2024
Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease
Srivastava S, Zhou H, Shenoi R, Morris M, Lainez-Mas B, Goedeke L, Rajendran B, Setia O, Aryal B, Kanasaki K, Koya D, Inoki K, Dardik A, Bell T, Fernández-Hernando C, Shulman G, Goodwin J. Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease. Science Advances 2024, 10: eadn6068. PMID: 39630889, PMCID: PMC11616692, DOI: 10.1126/sciadv.adn6068.Peer-Reviewed Original ResearchMeSH KeywordsAngiopoietin-Like Protein 4AnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease Models, AnimalEpithelial-Mesenchymal TransitionFibrosisHumansIntegrin beta1KidneyMicePodocytesConceptsAngiopoietin-like 4Diabetic kidney diseaseIntegrin B1Fibrogenic moleculesMutant miceSTING pathway activationIncreased fatty acid oxidationProgressive diabetic kidney diseaseDiabetic kidneyKidney diseaseReduced epithelial-to-mesenchymal transitionEpithelial-to-mesenchymal transitionFatty acid oxidationExpression of pro-inflammatory cytokinesTargeted pharmacological therapiesGene expressionMitochondrial damageEndothelial-to-mesenchymal transitionPro-inflammatory cytokinesPathway activationPharmacological therapyControl miceIntegrinAcid oxidationFibrogenic phenotype
2021
Molecular landscape and subtype-specific therapeutic response of nasopharyngeal carcinoma revealed by integrative pharmacogenomics
Ding R, Chen P, Rajendran B, Lyu X, Wang H, Bao J, Zeng J, Hao W, Sun H, Wong A, Valecha M, Yang E, Su S, Choi T, Liu S, Chan K, Yang L, Wu J, Miao K, Chen Q, Shim J, Xu X, Deng C. Molecular landscape and subtype-specific therapeutic response of nasopharyngeal carcinoma revealed by integrative pharmacogenomics. Nature Communications 2021, 12: 3046. PMID: 34031426, PMCID: PMC8144567, DOI: 10.1038/s41467-021-23379-3.Peer-Reviewed Original ResearchConceptsSarcomatoid carcinomaEpithelial-mesenchymal transitionNasopharyngeal carcinomaCarcinoma subtypesNeck cancer typesPatient-derived organoidCRT regimensDistinct molecular featuresMalignant headHigh morbidityTreatment regimensTherapeutic responseEC subtypesPathogenic mechanismsDrug responsivenessEGFR inhibitorsNPC subtypesCancer typesSubtypesCarcinomaPrecision oncologyDrug testsMolecular landscapeRegimensMicrotubule inhibitors
2020
NOTCH1 activation compensates BRCA1 deficiency and promotes triple-negative breast cancer formation
Miao K, Lei J, Valecha M, Zhang A, Xu J, Wang L, Lyu X, Chen S, Miao Z, Zhang X, Su S, Shao F, Rajendran B, Bao J, Zeng J, Sun H, Chen P, Tan K, Chen Q, Wong K, Xu X, Deng C. NOTCH1 activation compensates BRCA1 deficiency and promotes triple-negative breast cancer formation. Nature Communications 2020, 11: 3256. PMID: 32591500, PMCID: PMC7320176, DOI: 10.1038/s41467-020-16936-9.Peer-Reviewed Original ResearchMeSH KeywordsAllelesAnimalsAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCarcinogenesisCell DeathCell Line, TumorCheckpoint Kinase 1Disease ProgressionDNA Transposable ElementsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMice, KnockoutMitosisMutationReceptor, Notch1Signal TransductionTriple Negative Breast NeoplasmsConceptsTriple-negative breast cancerEpithelial-mesenchymal transitionHuman breast cancer tissuesBRCA1 mutation carriersBreast cancer tissuesBRCA1-deficient miceActivation of Notch1Breast cancer formationRefractory diseaseForm of Notch1Breast cancerMutation carriersHigh riskCancer tissuesClinical optionG2/M cell cycle checkpointFatal diseaseCell cycle checkpointsM cell cycle checkpointNotch1 activationBRCA1 deficiencyPhosphorylation of ATRNotch1Cancer formationCycle checkpoints