Chuan Wang

ORCID: 0000-0003-3811-7725
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About
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Research Areas
  • Peptidase Inhibition and Analysis
  • Cancer Immunotherapy and Biomarkers
  • Pancreatic and Hepatic Oncology Research
  • Immune Cell Function and Interaction
  • Immune cells in cancer
  • IgG4-Related and Inflammatory Diseases
  • Cancer, Hypoxia, and Metabolism
  • Lung Cancer Research Studies
  • Neuroendocrine Tumor Research Advances
  • Congenital Diaphragmatic Hernia Studies
  • Cancer Research and Treatments

University of Liverpool
2022-2023

Abstract Myofibroblastic cancer-associated fibroblast (myoCAF)–rich tumors generally contain few T cells and respond poorly to immune-checkpoint blockade. Although myoCAFs are associated with poor outcome in most solid tumors, the molecular mechanisms regulating myoCAF accumulation remain unclear, limiting potential for therapeutic intervention. Here, we identify ataxia-telangiectasia mutated (ATM) as a central regulator of phenotype. Differentiating myofibroblasts vitro cultured ex vivo...

10.1158/0008-5472.can-22-0435 article EN cc-by Cancer Research 2022-11-10

<div>Abstract<p>Myofibroblastic cancer-associated fibroblast (myoCAF)–rich tumors generally contain few T cells and respond poorly to immune-checkpoint blockade. Although myoCAFs are associated with poor outcome in most solid tumors, the molecular mechanisms regulating myoCAF accumulation remain unclear, limiting potential for therapeutic intervention. Here, we identify ataxia-telangiectasia mutated (ATM) as a central regulator of phenotype. Differentiating myofibroblasts...

10.1158/0008-5472.c.6514176.v1 preprint EN 2023-03-31

<div>Abstract<p>Myofibroblastic cancer-associated fibroblast (myoCAF)–rich tumors generally contain few T cells and respond poorly to immune-checkpoint blockade. Although myoCAFs are associated with poor outcome in most solid tumors, the molecular mechanisms regulating myoCAF accumulation remain unclear, limiting potential for therapeutic intervention. Here, we identify ataxia-telangiectasia mutated (ATM) as a central regulator of phenotype. Differentiating myofibroblasts...

10.1158/0008-5472.c.6514176 preprint EN 2023-03-31
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