ETIOPATHOGENESIS OF CANCER

Silent chronic inflammation is the necessary condition through which pathogens and IARC Group 1 carcinogens give rise to cancer: necessary, not sufficient, since only a minority of those exposed develop a neoplasm and risk is a function of duration and intensity. Three causal routes are distinguished — biological pathogens, chemical carcinogens, congenital DNA defects — the first two converging on inflammation while the third bypasses it.The 15-20% estimate of infection-attributable cancers is discussed as a methodological floor rather than a ceiling, since it counts only the agents actively searched for; the GBD 2023 cancer study itself states that several causally associated infectious diseases are not included in its estimates.The appendix examines five species with marked cancer resistance. In three the documented mechanism is anti-inflammatory: bat (dampened NLRP3 inflammasome with unchanged viral load), naked mole-rat (immunoregulatory HMM-HA, cancer incidence falling from 83% to 49% in the transgenic model), elephant (loss of necroptosis and pyroptosis genes). Bat and elephant converge on the same sensor family despite more than a hundred million years of separation. In two — whale and armadillo — the mechanism is instead genomic, showing that the chain can be broken at several points.A falsifiable prediction is stated: baseline inflammatory markers in these species have never been measured comparatively.