TL;DR
A novel autophagy-NF-κB-IL-6 axis governing senescence-independent SASP and the downstream inflammatory cascade in HNSCC is revealed, representing a promising therapeutic strategy to improve chemoradiotherapy plus immunotherapy efficacy.
Cellular senescence, a process characterized by the typically persistent cell-cycle arrest that occurs in response to DNA damage, plays a dual role in carcinogenesis. This complexity is predominantly influenced by the presence of senescent cancer-associated fibroblasts within the tumor microenvironment. While the induc...
Esophageal squamous cell carcinoma (ESCC) remains a formidable malignancy, with patients harboring programmed death ligand-1 (PD-L1)-negative tumors frequently exhibiting an "immune desert" phenotype and poor response to immune checkpoint blockade (ICB). Radiotherapy (RT), traditionally utilized for localized cytoreduc...
Ovarian cancer remains one of the most lethal gynecological malignancies, largely due to late diagnosis and the frequent development of resistance to platinum-based chemotherapy and taxanes. Increasing evidence implicates microRNAs as key regulators of drug response through their control of DNA damage response and repa...
Cellular senescence is a stress-responsive state marked by sustained proliferative arrest and changes in metabolism, chromatin organization, secretion, and immune signaling. In ovarian cancer (OC), platinum therapy and PARP inhibition can generate senescence-associated states with distinct consequences. Their effects d...
The dual-specificity tyrosine-regulated kinase DYRK1B is frequently expressed at elevated levels in solid tumors and has been implicated in cancer cell survival, therapy resistance, and cell cycle arrest. While DYRK1B is best known for maintaining quiescence, its broader impact on cancer cell phenotypic plasticity rema...
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