GENETICS, MOLECULAR-BIOLOGY AND COLORECTAL-CANCER
GENETICS, MOLECULAR-BIOLOGY AND COLORECTAL-CANCER
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DOI：
10.1016/0027-5107(93)90027-d
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发表时间：
1993-11-01
期刊：
影响因子：
--
通讯作者：
FINLAY, GJ
中科院分区：
文献类型：
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作者：
FINLAY, GJ
结直肠癌 (CRC) 的发展经历了几个组织学明确的阶段，反映了基因改变的连续获得。一些经常突变的基因已被确定，它们可能会导致遗传性和散发性癌症的发生（Bishop 和 Thomas，1990 年综述；Fearon 和 Vogelstein，1990 年；Fearon 和 Jones，1992 年；Hamilton，1992 年）。这项工作得出了一些概括。在癌症发展的最早可检测阶段就可以观察到突变。特定的基因往往会按照给定的顺序发生突变，但控制肿瘤形成的是关键数量的病变的积累。突变通过激活癌基因积极促进肿瘤特征，并通过失活抑癌基因消除对肿瘤特征的限制。
Colorectal cancer (CRC) develops through several histologically well-defined stages, reflecting the sequential acquisition of genetic alterations. Several frequently mutated genes have been identified which probably contribute to the development of both hereditary and sporadic cancer (reviewed in Bishop and Thomas, 1990; Fearon and Vogelstein, 1990; Fearon and Jones, 1992; Hamilton, 1992). Several generalizations emerge from this work. Mutations are observed in the earliest detectable stages of cancer development. Specific genes tend to be mutated in a given order, but it is the accumulation of a critical number of lesions which governs the appearance of neoplasia. Mutations actively promote neoplastic character by activating oncogenes and eliminate restraints on neoplastic character by inactivating tumour suppressor genes.