Douglas Hurst, Ph.D.
Assistant ProfessorUniversity of Alabama at Birmingham
Prior to receiving his degrees, Dr. Hurst served in the US Navy for 6 years as a SCUBA diver and nuclear mechanic onboard the fast attack nuclear submarine USS Grayling (SSN-646). After an honorable discharge from the Navy, Dr. Hurst earned a BS in Biochemistry and BA in Chemistry from the College of Charleston in Charleston, South Carolina where he published several papers from his undergraduate research related to the strong-base synthesis of heterocyclic aromatic compounds. He then received an individual pre-doctoral fellowship from the Department of Defense Breast Cancer Research Program entitled "Targeting Breast Cancer Membrane Metalloproteinases" under the mentorship of Dr. QX Amy Sang at Florida State University in Tallahassee, Florida. After completion of his PhD in Biochemistry, he moved to the University of Alabama at Birmingham where he obtained an individual Ruth L. Kirschstein post-doctoral fellowship from NIH (F32) entitled "Mechanistic Insight into BRMS1 Suppression of Metastasis" under the mentorship of Dr. Danny Welch. In December of 2010, he became an Assistant Professor in the Department of Pathology where his current studies are focused on understanding the molecular mechanisms of breast cancer metastasis.
The overall goal of his studies is to understand the molecular mechanisms of cancer metastasis. Many metastasis-associated genes are epigenetically regulated by chromatin structure. A major ongoing project in his group is to functionally characterize how SIN3 chromatin modification complexes regulate breast cancer progression and metastasis. SIN3 is a nuclear scaffold that recruits transcription factors, histone binding proteins, and protein modifying enzymes to specific sites of chromatin leading to epigenetic regulation of gene transcription. There are two paralogs of SIN3 in higher organisms that are located on different chromosomes. His group discovered that SIN3 paralogs, SIN3A and SIN3B, play divergent roles in regulating triple negative breast cancer progression and suggest that SIN3B expression is required for metastasis and SIN3A is a metastasis suppressor. His projects include basic molecular and cellular biology techniques using both in vitro and in vivo model systems to characterize the structural and functional units of SIN3 complexes. He has been funded extramurally by the American Cancer Society, METAvivor Research and Support, and the Elsa U. Pardee Foundation.
The overall goal of his studies is to understand the molecular mechanisms of cancer metastasis. Many metastasis-associated genes are epigenetically regulated by chromatin structure. A major ongoing project in his group is to functionally characterize how SIN3 chromatin modification complexes regulate breast cancer progression and metastasis. SIN3 is a nuclear scaffold that recruits transcription factors, histone binding proteins, and protein modifying enzymes to specific sites of chromatin leading to epigenetic regulation of gene transcription. There are two paralogs of SIN3 in higher organisms that are located on different chromosomes. His group discovered that SIN3 paralogs, SIN3A and SIN3B, play divergent roles in regulating triple negative breast cancer progression and suggest that SIN3B expression is required for metastasis and SIN3A is a metastasis suppressor. His projects include basic molecular and cellular biology techniques using both in vitro and in vivo model systems to characterize the structural and functional units of SIN3 complexes. He has been funded extramurally by the American Cancer Society, METAvivor Research and Support, and the Elsa U. Pardee Foundation.