hRAD54 gene and 1p high-resolution deletion-mapping analyses in oligodendrogliomas

被引:28
作者
Bello, MJ
de Campos, JM
Vaquero, J
Ruiz-Barnés, P
Kusak, ME
Sarasa, JL
Rey, JA
机构
[1] Hosp Univ La Paz, Dept Cirugia Expt, Lab Oncogenet Mol, Madrid, Spain
[2] CSIC, Inst Invest Biomed, Madrid, Spain
[3] Hosp Rio Hortega, Dept Neurosurg, Valladolid, Spain
[4] Clin Puerta de Hierro, Dept Neurosurg, Madrid, Spain
[5] Fdn Jimenez Diaz, Dept Neurosurg, Madrid, Spain
[6] Fdn Jimenez Diaz, Dept Anat Pathol, Madrid, Spain
关键词
D O I
10.1016/S0165-4608(99)00122-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The hRAD54 protein belongs to a superfamily of DNA helicases, and mutations in genes with DNA helicase function have been found to be responsible for cancer-prone syndromes (xeroderma pigmentosum, Bloom syndrome, Werner syndrome). hRAD54 thus could be a candidate modifier gene in tumors characterized by allelic imbalance at 1p32, the chromosome region in which this gene is located. Using a panel of 38 1p and five 1q markers, we therefore performed deletion-mapping analysis on a series of 35 oligodendrogliomas, which were also studied for mutations in the hRAD54 gene. Deletions of the short arm of chromosome 1 were evidenced in 26 tumors, mostly involving 1p36-1p13; all thus displayed loss of the 1p32 region. We used PCR/SSCP to examine all 18 exons of the hRAD54 gene for mutations in 25 tumors, but the mobility shifts detected corresponded to previously identified polymorphic changes: T-to-C transition at nucleotide 2865 (with no amino acid change) and at nucleotide 3008, at the 3' untranslated region. We conclude that hRAD54 gene alterations are not required for malignant transformation of oligodendrogliomas. (C) Elsevier Science, Inc., 1999. All Rights Reserved.
引用
收藏
页码:142 / 147
页数:6
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