LACK OF ALLELIC DELETION AND POINT MUTATION AS MECHANISMS OF P53 ACTIVATION IN HUMAN-MALIGNANT MELANOMA

被引:94
作者
CASTRESANA, JS
RUBIO, MP
VAZQUEZ, JJ
IDOATE, M
SOBER, AJ
SEIZINGER, BR
BARNHILL, RL
机构
[1] MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114
[2] MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114
[3] HARVARD UNIV,SCH MED,BOSTON,MA 02129
[4] UNIV NAVARRA,DEPT HISTOL & ANAT PATHOL,PAMPLONA,SPAIN
[5] MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114
[6] HARVARD UNIV,SCH MED,BOSTON,MA 02114
[7] HARVARD UNIV,SCH MED,BOSTON,MA 02115
[8] BRIGHAM & WOMENS HOSP,DEPT PATHOL DERMATOPATHOL,BOSTON,MA 02115
关键词
D O I
10.1002/ijc.2910550407
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
To investigate the role of the p53 tumor-suppressor gene in the development of human melanoma, loss of heterozygosity (LOH) of p53 was studied in 46 cases of melanoma by a polymerase-chain-reaction/restriction-fragment-length polymorphism (PCR/RFLP) analysis, and p53 mutations were assessed in 51 cases of melanoma by a polymerase-chain-reaction/ single-strand-conformation polymorphism (PCR/SSCP) analysis. Frozen tumors and paraffin samples were used in the study. We were not able to detect any allelic loss in 12 BstUI informative cases or any single mutation in exons 5 to 8 of the p53 gene. Our results, together with other findings at the DNA level, suggest that the p53 gene appears not to be commonly involved in the development of melanoma, at least by its most frequent mechanisms of deletion of one allele and/or mutation in the other. (C) 1993 Wiley-Liss, Inc.
引用
收藏
页码:562 / 565
页数:4
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