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目的与方法 :以永生化人支气管上皮细胞 (BEAS - 2B)受环磷酰胺、噻替哌诱导并发生癌性转化的细胞为模型 ,运用染色体G—显带技术 ,观察环磷酰胺、噻替哌的遗传毒作用引起的细胞转化过程中的染色体动态畸变。结果 :BEAS - 2B细胞染色体众数 46条 ,近二倍体 ,核型稳定 ,携带有M1,M2 ,M3三个标志染色体。环磷酰胺转化细胞 (BEAS -CP)为二倍体核型 ,丢失了 1个 14号染色体 ,增加了M 4异常染色体 ,该畸变可能与细胞转化的始动 ,促进和进展有关。噻替哌转化细胞 (BEAS-T)在培养过程中渐趋多倍体细胞 ,15代以后部分细胞的 14和 2 1号染色体各丢失 1条 ,BEAS -T 2 3代在软琼脂上形成克隆的细胞 (BEAS -ST)是多倍体细胞 ,并具有高频率的非稳定性畸变 ,BEAS -T 2 5代时为 3% ,BEAS -ST为 34 % ,多倍体背景上出现 2对巨型三着丝粒染色体。结论 :所发现的染色体畸变与细胞全面恶性转化之间存在明显关联
Purpose and Methods: Using immortalized human bronchial epithelial cells (BEAS-2B) as a model induced by cyclophosphamide, thiotepa and cancerous transformation, using chromosome G-banding technique to observe cyclophosphamide and thiophene The genetic toxicity of piperazine causes chromosome aberrations during cell transformation. RESULTS : The chromosome number of BEAS - 2B cells was 46, nearly diploid, karyotype stable and carrying three marker chromosomes M1, M2 and M3. Cyclophosphamide-transformed cells (BEAS-CP) is a diploid karyotype with one chromosome 14 missing and an abnormal M4 chromosome. This aberration may be related to the initiation, promotion and progression of cell transformation. BEAS-T cells gradually became polyploid during culture. After 15th generation, some cells lost 14 and 21 chromosomes 1 and BEAS-T 2 3 was cloned on soft agar. The cells (BEAS-ST) are polyploid and have a high frequency of unstable aberrations, 3% for BEAS-T25, 34% for BEAS-ST, and 2 pairs for giant polyploid backgrounds. Tricentric chromosomes. Conclusion: There is a clear correlation between the chromosome aberrations found and the overall malignant transformation of cells.