Thiagalingam S, Laken S, Willson J K, Markowitz S D, Kinzler K W, Vogelstein B, Lengauer C
Oncology Center, Program in Molecular Biology, Johns Hopkins University School of Medicine, 1650 Orleans Street, Baltimore, MD 21231, USA.
Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2698-702. doi: 10.1073/pnas.051625398. Epub 2001 Feb 13.
Losses of heterozygosity are the most common molecular genetic alteration observed in human cancers. However, there have been few systematic studies to understand the mechanism(s) responsible for losses of heterozygosity in such tumors. Here we report a detailed investigation of the five chromosomes lost most frequently in human colorectal cancers. A total of 10,216 determinations were made with 88 microsatellite markers, revealing 245 chromosomal loss events. The mechanisms of loss were remarkably chromosome-specific. Some chromosomes displayed complete loss such as that predicted to result from mitotic nondisjunction. However, more than half of the losses were associated with losses of only part of a chromosome rather than a whole chromosome. Surprisingly, these losses were due largely to structural alterations rather than to mitotic recombination, break-induced replication, or gene conversion, suggesting novel mechanisms for the generation of much of the aneuploidy in this common tumor type.
杂合性缺失是在人类癌症中观察到的最常见的分子遗传改变。然而,很少有系统的研究来了解此类肿瘤中杂合性缺失的机制。在此,我们报告了对人类结直肠癌中最常丢失的五条染色体的详细研究。使用88个微卫星标记进行了总共10216次测定,揭示了245次染色体丢失事件。丢失机制具有显著的染色体特异性。一些染色体显示出完全丢失,如预计由有丝分裂不分离导致的那样。然而,超过一半的丢失仅与染色体的一部分而非整条染色体的丢失相关。令人惊讶的是,这些丢失主要是由于结构改变,而非有丝分裂重组、断裂诱导复制或基因转换,这表明在这种常见肿瘤类型中产生许多非整倍体存在新的机制。