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甲基胆蒽诱导的小鼠肉瘤中c-myc癌基因在扩增时缺乏等位基因偏好性及缺失情况。

Lack of allelic preference in amplification and loss of the c-myc oncogene in methylcholanthrene-induced mouse sarcomas.

作者信息

Niwa O, Kominami R

机构信息

Department of Pathology, Hiroshima University.

出版信息

Jpn J Cancer Res. 1992 Nov;83(11):1192-7. doi: 10.1111/j.1349-7006.1992.tb02744.x.

Abstract

Sarcomas were induced in F1 mice between C57BL/6N and C3H/He strains by subcutaneous injection of methylcholanthrene. The c-myc oncogene was found to be amplified in 16 cases among 43 sarcomas of C57BL/6N x C3H/He mice and 1 case among 5 sarcomas of the reciprocal cross. The origin of the amplified allele was determined by the polymerase chain reaction single strand conformation polymorphism analysis. Among the 17 sarcomas, only one had both of the alleles amplified. The rest of the tumors carried the amplified c-myc allele coming either from C57BL/6N (9 cases) or from C3H/He (8 cases). These results indicate that the c-myc allele is amplified randomly in methylcholanthrene-induced mouse sarcomas irrespective of its origin, such as paternal or maternal allele and C57BL/6N or C3H/He allele. In addition to these changes, the unamplified c-myc oncogene was found to be lost in 12 cases out of the 17 sarcomas with the amplification.

摘要

通过皮下注射甲基胆蒽,在C57BL/6N和C3H/He品系的F1小鼠中诱发肉瘤。在C57BL/6N×C3H/He小鼠的43个肉瘤中有16例以及反向杂交的5个肉瘤中有1例发现c-myc癌基因被扩增。通过聚合酶链反应单链构象多态性分析确定扩增等位基因的来源。在这17个肉瘤中,只有一个两个等位基因都被扩增。其余肿瘤携带的扩增c-myc等位基因要么来自C57BL/6N(9例),要么来自C3H/He(8例)。这些结果表明,在甲基胆蒽诱发的小鼠肉瘤中,c-myc等位基因随机扩增,与其来源无关,如父本或母本等位基因以及C57BL/6N或C3H/He等位基因。除了这些变化外,在17个有扩增的肉瘤中,有12例未扩增的c-myc癌基因缺失。

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Parental origin effects in mice.小鼠中的亲本来源效应。
J Embryol Exp Morphol. 1986 Oct;97 Suppl:137-50.

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