CDKN2/p16基因在四种原发恶性肿瘤中存在状态的研究-东南大学学报医学版

CDKN2/p16基因在四种原发恶性肿瘤中存在状态的研究

单位：1.东南大学医学院生物学教研室,； 2.南京师范大学生命科学学院,； 3.南京八一医院全军肿瘤研究中心,

分类号：Q754, R734.2, R735, R737.9

出版年·卷·期（页码）：2001·20·第二期（71-74）

摘要：

目的：研究CDKN2/p16基因缺失和蛋白丢失在非小细胞肺癌、食管癌、胃癌、乳腺癌4种原发恶性肿瘤中的作用。方法：采用免疫组织化学法和多重PCR技术对68例(非小细胞肺癌31例，食管癌15例，胃癌13例，乳腺癌9例)原发肿瘤组织标本进行CDKN2/p16基因第一、第二外显子纯合缺失和p16蛋白表达丢失分析研究。结果：第一或(和)第二外显子总缺失率为13.2%(9/68)，蛋白丢失率为44%(30/68)，不同肿瘤组织标本的p16基因缺失率和蛋白丢失率差别很大。结论：CDKN2/p16基因是重要的多肿瘤抑制基因，在不同肿瘤组织中其失活方式不完全相同。

Objective To study CDKN2/p16 gene homozygous deletion and p16 protein loss in human primary.Methods Multiple PCR technique and immunohistochemical method were used to detect homozygous deletion of CDKN2/p16 gene exon 1,exon 2 and loss of p16 protein in 68 cases of primary cancers, including 31 non small cell lung cancers,15 esophageal carcinomas,13 gastric carcinomas and 9 breast cancers.Results Total rate of exon 1 or(and) exon 2 deletion was 13.2%(9/68).p16 protein loss rate was 44%(30/68).p16 gene deletion rates and p16 protein loss rates in various tumors were different.Conclusion CDKN2/p16 gene is an important inhibitory gene of many tumors.Mechanisms of CDKN2/p16 gene deletion are different in various tumors.

参考文献：

[1] Kamb A, GRUIS N·!A, WEAVER FELDHAUS J. A cell cycle regulator potentially involved in genesis of many tumor types. 1994(15). doi:10.1126/science.8153634
[2] Sambrook J. Molecular Cloning, 1989
[3] 王国丽, 杜传书, 林群娣. 非小细胞肺癌中p16INK4/CDKN2基因的缺失和点突变. 中华医学遗传学杂志1998(1)
[4] 周春晓, 孙建衡, 陆士新. 子宫内膜癌中CDKN2/p16基因缺失的研究, 1997(6)
[5] 金顺钱, 彭琼, 陆士新. 食管癌组织中MTS1/p16基因的缺失. 中华肿瘤杂志1998(1)
[6] LIGGET T W H Jr, SIDRANSKY D. Role of the P16 Tumor suppressor Gene in cancer. 1998(3)
[7] Nobori T, MIURA K, Wu D J. Deletion of the cyclin dependent kinase-4 inhibitor gene in multiple human cancers. 1993. doi:10.1038/368753a0
[8] Washimi O, NAGATAKE M, sada H. In vivo occurrence of p16(MTS1)and p15(MTS2)alterations preferentially in non-small cell lung cancers. 1995(55)
[9] Merlo A, HERMAN J G, Mao L. 5/CpG island methylation is associated with transcriptional silencing of tumor supressor p16/CDKN2/MTS1 in human cancers. 1995. doi:10.1038/nm0795-686
[10] HermanJG, MERLO A, Mao L. Inactivation of the CDKN2/p16/MTS1 gene is frequently associated with aberrant DNA methylation in all common human cancers, 1995(20)

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