2024
Growth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex
Aladelokun O, Lu L, Zheng J, Yan H, Jain A, Gibson J, Khan S, Johnson C. Growth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex. Human Genomics 2024, 18: 67. PMID: 38886847, PMCID: PMC11184737, DOI: 10.1186/s40246-024-00635-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAspartate-Ammonia LigaseCarbon-Nitrogen Ligases with Glutamine as Amide-N-DonorCell ProliferationColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticHCT116 CellsHeterograftsHumansMaleMiceReceptors, EstrogenReceptors, G-Protein-CoupledSex FactorsXenograft Model Antitumor AssaysConceptsFemale tumor-bearing miceFemale CRC patientsTumor-bearing miceCRC patientsTumor growthInferior survivalAssociated with inferior survivalMetabolic reprogrammingG protein-coupled estrogen receptorTriggering metabolic reprogrammingSustained tumor growthSuppressed tumor growthExpression of asparagine synthetaseCancer cell linesBackgroundSex-related differencesSurvival improvementImpact of sexFemale miceEstrogen receptorCancer growthTranslational relevanceRewiring of metabolic pathwaysCancer burdenMetabolic pathwaysAsparagine synthetaseCell surface RNAs control neutrophil recruitment
Zhang N, Tang W, Torres L, Wang X, Ajaj Y, Zhu L, Luan Y, Zhou H, Wang Y, Zhang D, Kurbatov V, Khan S, Kumar P, Hidalgo A, Wu D, Lu J. Cell surface RNAs control neutrophil recruitment. Cell 2024, 187: 846-860.e17. PMID: 38262409, PMCID: PMC10922858, DOI: 10.1016/j.cell.2023.12.033.Peer-Reviewed Original ResearchConceptsCell surfaceMammalian homologOuter cell surfaceRNA transportGlycan modificationsMammalian cellsSID-1Cellular functionsRecruitment to inflammatory sitesGlycoRNARNAMurine neutrophilsFunctional significanceNeutrophil recruitmentNeutrophil recruitment to inflammatory sitesBiological importanceCellsNeutrophil adhesionReduced neutrophil adhesionHomologyGlycansGenesInflammatory sitesRecruitmentEndothelial cells
2021
5‐Fluorouracil efficacy requires anti‐tumor immunity triggered by cancer‐cell‐intrinsic STING
Tian J, Zhang D, Kurbatov V, Wang Q, Wang Y, Fang D, Wu L, Bosenberg M, Muzumdar MD, Khan S, Lu Q, Yan Q, Lu J. 5‐Fluorouracil efficacy requires anti‐tumor immunity triggered by cancer‐cell‐intrinsic STING. The EMBO Journal 2021, 40: embj2020106065. PMID: 33615517, PMCID: PMC8013832, DOI: 10.15252/embj.2020106065.Peer-Reviewed Original ResearchConceptsAnti-tumor immunityTumor burdenSubsequent type I interferon productionHigh STING expressionIntratumoral T cellsT-cell depletionType I interferon productionI interferon productionLoss of STINGImmunocompetent hostsColorectal specimensT cellsSTING expressionBetter survivalHigh doseTherapeutic effectivenessHuman colorectal specimensMelanoma tumorsInterferon productionChemotherapeutic drugsMurine colonImmunityEfficacyStingsColon
2017
The DNA Methylcytosine Dioxygenase Tet2 Sustains Immunosuppressive Function of Tumor-Infiltrating Myeloid Cells to Promote Melanoma Progression
Pan W, Zhu S, Qu K, Meeth K, Cheng J, He K, Ma H, Liao Y, Wen X, Roden C, Tobiasova Z, Wei Z, Zhao J, Liu J, Zheng J, Guo B, Khan SA, Bosenberg M, Flavell RA, Lu J. The DNA Methylcytosine Dioxygenase Tet2 Sustains Immunosuppressive Function of Tumor-Infiltrating Myeloid Cells to Promote Melanoma Progression. Immunity 2017, 47: 284-297.e5. PMID: 28813659, PMCID: PMC5710009, DOI: 10.1016/j.immuni.2017.07.020.Peer-Reviewed Original ResearchConceptsImmunosuppressive functionMyeloid cellsIntratumoral myeloid cellsNon-hematologic malignanciesMyeloid-specific deletionTumor-associated macrophagesReduced tumor growthTumor-promoting functionsProinflammatory onesMyD88 pathwayMelanoma patientsCell depletionEffector TRole of TET2Methylcytosine dioxygenase TET2Mouse modelIL-1RMelanoma growthTherapeutic targetTumor growthTET2 expressionMelanoma progressionHematopoietic malignanciesMalignancyTET2miR-125b promotes MLL-AF9–driven murine acute myeloid leukemia involving a VEGFA-mediated non–cell-intrinsic mechanism
Liu J, Guo B, Chen Z, Wang N, Iacovino M, Cheng J, Roden C, Pan W, Khan S, Chen S, Kyba M, Fan R, Guo S, Lu J. miR-125b promotes MLL-AF9–driven murine acute myeloid leukemia involving a VEGFA-mediated non–cell-intrinsic mechanism. Blood 2017, 129: 1491-1502. PMID: 28053194, PMCID: PMC5356452, DOI: 10.1182/blood-2016-06-721027.Peer-Reviewed Original Research
2015
Oncogenic CXCL10 signalling drives metastasis development and poor clinical outcome
Wightman SC, Uppal A, Pitroda SP, Ganai S, Burnette B, Stack M, Oshima G, Khan S, Huang X, Posner MC, Weichselbaum RR, Khodarev NN. Oncogenic CXCL10 signalling drives metastasis development and poor clinical outcome. British Journal Of Cancer 2015, 113: 327-335. PMID: 26042934, PMCID: PMC4506383, DOI: 10.1038/bjc.2015.193.Peer-Reviewed Original ResearchConceptsClinical outcomesMetastatic potentialPoor clinical outcomePoor overall survivalMetastatic disease progressionExpression of CXCL10Renal cell carcinomaFunction of CXCL10Increased metastatic potentialIndividual tumor clonesTumor cell growthClinical data setsMetastatic diseaseOverall survivalMetastatic recurrenceCell carcinomaDifferent metastatic abilityCXCR3 pathwayCytokine profilingDisease progressionOncogenic axisCXCR3Metastasis developmentAvailable clinical data setsCXCL10
2012
Tumor Endothelial Inflammation Predicts Clinical Outcome in Diverse Human Cancers
Pitroda SP, Zhou T, Sweis RF, Filippo M, Labay E, Beckett MA, Mauceri HJ, Liang H, Darga TE, Perakis S, Khan SA, Sutton HG, Zhang W, Khodarev NN, Garcia JG, Weichselbaum RR. Tumor Endothelial Inflammation Predicts Clinical Outcome in Diverse Human Cancers. PLOS ONE 2012, 7: e46104. PMID: 23056240, PMCID: PMC3464251, DOI: 10.1371/journal.pone.0046104.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsBreast NeoplasmsCell Line, TumorCells, CulturedColonic NeoplasmsEndothelial CellsEndothelium, VascularFemaleGene Expression ProfilingGliomaHuman Umbilical Vein Endothelial CellsHumansInflammationKaplan-Meier EstimateLung NeoplasmsMaleMiceMiddle AgedMultivariate AnalysisNeoplasmsNeovascularization, PathologicOligonucleotide Array Sequence AnalysisTumor Necrosis Factor-alphaConceptsEndothelial inflammationEndothelial cellsOverall survivalHuman cancersDiverse human cancersExperimental modelTumor-associated endothelial cellsStromal inflammatory responsePathological prognostic factorsEndothelial-derived factorsPro-inflammatory cytokinesInflammatory gene expressionPathologic tissue specimensUntreated endothelial cellsVascular endothelial cellsMultiple human cancersInflammatory signatureHuman endothelial cellsPrognostic factorsClinical outcomesChronic inflammationInflammatory pathwaysLung cancerTumor necrosisInflammatory response
2011
MicroRNA Expression Characterizes Oligometastasis(es)
Lussier YA, Xing HR, Salama JK, Khodarev NN, Huang Y, Zhang Q, Khan SA, Yang X, Hasselle MD, Darga TE, Malik R, Fan H, Perakis S, Filippo M, Corbin K, Lee Y, Posner MC, Chmura SJ, Hellman S, Weichselbaum RR. MicroRNA Expression Characterizes Oligometastasis(es). PLOS ONE 2011, 6: e28650. PMID: 22174856, PMCID: PMC3236765, DOI: 10.1371/journal.pone.0028650.Peer-Reviewed Original ResearchConceptsOligometastatic patientsMetastasis-directed treatmentMetastasis-directed therapyHigh-dose radiotherapyPredictors of progressionMicroRNA-200 (miR-200) familyPolymetastatic progressionMetastatic diseasePatient selectionLocal treatmentCancer stagingMetastatic outcomeXenograft modelMicroRNA classifierPatientsPolymetastasesTumor samplesOligometastasesCell linesTreatmentProgressionBiological basisRadiotherapyExpressionTherapy