Investigators showed that, upon irradiation, interleukin-1α (IL-1α) not only polarized cancer-associated fibroblasts (CAFs) toward the inflammatory phenotype but also triggered oxidative DNA damage, thereby predisposing inflammatory CAFs to p53-mediated therapy-induced senescence, which in turn resulted in chemoradiotherapy resistance and disease progression.
[Cancer Cell]
7992332
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apa
50
1
171462
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