期刊文献+

8种人恶性淋巴瘤细胞系P16基因突变的研究 被引量:1

Mutations of P16 Gene in 8 Human Malignant Lymphoma Cell Lines
下载PDF
导出
摘要 为确定 P16基因与恶性淋巴瘤发生发展的关系 ,对 8种人恶性淋巴瘤细胞系中 P16基因突变情况进行研究。用银染 PCR- SSCP方法对 P16基因第二外显子突变情况进行研究 ,并对检出突变者用自动测序仪进行测序分析。检出1例纯合缺失 ,2例 P16基因第二外显子突变。测序分析发现 SU- DHL- 1P16基因第二外显子有 3处点突变 ,即密码子72的 GAC突变为 AAC,密码子 77的 GCT突变为 ACT,密码子 82与 83之间插入了一个 C。认为 P16基因在 B细胞恶性淋巴瘤细胞系中的突变率较高 ,提示其改变可能参与恶性淋巴瘤的发生发展。 In order to determine the relationship between P16 and the tumorigenesis of malignant lymphoma, silver stained PCR SSCP analysis and direct sequencing were used to evaluate the alterations of P16 gene in 8 human malignant lymphoma cell lines. A homolygous loss was found in SU DHL 9 while mutations of P16 exon 2 in SU DHL 1 and Daudi. Sequencing of the PCR product showed three point mutations in SU DHL 1, which were GAC to AAC in codon 72, GOT to ACT in codon 77, and a insertion of C between codon 82 and 83, respectively. This study suggested the mutations of P16 gene are highly frequent in B cell lymphoma cell lines and may play an important role in its tumorigenesis.
出处 《同济医科大学学报》 CAS CSCD 北大核心 2001年第3期229-231,共3页 Acta Universitatis Medicinae Tongji
基金 国家教委留学回国人员启动基金(No. 1995 - 135 )
关键词 P16基因 恶生淋巴瘤 基因突变 P16 gene malignant lymphoma cell lines
  • 相关文献

参考文献4

二级参考文献4

  • 1萨姆布鲁克 J,分子克隆实验指南,1995年
  • 2陈燕,国外医学输血及血液学分册,1994年,17卷,5期,260页
  • 3陈文杰,血液分子细胞生物学,1993年
  • 4杨天楹,临床血液学进展,1992年

共引文献7

同被引文献9

  • 1Rassidakis G Z, Georgakis G V, Dyaizo M, et al. Lack of c-kit (CD117) expression in CD30+ lymphomas and lymphomatoid papulosis[J]. Mod Pathol, 2004, 17(8) : 946-953.
  • 2Atanasio P, Xonia C V, Soraya T, et al. Imatinib mesylate (STI571) inhibits multiple myeloma cell proliferation and potentiates the effect of common anti myeloma agents[J]. British Joumal of Haematology, 2003, 123(5): 858-868.
  • 3Aldinucci D, Poletto D, Nanni P, et al. Hodgkin and Reed-Sternberg cells express functional c-kit receptors and interact with primary fibroblasts from Hodgkin's disease-involved lymph nodes through soluble and membrane-bound stem cell factor[J]. Br J Haematol, 2002, 118(4): 1055-1064.
  • 4Brauns T, Schuhewoher T, Dissmond J, et al. C-KIT expression in primary cutaneous T-cell lymphomas[J]. J Cutan Pathol, 2004, 31 : 577-582.
  • 5Gibson S L, Dai C Y, Lee H W, et al. Inhibition of colon tumor progression and angiogenesis by the INK4a/Arf locus[J]. Cancer Res, 2003, 63(4) : 742-746.
  • 6Maesawa C, Tamura G, Nishizuka S, et al. Inactivation of the CDKN2 gene by homozygous deletion and de novo methylation is associated with advanced stage esophageal squamous cell carcinoma[J]. Cancer Research, 1996, 56: 3875-3878.
  • 7Yamada Y, Kamihira S. Inactivation of tumor suppressor genes and the progression of adult T-cell leukemia-lymphoma [J]. Leuk Lymphoma, 2005, 46(11): 1553-1559.
  • 8Huang Q, Ai L, Zhang Z Y, et al. Promoter hypermethylation and protein expression of the P16 gene: analysis of 43 cases of B- cell primary gastric lymphomas from China[J]. Mod Pathol, 2004, 17(4): 416-422.
  • 9秦亚溱,陈珊珊,常艳,付家瑜,王新娟.STI571诱导K562细胞凋亡机制研究[J].中华血液学杂志,2002,23(6):289-292. 被引量:4

引证文献1

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部