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首页> 外文期刊>Journal of Cancer Research and Clinical Oncology >B-MYB-p53-related relevant regulator for the progression of clear cell renal cell carcinoma
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B-MYB-p53-related relevant regulator for the progression of clear cell renal cell carcinoma

机译:B-MYB-P53相关的相关稳压器,用于透明细胞肾细胞癌的进展

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摘要

Purpose To investigate the mRNA expression ofB-MYBandMDM2together with theirp53relatedness in clear cell renal cell carcinoma (ccRCC). Methods Genes were screened for their mRNA expression from 529 patients in a publicly available ccRCC cohort (TCGA). A cohort of 101 patients with ccRCC served as validation by qRT-PCR mRNA tissue expression analysis. Results Expression: B-MYBexpression was significantly higher in high-grade tumours (p 0.05). Survival:Multivariable Cox regression of the TCGA cohort revealedB-MYBupregulation and lowMDM2expression as predictors for an impaired overall survival (OS) (HR 1.97;p= 0.0003; HR 2.94,p< 0.0001) and progression-free survival (PFS) (HR 2.86;p= 0.0005; HR 1.58,p= 0.046). In the validation cohort, the results were confirmed for OS by univariable, but not multivariable regression: highB-MYBexpression (HR = 3.05,p= 0.035) and lowMDM2expression (HR 3.81,pvalue 0.036). Conclusion In ccRCC patients with high-grade tumours and advanced stages, highB-MYBexpression is common and is associated with poorer OS and PFS. These patients show a loss of their physiologicalB-MYB-p53network correlation, suggesting an additional, alternative regulatory, oncogenic mechanism. Assuming further characterization of its signalling pathways, B-MYB could be a potential therapy target for ccRCC.
机译:目的探讨B-myBandMDM2mRNA在肾透明细胞癌(ccRCC)中的表达及其相关性。方法从公开的ccRCC队列(TCGA)中的529例患者中筛选基因的mRNA表达。一组101例ccRCC患者通过qRT PCR mRNA组织表达分析进行验证。结果:B-myBe在高级别肿瘤中的表达显著增高(P0.05)。生存率:TCGA队列的多变量Cox回归显示,Db MyBupregration和低MDM2表达是受损总生存率(OS)和无进展生存率(PFS)的预测因子(HR 2.86;p=0.0005;HR 1.58,p=0.046)。在验证队列中,OS的结果通过单变量而非多变量回归得到证实:高B mybeexpression(HR=3.05,p=0.035)和低MDM2expression(HR 3.81,pvalue 0.036)。结论在患有高级别肿瘤和晚期的ccRCC患者中,高B myBe表达是常见的,并且与较差的OS和PFS相关。这些患者表现出生理性B-MYB-P53网络相关性缺失,这表明了一种额外的、替代性的调节致癌机制。假设其信号通路的进一步表征,B-MYB可能是ccRCC的潜在治疗靶点。

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  • 作者单位

    Heidelberg Univ Univ Med Ctr Mannheim Med Fac Mannheim Dept Urol &

    Urosurg Theodor Kutzer Ufer;

    Heidelberg Univ Univ Med Ctr Mannheim Med Fac Mannheim Dept Urol &

    Urosurg Theodor Kutzer Ufer;

    Heidelberg Univ Univ Med Ctr Mannheim Med Fac Mannheim Dept Urol &

    Urosurg Theodor Kutzer Ufer;

    Heidelberg Univ Univ Med Ctr Mannheim Med Fac Mannheim Dept Urol &

    Urosurg Theodor Kutzer Ufer;

    Heidelberg Univ Univ Med Ctr Mannheim Med Fac Mannheim Dept Urol &

    Urosurg Theodor Kutzer Ufer;

    Johannes Gutenberg Univ Mainz Inst Pathol Univ Med Ctr Mainz Germany;

    Heidelberg Univ Inst Pathol Univ Med Ctr Mannheim Mannheim Germany;

    Heidelberg Univ Univ Med Ctr Mannheim Med Fac Mannheim Dept Urol &

    Urosurg Theodor Kutzer Ufer;

    Heidelberg Univ Univ Med Ctr Mannheim Med Fac Mannheim Dept Urol &

    Urosurg Theodor Kutzer Ufer;

    Heidelberg Univ Univ Med Ctr Mannheim Med Fac Mannheim Dept Urol &

    Urosurg Theodor Kutzer Ufer;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学 ;
  • 关键词

    Kidney cancer; MYBL2; MDM2; Upstream regulation; Therapy target; Tumour marker;

    机译:肾癌;mybl2;mdm2;上游调节;治疗目标;肿瘤标志物;

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