Michalovitz D, Halevy O, Oren M
Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
J Cell Biochem. 1991 Jan;45(1):22-9. doi: 10.1002/jcb.240450108.
Although the case for p53 as a tumor suppressor gene appears very strong, one should still keep an open eye for the possibility that mutations in p53 do not necessarily imply a mere loss of "suppressor" activity. It is still possible that the presence of a p53 mutation in a tumor contributes, in a dominant positive manner, to tumorigenesis. In other words, certain p53 mutants may well be oncogenic in their own right, and carry distinct activities that promote growth deregulation and malignant progression. Elucidating this issue also has practical implications, since the nature of the resident mutations may greatly dictate the consequences of attempts to reintroduce wild-type (wt) p53 into particular types of tumor cells. There are two major obstacles along the road to meaningful answers: the limitations of the experimental systems used for evaluating the biological activities of wt and mutant p53 and a fundamental lack of knowledge about the relevant biochemistry of the p53 protein. These two aspects constitute primary experimental challenges for investigators in the field.
尽管p53作为一种肿瘤抑制基因的证据似乎非常确凿,但人们仍应密切关注p53突变不一定仅仅意味着“抑制”活性丧失的可能性。肿瘤中存在p53突变仍有可能以显性正性方式促进肿瘤发生。换句话说,某些p53突变体本身很可能具有致癌性,并具有促进生长失调和恶性进展的独特活性。阐明这个问题也具有实际意义,因为驻留突变的性质可能极大地决定了将野生型(wt)p53重新引入特定类型肿瘤细胞的尝试所产生的后果。在获得有意义答案的道路上存在两个主要障碍:用于评估wt和突变型p53生物学活性的实验系统的局限性,以及对p53蛋白相关生物化学的基本了解不足。这两个方面构成了该领域研究人员的主要实验挑战。