Comparative genomic hybridization reveals a specific pattern of chromosomal gains and losses during the genesis of colorectal tumors

Comparative genomic hybridization reveals a specific pattern of chromosomal gains and losses during the genesis of colorectal tumors
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DOI:
10.1002/(sici)1098-2264(199604)15:4
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发表时间:
1996-04
期刊:
影响因子:
3.5
通讯作者:
T. Ried;Regina Knutzen;R. Steinbeck;H. Blegen;E. Schröck;K. Heselmeyer;S. Du Manoir;G. Auer
T. Ried;Regina Knutzen;R. Steinbeck;H. Blegen;E. Schröck;K. Heselmeyer;S. Du Manoir;G. Auer
中科院分区:
生物学3区
文献类型:
--
作者:
T. Ried;Regina Knutzen;R. Steinbeck;H. Blegen;E. Schröck;K. Heselmeyer;S. Du Manoir;G. Auer

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比较基因组杂交被用来筛选DNA提取从组织学定义的组织切片从连续阶段的结直肠癌的染色体畸变。在正常上皮中未检测到畸变(n = 14)。7号染色体的获得在低级别腺瘤中作为单一事件发生(n = 14)。在高级别腺瘤(n = 12)中,30%的分析病例中存在7号和20号染色体的过度表达。转变为结肠癌(n = 16)的特点是出现多个染色体畸变。染色体1,13,20和染色体臂7 p和8 q的频繁获得,而染色体4和染色体臂8 p和18 q的反复代表性不足。通过DNA倍性测量和免疫组织化学染色分析用于CGH的相同组织切片,以定量增殖活性和p21/WAF-I和TP 53表达。我们观察到,粗异倍体和增殖活性增加是结直肠癌发生的早期事件,随后是TP 53过表达和在从高级别腺瘤到浸润性癌的进展过程中获得复发性染色体获得和丢失。基因染色体癌(1996)。© 1996 Wiley利斯公司
Comparative genomic hybridization was used to screen the DNA extracted from histologically defined tissue sections from consecutive stages of colorectal carcinogenesis for chromosomal aberrations. No aberrations were detected in normal epithelium (n = 14). Gain of chromosome 7 occurred as a single event in low‐grade adenomas (n = 14). In high‐grade adenomas (n = 12), an overrepresentation of chromosomes 7 and 20 was present in 30% of the cases analyzed. The transition to colon carcinomas (n = 16) was characterized by the emergence of multiple chromosomal aberrations. Chromosomes 1, 13, and 20 and chromosome arms 7p and 8q were frequently gained, whereas chromosome 4 and chromosome arms 8p and 18q were recurrently underrepresented. The same tissue sections that were used for CGH were analyzed by means of DNA‐ploidy measurements and immunohistochemical staining to quantify proliferative activity and p21/WAF‐I and TP53 expression. We observed that crude aneuploidy and increased proliferative activity are early events in colorectal carcinogenesis, followed by TP53 overexpression and the acquisition of recurrent chromosomal gains and losses during the progression from high‐grade adenomas to invasive carcinomas. Genes Chromosom Cancer (1996). © 1996 Wiley‐Liss, Inc.