论文部分内容阅读
本文对16例乳腺癌患者的肿瘤组织进行了染色体核型分析,其中12例进行了G带核型分析。结果表明乳腺癌细胞具有明显的染色体数目和结构异常。染色体数目以非整倍体为主,占81.48％。其中三倍体和四倍体数目范围最多见,其次为亚二倍体和超二倍体。染色体结构异常主要累及1,2,3,4,6和11号染色体。累及1号染色体的结构异常有6种类型,其断裂点在P~(13),q~(11—12),q~(21—22)。6号染色体异常的断裂点在6q~(22—24)。累及11号染色体的断裂点在11p~(13—15)和11q~(25)而累及3号染色体的断裂点在p~(25—26)。上述1,6,11和3号染色体的断裂点与细胞癌基因NRAS,SK,MYB,HRAS1,ETS和RAF1的定位相关。目前,许多实验表明癌基因的协同作用使正常细胞转化,本实验从细胞遗传学的角度为此理论提供了证据。
In this paper, the karyotype analysis of 16 cases of breast cancer patients were performed, of which 12 cases were G-band karyotype analysis. The results showed that breast cancer cells have obvious chromosome number and structural abnormalities. The number of chromosomes is mainly aneuploid, accounting for 81.48%. The triploid and tetraploid populations were the most common, followed by hypodiploid and hyperdiploid. Chromosome abnormalities mainly involved chromosomes 1, 2, 3, 4, 6 and 11. There are 6 types of structural abnormalities involving chromosome 1 with breakpoints in P13, q11-12, q21-22. The abnormal breakpoint of chromosome 6 is 6q~(22-24). The breakpoints of chromosome 11 involving 11p-13-15 and 11q-25 involved the breakpoint of chromosome 3 at p-25-26. The above-mentioned breakpoints of chromosomes 1, 6, 11 and 3 were associated with the localization of the cell oncogenes NRAS, SK, MYB, HRAS1, ETS and RAF1. At present, many experiments show that the synergy of oncogenes causes normal cells to transform. This experiment provides evidence for this theory from the perspective of cytogenetics.