Abstract PR11: Tissue-of-origin dictates the metabolic fate of branched chain amino acids in mutant Kras-driven cancers

Conclusions: Despite sharing an identical combination of mutations, mouse models of NSCLC and PDAC exhibit distinct phenotypes with regards to BCAA metabolism in tumors. The different fates of BCAAs in each of these tumor types might explain previously observed alterations in plasma BCAA levels and provides further insight into how tumors can influence whole body metabolic phenotypes in early cancer.1. Hu, J., et al. Heterogeneity of tumor-induced gene expression changes in the human metabolic network. Nature biotechnology 31, 522-529 (2013).2. Yuneva, M.O., et al. The Metabolic Profile of Tumors Depends on Both the Responsible Genetic Lesion and Tissue Type. Cell Metabolism 15, 157-170 (2012).3. Mayers, J.R., et al. Elevation of circulating branched-chain amino acids is an early event in human pancreatic adenocarcinoma development. Nature Medicine (2014).Citation Format: Jared R. Mayers, Margaret E. Torrence, Shawn M. Davidson, Thales Papagiannakopoulos, Allison N. Lau, Tyler Jacks, Matthew G. Vander Heiden. Tissue-of-origin dictates the metabolic fate of branched chain amino acids in mutant Kras-driven cancers. [abstract]. In: Proceedings of the AACR Special Conference: Metabolism and Cancer; Jun 7-10, 2015; Bellevue, WA. Philadelphia (PA): AACR; Mol Cancer Res 2016;14(1_Suppl):Abstractnr PR11.
Source: Molecular Cancer Research - Category: Cancer & Oncology Authors: Tags: Systemic Metabolic Alterations and Cancer: Oral Presentations - Proffered Abstracts Source Type: research