Role of active cell death (apoptosis) in multi-stage carcinogenesis
Role of active cell death (apoptosis) in multi-stage carcinogenesis
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DOI：
10.1016/0378-4274(95)03550-8
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发表时间：
1995-12-01
影响因子：
3.5
通讯作者：
Mullauer, L
中科院分区：
文献类型：
--
作者：
SchulteHermann, R;Bursch, W;Mullauer, L
主动细胞死亡是一种基因编码的细胞自我毁灭。在他莫昔芬处理后，存在形态学上不同类型的活性细胞死亡，例如肝中的细胞凋亡或人乳腺癌细胞中的自噬细胞死亡。（前）在大鼠肝脏肿瘤病变表现出增强的凋亡率，这往往会增加与恶性程度的增加。肿瘤促进剂和非遗传毒性致癌物抑制活性细胞死亡，从而增加（前）肿瘤细胞的积累并加速癌症的发展。另一方面，启动子撤回、禁食或应用负生长信号如转化生长因子β 1（TGF β 1）增强细胞凋亡，并可导致肿瘤前病变或肿瘤的选择性消退。
Active cell death is a genetically encoded self-destruction of a cell. There occur morphologically different types of active cell death, e.g. apoptosis in the liver or autophagic cell death in human mammary carcinoma cells after tamoxifen treatment. (Pre)neoplastic lesions in rat liver exhibit enhanced rates of apoptosis, which tend to increase with increasing malignancy. Tumor promoters and non-genotoxic carcinogens inhibit active cell death, thereby increasing the accumulation of (pre)neoplastic cells and accelerating the development of cancer. On the other hand promoter withdrawal, fasting or application of negative growth signals such as transforming growth factor beta 1 (TGF beta 1) enhance apoptosis and can lead to selective regression of preneoplastic lesions or tumors.