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• W2318839959 abstract "In 2011, an estimated 60,920 men and women will be diagnosed of which 13,120 will die of cancer of the kidney and renal pelvis. The current standard line of therapy includes surgery [partial or radical nephrectomy] or the use of molecular targeted agents such as antiangiogenic agents or immunotherapy. The common mutations found in renal cell carcinomas [RCC] are Von-Hippau Lindau [VHL] gene in clear cell RCC, c-met gene in papillary RCC type I, Fumarate hydratase [FH] gene in papillary type II or the Brit Hogg Dube’ [BHD] gene in chromophobe RCC. However there have been several studies indicating that some of the above genes like VHL can be silenced through promoter methylation as well. Hence, there has been an increasing focus on epigenetic modifications that can occur in RCCs, because of the possibility of reversing these epigenetic marks. There have been considerable reports on the use of agents such as histone deacetylase [HDAC] inhibitors or DNA methyl transferase inhibitors in different RCC cell lines or clinical trials. In this study, we looked at the HDAC expression and activity in matched tumor and non-tumor renal cell carcinoma tissue obtained from tissue procurement services at RPCI. Class I HDACs [HDAC 1, 2 and 3] and two members of class II HDACs [HDAC 4 and 5] are overexpressed in tumors compared to their non-tumor counterparts. In contrast, a class II member HDAC 6 level is lower in the tumor tissues relative to their non-tumor counterparts which corresponded to higher levels to acetylated α-tubulin in those tumors. However, these HDAC expression levels did not tend to have a correlation with grade or stage. We also established xenografts, that are implanted orthotopically and efforts are underway to obtain relatively faster growing tumors subcutaneously. Ongoing studies include defining the relation between expression and activity of HDACs in these tissues and the interaction and impact of other proteins with Class I and II HDACs [such as ER-α, Class III HDACs, VHL] in the context of common active pathways in tumors such as hypoxia [results of which will be available at the time of the meeting]. Further work also includes to look into other histone as well as DNA modifications, as well as enzymes that cause these modifications, in the matched tissues and to explore the potential use of histone or DNA modifying agents as part of RCC treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5016. doi:1538-7445.AM2012-5016" @default.
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• W2318839959 date "2012-04-15" @default.
• W2318839959 modified "2023-09-27" @default.
• W2318839959 title "Abstract 5016: Epigenetics in renal cell carcinoma" @default.
• W2318839959 doi "https://doi.org/10.1158/1538-7445.am2012-5016" @default.
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