ARE CELL NUMBER AND CELL-PROLIFERATION RISK-FACTORS FOR CANCER
ARE CELL NUMBER AND CELL-PROLIFERATION RISK-FACTORS FOR CANCER
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DOI：
10.1093/jnci/80.10.772
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发表时间：
1988-07-20
影响因子：
10.3
通讯作者：
WINICK, M
中科院分区：
文献类型：
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作者：
ALBANES, D;WINICK, M
相对而言，人们对人类致癌的机制知之甚少。在啮齿类动物中，热量限制强烈地抑制肿瘤的发展，并且有证据表明人类的癌症与体重之间存在正相关关系。生命早期的热量限制也被认为会永久地减少器官细胞。最近的一项关于成人身材和癌症发病率之间的联系同样暗示了在癌变过程中对生长和可能对早期营养的持久影响。据推测，癌症风险与增殖细胞的数量成正比，而增殖细胞的数量又取决于组织内细胞的数量和细胞分裂的速度。这一假设与人类癌变的几个方面是一致的，包括多阶段模型和大多数癌症的上皮起源。
Relatively little is known about the mechanisms underlying carcinogenesis in humans. Caloric restriction strongly inhibits the development of neoplasia in rodents, and there is evidence of a positive relationship between cancer and body weight in humans. Caloric restriction early in life is also known to permanently diminish organ cellularity. A recent link between adult stature and cancer incidence similarly implicates a lasting effect for growth and possibly for early nutrition in carcinogenesis. It is postulated that cancer risk is proportional to the number of proliferating cells, which in turn depends on both the number of cells and the rate of cell division within the tissue. This hypothesis is consistent with several aspects of human carcinogenesis, including multistage models and the epithelial origin of most cancers.