前列腺癌的DNA甲基化、分子遗传和连锁研究。

The Prostate. Supplement Pub Date : 1996-01-01
D F Jarrard, G S Bova, W B Isaacs
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引用次数: 0

摘要

分子生物学研究现在已经确定了一些重要的遗传和表观遗传机制,这些机制导致前列腺癌生长和分化基因的改变。除了DNA缺失和点突变外,DNA甲基化代表了肿瘤抑制基因或生长抑制基因失活的新范式。新基因的鉴定,包括前列腺癌易感位点,可以进一步了解前列腺癌的分子特征,并允许早期识别受影响的个体。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
DNA methylation, molecular genetic, and linkage studies in prostate cancer.

Molecular biologic studies have now identified a number of important genetic and epigenetic mechanisms that cause alterations in growth and differentiation genes in prostate cancer. In addition to DNA deletion and point mutation, DNA methylation represents a new paradigm for the inactivation of tumor suppressor or growth suppressor genes. The identification of new genes, including a prostate cancer susceptibility locus, may furnish further insight into the molecular characteristics of prostate cancer and permit the early identification of affected individuals.

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