Adami H O, Signorello L B, Trichopoulos D
Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
Semin Cancer Biol. 1998 Aug;8(4):255-62. doi: 10.1006/scbi.1998.0077.
We present an etiological model for breast cancer in humans, and we examine whether it accommodates the patterns of occurrence of this disease and the associated risk factors. The model has four components: (1) the likelihood of breast cancer occurrence depends on the number of cells at risk; (2) the number of target cells is partially determined early in life, perhaps even in utero; (3) while a pregnancy stimulates the replication of already initiated cells, it conveys long-term protection through structural changes, terminal cellular differentiation, and perhaps other mechanisms; and (4) in adult life, mammotropic hormones, in conjunction with their receptors, affect the number of target cells, the likelihood of retention of spontaneous somatic mutations, and the rate of expansion of initiated clones. The model accommodates several hypotheses but also allows new insights.
我们提出了一种人类乳腺癌的病因模型，并检验它是否符合这种疾病的发生模式及相关风险因素。该模型有四个组成部分：（1）乳腺癌发生的可能性取决于有风险的细胞数量；（2）目标细胞的数量在生命早期部分确定，甚至可能在子宫内就已确定；（3）虽然怀孕会刺激已启动细胞的复制，但它通过结构变化、终末细胞分化以及可能的其他机制提供长期保护；（4）在成年期，促乳激素与其受体共同作用，影响目标细胞的数量、自发体细胞突变保留的可能性以及启动克隆的扩增速率。该模型包含了几个假说，但也能带来新的见解。
