2024
EGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth.
Kuhlmann-Hogan A, Cordes T, Xu Z, Kuna R, Traina K, Robles-Oteiza C, Ayeni D, Kwong E, Levy S, Globig A, Nobari M, Cheng G, Leibel S, Homer R, Shaw R, Metallo C, Politi K, Kaech S. EGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth. Cancer Discovery 2024, 14: 524-545. PMID: 38241033, PMCID: PMC11258210, DOI: 10.1158/2159-8290.cd-23-0434.Peer-Reviewed Original ResearchLung adenocarcinomaGM-CSFEGFR-mutant lung adenocarcinomaGM-CSF secretionProinflammatory immune responseSuppress tumor progressionLocal immunosuppressionStatin therapyTherapeutic combinationsNovel therapiesTumor cellsTumor progressionTumor growthLung adenocarcinoma cellsEGFR phosphorylationImmune responseTransformed epitheliumCancer cellsInflammatory functionsEGFR signalingMacrophage metabolismAlveolar macrophagesIncreased cholesterol synthesisMetabolic supportOncogenic signalingEGFR-Driven Lung Adenocarcinomas Co-opt Alveolar Macrophage Metabolism and Function to Support EGFR Signaling and Growth.
Kuhlmann-Hogan A, Cordes T, Xu Z, Kuna R, Traina K, Robles-Oteíza C, Ayeni D, Kwong E, Levy S, Globig A, Nobari M, Cheng G, Leibel S, Homer R, Shaw R, Metallo C, Politi K, Kaech S. EGFR-Driven Lung Adenocarcinomas Co-opt Alveolar Macrophage Metabolism and Function to Support EGFR Signaling and Growth. Cancer Discovery 2024, of1-of22. PMID: 38270272, DOI: 10.1158/2159-8290.cd-23-0434.Peer-Reviewed Original ResearchLung adenocarcinomaGM-CSFEGFR-mutant lung adenocarcinomaT cell-based immunotherapyTransformed epitheliumOncogenic signalingGM-CSF secretionProinflammatory immune responseSuppress tumor progressionLocal immunosuppressionStatin therapyTherapeutic combinationsNovel therapiesTumor cellsTumor progressionTumor growthLung cancerLung adenocarcinoma cellsEGFR phosphorylationImmune responseImmunological supportCancer cellsInflammatory functionsAlveolar macrophagesIncreased cholesterol synthesis
2014
Immune-Based Antitumor Effects of BRAF Inhibitors Rely on Signaling by CD40L and IFNγ
Ho PC, Meeth KM, Tsui YC, Srivastava B, Bosenberg MW, Kaech SM. Immune-Based Antitumor Effects of BRAF Inhibitors Rely on Signaling by CD40L and IFNγ. Cancer Research 2014, 74: 3205-3217. PMID: 24736544, PMCID: PMC4063281, DOI: 10.1158/0008-5472.can-13-3461.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen-Presenting CellsAntineoplastic AgentsCD40 LigandCD4-Positive T-LymphocytesDrug Screening Assays, AntitumorIndolesInterferon-gammaMacrophagesMelanoma, ExperimentalMiceMice, TransgenicMutation, MissenseProto-Oncogene Proteins B-rafSignal TransductionSkin NeoplasmsSulfonamidesTumor MicroenvironmentConceptsTumor-infiltrating lymphocytesIFNγ expressionMyeloid cellsImmune stimulatory microenvironmentTh1 effector functionRegulatory T cellsAgonistic CD40 antibodyImmune-related changesTumor-bearing miceSuppress tumor growthIFNγ blockadeImmunologic changesAntitumor immunityAntitumor responseCD40 antibodyTumor regressionT cellsBRAF inhibitorsMurine modelEffector functionsImmunosuppressive featuresAntitumor effectsHost immunityMelanoma growthTumor growth