Overview
RESEARCH ABSTRACT
Studies from this laboratory identified cell surface expression of the molecular chaperone GRP78 as a major factor in prostate cancer and other malignancies. Cell surface GRP78 functions as a signaling receptor promoting tumor proliferation and suppressing apoptosis. Patients with a number of malignancies mount an autoimmune response to GRP78 and these antibodies, which bind to the NH2 terminal domains of GRP78, are receptor agonists whose appearance is a marker of poor prognosis. More recently, we have shown that antibodies directed against the COOH-terminal domain of GRP78 are receptor antagonists which may have therapeutic potential for treating patients whose tumors express GRP78 on the cell surface.
Studies from this laboratory identified cell surface expression of the molecular chaperone GRP78 as a major factor in prostate cancer and other malignancies. Cell surface GRP78 functions as a signaling receptor promoting tumor proliferation and suppressing apoptosis. Patients with a number of malignancies mount an autoimmune response to GRP78 and these antibodies, which bind to the NH2 terminal domains of GRP78, are receptor agonists whose appearance is a marker of poor prognosis. More recently, we have shown that antibodies directed against the COOH-terminal domain of GRP78 are receptor antagonists which may have therapeutic potential for treating patients whose tumors express GRP78 on the cell surface.
Current Duke Appointments & Affiliations
Professor Emeritus of Pathology
·
2025 - Present
Pathology,
Clinical Science Departments
Recent Scholarly Works
Retraction notice to "A novel receptor function for the heat shock protein Grp78: silencing of Grp78 gene expression attenuates α2M*-induced signalling" [Cellular Signalling 16 (2004) 929-938].
Journal article Cell Signal · August 2026 Full text Link to item CiteRetraction notice to " Induction of mitogenic signalling in the 1LN prostate cell line on exposure to submicromolar concentrations of cadmium" [Cellular Signalling 15 (2003) 1059-1070].
Journal article Cell Signal · August 2026 Full text Link to item CiteRetraction notice to "The cAMP-activated GTP exchange factor, Epac1 upregulates plasma membrane and nuclear Akt kinase activities in 8-CPT-2-O-Me-cAMP-stimulated macrophages: Gene silencing of the cAMP-activated GTP exchange Epac1 prevents 8-CPT-2-O-Me-cAMP activation of Akt activity in macrophages" [Cellular Signalling 20 (2008) 1459-1470].
Journal article Cell Signal · August 2026 Full text Link to item CiteRecent Grants
Development of an Optimized Human Antibody to a Novel Target for the Treatment of Fibrotic Diseases
ResearchPrincipal Investigator · Awarded by North Carolina Biotechnology Center · 2019 - 2020Tension-Stat3-miR-mediated Metastasis
ResearchInvestigator · Awarded by City of Hope · 2015 - 2017Clinical Oncology Research Career Development Program
ResearchMentor · Awarded by National Institutes of Health · 2009 - 2015View All Grants
Education
Duke University ·
1973
M.D.
Duke University ·
1972
Ph.D.