Barry I. Hudson, Ph.D.
Research Assistant Professor of Medicine
Description of Research
Dr. Hudson’s research on understanding molecular and cellular mechanisms of receptor mediated effects underlying disease states including various cancers, diabetes, and vascular disease. In particular, our research efforts are focused on the role of the Receptor for Advanced Glycation End-products (RAGE) in these disease settings, in particular in cancer. Our laboratory investigates the mechanisms regulating RAGE at the molecular and cellular level and performs translational studies investigating the role of RAGE as a biomarker for various disease states.
In the last few years our research has increasingly focused on the investigation of the role of RAGE and its role in cancer progression and metastasis. We have found that blocking RAGE signaling may be an attractive therapeutic target for reducing tumorigenesis and metastasis. Work from our lab has demonstrated that by blocking RAGE signaling, this results in reducing tumor growth and metastasis. Furthermore, we have shown activation of RAGE signaling results in profound changes in cellular properties strongly associated with the metastatic process including increased cell migration & invasion, proliferation and resistance to apoptosis. To this end we have developed a strong collaboration with the research group of Joyce Slingerland where we have tested blocking RAGE signaling in breast cancer metastatic models. We are currently expanding this research to study the effects of RAGE on tumor/stromal interactions through collaborations with Marc Lippman’s research group. Additionally, we are currently funded by an American Cancer Society (ACS) Institutional Research Grant to focus on the role of RAGE in metastasis. Our future goals are to explore the mechanisms driving these observations and test therapeutics targeted to RAGE for use in treating breast and other cancer metastasis.
- Discovered and characterized the signaling mechanisms of RAGE that drive migration and invasion of tumor cells.
- Discovered and mapped the repertoire of alternatively spliced isoforms of RAGE which include soluble decoy and signaling deficient isoforms that act as inhibitory mechanisms in cancer cells.
- Demonstrated a role for RAGE in breast cancer metastasis
- Has designed new approaches to inhibit RAGE currently being tested in metastatic models.
Selected Cancer-Related Publications
- Jules J, Maiguel D, Hudson BI. Alternative Splicing of the RAGE Cytoplasmic Domain Regulates Cell Signaling and Function. PLoS One 8:e78267,2013 Read more »
Collaborating in the Multidisciplinary Research Program(s):