Stephen Y. Chih

ORCID: 0000-0003-4397-6065
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About
Contact & Profiles
Research Areas
  • Ferroptosis and cancer prognosis
  • Immune cells in cancer
  • Cell death mechanisms and regulation
  • Cell Adhesion Molecules Research
  • Glioma Diagnosis and Treatment
  • Barrier Structure and Function Studies
  • Microtubule and mitosis dynamics
  • Phagocytosis and Immune Regulation
  • Multiple Myeloma Research and Treatments
  • Cancer-related molecular mechanisms research
  • Circular RNAs in diseases
  • Drug Transport and Resistance Mechanisms
  • Cancer, Lipids, and Metabolism
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Hippo pathway signaling and YAP/TAZ
  • Cancer, Hypoxia, and Metabolism
  • Melanoma and MAPK Pathways
  • Cancer Treatment and Pharmacology

Penn State Milton S. Hershey Medical Center
2020-2025

University of California, Santa Barbara
2021

Abstract Tumor necrosis commonly exists and predicts poor prognoses in many cancers. Although it is thought to result from chronic ischemia, the underlying nature mechanisms driving involved cell death remain obscure. Here, we show that glioblastoma (GBM) involves neutrophil-triggered ferroptosis. In a hyperactivated transcriptional coactivator with PDZ-binding motif-driven GBM mouse model, neutrophils coincide temporally spatially. Neutrophil depletion dampens necrosis. Neutrophils isolated...

10.1038/s41467-020-19193-y article EN cc-by Nature Communications 2020-10-27

Abstract The association of necrosis in tumors with poor prognosis implies a potential tumor-promoting role. However, the mechanisms underlying cell death this context and how damaged tissue contributes to tumor progression remain unclear. Here, we identified p38 mitogen-activated protein kinases (p38 MAPK, a.k.a. p38) as key player promoting inflammatory response ischemic stress associated necrotic tumors. We found that glioblastoma (GBM) cells expressing patient-derived Kirsten rat sarcoma...

10.1038/s41419-025-07335-3 article EN cc-by Cell Death and Disease 2025-01-14

Tumor necrosis is a poor prognostic marker in glioblastoma (GBM) and variety of other solid cancers. Accumulating evidence supports that could facilitate tumor progression resistance to therapeutics. GBM typically first detected by magnetic resonance imaging (MRI), after prominent has already formed. Therefore, radiological appearances early formation the temporal-spatial development alongside remain poorly understood. This knowledge gap leads lack reliable radiographic diagnostic/prognostic...

10.3389/fonc.2022.993649 article EN cc-by Frontiers in Oncology 2022-10-14

Abstract Glioblastoma (GBM) is the most common malignant primary brain tumor. The median survival less than two years. mesenchymal (MES) subtype of GBM particularly associated with treatment resistance, poor prognosis, and enriched infiltration immune cells, including tumor-associated microglia and/or macrophages (TAMs). Despite promising results in preclinical studies, clinical trials targeting TAMs have been unsuccessful. Necrosis a hallmark correlates unfavorable outcomes, but how...

10.1158/1538-7445.am2024-188 article EN Cancer Research 2024-03-22

Abstract Necrosis is commonly found in various solid tumors and predicts worse outcome. Chronic ischemia can initiate tumor necrosis, however, how the damaged tissue further expands unclear. Previous studies that neutrophils associate with necrosis could contribute development glioblastoma (GBM) through transferring myeloperoxidase-containing granules into cells inducing cell ferroptosis. How neutrophilic granule transfer occurs unknown. Here, an unbiased small molecule screen, we statins...

10.1158/1538-7445.am2024-5994 article EN Cancer Research 2024-03-22

Abstract Glioblastoma multiforme (GBM) is the most common and aggressive brain tumor in adults. Despite association of necrosis a poor prognosis GBM, mechanisms underlying formation remain unclear, likely due to lack appropriate experimental models examine development necrosis. In our study, we developed mouse with by intracranially injecting human GBM cells expressing KRAS or PI3K active mutants into immunodeficient mice. Surprisingly, despite all tumors displayed similar sizes, control an...

10.1158/1538-7445.am2024-393 article EN Cancer Research 2024-03-22
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