(1) Background: We consider dormant, pre-cancerous states prevented from developing into cancer by the immune system. Inflammatory morbidity may compromise the immune system and cause the pre-cancer to escape into an actual cancerous development. The immune deficiency described is general, but the results may vary across specific cancers due to different variances (2) Methods: We formulate a general conceptual model to perform rigorous in silico consequence analysis. Relevant existing data for myeloproliferative malignancies from the literature are used to calibrate the in silico computations. (3) Results and conclusions: The hypothesis suggests a common physiological origin for many clinical and epidemiological observations in relation to cancers in general. Examples are the observed age-dependent prevalence for hematopoietic cancers, a general mechanism-based explanation for why the risk of cancer increases with age, and how somatic mutations in general, and specifically seen in screenings of citizens, sometimes are non-increased or even decrease when followed over time. The conceptual model is used to characterize different groups of citizens and patients, describing different treatment responses and development scenarios.
Keywords: aging; cancer; comorbidity; immuno-competition; inflammation; myeloproliferative neoplasms.