2024
Preclinical in vitro and in vivo activity of the RAF/MEK clamp avutometinib in combination with FAK inhibition in uterine carcinosarcomas
Demirkiran C, Greenman M, Bellone S, McNamara B, Hartwich T, Manavella D, Mutlu L, Zipponi M, Yang-Hartwich Y, Yang K, Ratner E, Schwartz P, Coma S, Pachter J, Santin A. Preclinical in vitro and in vivo activity of the RAF/MEK clamp avutometinib in combination with FAK inhibition in uterine carcinosarcomas. Gynecologic Oncology 2024, 187: 12-20. PMID: 38703673, DOI: 10.1016/j.ygyno.2024.04.010.Peer-Reviewed Original ResearchFocal adhesion kinaseUC cell linesWhole-exome-sequencingFAK inhibitorCell linesFocal adhesion kinase inhibitionPhosphorylated (p)‑FAKWestern blot assayRAF/MEK inhibitionUterine carcinosarcomaRAS/MAPK pathway genesPreclinical in vitroBlot assayVS-4718Cell cycle assayGenetic landscapePathway genesMAP2KGenetic alterationsDecreased p-ERKCycle assaySuperior tumor growth inhibitionBiologically aggressive tumorsGrowth inhibitionIn vitro activity
2022
Clozapine Long-Term Treatment Might Reduce Epigenetic Age Through Hypomethylation of Longevity Regulatory Pathways Genes
Pérez-Aldana B, Martínez-Magaña J, Mayén-Lobo Y, de Montellano D, Aviña-Cervantes C, Ortega-Vázquez A, Genis-Mendoza A, Sarmiento E, Soto-Reyes E, Juárez-Rojop I, Tovilla-Zarate C, González-Castro T, Nicolini H, López-López M, Monroy-Jaramillo N. Clozapine Long-Term Treatment Might Reduce Epigenetic Age Through Hypomethylation of Longevity Regulatory Pathways Genes. Frontiers In Psychiatry 2022, 13: 870656. PMID: 35664466, PMCID: PMC9157596, DOI: 10.3389/fpsyt.2022.870656.Peer-Reviewed Original ResearchPathway genesDNA methylomeEpigenetic ageProtein-protein interactionsLong-term treatmentDifferential methylation sitesInfinium MethylationEPIC BeadChipMethylation sitesPsychopharmacological treatmentMethylationEPIC BeadChipContinuous clozapine treatmentDrug-naive patientsGenesMethylomeYears of treatmentLower mortality rateChronological ageCLZ treatmentClozapine treatmentMale patientsDelta agePsychiatric disordersPatientsPsychotic disordersMortality rateUntargeted metabolomics analysis of esophageal squamous cell cancer progression
Yang T, Hui R, Nouws J, Sauler M, Zeng T, Wu Q. Untargeted metabolomics analysis of esophageal squamous cell cancer progression. Journal Of Translational Medicine 2022, 20: 127. PMID: 35287685, PMCID: PMC8919643, DOI: 10.1186/s12967-022-03311-z.Peer-Reviewed Original ResearchConceptsEsophageal squamous cell carcinomaPhosphatidylserine synthase 1Metabolic pathway genesGene Set Enrichment AnalysisESCC progressionMetabolic pathwaysGlycerophospholipid metabolismPathway genesTumor/node/metastasis stageStage IIMRNA expressionSquamous cell cancer progressionSquamous cell carcinomaKey metabolic pathwaysAdjacent cancerous tissuePotential therapeutic targetCharacteristic curve analysisGood diagnostic valueTandem mass spectrometry analysisCancer Genome AtlasKyoto EncyclopediaMass spectrometry analysisExpression heatmapsPathway databasesPoor prognosis
2021
Molecular Genetics and Complex Inheritance of Congenital Heart Disease
Diab NS, Barish S, Dong W, Zhao S, Allington G, Yu X, Kahle KT, Brueckner M, Jin SC. Molecular Genetics and Complex Inheritance of Congenital Heart Disease. Genes 2021, 12: 1020. PMID: 34209044, PMCID: PMC8307500, DOI: 10.3390/genes12071020.Peer-Reviewed Original ResearchConceptsHigh-throughput genomic technologiesHigh-throughput sequencingGenetic architectureCHD familyGenetic variationSophisticated analysis strategiesCilia genesComplex inheritancePathway genesDe novo mutationsGenomic technologiesCauses of CHDMolecular geneticsBiological pathwaysMolecular diagnosisNumber variationsVEGF pathway genesGenesChromatinMutationsNovo mutationsGenetic etiologyTransmitted mutationsGenetic explanationSequencingProtein neddylation as a therapeutic target in pulmonary and extrapulmonary small cell carcinomas
Norton J, Augert A, Eastwood E, Basom R, Rudin C, MacPherson D. Protein neddylation as a therapeutic target in pulmonary and extrapulmonary small cell carcinomas. Genes & Development 2021, 35: 870-887. PMID: 34016692, PMCID: PMC8168556, DOI: 10.1101/gad.348316.121.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasic Helix-Loop-Helix Transcription FactorsCarcinoma, Small CellCell DeathCell Line, TumorCOP9 Signalosome ComplexCyclopentanesDisease Models, AnimalGene Expression Regulation, NeoplasticHeterograftsHumansLung NeoplasmsMiceNEDD8 ProteinNeuroendocrine CellsProteinsPyrimidinesRepressor ProteinsSequence DeletionConceptsSmall cell lung carcinomaSmall cell carcinomaExtrapulmonary small cell carcinomaNeddylation inhibitionCell carcinomaCell statesGenome-scale CRISPR/Therapeutic targetPatient-derived xenograft modelsCell linesDeletion of componentsSolid tumor malignanciesCell lung carcinomaNovel therapeutic approachesPotential therapeutic targetSuppressor screenSCLC cell linesCOP9 signalosomeProtein neddylationCRISPR/Genetic suppressionPathway genesPDX modelsMajor regulatorLung carcinomaProgressive myoclonus epilepsies—Residual unsolved cases have marked genetic heterogeneity including dolichol-dependent protein glycosylation pathway genes
Courage C, Oliver KL, Park EJ, Cameron JM, Grabińska KA, Muona M, Canafoglia L, Gambardella A, Said E, Afawi Z, Baykan B, Brandt C, di Bonaventura C, Chew HB, Criscuolo C, Dibbens LM, Castellotti B, Riguzzi P, Labate A, Filla A, Giallonardo AT, Berecki G, Jackson CB, Joensuu T, Damiano JA, Kivity S, Korczyn A, Palotie A, Striano P, Uccellini D, Giuliano L, Andermann E, Scheffer IE, Michelucci R, Bahlo M, Franceschetti S, Sessa WC, Berkovic SF, Lehesjoki AE. Progressive myoclonus epilepsies—Residual unsolved cases have marked genetic heterogeneity including dolichol-dependent protein glycosylation pathway genes. American Journal Of Human Genetics 2021, 108: 722-738. PMID: 33798445, PMCID: PMC8059372, DOI: 10.1016/j.ajhg.2021.03.013.Peer-Reviewed Original ResearchConceptsPME genesProgressive myoclonus epilepsyWhole-exome sequencingPrevious genetic analysisGroup of genesVariety of proteinsPrevious disease associationsUnrelated individualsCopy number changesProtein glycosylationPathway genesEndosomal functionGenetic analysisDisease-causing variantsGenesLikely disease-causing variantsAdditional family membersGenetic heterogeneityHeterogeneous rare diseasesUnsolved casesDisease associationsNovel causeMyoclonus epilepsyHeterozygous variantsHomozygous variantHypermutated phenotype in gliosarcoma of the spinal cord
Hong CS, Kuzmik GA, Kundishora AJ, Elsamadicy AA, Koo AB, McGuone D, Blondin NA, DiLuna ML, Erson-Omay EZ. Hypermutated phenotype in gliosarcoma of the spinal cord. Npj Precision Oncology 2021, 5: 8. PMID: 33580181, PMCID: PMC7881101, DOI: 10.1038/s41698-021-00143-w.Peer-Reviewed Original ResearchSpinal cordWhole-exome sequencingLow-grade brain gliomasVariant of glioblastomaLow-grade gliomasTumor anteriorAdjuvant radiationNeurological deficitsSomatic single nucleotide variationsPoor prognosisGrade gliomasTemozolomide treatmentBrain gliomasGliosarcomaMicrosatellite stabilityCordSomatic mutationsHypermutator phenotypeGliomasComprehensive genetic characterizationGenomic mechanismsSingle nucleotide variationsPhenotypeFirst reportPathway genesA mosquito small RNA genomics resource reveals dynamic evolution and host responses to viruses and transposons
Ma Q, Srivastav SP, Gamez S, Dayama G, Feitosa-Suntheimer F, Patterson EI, Johnson RM, Matson EM, Gold AS, Brackney DE, Connor JH, Colpitts TM, Hughes GL, Rasgon JL, Nolan T, Akbari OS, Lau NC. A mosquito small RNA genomics resource reveals dynamic evolution and host responses to viruses and transposons. Genome Research 2021, 31: gr.265157.120. PMID: 33419731, PMCID: PMC7919454, DOI: 10.1101/gr.265157.120.Peer-Reviewed Original ResearchConceptsPIWI-interacting RNAsGenomic resourcesMosquito cell culturesSmall RNA regulatory pathwaysSmall RNA expression profilesPIWI pathway genesRNA regulatory pathwaysSatellite DNA repeatsSmall RNA profilesCapacity of mosquitoesRNA interference (RNAi) pathwayRNA expression profilesImportant mosquito speciesTransposon activityGenome integritySiRNA populationsDNA repeatsInterference pathwayCluster lociCell culturesEvolutionary dynamicsPathway genesRegulatory pathwaysMosquito cellsExpression profiles
2020
Analysis of the Transcriptome: Regulation of Cancer Stemness in Breast Ductal Carcinoma In Situ by Vitamin D Compounds
Shan N, Minden A, Furmanski P, Bak M, Cai L, Wernyj R, Sargsyan D, Cheng D, Wu R, Kuo H, Li S, Fang M, Maehr H, Kong A, Suh N. Analysis of the Transcriptome: Regulation of Cancer Stemness in Breast Ductal Carcinoma In Situ by Vitamin D Compounds. Cancer Prevention Research 2020, 13: 673-686. PMID: 32467291, PMCID: PMC7415686, DOI: 10.1158/1940-6207.capr-19-0566.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsCarcinoma, Ductal, BreastCarcinoma, Intraductal, NoninfiltratingCell Line, TumorCell ProliferationDatasets as TopicDisease ProgressionDNA MethylationDown-RegulationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplastic Stem CellsRNA-SeqSignal TransductionUp-RegulationVitamin DConceptsCancer stem-like cellsStem-like cellsInvasive ductal carcinomaVitamin D compoundsNext-generation RNA sequencingCancer stem cell-like populationsGlobal transcriptomic analysisStem cell-like populationIngenuity Pathway AnalysisDuctal carcinomaCell-like populationD compoundsTranscriptomic analysisVitamin DGene methylation statusRNA sequencingEpithelial-mesenchymal transitionGlobal profilingPathway genesBreast cancer stem-like cellsCanonical pathwaysNegative regulatorUpstream regulatorPathway analysisNew breast cancer diagnoses
2019
Elevated CO2 regulates the Wnt signaling pathway in mammals, Drosophila melanogaster and Caenorhabditis elegans
Shigemura M, Lecuona E, Angulo M, Dada LA, Edwards MB, Welch LC, Casalino-Matsuda SM, Sporn PHS, Vadász I, Helenius IT, Nader GA, Gruenbaum Y, Sharabi K, Cummins E, Taylor C, Bharat A, Gottardi CJ, Beitel GJ, Kaminski N, Budinger GRS, Berdnikovs S, Sznajder JI. Elevated CO2 regulates the Wnt signaling pathway in mammals, Drosophila melanogaster and Caenorhabditis elegans. Scientific Reports 2019, 9: 18251. PMID: 31796806, PMCID: PMC6890671, DOI: 10.1038/s41598-019-54683-0.Peer-Reviewed Original ResearchConceptsLarge-scale transcriptomic studyAvailable transcriptomic datasetsCell linesWnt pathway genesOrganismal functionDrosophila melanogasterElevated CO2Different tissue originsTranscriptomic studiesBronchial cell lineCO2 elevationTranscriptomic datasetsGenomic responsesHuman bronchial cell linePathway genesGene expressionDifferent tissuesGenesHigh CO2Tissue originMammalsSkeletal musclePathwayCaenorhabditisMelanogasterSecond-Hit Somatic Mutations in Mevalonate Pathway Genes Underlie Porokeratosis
Atzmony L, Choate KA. Second-Hit Somatic Mutations in Mevalonate Pathway Genes Underlie Porokeratosis. Journal Of Investigative Dermatology 2019, 139: 2409-2411. PMID: 31753123, PMCID: PMC7962864, DOI: 10.1016/j.jid.2019.07.723.Peer-Reviewed Original ResearchSolid pseudopapillary neoplasms of the pancreas are dependent on the Wnt pathway
Selenica P, Raj N, Kumar R, Brown D, Arqués O, Reidy D, Klimstra D, Snuderl M, Serrano J, Palmer H, Weigelt B, Reis‐Filho J, Scaltriti M. Solid pseudopapillary neoplasms of the pancreas are dependent on the Wnt pathway. Molecular Oncology 2019, 13: 1684-1692. PMID: 30972907, PMCID: PMC6670010, DOI: 10.1002/1878-0261.12490.Peer-Reviewed Original ResearchConceptsSolid pseudopapillary neoplasmWnt pathwayLow‐complexity genomeWnt pathway genesPseudopapillary neoplasmSubtypes of pancreatic tumorsPrimary SPNPathway genesGenomic lesionsNuclear accumulationAdvanced stage diseaseEpithelial cell originSomatic mutationsWntGenomeMethylomeExpression levelsIndolent tumorsGenesPathwayPancreatic tumorsStage diseaseMutationsCell originClinical studiesH19 lncRNA identified as a master regulator of genes that drive uterine leiomyomas
Cao T, Jiang Y, Wang Z, Zhang N, Al-Hendy A, Mamillapalli R, Kallen AN, Kodaman P, Taylor HS, Li D, Huang Y. H19 lncRNA identified as a master regulator of genes that drive uterine leiomyomas. Oncogene 2019, 38: 5356-5366. PMID: 31089260, PMCID: PMC6755985, DOI: 10.1038/s41388-019-0808-4.Peer-Reviewed Original ResearchConceptsSingle nucleotide polymorphismsKey pathway genesGenome-scale studiesGenome-wide transcriptomeExtracellular matrixMethylation profiling analysisRegulation of expressionKey driver genesH19 single nucleotide polymorphismsEpigenetic modificationsMaster regulatorPathway genesTET expressionExpression changesExpression of H19H19 lncRNADriver genesProfiling analysisGenesH19Smooth muscle cellsUnifying mechanismMuscle cellsNovel target therapiesLncRNAs
2017
GRAPE: a pathway template method to characterize tissue-specific functionality from gene expression profiles
Klein MI, Stern DF, Zhao H. GRAPE: a pathway template method to characterize tissue-specific functionality from gene expression profiles. BMC Bioinformatics 2017, 18: 317. PMID: 28651562, PMCID: PMC5485588, DOI: 10.1186/s12859-017-1711-z.Peer-Reviewed Original ResearchConceptsGene expression profilesExpression profilesIndividual gene expression profilesTissue-specific functionalityEnrichment-based methodsPathway scoresGene expression levelsBatch effectsPathway genesPresent genesPerturbed pathwaysPathway expressionExpression levelsIndividual samplesTissue typesPathwayGenesTCGA subtypesAbnormal pathwaysIndependent datasetsBreast cancer subtypesNon-competitive approachIndividual tumorsCancer subtypesGrapes
2016
Metformin alters DNA methylation genome-wide via the H19/SAHH axis
Zhong T, Men Y, Lu L, Geng T, Zhou J, Mitsuhashi A, Shozu M, Maihle NJ, Carmichael GG, Taylor HS, Huang Y. Metformin alters DNA methylation genome-wide via the H19/SAHH axis. Oncogene 2016, 36: 2345-2354. PMID: 27775072, PMCID: PMC5415944, DOI: 10.1038/onc.2016.391.Peer-Reviewed Original ResearchConceptsS-adenosylhomocysteine hydrolaseDNA methylation genomeGenome-wide alterationsNovel mechanismSubset of genesDNA methyltransferase 3BMethylation genomeDNA methylationEpigenetic dysregulationPathway genesMolecular basisAMPK activationLet-7Methyltransferase 3BMolecular mechanismsEndometrial cancer tissue samplesH19 knockdownGene methylationCell proliferationCancer tissue samplesCancer cellsNormal cellsConcomitant inhibitionGenesMethylationIRF5 and IRF5 Disease-Risk Variants Increase Glycolysis and Human M1 Macrophage Polarization by Regulating Proximal Signaling and Akt2 Activation
Hedl M, Yan J, Abraham C. IRF5 and IRF5 Disease-Risk Variants Increase Glycolysis and Human M1 Macrophage Polarization by Regulating Proximal Signaling and Akt2 Activation. Cell Reports 2016, 16: 2442-2455. PMID: 27545875, PMCID: PMC5165654, DOI: 10.1016/j.celrep.2016.07.060.Peer-Reviewed Original ResearchMeSH KeywordsAcetylmuramyl-Alanyl-IsoglutamineAdjuvants, ImmunologicAnimalsCell DifferentiationGene Expression RegulationGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitInterferon Regulatory FactorsInterleukin-1 Receptor-Associated KinasesIntracellular Signaling Peptides and ProteinsMacrophagesMiceMice, Inbred C57BLMice, KnockoutMutationNod2 Signaling Adaptor ProteinPrimary Cell CultureProtein BindingProto-Oncogene Proteins c-aktReceptor-Interacting Protein Serine-Threonine Kinase 2Signal TransductionTNF Receptor-Associated Factor 6ConceptsInterferon regulatory factor 5Akt2 activationPro-inflammatory cytokinesM1 macrophage polarizationGlycolytic pathway genesHuman macrophagesDisease-associated polymorphismsM1 polarizationMacrophage polarizationInflammatory M1 macrophage polarizationPathway genesProximal signalingOligomerization domainRegulatory factor 5Glycolytic pathwayEnhanced glycolysisGenetic variantsGlycolysisMetabolic outcomesIRF5 expressionM1 macrophagesCentral mediatorFactor 5CytokinesMacrophagesRASopathy Gene Mutations in Melanoma
Halaban R, Krauthammer M. RASopathy Gene Mutations in Melanoma. Journal Of Investigative Dermatology 2016, 136: 1755-1759. PMID: 27236105, PMCID: PMC4992636, DOI: 10.1016/j.jid.2016.05.095.Peer-Reviewed Original ResearchConceptsRASopathy mutationsRAS/mitogen-activated protein kinaseRAS/mitogen-activated protein kinase (MAPK) pathwayMitogen-activated protein kinase pathwayMitogen-activated protein kinaseProtein kinase pathwayAmino acid substitutionsNext-generation sequencingProtein kinasePathway genesKinase pathwaySequencing dataDriver genesAcid substitutionsGenomic abnormalitiesMutationsLegius syndromeGenesAbundant mutationsGermline mutationsGene mutationsPathwaySignificant overlapKinaseMelanomagenesisDNA methylation changes in extracellular remodeling pathway genes during the transformation of human mesenchymal stem cells
Kim T, Park S, Kim H, Ahuja N, Yi J. DNA methylation changes in extracellular remodeling pathway genes during the transformation of human mesenchymal stem cells. Genes & Genomics 2016, 38: 611-617. DOI: 10.1007/s13258-016-0402-x.Peer-Reviewed Original ResearchTranscriptional silencingPathway genesECM genesMesenchymal compartmentStem cell model systemPromoter DNA hypermethylationPromoter hypermethylationDNA methylation changesGene expression profile dataEssential structural componentKey cellular eventsExpression profile dataImportant functional roleExtracellular matrix moleculesColon cancer cell linesCell model systemHuman mesenchymal stem cellsMethylation patternsMethylation changesTranscription-polymerase chain reaction analysisDNA hypermethylationEpigenetic alterationsReverse transcription-polymerase chain reaction analysisHuman malignancesCellular events
2014
Evaluating the ovarian cancer gonadotropin hypothesis: A candidate gene study
Lee AW, Tyrer JP, Doherty JA, Stram DA, Kupryjanczyk J, Dansonka-Mieszkowska A, Plisiecka-Halasa J, Spiewankiewicz B, Myers EJ, Study A, Group A, Chenevix-Trench G, Fasching PA, Beckmann MW, Ekici AB, Hein A, Vergote I, Van Nieuwenhuysen E, Lambrechts D, Wicklund KG, Eilber U, Wang-Gohrke S, Chang-Claude J, Rudolph A, Sucheston-Campbell L, Odunsi K, Moysich KB, Shvetsov YB, Thompson PJ, Goodman MT, Wilkens LR, Dörk T, Hillemanns P, Dürst M, Runnebaum IB, Bogdanova N, Pelttari LM, Nevanlinna H, Leminen A, Edwards RP, Kelley JL, Harter P, Schwaab I, Heitz F, du Bois A, Orsulic S, Lester J, Walsh C, Karlan BY, Hogdall E, Kjaer SK, Jensen A, Vierkant RA, Cunningham JM, Goode EL, Fridley BL, Southey MC, Giles GG, Bruinsma F, Wu X, Hildebrandt MA, Lu K, Liang D, Bisogna M, Levine DA, Weber RP, Schildkraut JM, Iversen ES, Berchuck A, Terry KL, Cramer DW, Tworoger SS, Poole EM, Olson SH, Orlow I, Bandera EV, Bjorge L, Tangen IL, Salvesen HB, Krakstad C, Massuger LF, Kiemeney LA, Aben KK, van Altena AM, Bean Y, Pejovic T, Kellar M, Le ND, Cook LS, Kelemen LE, Brooks-Wilson A, Lubinski J, Gronwald J, Cybulski C, Jakubowska A, Wentzensen N, Brinton LA, Lissowska J, Yang H, Nedergaard L, Lundvall L, Hogdall C, Song H, Campbell IG, Eccles D, Glasspool R, Siddiqui N, Carty K, Paul J, McNeish IA, Sieh W, McGuire V, Rothstein JH, Whittemore AS, McLaughlin JR, Risch HA, Phelan CM, Anton-Culver H, Ziogas A, Menon U, Ramus SJ, Gentry-Maharaj A, Harrington P, Pike MC, Modugno F, Rossing MA, Ness RB, Pharoah PD, Stram DO, Wu AH, Pearce CL. Evaluating the ovarian cancer gonadotropin hypothesis: A candidate gene study. Gynecologic Oncology 2014, 136: 542-548. PMID: 25528498, PMCID: PMC4892108, DOI: 10.1016/j.ygyno.2014.12.017.Peer-Reviewed Original ResearchConceptsOvarian cancer riskOvarian Cancer StudyCancer riskGene-level associationsOnly modest associationsUnconditional logistic regressionCancer studiesHormone-related diseasesPathway genesGonadotropin hypothesisEtiologic roleGenome-wide significant associationOvarian cancerProstate cancerLarger sample sizeGonadotropinSignificant associationDisease riskModest associationLogistic regressionGene-level testsHigh-penetrance susceptibility genesCandidate gene studiesStrong genetic basisUnderstanding of biology
2013
Polymorphisms in DNA repair pathway genes, body mass index, and risk of non‐Hodgkin lymphoma
Chen Y, Zheng T, Lan Q, Kim C, Qin Q, Foss F, Chen X, Holford T, Leaderer B, Boyle P, Wang C, Dai M, Liu Z, Ma S, Chanock SJ, Rothman N, Zhang Y. Polymorphisms in DNA repair pathway genes, body mass index, and risk of non‐Hodgkin lymphoma. American Journal Of Hematology 2013, 88: 606-611. PMID: 23619945, PMCID: PMC3902049, DOI: 10.1002/ajh.23463.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overBody Mass IndexCase-Control StudiesDNA RepairDNA-Binding ProteinsExodeoxyribonucleasesFemaleGenotypeHumansLymphoma, Large B-Cell, DiffuseLymphoma, Non-HodgkinMiddle AgedPolymorphism, GeneticRecQ HelicasesRisk FactorsUbiquitin-Protein LigasesWerner Syndrome HelicaseX-ray Repair Cross Complementing Protein 1Xeroderma Pigmentosum Group D ProteinConceptsBody mass indexNon-Hodgkin lymphomaDNA repair pathway genesCT/TTMass indexNHL riskPopulation-based case-control studyRisk of NHLDiffuse large B-cell lymphomaGT/TT genotypesLarge B-cell lymphomaAC/CCT-cell lymphomaCase-control studyB-cell lymphomaConnecticut womenTT genotypeGG genotypePathway genesLymphomaCommon genetic variationWomenRiskSignificant interaction
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