2025
The multilayered transcriptional architecture of glioblastoma ecosystems
Nomura M, Spitzer A, Johnson K, Garofano L, Nehar-belaid D, Galili Darnell N, Greenwald A, Bussema L, Oh Y, Varn F, D’Angelo F, Gritsch S, Anderson K, Migliozzi S, Gonzalez Castro L, ChowdhFury T, Robine N, Reeves C, Park J, Lipsa A, Hertel F, Golebiewska A, Niclou S, Nusrat L, Kellet S, Das S, Moon H, Paek S, Bielle F, Laurenge A, Di Stefano A, Mathon B, Picca A, Sanson M, Tanaka S, Saito N, Ashley D, Keir S, Ligon K, Huse J, Yung W, Lasorella A, Verhaak R, Iavarone A, Suvà M, Tirosh I. The multilayered transcriptional architecture of glioblastoma ecosystems. Nature Genetics 2025, 57: 1155-1167. PMID: 40346361, PMCID: PMC12081307, DOI: 10.1038/s41588-025-02167-5.Peer-Reviewed Original ResearchConceptsCell typesSingle-nucleus RNA sequencingDiversity of cellular statesMalignant cell statesGene expression programsTumor DNA sequencingDNA sequencesTranscriptional architectureCellular statesTranscriptional heterogeneityRNA sequencingCell statesCellular heterogeneityExpression programsGenetic aberrationsRecurrent GBM samplesPathway activationLayer of heterogeneityNeuronal-likeNonmalignant cell typesGBM samplesTherapeutic resistanceSequenceEcosystemCell-like
2024
The amalgam of naive CD4+ T cell transcriptional states is reconfigured by helminth infection to dampen the amplitude of the immune response
Even Z, Meli A, Tyagi A, Vidyarthi A, Briggs N, de Kouchkovsky D, Kong Y, Wang Y, Waizman D, Rice T, De Kumar B, Wang X, Palm N, Craft J, Basu M, Ghosh S, Rothlin C. The amalgam of naive CD4+ T cell transcriptional states is reconfigured by helminth infection to dampen the amplitude of the immune response. Immunity 2024, 57: 1893-1907.e6. PMID: 39096910, PMCID: PMC11421571, DOI: 10.1016/j.immuni.2024.07.006.Peer-Reviewed Original ResearchT cell receptorImmune responseNaive CD4<sup>+</sup> T cellsCD4<sup>+</sup> T cellsIFN-IHelminth infectionsNippostrongylus brasiliensis infectionDecreased immune responseType I interferonNaive TT cellsMemory-likeUnrelated antigensTranscriptional changesExtracellular matrixSPF miceCell receptorsI interferonGerm-freeResponse to certain environmental cuesInfectionMiceFunctional changesCell transcriptional statesTranscriptional heterogeneityEpigenetic heterogeneity hotspots in human liver disease progression
Hlady R, Zhao X, Khoury L, Wagner R, Luna A, Pham K, Pyrosopoulos N, Jain D, Wang L, Liu C, Robertson K. Epigenetic heterogeneity hotspots in human liver disease progression. Hepatology 2024, 81: 1197-1210. PMID: 39028883, PMCID: PMC11742070, DOI: 10.1097/hep.0000000000001023.Peer-Reviewed Original ResearchEpigenetic heterogeneityGenome-wide profiling of DNA methylationProfiling of DNA methylationDNA methylation landscapeGenome-wide profilingGene expression heterogeneityCopy number variationsMethylation landscapeOnset of liver cancerDNA methylationLiver disease developmentPhenotypic effectsNumber variationsGenetic heterogeneityTranscriptional heterogeneityFunctional screeningLiver disease progressionCopy numberExpression heterogeneityGene expressionTumor suppressorHuman diseasesGenesPathological phenotypesKey pathways
2021
Single-Cell Transcriptional Heterogeneity of Neutrophils During Acute Pulmonary Cryptococcus neoformans Infection
Deerhake ME, Reyes EY, Xu-Vanpala S, Shinohara ML. Single-Cell Transcriptional Heterogeneity of Neutrophils During Acute Pulmonary Cryptococcus neoformans Infection. Frontiers In Immunology 2021, 12: 670574. PMID: 33995406, PMCID: PMC8116703, DOI: 10.3389/fimmu.2021.670574.Peer-Reviewed Original ResearchConceptsPulmonary Cryptococcus neoformans infectionDistinct neutrophil subsetsCryptococcus neoformans infectionRole of neutrophilsLigand-receptor analysisCytokine gene expressionFirst-line defensePulmonary cryptococcosisNeoformans infectionDendritic cellsNeutrophil subsetsNeutrophil heterogeneityNeutrophil functionImmune cellsCell transcriptional heterogeneityAlveolar macrophagesNeutrophilsFungal infectionsCryptococcus neoformansInfectionSingle-cell transcriptional analysisGene expressionGenerate ROSOxidative stress signatureTranscriptional heterogeneity
2020
A unifying paradigm for transcriptional heterogeneity and squamous features in pancreatic ductal adenocarcinoma
Hayashi A, Fan J, Chen R, Ho Y, Makohon-Moore A, Lecomte N, Zhong Y, Hong J, Huang J, Sakamoto H, Attiyeh M, Kohutek Z, Zhang L, Boumiza A, Kappagantula R, Baez P, Bai J, Lisi M, Chadalavada K, Melchor J, Wong W, Nanjangud G, Basturk O, O’Reilly E, Klimstra D, Hruban R, Wood L, Overholtzer M, Iacobuzio-Donahue C. A unifying paradigm for transcriptional heterogeneity and squamous features in pancreatic ductal adenocarcinoma. Nature Cancer 2020, 1: 59-74. PMID: 35118421, PMCID: PMC8809486, DOI: 10.1038/s43018-019-0010-1.Peer-Reviewed Original ResearchConceptsExpression profilesSquamous featuresPancreatic cancerChromatin modifier genesCancer expression profilesMetastatic pancreatic cancerEvolution of pancreatic cancerBasal-like phenotypeBasal-like subtypePhylogenetic studiesChromatin modifiersEvolutionary analysisPancreatic ductal adenocarcinomaTranscriptional heterogeneityModifier genesIntercellular heterogeneitySubclonal populationsSquamous histologyMYC amplificationGlandular tumorsSomatic mutationsSquamous morphologyClonal mutationsDuctal adenocarcinomaHistologic correlation
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