@article{(Open Science Index):https://publications.waset.org/pdf/10001486,
	  title     = {VHL, PBRM1 and SETD2 Genes in Kidney Cancer: A Molecular Investigation},
	  author    = {Rozhgar A. Khailany and  Mehri Igci and  Emine Bayraktar and  Sakip Erturhan and  Metin Karakok and  Ahmet Arslan},
	  country	= {},
	  institution	= {},
	  abstract     = {Kidney cancer is the most lethal urological cancer
accounting for 3% of adult malignancies. VHL, a tumor-suppressor
gene, is best known to be associated with renal cell carcinoma
(RCC). The VHL functions as negative regulator of hypoxia inducible
factors. Recent sequencing efforts have identified several novel
frequent mutations of histone modifying and chromatin remodeling
genes in ccRCC (clear cell RCC) including PBRM1 and SETD2. The
PBRM1 gene encodes the BAF180 protein, which involved in
transcriptional activation and repression of selected genes. SETD2
encodes a histone methyltransferase, which may play a role in
suppressing tumor development. In this study, RNAs of 30 paired
tumor and normal samples that were grouped according to the types
of kidney cancer and clinical characteristics of patients, including
gender and average age were examined by RT-PCR, SSCP and
sequencing techniques. VHL, PBRM1 and SETD2 expressions were
relatively down-regulated. However, statistically no significance was
found (Wilcoxon signed rank test, p>0.05). Interestingly, no mutation
was observed on the contrary of previous studies. Understanding the
molecular mechanisms involved in the pathogenesis of RCC has
aided the development of molecular-targeted drugs for kidney cancer.
Further analysis is required to identify the responsible genes rather
than VHL, PBRM1 and SETD2 in kidney cancer.},
	    journal   = {International Journal of Medical and Health Sciences},
	  volume    = {9},
	  number    = {5},
	  year      = {2015},
	  pages     = {423 - 426},
	  ee        = {https://publications.waset.org/pdf/10001486},
	  url   	= {https://publications.waset.org/vol/101},
	  bibsource = {https://publications.waset.org/},
	  issn  	= {eISSN: 1307-6892},
	  publisher = {World Academy of Science, Engineering and Technology},
	  index 	= {Open Science Index 101, 2015},
	}