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Lack of allelic deletion and point mutation as mechanisms of p53 activation in human malignant melanoma
Author(s) -
Castresana Javier S.,
Rubio MariPaz,
Seizinger Bernd R.,
Vàzquez J. Jaime,
Idoate Miguel,
Sober Arthur J.,
Barnhill Raymond L.
Publication year - 1993
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910550407
Subject(s) - loss of heterozygosity , point mutation , single strand conformation polymorphism , biology , polymerase chain reaction , melanoma , exon , restriction fragment length polymorphism , allele , mutation , microbiology and biotechnology , tumor suppressor gene , genetics , gene , polymerase , cancer research , carcinogenesis
Abstract 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 BstU1 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.