Faculty : Departmental- Primary

Barry I. Hudson, PhD

Dr. Hudson’s research focusses 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.

Current efforts in the lab are focused on the role of RAGE in breast cancer metastasis, and the role of in tumor intrinsic and stromal mechanisms. Further we are investigating whether blocking RAGE signaling may be an attractive therapeutic target for reducing tumorigenesis and metastasis. We are also studying the mechanistic regulation of RAGE in the cell and the role of ectodomain shedding in this process.

The long-term goals of the Hudson Lab are to investigate the role of receptor regulation and signal transduction in endocrine-related diseases. These investigations will extend to RAGE and other novel receptor/signaling isoforms and their role in these disease states. This research will provide further understanding of receptor function and signaling and could lead to the development of novel targeted therapeutics.

Click here for information on: DOD Funds Study of Link between Diabetes and Breast Cancer

Biographical Information

BSc University of Leeds, 1996

PhD University of Leeds, 2001

Postdoctoral: Department of Surgery, Columbia University (2002-2005)

Associate Research Scientist: Department of Surgery, Columbia University (2005-2010)
Research Assistant Professor: Division of Endocrinology (2010)

Professional Affiliations

University of Miami Sylvester Comprehensive Cancer Center

Select Publications

  • Wang L, Rundek T, Beecham A, Hudson B, Blanton SH, Zhao H, Sacco RL, Dong C. (2014) Genome-wide interaction study identifies RCBTB1 as a modifier for smoking effect on carotid intima-media thickness. ATVB 34(1):219-25.
  • Jules J, Miaguel D, Hudson BI. (2013) Alternative splicing of the RAGE cytoplasmic domain regulates cell signaling and function. PLOS ONE 8;8(11):e78267.
  • Ma W, Rai V, Hudson BI, Song F, Schmidt AM, Barile GR. (2012) RAGE binds C1q and enhances C1q-mediated phagocytosis.Cell Immunol. 274(1-2):72-82.
  • Hudson BI, Moon YP, Kalea AZ, Khatri M, Marquez C, Schmidt AM, Paik MC, Yoshita M, Sacco RL, DeCarli C, Wright CB, Elkind MS (2011) Association of serum soluble receptor for advanced glycation end-products with subclinical cerebrovascular disease: the Northern Manhattan Study (NOMAS). Atherosclerosis. 216(1):192-8.
  • Godier-Furnémont A, Martens T, Koeckert M, Wan L, Parks J, Arai K, Zhang G, Hudson BI, Homma S, Vunjak-Novakovic G. (2011) Composite Scaffold Provides a Cell Delivery Platform for Cardiovascular Repair. PNAS 108(19):7974-9.
  • Kalea AZ, See F, Harja E, Arriero M, Schmidt AM, Hudson BI. (2010). Alternatively spliced RAGEv1 inhibits tumorigenesis through suppression of JNK signaling. Cancer Res. 70(13):5628-38.
  • Kalea AZ, Reininger N, Yang H, Arriero M, Schmidt AM, Hudson BI. (2009) Alternative splicing of the murine Receptor for Advanced Glycation End-products (RAGE) gene. FASEB J, 23:1766-74
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