2021
PARP inhibitors in head and neck cancer: Molecular mechanisms, preclinical and clinical data
Moutafi M, Economopoulou P, Rimm D, Psyrri A. PARP inhibitors in head and neck cancer: Molecular mechanisms, preclinical and clinical data. Oral Oncology 2021, 117: 105292. PMID: 33862558, DOI: 10.1016/j.oraloncology.2021.105292.Peer-Reviewed Original ResearchConceptsPoly (ADP-ribose) polymerase (PARP) inhibitorsCheckpoint inhibitorsCell death 1 (PD-1) checkpoint inhibitorsDeath-1 checkpoint inhibitorsDeath ligand 1 (PD-L1) expressionPARP inhibitorsPD-1 checkpoint inhibitorsNeck squamous cell carcinomaCornerstone of treatmentLigand 1 expressionImmune modulating effectsSquamous cell carcinomaSuccessful treatment outcomeDesign of trialsOutcome of therapyTreatment landscapeCell carcinomaNeck cancerTreatment outcomesClinical dataTherapeutic strategiesDNA damageRecent approvalImmune primingNucleotide excision repair
2020
Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition
Gale M, Li Y, Cao J, Liu ZZ, Holmbeck MA, Zhang M, Lang SM, Wu L, Do Carmo M, Gupta S, Aoshima K, DiGiovanna MP, Stern DF, Rimm DL, Shadel GS, Chen X, Yan Q. Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition. Cancer Research 2020, 80: 524-535. PMID: 31690671, PMCID: PMC7002225, DOI: 10.1158/0008-5472.can-18-3985.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBreast NeoplasmsCell ProliferationDrug Resistance, NeoplasmEnzyme InhibitorsFemaleHumansMiceMice, Inbred NODMice, SCIDMitochondrial Proton-Translocating ATPasesOligomycinsReceptor, ErbB-2TrastuzumabTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsResistant cellsHER2-Targeted TherapyTrastuzumab-resistant tumorsNew therapeutic strategiesNovel potential targetDrug-free mediumAntibody therapySynthase inhibitionLow doseTherapeutic strategiesTrastuzumabBreast tumorsHER2TherapyAcquired ResistanceTumorsPotential targetMitochondrial respirationCellsSelective dependencyInhibitionMinimal changesNovel vulnerabilitiesATP synthase inhibitionOligomycin A
2009
Residual breast cancers after conventional therapy display mesenchymal as well as tumor-initiating features
Creighton CJ, Li X, Landis M, Dixon JM, Neumeister VM, Sjolund A, Rimm DL, Wong H, Rodriguez A, Herschkowitz JI, Fan C, Zhang X, He X, Pavlick A, Gutierrez MC, Renshaw L, Larionov AA, Faratian D, Hilsenbeck SG, Perou CM, Lewis MT, Rosen JM, Chang JC. Residual breast cancers after conventional therapy display mesenchymal as well as tumor-initiating features. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 13820-13825. PMID: 19666588, PMCID: PMC2720409, DOI: 10.1073/pnas.0905718106.Peer-Reviewed Original ResearchConceptsBreast cancerConventional treatmentHigh tumor-initiating potentialResidual breast cancerBreast cancer patientsCell surface antigen profileLong-term survivalHuman breast tumorsBreast cancer cellsTumor-initiating cellsTumor-initiating potentialEndocrine therapyGene expression signaturesCancer patientsTumor cell populationClinical significanceMolecular subtypesTherapeutic strategiesMesenchymal markersMetalloproteinase-2Breast tumorsSubpopulation of cellsAntigen profileMesenchymal featuresTumor tissue