Tumor-Promoting Inflammation Module

A conserved mechanism module for the enabling characteristic of cancer (Hanahan & Weinberg): tumor-promoting inflammation. Chronic inflammation fosters multiple hallmark capabilities by supplying the tumor microenvironment with bioactive molecules. The conserved causal chain runs from an inflammatory stimulus (chronic infection, autoimmune or irritant-driven chronic inflammation, obesity-associated inflammation, or inflammation elicited by the incipient neoplasm itself) through recruitment and activation of innate and adaptive immune cells - tumor-associated macrophages, neutrophils, mast cells, and lymphocytes - that establish a pro-tumorigenic inflammatory microenvironment. These cells secrete growth factors, pro-angiogenic factors (VEGF), matrix-remodeling proteases (MMPs), reactive oxygen species that are themselves mutagenic, and cytokines (TNF, IL-6) that activate pro-survival/proliferative NF-kB and STAT3 signaling in tumor cells. The net effect is promotion of proliferation, survival, angiogenesis, invasion, and further genomic instability. Individual disorder entries declare conformance via conforms_to, substituting the tumor-type-specific inflammatory driver (e.g., Helicobacter pylori gastritis preceding gastric cancer, inflammatory bowel disease preceding colitis-associated colorectal cancer, viral hepatitis preceding hepatocellular carcinoma). This module complements immune_checkpoint_blockade, which models the adaptive immune-evasion arm.