2024
High-throughput characterization of functional variants highlights heterogeneity and polygenicity underlying lung cancer susceptibility
Long E, Patel H, Golden A, Antony M, Yin J, Funderburk K, Feng J, Song L, Hoskins J, Amundadottir L, Hung R, Amos C, Shi J, Rothman N, Lan Q, Consortium I, Choi J. High-throughput characterization of functional variants highlights heterogeneity and polygenicity underlying lung cancer susceptibility. American Journal Of Human Genetics 2024, 111: 1405-1419. PMID: 38906146, PMCID: PMC11267514, DOI: 10.1016/j.ajhg.2024.05.021.Peer-Reviewed Original ResearchGenome-wide association studiesGenome-wide association study lociFunctional variantsTranscriptional activityAllelic transcriptional activityLung cancer susceptibilityRisk-associated lociPotential functional variantsCell type-specific expressionRisk-associated variantsLung cancer cell growthNon-protein-codingComprehensive functional analysisTranscription factor analysisCancer susceptibilityCancer cell growthGWAS lociEpigenomic dataCRISPR interferenceAssociation studiesLinkage disequilibriumAllelic effectsSignificant variantsGenetic variantsSusceptibility genesAn emerging antibacterial nanovaccine for enhanced chemotherapy by selectively eliminating tumor-colonizing bacteria
Chen L, Kang Z, Shen J, Zhao R, Miao Y, Zhang L, Zheng Z, Zhang Z, Liu N, Wang C, Fang H, Zhou J, Wang Y, Liu Z, Yang Y, Chen Q. An emerging antibacterial nanovaccine for enhanced chemotherapy by selectively eliminating tumor-colonizing bacteria. Science Bulletin 2024, 69: 2565-2579. PMID: 38918142, DOI: 10.1016/j.scib.2024.06.016.Peer-Reviewed Original ResearchConceptsF. nucleatumColorectal cancerEffective antigen presentationEnhance chemotherapy efficacyT cell activationReduce cancer metastasisPoor treatment outcomesIncreased cancer cell growthCancer cell growthOral anaerobesDendritic cellsFusobacterium nucleatumChemotherapy efficacyAntitumor effectAntigen presentationBiomimetic nanovaccinesEnhanced chemotherapyNanovaccineAlum adjuvantCpG oligonucleotidesTreatment outcomesImmune responseImmune progressionTherapeutic effectVaccine effectiveness
2022
APOBEC mutagenesis and selection for NFE2L2 contribute to the origin of lung squamous-cell carcinoma
Cannataro VL, Kudalkar S, Dasari K, Gaffney SG, Lazowski HM, Jackson LK, Yildiz I, Das RK, Rothberg BE, Anderson KS, Townsend JP. APOBEC mutagenesis and selection for NFE2L2 contribute to the origin of lung squamous-cell carcinoma. Lung Cancer 2022, 171: 34-41. PMID: 35872531, PMCID: PMC10126952, DOI: 10.1016/j.lungcan.2022.07.004.Peer-Reviewed Original ResearchConceptsCytidine deaminationMutagenic processesDefective homologous recombinationGenomic sequencesHomologous recombinationAttractive potential targetAPOBEC mutagenesisLung squamous cell carcinomaDeamination activityCancer cell growthAPOBEC proteinsAPOBEC activityCell growthCellular proliferationNFE2L2MutationsMolecular investigationsCancer effectsPotential targetMolecular variantsAPOBECSurvival of cancerSquamous cell carcinomaDeaminationVariantsPUMILIO proteins promote colorectal cancer growth via suppressing p21
Gong Y, Liu Z, Yuan Y, Yang Z, Zhang J, Lu Q, Wang W, Fang C, Lin H, Liu S. PUMILIO proteins promote colorectal cancer growth via suppressing p21. Nature Communications 2022, 13: 1627. PMID: 35338151, PMCID: PMC8956581, DOI: 10.1038/s41467-022-29309-1.Peer-Reviewed Original ResearchConceptsColorectal cancerAOM/DSS modelIntestine-specific knockoutColitis-associated cancerHuman CRC cellsOrthotopic colon cancer modelColorectal cancer growthG1/S transitionHuman colorectal cancerColorectal tumor growthColon cancer modelCancer cell growthCRC progressionCRC cellsIntravenous injectionTherapeutic targetCancer growthCancer modelTumor growthSignificant decreaseS transitionDirect targetP21 mRNACancerDSS model
2021
Knocking down claudin receptors leads to a decrease in prostate cancer cell migration, cell growth, cell viability and clonogenic cell survival
Liu Q, Shen H, Naguib A, Weiss RM, Martin DT. Knocking down claudin receptors leads to a decrease in prostate cancer cell migration, cell growth, cell viability and clonogenic cell survival. Molecular Biomedicine 2021, 2: 31. PMID: 35006480, PMCID: PMC8607359, DOI: 10.1186/s43556-021-00053-0.Peer-Reviewed Original ResearchProstate cancer cell growthCancer cell growthProstate cancer cellsProstate cancerLNCaP cellsCommon solid organ malignancyHuman prostate cancer specimensProstate cancer cell migrationSolid organ malignanciesAdvanced prostate cancerCancer cellsHuman prostate cancer cellsNormal human prostate cellsMetastatic human prostate cancer cellsProstate cancer specimensHuman prostate cellsCell growthNew molecular targetsCell viabilityCell migrationCancer cell migrationClaudin receptorsOrgan malignanciesProstate cancer PC3Clonogenic cell survivalA Polyphenol-Rich Extract of Olive Mill Wastewater Enhances Cancer Chemotherapy Effects, While Mitigating Cardiac Toxicity
Albini A, Festa M, Ring N, Baci D, Rehman M, Finzi G, Sessa F, Zacchigna S, Bruno A, Noonan D. A Polyphenol-Rich Extract of Olive Mill Wastewater Enhances Cancer Chemotherapy Effects, While Mitigating Cardiac Toxicity. Frontiers In Pharmacology 2021, 12: 694762. PMID: 34434106, PMCID: PMC8381749, DOI: 10.3389/fphar.2021.694762.Peer-Reviewed Original ResearchHearts of miceSide effectsRat cardiomyocytesPotential cardioprotective activityEffect of chemotherapyProstate cancer xenograftsAdverse side effectsColon cancer cell growthCancer cell growthPolyphenol-rich extractAnti-oxidant activityAnti-cancer activityCardiovascular preventionCardioprotective effectsTumor weightCardiac toxicityCancer patientsCardiovascular toxicityCancer xenograftsCardioprotective roleProtective effectCancer chemotherapy effectsMouse pupsCardioprotective activityChemotherapy effectMutant-selective degradation by BRAF-targeting PROTACs
Alabi S, Jaime-Figueroa S, Yao Z, Gao Y, Hines J, Samarasinghe KTG, Vogt L, Rosen N, Crews CM. Mutant-selective degradation by BRAF-targeting PROTACs. Nature Communications 2021, 12: 920. PMID: 33568647, PMCID: PMC7876048, DOI: 10.1038/s41467-021-21159-7.Peer-Reviewed Original ResearchConceptsInhibitor-based therapyBRAF inhibitor-based therapiesBRAF missense mutationsCancer cell growthBRAF V600Current treatmentNew therapiesTherapeutic windowXenograft modelBRAF mutantMutant BRAFVivo efficacyDrug modalitiesRaf family membersProteolysis targeting chimera (PROTAC) technologyTherapyBRAFMissense mutationsFamily membersBRAFWTCell growthDegree of selectivityInactivated conformationPatientsV600
2019
Activation of the Unfolded Protein Response Pathway in Cytotoxic T Cells: A Comparison Between in vitro Stimulation, Infection, and the Tumor Microenvironment.
Kerr SR, Katz SG. Activation of the Unfolded Protein Response Pathway in Cytotoxic T Cells: A Comparison Between in vitro Stimulation, Infection, and the Tumor Microenvironment. The Yale Journal Of Biology And Medicine 2019, 92: 675-685. PMID: 31866782, PMCID: PMC6913815.Peer-Reviewed Original ResearchConceptsUnfolded protein responseProtein responseUnfolded protein response pathwayProtein response pathwayPathogen responseLower organismsResponse pathwaysCancer cell growthIRE1αCell growthIntracellular receptorsSecretory cellsPrecise roleCytotoxic T cellsPivotal roleT cellsCellsTumor microenvironmentEukaryotesHomologReceptorsContext of developmentOrganismsRoleApoptosisLoss of thymidine kinase 1 inhibits lung cancer growth and metastatic attributes by reducing GDF15 expression
Malvi P, Janostiak R, Nagarajan A, Cai G, Wajapeyee N. Loss of thymidine kinase 1 inhibits lung cancer growth and metastatic attributes by reducing GDF15 expression. PLOS Genetics 2019, 15: e1008439. PMID: 31589613, PMCID: PMC6797230, DOI: 10.1371/journal.pgen.1008439.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAdultAgedAnimalsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationDatasets as TopicDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGrowth Differentiation Factor 15HumansLungLung NeoplasmsMaleMiceMiddle AgedNeoplasm Recurrence, LocalPrognosisSurvival AnalysisThymidine KinaseTranscription FactorsXenograft Model Antitumor AssaysConceptsShort hairpin RNALUAD cellsMetastatic attributesRho GTPase activityMAP kinase pathwayEctopic expressionGTPase activityTranscriptional overexpressionKinase pathwayKinase 1Cancer cell growthGenetic knockdownProfiling-based approachDifferentiation factor 15Hairpin RNALung adenocarcinoma patientsLung cancer growthCell growthLUAD therapyDownstream mediatorLUAD tumorsLUAD growthKey hallmarksReduced expressionDependent mannerSynergistic inhibition of GP130 and ERK signaling blocks chemoresistant bladder cancer cell growth
Li X, He S, Tian Y, Weiss RM, Martin DT. Synergistic inhibition of GP130 and ERK signaling blocks chemoresistant bladder cancer cell growth. Cellular Signalling 2019, 63: 109381. PMID: 31374291, DOI: 10.1016/j.cellsig.2019.109381.Peer-Reviewed Original ResearchMeSH KeywordsButadienesCarcinoma, Transitional CellCell Line, TumorCell MovementCell SurvivalDrug Resistance, NeoplasmDrug SynergismEnzyme InhibitorsGene Expression Regulation, NeoplasticGlycoproteinsHumansHydrazinesMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1NitrilesQuinoxalinesUrinary Bladder NeoplasmsConceptsChemoresistant bladder cancerBladder cancer cellsBladder cancerInterleukin-6Clinical outcomesMultidrug resistanceGemcitabine-resistant bladder cancer cellsBladder cancer cell growthMajor treatment obstacleMetastatic bladder cancerPI3K/Akt/mTOR signalingCancer cellsResistant bladder cancer cellsPoor clinical outcomeAkt/mTOR SignalingSynergistic inhibitionNovel therapeutic strategiesPotential therapeutic targetMEK/ERK signalingCancer cell growthRaf/MEK/ERK signalingRole of gp130Therapeutic strategiesTreatment obstaclesTherapeutic targetGlucose Metabolic Reprogramming and Cell Proliferation Arrest in Colorectal Micropapillary Carcinoma
Vyas M, Patel N, Celli R, Wajapeyee N, Jain D, Zhang X. Glucose Metabolic Reprogramming and Cell Proliferation Arrest in Colorectal Micropapillary Carcinoma. Gastroenterology Research 2019, 12: 128-134. PMID: 31236153, PMCID: PMC6575135, DOI: 10.14740/gr1145.Peer-Reviewed Original ResearchColorectal micropapillary carcinomaGlucose transporter 1Micropapillary carcinomaGlucose metabolic reprogrammingColorectal carcinomaGlandular componentMetabolic reprogrammingGlycogen metabolismFrequent lymphovascular invasionCancer cell growthMPC therapyLymphovascular invasionTumor cell survivalAggressive variantPoor outcomeCell cycle arrestColon cancer cellsKi-67Glycogen metabolizing enzymesMetabolizing enzymesCarcinomaTransporter 1Cell proliferation arrestHCT116 colon cancer cellsReal-time PCR analysis
2018
Tumor Cell Autonomous RON Receptor Expression Promotes Prostate Cancer Growth Under Conditions of Androgen Deprivation
Brown NE, Paluch AM, Nashu MA, Komurov K, Waltz SE. Tumor Cell Autonomous RON Receptor Expression Promotes Prostate Cancer Growth Under Conditions of Androgen Deprivation. Neoplasia 2018, 20: 917-929. PMID: 30121008, PMCID: PMC6098205, DOI: 10.1016/j.neo.2018.07.003.Peer-Reviewed Original ResearchMeSH KeywordsAndrogensAnimalsApoptosisbeta CateninBiomarkersCell ProliferationGene Expression Regulation, NeoplasticHumansImmunohistochemistryMaleMiceNF-kappa BProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantReceptor Protein-Tyrosine KinasesReceptors, AndrogenSignal TransductionTranscriptional Regulator ERGConceptsCastration-resistant prostate cancerAndrogen receptor reactivationProstate cancerAndrogen deprivationReceptor reactivationAndrogen receptor nuclear localizationHormone-refractory prostate cancerProstate cancer cell growthAR-responsive genesCurrent treatment strategiesCastration-resistant growthProstate cancer growthRON receptor tyrosine kinaseProstate cancer progressionHuman hormone-refractory prostate cancersCancer cell growthProstate cancer cellsMurine prostate cancer cellsDeprivation therapyCRPC therapyCRPC cellsMechanisms of resistanceAndrogen receptorTreatment strategiesRON overexpressionChapter 16 Reflections on the Present and Future State of Lung Cancer Research and Management
Detterbeck F, Tanoue L. Chapter 16 Reflections on the Present and Future State of Lung Cancer Research and Management. 2018, 243-249. DOI: 10.1016/b978-0-323-48565-4.00016-3.Peer-Reviewed Original ResearchStereotactic body radiotherapyLung cancer researchCancer cell growthNew trial designsSurgical resectionUnresectable tumorsCurative treatmentBody radiotherapyLung cancerTobacco addictionTrial designSmall cohortBiologic driversResearch endpointsMinimal toxicityEarly detectionInvasive surgeryTumor's abilityTreatmentRadiotherapyCancer researchCell growthNew optionsMajor advancesMinor events
2017
Extracellular renalase protects cells and organs by outside‐in signalling
Wang Y, Safirstein R, Velazquez H, Guo X, Hollander L, Chang J, Chen T, Mu J, Desir GV. Extracellular renalase protects cells and organs by outside‐in signalling. Journal Of Cellular And Molecular Medicine 2017, 21: 1260-1265. PMID: 28238213, PMCID: PMC5487909, DOI: 10.1111/jcmm.13062.Peer-Reviewed Original ResearchConceptsProtective effectNovel therapeutic strategiesCancer cell growthBlood pressureOrgan injuryJAK/STATHeart rateTherapeutic strategiesToxic injuryCytoprotective actionMitogen-activated protein kinase pathwayRenalaseTranslational opportunitiesTumor cellsCellular actionsProtein kinase BInitial reportProtein kinase pathwayInjuryKinase BOrgansKinase pathwayGrowth-related genesCell growthExtracellular renalase
2016
HOXB13 and other high penetrant genes for prostate cancer
Pilie P, Giri V, Cooney K. HOXB13 and other high penetrant genes for prostate cancer. Asian Journal Of Andrology 2016, 18: 530-532. PMID: 27034017, PMCID: PMC4955175, DOI: 10.4103/1008-682x.175785.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsHereditary cancer syndromesMismatch repair genesCancer syndromesGermline mutationsProstate cancerMultiple primary malignanciesOvarian cancer syndromeCancer family syndromeDeleterious germline mutationsRare tumor typeCancer cell growthRepair genesHigh-penetrance genesPenetrant germline mutationsPrimary malignancyCommon cancerLi-FraumeniKey tumor suppressor genesFamily syndromeCancer tissuesHereditary breastTumor typesSyndromeCancer typesCancer
2013
An Essential Requirement for the SCAP/SREBP Signaling Axis to Protect Cancer Cells from Lipotoxicity
Williams K, Argus J, Zhu Y, Wilks M, Marbois B, York A, Kidani Y, Pourzia A, Akhavan D, Lisiero D, Komisopoulou E, Henkin A, Soto H, Chamberlain B, Vergnes L, Jung M, Torres J, Liau L, Christofk H, Prins R, Mischel P, Reue K, Graeber T, Bensinger S. An Essential Requirement for the SCAP/SREBP Signaling Axis to Protect Cancer Cells from Lipotoxicity. Cancer Research 2013, 73: 2850-2862. PMID: 23440422, PMCID: PMC3919498, DOI: 10.1158/0008-5472.can-13-0382-t.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell CycleCell Line, TumorCell ProliferationFatty Acid SynthasesGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsMiceMice, Inbred NODModels, StatisticalNeoplasm TransplantationNeoplasmsSignal TransductionStearoyl-CoA DesaturaseSterolsConceptsSterol regulatory element-binding proteinsFatty acid synthesisSREBP activityCellular growthFatty acid poolKey transcriptional regulatorCancer cellsFatty acid desaturationAcid synthesisAcid poolElement-binding proteinMetabolic flux analysisTranscriptional regulatorsLipid biosynthesisNovel mechanistic explanationStearoyl-CoA desaturase-1Fatty acid synthase activityCancer metabolismCancer cell growthSignaling AxisCell growthFlux analysisSynthase activityDesaturase 1Lipid profiling
2012
Lin28 regulates HER2 and promotes malignancy through multiple mechanisms
Feng C, Neumeister V, Ma W, Xu J, Lu L, Bordeaux J, Maihle NJ, Rimm DL, Huang Y. Lin28 regulates HER2 and promotes malignancy through multiple mechanisms. Cell Cycle 2012, 11: 2486-2494. PMID: 22713243, DOI: 10.4161/cc.20893.Peer-Reviewed Original ResearchConceptsHuman epidermal growth factor receptor 2HER2 expressionLin28 expressionEpidermal growth factor receptor 2Growth factor receptor 2Primary breast tumorsFactor receptor 2Cancer cell growthMajor therapeutic targetMultiple mechanismsAdvanced human malignanciesClinical outcomesPoor prognosisBreast cancerReceptor 2Therapeutic targetBreast tumorsNovel mechanistic insightsHuman malignanciesLin28 overexpressionReceptor tyrosine kinasesCancerCell proliferationHuman cancersPowerful predictorEffect of KRAS Oncogene Substitutions on Protein Behavior: Implications for Signaling and Clinical Outcome
Ihle NT, Byers LA, Kim ES, Saintigny P, Lee JJ, Blumenschein GR, Tsao A, Liu S, Larsen JE, Wang J, Diao L, Coombes KR, Chen L, Zhang S, Abdelmelek MF, Tang X, Papadimitrakopoulou V, Minna JD, Lippman SM, Hong WK, Herbst RS, Wistuba II, Heymach JV, Powis G. Effect of KRAS Oncogene Substitutions on Protein Behavior: Implications for Signaling and Clinical Outcome. Journal Of The National Cancer Institute 2012, 104: 228-239. PMID: 22247021, PMCID: PMC3274509, DOI: 10.1093/jnci/djr523.Peer-Reviewed Original ResearchMeSH KeywordsAspartic AcidCarcinoma, Non-Small-Cell LungCell Line, TumorClinical Trials, Phase II as TopicCysteineDisease-Free SurvivalGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, rasGenetic VectorsGlycineHumansImmunoblottingImmunoprecipitationKaplan-Meier EstimateLentivirusLung NeoplasmsMicroarray AnalysisMolecular Targeted TherapyMutationProto-Oncogene Proteins c-aktRandomized Controlled Trials as TopicSignal TransductionTOR Serine-Threonine KinasesTreatment OutcomeValineConceptsNon-small cell lung cancerKirsten rat sarcoma viral oncogene homologProgression-free survivalNSCLC cell linesWild-type KRASMutant KRASRefractory non-small cell lung cancerWorse progression-free survivalRat sarcoma viral oncogene homologRas2 Kirsten rat sarcoma viral oncogene homologSarcoma viral oncogene homologKaplan-Meier curvesCell lung cancerReverse-phase protein array studiesKRas proteinsHuman bronchial epithelial cellsCancer cell growthPatient tumor samplesCell linesImmortalized human bronchial epithelial cellsBronchial epithelial cellsProtein array studiesTumor gene expressionEvaluable patientsClinical outcomes
2010
Combination Treatment with MEK and AKT Inhibitors Is More Effective than Each Drug Alone in Human Non-Small Cell Lung Cancer In Vitro and In Vivo
Meng J, Dai B, Fang B, Bekele BN, Bornmann WG, Sun D, Peng Z, Herbst RS, Papadimitrakopoulou V, Minna JD, Peyton M, Roth JA. Combination Treatment with MEK and AKT Inhibitors Is More Effective than Each Drug Alone in Human Non-Small Cell Lung Cancer In Vitro and In Vivo. PLOS ONE 2010, 5: e14124. PMID: 21124782, PMCID: PMC2993951, DOI: 10.1371/journal.pone.0014124.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBenzimidazolesCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell SurvivalDose-Response Relationship, DrugDrug SynergismFemaleHeterocyclic Compounds, 3-RingHumansLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMitogen-Activated Protein Kinase KinasesProto-Oncogene Proteins c-aktSignal TransductionSurvival AnalysisTumor BurdenXenograft Model Antitumor AssaysConceptsNon-small cell lung cancerCell lung cancerCombination of AZD6244Lung cancer cell linesCombination therapyLung cancerCancer cell linesTumor growthTumor tissueHuman non-small cell lung cancerLung cancer cell growthCell linesHuman lung cancer cell linesSingle drug treatmentSynergistic antitumor activityHuman lung tumorsAnimal survival timeMean animal survival timeCancer cell growthXenograft tumor growthP-AKT expressionLung tumorsDrug treatmentDrug combinationsSurvival time
2009
Wound Fluid Induces Cancer Cell Growth: A Mechanism for Recurrence?
Adelson K, Bahadur U, Halpern M, Hauptman E, Barginear M, Bleiweiss I, Ting J, Weltz C, Coomer C, Raptis G, Germain D. Wound Fluid Induces Cancer Cell Growth: A Mechanism for Recurrence? Cancer Research 2009, 69: 3146-3146. DOI: 10.1158/0008-5472.sabcs-09-3146.Peer-Reviewed Original ResearchResidual diseaseLocal recurrenceCancer cell growthBreast cancer cellsWound fluidCancer cell linesAbdominal drainMastectomy patientsSame patientCancer cellsAbdominal flap reconstructionBilateral mastectomy patientsUnilateral mastectomy patientsDifferent breast cancer cell linesBreast cancer cell linesCell linesOccult metastasesCytokine profileSurgical resectionBilateral mastectomyLymph nodesInflammatory componentUnilateral mastectomyPrimary tumorAbdominal fluid
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