结直肠癌中的TP53肿瘤抑制基因。I. 17号染色体上的基因改变。
The TP53 tumour suppressor gene in colorectal carcinomas. I. Genetic alterations on chromosome 17.
作者信息
Meling G I, Lothe R A, Børresen A L, Graue C, Hauge S, Clausen O P, Rognum T O
机构信息
Institute of Forensic Medicine, National Hospital, University of Oslo, Norway.
出版信息
Br J Cancer. 1993 Jan;67(1):88-92. doi: 10.1038/bjc.1993.14.
In 231 colorectal carcinomas, allele variation at four restriction fragments length polymorphisms (RFLP) loci on chromosome 17 have been studied by Southern analysis. Heterozygous loss of the TP53 gene was found in 68% (129/189) of the carcinomas informative on both chromosome arms. In 41% (77/189) of the carcinomas the loss was found only on 17p. Two probes were used to detect alterations on 17p, pBHP53 and pYNZ22. When loss was demonstrated with pYNZ22, pBHP53 also always showed loss (n = 45), whereas when loss was demonstrated with pBHP53, only 45 of 54 (83%) showed loss with pYNZ22. Loss on 17q was found in 34% (64/189) of the carcinomas, and 6% (12/189) had loss on this chromosome arm, only. Loss on 17q was significantly associated with loss on 17p (P < 0.01). These data confirm that the TP53 gene is the target of loss on chromosome arm 17p in colorectal carcinomas, and demonstrate that loss of the TP53 gene is most frequently part of limited, subchromosomal loss. Furthermore, the results do not suggest any additional tumour suppressor gene(s) on chromosome 17 involved in colorectal carcinogenesis.
对231例结肠直肠癌患者，通过Southern分析研究了17号染色体上四个限制性片段长度多态性（RFLP）位点的等位基因变异。在两条染色体臂均有信息的癌组织中，68%（129/189）发现TP53基因杂合性缺失。在41%（77/189）的癌组织中，仅在17p上发现缺失。使用两个探针检测17p上的改变，即pBHP53和pYNZ22。当用pYNZ22证明有缺失时，pBHP53也总是显示缺失（n = 45），而当用pBHP53证明有缺失时，54例中只有45例（83%）用pYNZ22显示缺失。在34%（64/189）的癌组织中发现17q缺失，仅6%（12/189）的癌组织在此染色体臂上有缺失。17q缺失与17p缺失显著相关（P < 0.01）。这些数据证实TP53基因是结肠直肠癌中17p染色体臂缺失的靶点，并表明TP53基因缺失最常见的是有限的亚染色体缺失的一部分。此外，结果并未提示17号染色体上有任何其他参与结肠直肠癌发生的肿瘤抑制基因。
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