前列腺癌患者NBS1基因3′-UTR中microrna -629结合位点的群体特异性遗传变异

Q3 Pharmacology, Toxicology and Pharmaceutics Journal of Experimental Therapeutics and Oncology Pub Date : 2017-09-01
Ammad Ahmad Farooqi, Syed M Kamran Majeed, Qaisar Mansoor, Muhammad Ismail
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引用次数: 0

摘要

目的:前列腺癌是一种基因组复杂的疾病,最近出现的科学证据正在为现有的肿瘤学知识库增加新的信息。前列腺癌细胞在雄激素存在或不存在的情况下巧妙地重新连接信号级联。我们没有更好的基于癌症患者的蛋白质组和基因组的患者相关信息。方法:本实验室采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)分析方法,对100例前列腺癌患者和100例无临床病史的健康人的NBS1基因3′UTR C/T和A/G多态性进行了研究。结果:rs13312986 A>G基因型患者AA率为78%,对照组为80%。患者为21%,对照组为20%。患者中GG为1%,对照组中未检出GG。患者A等位基因频率为0.885%,对照组为0.9%。G的等位基因频率在患者中为0.115%,在对照组中为0.1%。对于rs14448 T>C基因型,患者中TC为23%,对照组中为20%。患者TT为77%,对照组为80%。在患者和对照组中均未检测到CC。患者T等位基因为0.885%,对照组为0.9%。C等位基因在患者中为0.115%,在对照组中为0.1% +。结论:未来的研究必须集中在更深入和详细的机制上,因为对NBS1的miRNA调控的研究还不完全,而对这些联系的探索是临床肿瘤学中最令人兴奋的领域之一。
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Population-specific genetic variation at microRNA-629-binding site in the 3'-UTR of NBS1 gene in prostate cancer patients.

Objective: Prostate cancer is a genomically complex disease and recently emerging scientific evidence is adding new pieces of information into existing pool of knowledge of oncology. Prostate cancer cells tactfully rewire signaling cascades in presence or absence of androgen. We do not have finer proteome and genome based patient related information of our cancer patients.

Methodology: In the present laboratory research, we studied 3' UTR C/T and A/G polymorphism in NBS1 gene in 100 prostate cancer patients and 100 healthy individuals without any previous clinical history, using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis.

Results: For rs13312986 A&#62;G genotypes, AA was 78% in patients and 80% in controls. AG was 21% in patients and 20% in controls. GG was 1% in patients and none was detected in control. Allelic frequencies for A was 0.885% in patients and 0.9% in controls. Allelic frequencies for G were 0.115% in patients and 0.1% in controls. For rs14448 T&#62;C genotypes, TC was 23% in patients and 20% in controls. TT was 77% in patients and 80% in controls. CC was not detected either in patients or controls. T allele was 0.885% in patients and 0.9% in controls. C allele was 0.115% in patients and 0.1%-+ in controls.

Conclusions: Future studies must converge on deeper and detailed mechanisms, as miRNA regulation of NBS1 is incompletely studied and exploration of these connections constitutes one of the most exciting areas in clinical oncology.

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