu TP, Gimple RC, Li Z, Prager BC, Wu Q, Yu Y, Wang P, Wang Y, Gorkin DU, Zhang C, Dowiak AV, Lin K, Zeng C, Sui Y, Kim LJY, Miller TE, Jiang L, Lee-Poturalski C, Huang Z, Fang X, Zhai K, Mack SC, Sander M, Bao S, Kerstetter-Fogle AE, Sloan AE, Xiao AZ, Rich JN. N 6 -methyladenine DNA Modification in Glioblastoma. Cell 2018, 175: 1228-1243.e20. PMID: 30392959, PMCID: PMC6433469, DOI: 10.1016/j.cell.2018.10.006.Peer-Reviewed Original ResearchMeSH KeywordsAdenineAdultAgedAlkB Homolog 1, Histone H2a DioxygenaseAnimalsAstrocytesBrain NeoplasmsCell HypoxiaChildDNA MethylationEpigenomicsFemaleGlioblastomaHeterochromatinHistonesHumansKaplan-Meier EstimateMaleMiceMiddle AgedNeoplastic Stem CellsRNA InterferenceRNA, Small InterferingTumor Suppressor Protein p53ConceptsDNA modificationsHeterochromatic histone modificationsRegulation of transcriptionNovel DNA modificationChromatin accessibilityEpigenetic marksHistone modificationsTranscriptional silencingEpigenetic modificationsGenetic driversHuman diseasesOncogenic pathwaysTumor cell proliferationPotential therapeutic targetALKBH1Cell proliferationTumor-bearing miceCritical roleTherapeutic targetDNAHuman tissuesHuman glioblastoma modelGlioblastoma modelGlioblastomaSilencingRole of eIF3a in 4-amino-2-trifluoromethyl-phenyl retinate-induced cell differentiation in human chronic myeloid leukemia K562 cells
Li G, Wang K, Li Y, Ruan J, Wang C, Qian Y, Zu S, Dai B, Meng Y, Zhou R, Ge J, Chen F. Role of eIF3a in 4-amino-2-trifluoromethyl-phenyl retinate-induced cell differentiation in human chronic myeloid leukemia K562 cells. Gene 2018, 683: 195-209. PMID: 30340049, DOI: 10.1016/j.gene.2018.10.035.Peer-Reviewed Original ResearchConceptsMyeloid differentiation marker CD11bCyclin D1Trans retinoic acid (ATRA) derivativeK562 cellsAnti-tumor effectsChronic myeloid leukemia K562 cellsMyeloid leukemia cell differentiationRetinoic acid derivativesCell differentiationG0/G1 phaseExpression of eIF3aC-MycHuman chronic myeloid leukemia K562 cellsDifferentiation marker CD11bTumor cell proliferationRole of eIF3aActivation of ERK1/2Marker CD11bCML cellsLeukemia cell differentiationP-ERKLeukemia K562 cellsPhenyl retinateP-RafEIF3a expressionObesity promotes resistance to anti-VEGF therapy in breast cancer by up-regulating IL-6 and potentially FGF-2
Incio J, Ligibel JA, McManus DT, Suboj P, Jung K, Kawaguchi K, Pinter M, Babykutty S, Chin SM, Vardam TD, Huang Y, Rahbari NN, Roberge S, Wang D, Gomes-Santos IL, Puchner SB, Schlett CL, Hoffmman U, Ancukiewicz M, Tolaney SM, Krop IE, Duda DG, Boucher Y, Fukumura D, Jain RK. Obesity promotes resistance to anti-VEGF therapy in breast cancer by up-regulating IL-6 and potentially FGF-2. Science Translational Medicine 2018, 10 PMID: 29540614, PMCID: PMC5936748, DOI: 10.1126/scitranslmed.aag0945.Peer-Reviewed Original ResearchConceptsVEGF therapyInterleukin-6Breast cancerMouse modelAnti-vascular endothelial growth factor therapyEndothelial growth factor therapyTumor vasculatureAnti-VEGF therapyAnti-VEGF treatmentIL-6 blockadeGrowth factor therapyIL-6 productionFGF-2Up-regulates IL-6Second mouse modelFGF-2 expressionTumor cell proliferationFactor therapyGrowth factor 2Proinflammatory factorsMetastatic sitesBC patientsObese miceReceptor inhibitionSystemic concentrationsGlutamine metabolism via glutaminase 1 in autosomal-dominant polycystic kidney disease
Soomro I, Sun Y, Li Z, Diggs L, Hatzivassiliou G, Thomas AG, Rais R, Parker SJ, Slusher BS, Kimmelman AC, Somlo S, Skolnik EY. Glutamine metabolism via glutaminase 1 in autosomal-dominant polycystic kidney disease. Nephrology Dialysis Transplantation 2018, 33: 1343-1353. PMID: 29420817, PMCID: PMC6070111, DOI: 10.1093/ndt/gfx349.Peer-Reviewed Original ResearchConceptsCyst growthCB-839Mouse modelGlutaminase 1Glutamine metabolismAutosomal dominant polycystic kidney disease cellsAutosomal dominant polycystic kidney diseaseCyst-lining epithelial cellsNormal human kidneyCompensatory metabolic changesInhibited mammalian targetPolycystic kidney diseaseCyst-lining epitheliaTumor cell proliferationKidney diseaseAnimal modelsGLS1 inhibitionHuman ADPKD kidneysHuman kidneyMammalian targetVariable outcomesCyst formationMetabolic changesADPKDMetabolism of glutamine
2017
Demethylation Therapy as a Targeted Treatment for Human Papillomavirus–Associated Head and Neck Cancer
Biktasova A, Hajek M, Sewell A, Gary C, Bellinger G, Deshpande HA, Bhatia A, Burtness B, Judson B, Mehra S, Yarbrough WG, Issaeva N. Demethylation Therapy as a Targeted Treatment for Human Papillomavirus–Associated Head and Neck Cancer. Clinical Cancer Research 2017, 23: 7276-7287. PMID: 28916527, DOI: 10.1158/1078-0432.ccr-17-1438.Peer-Reviewed Original ResearchConceptsClinical trialsHNSCC cellsMatrix metalloproteinasesHuman papillomavirus-associated headNeck squamous cell carcinomaSquamous cell carcinomaAbility of HPVClin Cancer ResTumor cell proliferationNeck cancer cellsWindow trialsCell carcinomaEffective therapyPreclinical modelsHPVHPV oncogenesMouse modelMouse blood vesselsDNA demethylating agentHNSCCXenografted tumorsHPV genesIFN responseTherapyTumor samplesNicotine Prevents and Reverses Paclitaxel-Induced Mechanical Allodynia in a Mouse Model of CIPN
Kyte S, Toma W, Bagdas D, Meade J, Schurman L, Lichtman A, Chen Z, Del Fabbro E, Fang X, Bigbee J, Damaj M, Gewirtz D. Nicotine Prevents and Reverses Paclitaxel-Induced Mechanical Allodynia in a Mouse Model of CIPN. Journal Of Pharmacology And Experimental Therapeutics 2017, 364: 110-119. PMID: 29042416, PMCID: PMC5738719, DOI: 10.1124/jpet.117.243972.Peer-Reviewed Original ResearchConceptsChemotherapy-induced peripheral neuropathyPaclitaxel-induced mechanical allodyniaMechanical allodyniaPeripheral neuropathyMouse modelTreatment of CIPNLewis lung carcinoma tumor growthIntraepidermal nerve fiber lossPaclitaxel-induced peripheral neuropathyH460 non-small cell lung cancer cellsNon-small cell lung cancer cellsLung tumor cell proliferationNerve fiber dysfunctionNicotinic acetylcholine receptor subtypesCell lung cancer cellsChronic nicotine administrationNerve fiber lossChronic nicotine treatmentMale C57BL/6J miceAcetylcholine receptor subtypesLung cancer cellsProliferation of A549Receptor-mediated pathwayTumor cell proliferationCIPN treatment
2016
Tumor-associated macrophages drive spheroid formation during early transcoelomic metastasis of ovarian cancer
Yin M, Li X, Tan S, Zhou HJ, Ji W, Bellone S, Xu X, Zhang H, Santin AD, Lou G, Min W. Tumor-associated macrophages drive spheroid formation during early transcoelomic metastasis of ovarian cancer. Journal Of Clinical Investigation 2016, 126: 4157-4173. PMID: 27721235, PMCID: PMC5096908, DOI: 10.1172/jci87252.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsErbB ReceptorsFemaleHeterograftsHumansIntercellular Adhesion Molecule-1Macrophage-1 AntigenMacrophagesMiceMice, NudeNeoplasm MetastasisNeoplasm ProteinsNeoplasm TransplantationOvarian NeoplasmsSpheroids, CellularVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1ConceptsTumor-associated macrophagesOvarian cancerTranscoelomic metastasisTumor cellsICAM-1Mouse modelEpithelial ovarian cancerOvarian cancer growthOvarian cancer metastasisSpheroid formationOvarian cancer progressionVEGF/VEGFRTumor cell proliferationPharmacological blockadeMetastatic cancerColon cancerCancer growthMetastasisAntibody neutralizationTumor growthCancerClinical pathologyCancer metastasisCancer progressionΑMβ2 integrinCalcium-Sensing Receptor Promotes Breast Cancer by Stimulating Intracrine Actions of Parathyroid Hormone–Related Protein
Kim W, Takyar FM, Swan K, Jeong J, VanHouten J, Sullivan C, Dann P, Yu H, Fiaschi-Taesch N, Chang W, Wysolmerski J. Calcium-Sensing Receptor Promotes Breast Cancer by Stimulating Intracrine Actions of Parathyroid Hormone–Related Protein. Cancer Research 2016, 76: 5348-5360. PMID: 27450451, PMCID: PMC5026591, DOI: 10.1158/0008-5472.can-15-2614.Peer-Reviewed Original ResearchConceptsMMTV-PyMT miceBreast cancer cellsCaSR activationBone metastasesBreast cancerInhibited tumor cell proliferationOsteolytic bone metastasesCancer cellsHuman breast cancer cell linesCalcium-sensing receptorHuman breast cancer cellsHormone-related proteinTransgenic mouse modelBreast cancer cell linesMMTV-PyMT transgenic mouse modelBreast cancer progressionTumor cell proliferationTumor cell growthCancer cell linesPTHrP levelsTissue-specific disruptionHigh extracellular concentrationsPTHrP productionCASR genePTHrP expressionPhase I study of safety and tolerability of sunitinib in combination with sirolimus in patients with refractory solid malignancies and determination of VEGF (VEGF-A) and soluble VEGF-R2 (sVEGFR2) in plasma
Li J, Kluger H, Devine L, Lee JJ, Kelly WK, Rink L, Saif MW. Phase I study of safety and tolerability of sunitinib in combination with sirolimus in patients with refractory solid malignancies and determination of VEGF (VEGF-A) and soluble VEGF-R2 (sVEGFR2) in plasma. Cancer Chemotherapy And Pharmacology 2016, 77: 1193-1200. PMID: 27103123, DOI: 10.1007/s00280-016-3033-7.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntineoplastic Combined Chemotherapy ProtocolsDose-Response Relationship, DrugDrug Administration ScheduleFemaleHumansIndolesMaleMaximum Tolerated DoseMiddle AgedNeoplasmsPyrrolesSirolimusSunitinibTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Young AdultConceptsRenal cell carcinomaComplete responseFourth cohortVEGF productionOral small-molecule inhibitorApparent pharmacokinetic interactionMedian age 57Prior systemic therapyRefractory solid malignanciesResidual renal massTolerability of sunitinibHand-foot syndromeHalf of patientsLymph node dissectionCombination of sunitinibPhase 1 studyDose of sunitinibOral mTOR inhibitorDose/scheduleUnknown compensatory mechanismsCycle 1Multiple receptor tyrosine kinasesAnti-tumor activityEpithelial growth factor receptor (EGFR) signalingTumor cell proliferation
2015
Small‐Molecule‐Mediated Degradation of the Androgen Receptor through Hydrophobic Tagging
Gustafson J, Neklesa T, Cox C, Roth A, Buckley D, Tae H, Sundberg T, Stagg D, Hines J, McDonnell D, Norris J, Crews C. Small‐Molecule‐Mediated Degradation of the Androgen Receptor through Hydrophobic Tagging. Angewandte Chemie 2015, 127: 9795-9798. DOI: 10.1002/ange.201503720.Peer-Reviewed Original ResearchSelective androgen receptor degradersAndrogen receptorAR mutationsAndrogen-dependent prostate cancer cell lineSecond-generation AR antagonistsAR degradationProstate tumor cell proliferationProstate cancer cell linesAR target genesTumor cell proliferationAntitumor chemotherapeutic agentsCancer cell linesAR antagonistsChemotherapeutic agentsCell proliferationAR ligandsCell linesAntagonistTumor strategyResistance mechanismsReceptorsRecent studiesProliferationTarget genesDependent transcription
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