DNA methylation, molecular genetic, and linkage studies in prostate cancer

DNA methylation, molecular genetic, and linkage studies in prostate cancer
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前列腺癌中的 DNA 甲基化、分子遗传学和连锁研究

DOI:
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发表时间:
1996
期刊:
The Prostate. Supplement
影响因子:
--
通讯作者:
W. Isaacs
W. Isaacs
中科院分区:
--
文献类型:
--
作者:
D. Jarrard;G. Bova;W. Isaacs

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分子生物学研究现已确定了许多导致前列腺癌生长和分化基因改变的重要遗传和表观遗传机制。除了DNA缺失和点突变之外,DNA甲基化代表了肿瘤抑制或生长抑制基因失活的新范例。包括前列腺癌易感位点在内的新基因的鉴定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。 © 1996 Wiley-Liss, Inc.
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. © 1996 Wiley‐Liss, Inc.
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DOI: --
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