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Lack of allelic deletion and point mutation as mechanisms of p53 activation in human malignant melanoma.

作者信息

Castresana J S, Rubio M P, Vázquez J J, Idoate M, Sober A J, Seizinger B R, Barnhill R L

机构信息

Molecular Neuro-Oncology Laboratory, Massachusetts General Hospital, Charlestown 02129.

出版信息

Int J Cancer. 1993 Oct 21;55(4):562-5. doi: 10.1002/ijc.2910550407.

DOI:10.1002/ijc.2910550407
PMID:8104906
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 12BstUI 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.

摘要

相似文献

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Lack of allelic deletion and point mutation as mechanisms of p53 activation in human malignant melanoma.
Int J Cancer. 1993 Oct 21;55(4):562-5. doi: 10.1002/ijc.2910550407.
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Chromosome 17 allelic loss and NF1-GRD mutations do not play a significant role as molecular mechanisms leading to melanoma tumorigenesis.17号染色体等位基因缺失和NF1 - GRD突变作为导致黑色素瘤肿瘤发生的分子机制,并未发挥重要作用。
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Detection of loss of heterozygosity of p53 gene in paraffin-embedded breast cancers by non-isotopic PCR-SSCP.
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Frequent TP53 gene alterations (mutation, allelic loss, nuclear accumulation) in primary non-small cell lung cancer.原发性非小细胞肺癌中频繁出现的TP53基因改变(突变、等位基因缺失、核内积聚)
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Polymerase chain reaction-based approaches for detection of allelic loss in the p53 tumor suppressor gene in colon neoplasms.基于聚合酶链反应的方法检测结肠肿瘤中p53肿瘤抑制基因的等位基因缺失。
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