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运用定量实时聚合酶链反应法研究γ射线诱导的小鼠胸腺淋巴瘤中c-myc的DNA拷贝数与mRNA表达水平之间缺乏相关性

Lack of correlation between DNA copy number and mRNA expression levels of c-myc in gamma-radiation-induced mouse thymic lymphomas by using quantitative real-time PCR.

作者信息

Santos J, Vaquero C, Reyes J, López-Nieva P, Matabuena M, Villa M, Fernández P, Fernández-Piqueras J

机构信息

Laboratorio de Genética Molecular Humana, Departamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Spain.

出版信息

Clin Transl Oncol. 2006 May;8(5):349-53. doi: 10.1007/s12094-006-0181-y.

DOI:10.1007/s12094-006-0181-y
PMID:16760010
Abstract

BACKGROUND

It is well documented that over-expression of the c-myc proto-oncogene occurs in the vast majority of mouse thymic lymphomas induced by gamma-irradiation, evidencing the importance of this gene in T-cell lymphomagenesis. However, it remains unknown whether elevated levels of c-myc expression are driven by extra c-myc copy numbers.

MATERIALS AND METHODS

Here we use a quantitative test on the basis of real-time PCR to determine the cellular copy number of c-myc in a set of 14 g-radiation- induced thymic lymphomas obtained from (C57BL/6J x BALB/cJ) F1 hybrid mice with increased mRNA c-myc expression.

RESULTS

Since 5 out of 14 (35.7%) cases had no extra copy numbers of c-myc, gene amplification was obviously not the cause of c-myc over-expression in these tumours. In the remaining 9 tumours, c-myc over-expression was also accompanied with extra DNA copy numbers. Therefore, c-myc amplification might be a consequence of the genomic instability subsequent to the up-regulation of c-myc. However, linear regression analysis showed a lack of correlation between increasing DNA copy numbers and mRNA over expression of c-myc in these tumours (r = 0.029, p = 0.94).

CONCLUSION

De-regulation of c-myc does not necessarily imply amplification of this gene in these tumours. This report is, to our knowledge, the first one comparing c-myc amplification with expression in lymphomas of the T-cell lineage.

摘要

背景

有充分文献记载,在绝大多数由γ射线诱导的小鼠胸腺淋巴瘤中,c-myc原癌基因过度表达,这证明了该基因在T细胞淋巴瘤发生中的重要性。然而,c-myc表达水平升高是否由额外的c-myc拷贝数驱动仍不清楚。

材料与方法

在此,我们基于实时PCR进行定量检测,以确定从(C57BL/6J×BALB/cJ)F1杂交小鼠获得的一组14个γ射线诱导的胸腺淋巴瘤中c-myc的细胞拷贝数,这些淋巴瘤的mRNA c-myc表达增加。

结果

由于14例中有5例(35.7%)没有c-myc的额外拷贝数,基因扩增显然不是这些肿瘤中c-myc过度表达的原因。在其余9个肿瘤中,c-myc过度表达也伴随着额外的DNA拷贝数。因此,c-myc扩增可能是c-myc上调后基因组不稳定的结果。然而,线性回归分析显示,在这些肿瘤中,DNA拷贝数增加与c-myc的mRNA过度表达之间缺乏相关性(r = 0.029,p = 0.94)。

结论

在这些肿瘤中,c-myc失调不一定意味着该基因扩增。据我们所知,本报告是第一篇比较T细胞系淋巴瘤中c-myc扩增与表达的报告。

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Defective expression of Notch1 and Notch2 in connection to alterations of c-Myc and Ikaros in gamma-radiation-induced mouse thymic lymphomas.在γ射线诱导的小鼠胸腺淋巴瘤中,Notch1和Notch2的表达缺陷与c-Myc和Ikaros的改变有关。
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