Figure 1.

Diagrammatic representation of the hypothesis for the causation of young-onset carcinogenesis. The risk for young-onset cancer begins in utero with exposure of the foetus to maternal, stressors. The possibility of a paternal contribution through the damaging effects of stressors on the sperm are considered and warrant consideration. Exposure to the same stressors, during adolescence or young adulthood, facilitates a re-activation of these ‘responses designed to be protective’ but ultimately resulting in a loss of regulation at a metabolic and/or genetic level culminating in the evolution of the neoplastic process as a result of a cumulative effect with environmental and other genetic factors.