Poor clinical significance of p53 gene polymorphism in acute myeloid leukemia

被引:25
作者
Nakano, Y
Naoe, T [1 ]
Kiyoi, H
Kunishima, S
Minami, S
Miyawaki, S
Asou, N
Kuriyama, K
Saito, H
Ohno, R
机构
[1] Nagoya Univ, Sch Med, Dept Infect Dis, Nagoya, Aichi 4668560, Japan
[2] Japanese Red Cross Aichi Blood Ctr, Dept Med, Seto, Japan
[3] Japanese Red Cross Nagoya First Hosp, Dept Med, Nagoya, Aichi, Japan
[4] Saiseikai Maebashi Hosp, Dept Med, Maebashi, Gumma, Japan
[5] Kumamoto Univ, Sch Med, Dept Internal Med 2, Kumamoto 860, Japan
[6] Nagasaki Univ, Sch Med, Inst Atom Dis, Dept Hematol, Nagasaki 852, Japan
[7] Nagoya Univ, Sch Med, Dept Internal Med 1, Nagoya, Aichi 466, Japan
[8] Hamamatsu Univ Sch Med, Dept Med 3, Hamamatsu, Shizuoka 43131, Japan
关键词
acute myeloid leukemia; p53; polymorphism; cancer susceptibility; loss of heterozygosity; prognosis;
D O I
10.1016/S0145-2126(99)00187-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The cancer susceptibility according to the p53 polymorphism at codon 72 has been in controversy. In this study, the clinical significance of p53 polymorphism in de novo acute myeloid leukemia (AML) was examined. Although the allelic frequency of Arg in 200 patients with AML (64.3%) tended to be greater than that in normal controls (56.6%), these frequencies were within the normal range according to the previous data in Japan (from 59.9 to 65.3%). p53 mutations, found in nine (4.5%) of the 200 patients, were not related to the polymorphism. Six of 93 patients showing heterozygosity at codon 72 had allelic imbalance according to the polymerase chain reaction assay, which occurred in either allele and was associated with p53 mutation and poor prognosis (P = 0.01). However, the p53 polymorphism was not associated with clinical features, complete remission rates or prognosis of AML. These results indicate that the p53 genotype at codon 72 is useful to detect loss of heterozygosity but not associated with risk, pathophysiology or therapeutic response of AML. (C) 2000 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:349 / 352
页数:4
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