(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.
（1）背景：我们关注的是处于休眠状态的癌前病变，这些病变通常被免疫系统抑制而未能发展为癌症。炎症性疾病可能削弱免疫系统功能，导致癌前病变突破免疫监控，进展为实际癌症。这种免疫缺陷具有普遍性，但由于不同癌症存在特异性差异，其具体影响可能因癌种而异。（2）方法：我们构建了一个通用概念模型进行严谨的计算机模拟结果分析。通过文献中骨髓增殖性肿瘤的相关现有数据对计算机模拟计算进行参数校准。（3）结果与结论：该假说为多种癌症相关的临床与流行病学观察提供了共同的生理学起源解释。具体例证包括：造血系统肿瘤随年龄增长而发病率上升的现象、癌症风险随年龄增长而增加的普适性机制解释，以及通过长期随访发现，普通体细胞突变（特别是公民筛查中发现的突变）有时并未增加甚至减少的观察结果。该概念模型可用于划分不同特征的公民与患者群体，描述其差异化的治疗反应与疾病发展轨迹。
肿瘤(癌症)患者之家