Aug 2026· Oncogene· Vol 45, pp. 4051 - 4064· 0 citations· 40 references
Medicine
TL;DR
This study unveils an MDK-TRPA1 + CAF-mediated mechanism of ICB resistance in GC and highlights the WNT5A-SPP1+ macrophage pathway as a promising target to overcome immunotherapy resistance.
Abstract Background Checkpoint blockade (CPB) has limited efficacy in patients with colorectal cancer (CRC), warranting improved therapeutic strategies capable of remodeling the tumor microenvironment. Stem-like TCF1+CD8+ T cells, cytotoxic CD8+ T cells, and lymphoid aggregates have been associated with CPB responsiven...
C. Minnar, Masaya Miyamoto, Asma S. Khelifa et al.· Journal for ImmunoTherapy of...· 0 citations
It is shown that MDSCs accelerate ESCC growth in both immunocompetent and T cell-deficient mice, indicating an intrinsic tumor-promoting program and targeting this pathway may complement T cell-focused therapies in ESCC.
Guo-Hui Qin, Ping-Chuan Ma, Sha-Sha Liu et al.· Cancer Immunology and Immuno...· 0 citations
Cancer-associated fibroblasts (CAFs) are key regulators of tumor progression and therapeutic response in pancreatic ductal adenocarcinoma (PDAC). While CAF-mediated immune modulation has been extensively studied, it remains poorly understood whether adaptive immune cells reciprocally shape CAF heterogeneity and funct...
Jessica Hung, Stephanie L. Silveria, Jenna Vickery et al.· Cancer Research· 0 citations
This work reveals that POSTN + CAFs establish an immunosuppressive TME and are associated with ICB non-response in GC by remodeling lipid metabolism through the ITGB1-PI3K/AKT/mTOR-PPARγ axis, a finding that underscores the therapeutic value of intervening in this specific CAF-macrophage metabolic crosstalk.
Qin Ding, Zi-Teng Li, Rui-Wen Liu et al.· Redox Biology· 0 citations