Migliore Lucia, Migheli Francesca, Spisni Roberto, Coppedè Fabio
Department of Human and Environmental Sciences, University of Pisa, Street S. Giuseppe 22, 56126 Pisa, Italy.
J Biomed Biotechnol. 2011;2011:792362. doi: 10.1155/2011/792362. Epub 2011 Feb 14.
Most of the colorectal cancer (CRC) cases are sporadic, only 25% of the patients have a family history of the disease, and major genes causing syndromes predisposing to CRC only account for 5-6% of the total cases. The following subtypes can be recognized: MIN (microsatellite instability), CIN (chromosomal instability), and CIMP (CpG island methylator phenotype). CIN occurs in 80-85% of CRC. Chromosomal instability proceeds through two major mechanisms, missegregation that results in aneuploidy through the gain or loss of whole chromosomes, and unbalanced structural rearrangements that lead to the loss and/or gain of chromosomal regions. The loss of heterozygosity that occur in the first phases of the CRC cancerogenesis (in particular for the genes on 18q) as well as the alteration of methylation pattern of multiple key genes can drive the development of colorectal cancer by facilitating the acquisition of multiple tumor-associated mutations and the instability phenotype.
大多数结直肠癌(CRC)病例为散发性,仅有25%的患者有该病家族史,而导致易患CRC综合征的主要基因仅占总病例数的5-6%。可识别出以下亚型:微卫星不稳定性(MIN)、染色体不稳定性(CIN)和CpG岛甲基化表型(CIMP)。80-85%的CRC发生CIN。染色体不稳定性通过两种主要机制进行,一种是错配分离,通过整条染色体的增减导致非整倍体,另一种是不平衡的结构重排,导致染色体区域的丢失和/或增加。在CRC发生的第一阶段出现的杂合性缺失(特别是18q上的基因)以及多个关键基因甲基化模式的改变,可通过促进获得多个肿瘤相关突变和不稳定性表型来推动结直肠癌的发展。