Pathology and Laboratory Medicine

William D. Hill, Ph.D.

hillwi@musc.edu

My lab focuses on stem cells and bone homeostasis. One of the primary areas of research is the role of the cytokine CXCL12 and its proteolytic metabolites that have separate biological activity. This not only has an impact on bone biology with aging, but has implications in many other areas, such as immunology and cancer biology. We also study age-associated changes in the epigenetic regulation of stem cells, in particular miRNAS. Our lab has a strong clinical translational focus.

Hainan Lang, Ph.D.

langh@musc.edu

Please a complete list of published work in MyBibliography.
More information about my lab can be found by accessing this document (PDF)

Demetri Spyropoulos, Ph.D.

spyropdd@musc.edu

Our work focuses on endocrine disrupting chemicals and precision medical models: Gene-by-Environment interactions as they pertain to Developmental health trajectories and Age-related degenerative diseases. Obesity, metabolism, MSC differentiation (bone, muscle, fat), neurodegeneration and behavior. Patient-derived preserved tissues as a model for the study and treatment of diseases.
See my MUSC Directory information.
See a story about Dr. Spyropoulos' research in a publication by the Gulf of Mexico Research Initiative.

David P. Turner, Ph.D.

turnerda@musc.edu

Specific populations defined by lifestyle factors such as diet, obesity and physical inactivity often bear a greater cancer burden. The impact of these interrelated social, demographic and environmental consequences on the biologic make up of tumors remains largely undefined (reviewed by the PI1, 2). Through NCI supported research (U54CA210962; R21CA176135; R21CA194469), we have data to support a unique paradigm wherein lifestyle-associated advanced glycation end products (AGEs) represent a common biological element within health disparity influences that can impact neoplastic growth. We are now exposed to AGEs every day through the lives we lead and the foods we eat. The typical highly processed western diet, high in sugar, protein and fat, is AGE laden now contributing as much as 30% of the AGEs that accumulate within the body3-6. AGEs function as ligand to the transmembrane receptor for AGE (RAGE) which is a potent regulator of transcription factor mediated paracrine signaling and is positively associated with poor outcome7-9. Our studies show that AGEs positively correlate with elevated RAGE in prostate tumors with the highest levels occurring in more aggressive disease and men with African ancestry10. A key finding shows that chronic consumption of dietary-AGEs accelerates prostate tumor growth and is dependent upon stromal RAGE expression. Tumor epithelial cells manipulate their surrounding environment to promote cancer associated fibroblast (CAF) mediated secretion of growth factors, cytokines and chemokines which creates a pro-tumorigenic milieu11-13. Dietary-AGE activation of RAGE caused a regulatory program of 'activated' stroma which was defined by increased recruitment of MYC expressing CAFs and tumor associated macrophages (TAMs). Fibroblasts and macrophages isolated from AGE fed mice retained their tumor promoting abilities in ex vivo cultures. Tumor associated stromal cells also adopt distinct metabolic profiles which function to maintain the energy requirements needed for cell differentiation and functionality11, 14. Whole genome analysis of excised tumors from the high AGE fed mice show that chronic consumption of AGEs impacts oxidative and glycolytic metabolism through the differential expression of MYC metabolic target genes. Our long-term objective is to define the mechanistic implications of AGEs on tumor biology and its contribution to cancer outcomes.
Watch a TEDxCharleston presentation by Dr. Turner