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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.
The deletion and mutation of tumor suppressor genes P53 and P16 and the appearance of Bcl-2/JH fusion gene are the molecular biological causes of malignant lymphoma. P53 and P16 genes are also important genes that induce apoptosis of lymphoma cells, and Bcl- Gene 2 is an important gene that inhibits apoptosis of lymphoma cells. In order to study the changes in the structure of these three genes, nine human malignant lymphoma cell lines were assayed using PCR-SSCP and PCR amplification product sequencing methods. - Point mutations in the P53 gene were found in six malignant lymphoma cell lines of DHL-1, SU-DHL-4, SU-DHL-6, SU-DHL-8, and SU-DHL-10,8392, respectively, at 5,6, Exon 7; SU-DHL-9 has a homozygous deletion of the P16 gene, while the SU-DHL-1 and Daudi cell lines have a mutation in exon 2 of the P16 gene, and the SU-DHL-1 sequencing result is a password. The GAC mutation of subgenome 30 was AAC, the GCT mutation at codon 35 was ACT, and the Bcl2-2/JH gene was inserted between codons 40 and 41 with a C:SU-DHL-4 and SU-DHL-6 motif. The changes in gene structure occurred in the malignant lymphoma cell line and its significance in development.