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人类结直肠癌中肿瘤抑制基因位点的杂合性缺失

Loss of heterozygosity of tumour suppressor gene loci in human colorectal carcinoma.

作者信息

Iacopetta B, DiGrandi S, Dix B, Haig C, Soong R, House A

机构信息

University Department of Surgery, Queen Elizabeth II Medical Centre, Nedlands, Australia.

出版信息

Eur J Cancer. 1994;30A(5):664-70. doi: 10.1016/0959-8049(94)90541-x.

Abstract

We used Southern blot analysis and polymerase chain reaction-based techniques to examine deletions of tumour suppressor gene loci in 91 primary colorectal tumours. The tumour suppressor genes studied were MCC and APC on chromosome 5q, p53 on chromosome 17p, DCC on chromosome 18q, and the putative suppressor gene nm23-H1 on chromosome 17q. The most frequent allelic loss observed was in chromosome 17p with 76% (68/89) of informative tumours showing loss of heterozygosity at this locus, followed by 34% (19/55) for DCC, 31% (12/39) for MCC, 17% (9/53) for APC and 16% (3/19) for nm23. No significant differences in the frequency of these suppressor gene allelic losses were observed between Dukes B and C stage adenocarcinomas.

摘要

我们采用Southern印迹分析和基于聚合酶链反应的技术,检测了91例原发性结肠直肠癌肿瘤抑制基因位点的缺失情况。所研究的肿瘤抑制基因包括位于5号染色体长臂上的MCC和APC基因、位于17号染色体短臂上的p53基因、位于18号染色体长臂上的DCC基因以及位于17号染色体长臂上的假定抑制基因nm23-H1。观察到的最常见等位基因缺失发生在17号染色体短臂,76%(68/89)的信息丰富肿瘤在此位点显示杂合性缺失,其次是DCC为34%(19/55)、MCC为31%(12/39)、APC为17%(9/53)、nm23为16%(3/19)。在Dukes B期和C期腺癌之间,未观察到这些抑制基因等位基因缺失频率的显著差异。

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