人恶性淋巴瘤细胞系P53，P16，Bcl-2／JH基因的研究

抑癌基因P53,P16的缺失和突变以及Bcl-2/JH融合基因的出现是恶性淋巴瘤发生的分子生物学病因,P53和P16基因亦是诱导淋巴瘤细胞凋亡的重要基因,而Bcl-2基因是抑制淋巴瘤细胞凋亡的重要基因,为研究这三种基因结构的变化,用PCR-SSCP,以及PCR扩增产物序列测定的方法测定了人九种恶性淋巴瘤细胞系,发现SU-DLH-1,SU-DHL-4,SU-DHL-6,SU-DHL-8,SU-DHL-10,8392六种恶性淋巴瘤细胞系有P53基因的点突变,分别在5,6,7外显子;SU-DHL-9有P16基因的纯合缺失,而SU-DHL-1和Daudi细胞系有P16基因的第2外显子的突变,SU-DHL-1的测序结果为密码子30的GAC突变为AAC,密码子35的GCT突变为ACT,密码子40与41之间插人了一个C:SU-DHL-4和SU-DHL-6出现Bcl2-2/JH基因,讨论了基因结构的变化在恶性淋巴瘤细胞系发生,发展中的意义.

Study on P53, P16, Bcl-2/JH Genes in Human Malignant Lymphoma Cell Lines

The pathogenicity of molecular biology in malignant lymphoma shows the deletion and mutation of P53 and P16 which are carcinoma suppressor genes and formation of Bcl-2/JH fusion gene. As the same time, P53 and P16 are important genes which can suppress the apoptosis of lymphoma cells. Also, Bcl-2/JH is an important gene which can induce the apoptosis of ones. In order to studying the constitutional changes of these three kinds of gene, PCR-SSCP and PCR sequencing were used for 9 kinds of human malignant lymphoma cell line. It found that 7 kinds of cell line including SDHL-1, SU-DHL-4, SU-DHL-6, SU-DHL-8, SU-DHL-10, 8392 and Daudi had point mutations of P53 gene. They emerged in 5, 6, 7 exons respectively. SU-DHL-9 had homozygous deletion of P16 gene. Meanwhile, SU-DHL-1 and Daudi cell lines had mutation of the second exon of P16 gene GAC in codon 30 mutated into AAC. GCT in codon 35 mutated into ACT. Between codon 40 and 41, C was inserted. SU-DHL-4 and SU-DHL-6 was accord with Bcl-2/JH fusion genes. The significance of gene constitutional changes which effected on pathogenesis, development of malignant lymphoma cell lines was discussed.