Accession Number : AD1010167


Title :   BUD31 and Lipid Metabolism: A New Potential Therapeutic Entry Point for Myc-Driven Breast Cancer


Descriptive Note : Technical Report,01 Feb 2015,31 Jan 2016


Corporate Author : Baylor College of Medicine Houston United States


Personal Author(s) : Kurley,Sarah


Full Text : http://www.dtic.mil/dtic/tr/fulltext/u2/1010167.pdf


Report Date : 01 Feb 2016


Pagination or Media Count : 9


Abstract : Myc activation is common in breast cancer, correlated with triple negative disease, and associated with mortality. Thus, understanding Myc-driven breast cancer will facilitate knowledge of triple negative disease, a subtype of breast cancer with poor outcome and limited treatment options. Our laboratory has performed a genome-wide RNAi screen to identify genes that are required to tolerate Myc activation. Through this screen, we have identified BUD31, a poorly understood gene, and components of the fatty acid oxidation pathway (FAMs) as required for tolerance of Myc driven stress. Our goal herein is to test the hypothesis that BUD31 and FAMs may be putative new therapeutic entry points for Myc-driven breast cancer. Within this period of performance, we have published a manuscript in Nature detailing a role for BUD31 in splicing and shown more broadly that splicing is a viable therapeutic intervention point for myc-driven breast cancer. The connection betweenBUD31 and FAMs still remains unclear. Nevertheless, in support of our hypothesis and data, others have more recently published and presented mechanisms whereby fatty acid oxidation is a point of treatment sensitivity in triple negative breast cancer (TNBC). Their and our initial findings suggest that FAMs and downstream pathways may be particularly important for metastatic TNBC. As metastasis is the leading cause of breast cancer patient mortality, we believe this avenue warrants further attention.


Descriptors :   breast cancer , Lipid metabolism , Fatty acids , therapy , genes , activation , oxidation , ribonucleic acids , metastasis , interactions


Distribution Statement : APPROVED FOR PUBLIC RELEASE