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在受辐射的李-佛美尼综合征淋巴母细胞系中，G1/S细胞周期阻滞无缺陷。

No defect in G1/S cell cycle arrest in irradiated Li-Fraumeni lymphoblastoid cell lines.

作者信息

Williams K J, Heighway J, Birch J M, Norton J D, Scott D

机构信息

CRC Department of Cancer Genetics, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester, UK.

出版信息

Br J Cancer. 1996 Sep;74(5):698-703. doi: 10.1038/bjc.1996.424.

DOI:10.1038/bjc.1996.424
PMID:8795570
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2074690/
Abstract

The radiation response of Epstein-Barr virus (EBV)-immortalised lymphoblastoid cell lines derive from Li-Fraumeni syndrome (LFS) and LFS-like individuals was investigated. Cells from all LFS and LFS-like cases showed an accumulation of p53 protein following 137Cs gamma-irradiation, which was associated with cell cycle arrest at the G1/S border. This response was indistinguishable from that seen in cells derived from normal individuals, and occurred in cases with missense mutations in the TP53 gene at codons 175, 180, 220 and 248 and also in two LFS-like individuals with no TP53 mutation. Previous studies using lymphocytes and fibroblasts from LFS individuals have demonstrated abnormal radiation responses in these cells. This suggest cell type specificity in the contribution of a mutant p53 protein to phenotype.

摘要

对源自李-佛美尼综合征（LFS）及LFS样个体的爱泼斯坦-巴尔病毒（EBV）永生化淋巴母细胞系的辐射反应进行了研究。所有LFS及LFS样病例的细胞在经137Csγ射线照射后均出现p53蛋白积累，这与细胞周期在G1/S边界处停滞有关。这种反应与正常个体来源的细胞中所见的反应无法区分，并且在TP53基因密码子175、180、220和248处存在错义突变的病例以及两名无TP53突变的LFS样个体中也会发生。先前使用LFS个体的淋巴细胞和成纤维细胞进行的研究已证明这些细胞中存在异常的辐射反应。这表明突变型p53蛋白对表型的贡献存在细胞类型特异性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dada/2074690/6fccbd074279/brjcancer00021-0040-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dada/2074690/73a8ab28ab0e/brjcancer00021-0038-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dada/2074690/6fccbd074279/brjcancer00021-0040-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dada/2074690/73a8ab28ab0e/brjcancer00021-0038-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dada/2074690/6fccbd074279/brjcancer00021-0040-a.jpg

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引用本文的文献

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Li-Fraumeni syndrome--a molecular and clinical review.

本文引用的文献

1
Mutant p53 proteins have diverse intracellular abilities to oligomerize and activate transcription.突变型p53蛋白具有多种在细胞内形成寡聚体并激活转录的能力。
Oncogene. 1993 Jul;8(7):1815-24.
2
Role of the p53 tumor suppressor gene in cell cycle arrest and radiosensitivity of Burkitt's lymphoma cell lines.p53肿瘤抑制基因在伯基特淋巴瘤细胞系的细胞周期阻滞和放射敏感性中的作用。
Cancer Res. 1993 Oct 15;53(20):4776-80.
3
Several mutant p53 proteins detected in cancer-prone families with Li-Fraumeni syndrome exhibit transdominant effects on the biochemical properties of the wild-type p53.
李-弗劳梅尼综合征——分子与临床综述
Br J Cancer. 1997;76(1):1-14. doi: 10.1038/bjc.1997.328.
在患有李-弗劳梅尼综合征的癌症高发家族中检测到的几种突变型p53蛋白对野生型p53的生化特性表现出反式显性效应。
Oncogene. 1993 Sep;8(9):2449-56.
4
p21 is a universal inhibitor of cyclin kinases.p21是细胞周期蛋白激酶的通用抑制剂。
Nature. 1993 Dec 16;366(6456):701-4. doi: 10.1038/366701a0.
5
Cytogenetic response to G2-phase X irradiation in relation to DNA repair and radiosensitivity in a cancer-prone family with Li-Fraumeni syndrome.与李-佛美尼综合征这一癌症易感家族中的DNA修复及放射敏感性相关的G2期X射线照射的细胞遗传学反应
Radiat Res. 1993 Nov;136(2):236-40.
6
WAF1, a potential mediator of p53 tumor suppression.WAF1，一种p53肿瘤抑制的潜在介导因子。
Cell. 1993 Nov 19;75(4):817-25. doi: 10.1016/0092-8674(93)90500-p.
7
Prevalence and diversity of constitutional mutations in the p53 gene among 21 Li-Fraumeni families.21个李-弗劳梅尼家族中p53基因胚系突变的患病率及多样性
Cancer Res. 1994 Mar 1;54(5):1298-304.
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How loops, beta sheets, and alpha helices help us to understand p53.环、β折叠和α螺旋如何帮助我们理解p53。
Cell. 1994 Aug 26;78(4):543-6. doi: 10.1016/0092-8674(94)90519-3.
9
The p21 inhibitor of cyclin-dependent kinases controls DNA replication by interaction with PCNA.细胞周期蛋白依赖性激酶的p21抑制剂通过与增殖细胞核抗原相互作用来控制DNA复制。
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