The ras gene family and human carcinogenesis

作者: Johannes L. Bos

DOI: 10.1016/0165-1110(88)90004-8

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摘要: It has been well established that specific alterations in members of the ras gene family, H-ras, K-ras and N-ras, can convert them into active oncogenes. These are either point mutations occurring codon 12, 13 or 61 or, alternatively, a 5- to 50-fold amplification wild-type gene. Activated oncogenes have found significant proportion all tumors but incidence varies considerably with tumor type: it is relatively frequent (20-40%) colorectal cancer acute myeloid leukemia, absent present only rarely in, for example, breast stomach cancer. No correlation found, yet, between presence absence an activated clinical biological features malignancy. The activation one step multistep process formation. mutated genes benign polyps colon indicates be early event, possibly even initiating event. However, also occur later course carcinogenesis initiate instance transition polyp malignant carcinoma primary melanoma metastatic tumor. Apparently, not obligatory event when occurs contribute both advanced stages human carcinogenesis.

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