Harrington E A, Fanidi A, Evan G I
Biochemistry of the Cell Nucleus Laboratory, Imperial Cancer Research Fund, London, UK.
Curr Opin Genet Dev. 1994 Feb;4(1):120-9. doi: 10.1016/0959-437x(94)90100-7.
Several recent studies have implicated oncogenes and tumour suppressor genes in the regulation of programmed cell death (apoptosis). Lesions in the cell death pathway appear to be important in both carcinogenesis and the evolution of drug resistance in tumours. They include deregulated expression of genes such as bcl-2, loss of p53, and autocrine activation of anti-apoptotic signal transduction pathways. Paradoxically, a number of dominant oncogenes appear to act as potent inducers of apoptosis. This suggests that the pathways of cell proliferation and cell death may be tightly coupled, an idea that may have dramatic implications for models of oncogene co-operation and carcinogenesis.
最近的几项研究表明，癌基因和肿瘤抑制基因参与了程序性细胞死亡（凋亡）的调控。细胞死亡途径中的损伤在肿瘤发生和肿瘤耐药性演变中似乎都很重要。这些损伤包括bcl-2等基因的表达失调、p53缺失以及抗凋亡信号转导途径的自分泌激活。矛盾的是，一些显性癌基因似乎可作为凋亡的有效诱导剂。这表明细胞增殖和细胞死亡途径可能紧密相连，这一观点可能对癌基因协同作用和肿瘤发生模型产生重大影响。
