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人结直肠癌中c-Ki-ras-2原癌基因的差异激活

Differential activation of the c-Ki-ras-2 proto-oncogene in human colorectal carcinoma.

作者信息

Halatsch M E, Hirsch-Ernst K I, Weinel R J, Kahl G F

机构信息

Department of Toxicology, Georg-August-University, Göttingen, Germany.

出版信息

Anticancer Res. 1998 Jul-Aug;18(4A):2323-5.

PMID:9703874
Abstract

In colorectal carcinoma, c-Ki-ras-2 mutations predominantly occur in codon 12 and, to a considerably lesser extent, in codon 13. To our knowledge, involvement of codon 61 in c-Ki-ras-2 has been reported only once among the large number of colon cancers investigated altogether. In this study, five human primary colorectal carcinomas were analyzed for the presence of activating c-Ki-ras-2 point mutations in codon 12, 13, and 61. Tumor DNAs were amplified by PCR and subsequently hybridized to a panel of synthetic oligonucleotides representing the complete spectrum of possible mutations. In two of the five tumors, mutations involving codons 13 and 61, respectively, were detected. These data extend previous findings that point mutation of codon 61 may be an improbable yet possible event leading to activation of c-Ki-ras-2 in colorectal carcinoma.

摘要

在结直肠癌中,c-Ki-ras-2突变主要发生在第12密码子,在第13密码子发生的程度要小得多。据我们所知,在总共大量研究的结肠癌中,仅报道过1次c-Ki-ras-2第61密码子受累情况。在本研究中,分析了5例人类原发性结直肠癌中第12、13和61密码子激活型c-Ki-ras-2点突变的存在情况。肿瘤DNA通过PCR扩增,随后与一组代表所有可能突变谱的合成寡核苷酸杂交。在5例肿瘤中的2例中,分别检测到涉及第13和61密码子的突变。这些数据扩展了先前的发现,即第61密码子的点突变可能是导致结直肠癌中c-Ki-ras-2激活的一个不太可能但有可能的事件。

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