The senescence-associated secretory phenotype (SASP) drives tumor progression through a multifaceted molecular network—comprising cytokines (IL-6, IL-8), chemokines (CXCL1, CCL2), proteases (MMPs), and growth factors (VEGF, TGF-β)—that remodels the tumor microenvironment (TME) into a pro-carcinogenic niche (69). The gene discussed is CXCL1; the disease is neoplasm.