Research will focus on understanding the role of CD47 in cancer and developing strategies to enhance responses to conventional cancer therapeutics and immunotherapy by targeting CD47 interactions with its extracellular ligands. The objective is to enhance therapeutic responses while reducing dose-limiting side effects. Approaches include in vitro investigation of CD47-dependent signal transduction in tumor cells and relevant cells in the tumor microenvironment including immune and vascular cells. Syngeneic mouse tumor models will be used to validate novel mechanism to control tumor growth and opportunities to apply CD47-target therapeutics.
The Biochemical Pathology Section has identified thrombospondin-1 signaling through its receptor CD47 as a major regulator of cell and tissue responses to stress (Antioxid. Redox Signal. 27(12):771-773, 2017). In nonmalignant cells CD47 regulates global metabolism, autophagy, and stem cell transcription factors. Therapeutic blockade of CD47 thereby protects nonmalignant tissues, but the same treatment sensitizes tumors to cytotoxic therapies. We have identified a critical role of CD8 T cells in the latter activity (Cancer Res. 74(23):6771-6783, 2014).
Interested candidates must have a Ph.D. and/or an MD and have less than 3 years of postdoctoral experience and a minimum of one first-authorship manuscript in a leading peer-reviewed journal. A strong background in cellular and molecular biology techniques is required, and experience with murine models of cancer is desirable. This is a time-limited renewable appointment with stipend commensurate with experience.
Applicants should submit a cover letter describing their research experience and interests, CV including bibliography and contact information for three references to: Dr. David Roberts Email: drobertsmail.nih.gov
This position is subject to a background investigation. The NIH is dedicated to building a diverse community in its training and employment programs.