Gregory A. Clines, MD, PhD

Gregory_Clines_01Assistant Professor of Medicine and Cell, Developmental and Integrative Biology
Endocrinology Section, Birmingham VA Medical Center Medical Service

Physical Address:
BDB 730
1808 7th Avenue South
Birmingham, AL 35294-0012

Email: This email address is being protected from spambots. You need JavaScript enabled to view it.

Training
M.D., University of Texas Southwestern Medical School, Dallas, TX, 1999
Ph.D., University of Texas Southwestern Medical Center, Dallas, TX, 1999

Internship and Residency
Internal Medicine, Duke University Medical Center, Durham, NC, 2002

Fellowship
Endocrinology, Diabetes & Metabolism, University of Virginia, Charlottesville, VA, 2005

Certifications
American Board of Internal Medicine, 2002, 2012
American Board of Internal Medicine/Endocrinology, Diabetes and Metabolism, 2005

Clinical Interests
Metabolic and Genetic Bone Diseases, Disorders of Mineral Metabolism, General Endocrinology

Research Interests
Bone undergoes continuous remodeling that is coordinated by the bone forming osteoblasts and the bone resorbing osteoclasts. Diseases such as bone metastasis, a devastating complication of breast and prostate cancer, disrupt bone remodeling and increase fracture risk. My laboratory investigates how the metastasis of tumor cells to bone alters the bone microenvironment and how factors secreted by the osteoblast provide an environment for tumor cells to flourish. We have found that DKK1, an inhibitor of Wnt signaling secreted by both cancer cells and osteoblasts, is inversely related to osteoblast activity in bone metastasis. Using animal models of bone metastasis, we are investigating mechanisms of DKK1 regulation by osteoblasts and cancer cells themselves. Understanding the role of DKK1 and other modulators of Wnt signaling will facilitate the development of novel therapies to prevent and treat bone metastasis.

Another research focus of the laboratory is uncovering mechanisms of altered bone homeostasis in cystic fibrosis (CF). CF-related bone disease is associated with reduced bone mineral density, increased fracture risk, reduced bone formation and enhanced osteoclastic bone resorption. We have discovered that Cftr, the gene mutated in CF, is expressed principally in the osteoblast in bone and that inactivation of this gene delays osteoblast differentiation and downregulates Wnt signaling. The future goals of this project are to better define the osteoblast signaling pathways regulated by CFTR, determine CFTR interacting partners in the osteoblast, and develop animal models of CF bone disease.