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University of Colorado Cancer Center

University of Colorado Cancer Center, A National Cancer Institute-designated Comprehensive Cancer Center

Steve Anderson, PhD



Molecular Biology


University of Colorado Anschutz Medical Campus


Must have completed one year of college

Number of Openings: 1


The summer student would work on a project regarding the molecular basis of altered tumor metabolism.
My lab is interested in signaling pathways that regulate mammary gland development and tumorigenesis. Our interest in mammary gland development has been stimulated by our studies of the MMTV-myr-Akt1 transgneic mice in which we observed that expression of activated Akt1 stimulated the precocious appearance of cytoplasmic lipid droplets during pregnancy.  This stimulated us to examine the molecular switches in mice that regulate lipid biosynthesis at secretory activation, the transition from pregnancy to lactation.  The major source of calories in mouse milk is present in the fat component, which is important for development of the nervous system as well as normal growth.  The magnitude of the contribution of the fat present in mouse milk is revealed by the fact that an average mouse will secrete her entire body weight in milk fat in approximately 21 days of lactation.  This fat is either derived from dietary fat, or is synthesized de novo from glucose. We are using genetically modified mice to examine the roles of various signaling molecules and transcription factors in regulating lipid biosynthesis in the lactating mammary gland.
Tumor cells are known to display an altered metabolism that is characterized by increased glucose uptake, an increase in glycolysis, and the increased secretion of lactate, a waste product of glycolysis.  We have been examining the effect of altering the expression of the hexose transporter GLUT1 upon tumorigenesis in vivo.  Inhibiting expression of GLUT1 decreases the initial growth of tumors in vivo, while overexpressing GLUT1 enhances tumor growth.  We recently have used Cre recombinase to excise GLUT1 from transgenic mice expressing an activated oncogene and have observed a complete suppression of mammary tumorigenesis, even in mice that have lost just a single alelle of GLUT1.  This indicates that GLUT1 and glucose are absolutely critical in mammary tumorigenesis induced by the Neu/ErbB2 oncogene.  We continue to probe the role of glucose in tumor metabolism and how modifying glucose flux may alter tumor growth. 



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