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[化学诱导致癌作用的分子机制]

[Molecular mechanisms of chemically induced carcinogenesis].

作者信息

Palut D, Kostka G, Adamczyk M

机构信息

Zakład Toksykologii Srodowiskowej, Państwowy Zakład Higieny, Warszawa.

出版信息

Rocz Panstw Zakl Hig. 1998;49(1):35-54.

PMID:9734231
Abstract

In this review recent point of view concerning the molecular mechanisms of chemically induced carcinogenesis is presented. The new and promising trends of neoplasia investigations are based on discovery of protooncogenes and tumor suppressor genes, which maintain tissue homeostasis by controlling cellular proliferation and differentiation. It is generally recognised, that mutations induced by genotoxic carcinogens, particularly those resulting in activation of protooncogenes and inactivation of suppressor genes, play a crucial role in the initiation step of multistage process of tumorigenesis. Tumor promotion is recognized as a process whereby initiated cells are stimulated to selective growth and then, to develop into the cancer during progression step. Tumor promotion can be affected by many nongenotoxic carcinogens. In this review the attention is given to the mutational activation of the c-ras oncogenes and inactivation of p53 suppressor gene in rodent and human cancers by genotoxic carcinogens. Moreover, the significance of nongenotoxic carcinogens and the mechanisms by which these compounds may accelerate tumorigenesis are discussed.

摘要

本综述介绍了有关化学诱导致癌作用分子机制的最新观点。肿瘤形成研究的新趋势和有前景的趋势基于原癌基因和肿瘤抑制基因的发现,这些基因通过控制细胞增殖和分化来维持组织稳态。人们普遍认识到,遗传毒性致癌物诱导的突变,尤其是那些导致原癌基因激活和抑制基因失活的突变,在肿瘤发生多阶段过程的起始步骤中起着关键作用。肿瘤促进被认为是一个过程,在此过程中,起始细胞被刺激选择性生长,然后在进展阶段发展成癌症。许多非遗传毒性致癌物可影响肿瘤促进。本综述关注遗传毒性致癌物在啮齿动物和人类癌症中导致的c-ras癌基因的突变激活和p53抑制基因的失活。此外,还讨论了非遗传毒性致癌物的重要性以及这些化合物可能加速肿瘤发生的机制。

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