Gregory Brent

Gregory A. Brent, MD

Professor in Residence, Department of Medicine, Department of Physiology
Chair, Department of Medicine, Veterans Affairs Greater Los Angeles Healthcare System

Languages

English

Specialty

Endocrinology

Institutional Affiliation

Veterans Affairs Greater Los Angeles Healthcare System

Education

Fellowships

Endocrinology, Brigham and Women's Hospital, 1985 - 1986
Molecular Biology, Massachusetts General Hospital, and Genetics, Harvard Medical School, 1986 - 1989
Medicine, Harvard Medical School, 1985 - 1987

Internship

Internal Medicine, Wadsworth VA Medical Center, UCLA, 1981 - 1982

Degree

MD, University of Southern California, 1981

Residencies

Chief Resident, Internal Medicine, Wadsworth VA Medical Center, UCLA, 1984 - 1985
Internal Medicine, Wadsworth VA Medical Center, UCLA, 1982 - 1984

Board Certifications

Endocrinology, Diabetes and Metabolism, American Board of Internal Medicine, 1987
Internal Medicine, American Board of Internal Medicine, 1984

Contact Information

Clinical Interests

Thyroid Diseases

Scientific Interests

Dr. Gregory Brent's laboratory focuses on understanding gene regulation by nuclear acting hormones, especially thyroid hormone (T3) and retinoic acid (RA), which combine with nuclear receptors (RAR and TR). He studies the regulation and co-regulation of genes by T3 and RA as influenced by the DNA response element(s), the specific TR and RAR receptor isoforms available, nuclear receptor partners, ligand(s) concentration, and response co-activators and co-repressors. He studies T3 and RA influences on metabolism and gene regulation in hormone-dependent cancer. The sodium/iodide symporter (NIS) gene is normally expressed in the thyroid and the lactating breast. Brent has studied factors associated with reduced expression of NIS in thyroid cancer and approaches to augment NIS expression in breast cancer. He has identified RA regulation of the NIS gene in breast cancer cell lines and in vivo models through modification of signal transduction pathways. He has studied in vitro and in vivo models to promote radioiodine uptake into breast cancer after systemic treatment with retinoids. He is currently mapping signal transduction pathways in thyroid and breast cancer modified by RA treatment, with the goal of improving radioiodine therapy.

Highlighted Publications

Kogai T, Liu YY, Mody K, Shamsian DV, Brent GA. Regulation of sodium iodide symporter gene expression by Rac1/p38Beta mitogen-activated protein kinase signaling pathway in MCF-7 breast cancer cells. J Biol Chem. 2012 Jan 27;287(5):3292-300. Epub 2011 Dec 8

Ohashi E, Kogai T, Kagechika H, Brent GA. Activation of the PI3 kinase pathway by retinoic acid mediates sodium/iodide symporter induction and iodide transport in MCF-7 breast cancer cells. Cancer Res. 2009 Apr 15;69(8):3443-50. Epub 2009 Apr 7

Kogai T, Ohashi E, Jacobs MS, Sajid-Crockett S, Fisher ML, Kanamoto Y, Brent GA. Retinoic acid stimulation of the sodium/iodide symporter in MCF-7 breast cancer cells is mediated by the insulin growth factor-I/phosphatidylinositol 3-kinase and p38 mitogen-activated protein kinase signaling pathways. J Clin Endocrinol Metab. 2008 May;93(5):1884-92. Epub 2008 Mar 4

Kogai T, Sajid-Crockett S, Newmarch LS, Liu YY, Brent GA. Phosphoinositide-3-kinase inhibition induces sodium/iodide symporter expression in rat thyroid cells and human papillary thyroid cancer cells. J Endocrinol. 2008 Nov;199(2):243-52. Epub 2008 Sep 1

Kogai T, Ohashi E, Jacobs MS, Sajid-Crockett S, Fisher ML, Kanamoto Y, Brent GA. Retinoic acid stimulation of the sodium/iodide symporter in MCF-7 breast cancer cells is mediated by the insulin growth factor-I/phosphatidylinositol 3-kinase and p38 mitogen-activated protein kinase signaling pathways. J Clin Endocrinol Metab. 2008 May;93(5):1884-92. Epub 2008 Mar 4.