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人类癌症中nm23的体细胞等位基因缺失。

Somatic allelic deletion of nm23 in human cancer.

作者信息

Leone A, McBride O W, Weston A, Wang M G, Anglard P, Cropp C S, Goepel J R, Lidereau R, Callahan R, Linehan W M

机构信息

Laboratories of Pathology, National Cancer Institute, NIH, Bethesda, Maryland 20892.

出版信息

Cancer Res. 1991 May 1;51(9):2490-3.

PMID:2015608
Abstract

Tumor progression to the metastatic phenotype is accompanied in certain cell types by reduced expression of the nm23 gene. We have localized human nm23-H1 to chromosome 17 by somatic cell hybrid analysis. Regional localization in the CEPH database and in situ hybridization is reported. Somatic allelic deletion of nm23-H1 was observed in human breast, renal, colorectal, and lung carcinoma DNA samples, as compared to DNA from matched normal tissues. A homozygous deletion of nm23-H1 was observed in a lymph node metastasis of a colorectal carcinoma, indicating that nm23-H1 can be recessively inactivated. The data identify nm23-H1 as a novel, independent locus for allelic deletion in human cancer, a characteristic shared with previously described suppressor genes.

摘要

在某些细胞类型中,肿瘤向转移表型的进展伴随着nm23基因表达的降低。我们通过体细胞杂交分析将人类nm23-H1基因定位于17号染色体。报告了在CEPH数据库中的区域定位和原位杂交结果。与匹配的正常组织的DNA相比,在人类乳腺癌、肾癌、结直肠癌和肺癌的DNA样本中观察到nm23-H1的体细胞等位基因缺失。在一例结直肠癌的淋巴结转移中观察到nm23-H1的纯合缺失,表明nm23-H1可以隐性失活。这些数据确定nm23-H1是人类癌症中一个新的、独立的等位基因缺失位点,这是与先前描述的抑癌基因共有的特征。

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