MUSC Hollings Cancer Center

Developmental Cancer Therapeutics Research Program

DCTThe scientific goal of the Hollings Cancer Center Developmental Cancer Therapeutics Program is to discover and characterize unique agents and pathways that will impact the development of more effective cancer therapies and to translate these discoveries into clinical applications by using proof-of-principle, early phase clinical and correlative science studies.
The Developmental Cancer Therapeutics Program is co-led by Kenneth D. Tew, PhD, and Carolyn D. Britten, MD. This program is organized around three themes of scientific investigation and is a central hub where therapeutic-focused discoveries across all Hollings Cancer Center programs are translated into clinical studies.  The three themes are: 1) Elucidation of Cellular Signaling Pathways; 2) Modulation of Redox and Cellular Stress Response; and 3) Development of Small Molecule Chemotherapeutic Agents.

Program Leaders
Kenneth D. Tew, PhD
Carolyn D. Britten, MD

Developmental Cancer Therapeutics Members


FEATURED RESEARCH PROJECT

A highly-interactive group of Developmental Cancer Therapeutics Program investigators focuses on the role of the PIM family of kinases in carcinogenesis and cancer therapy. These highly-regulated serine-threonine kinases are expressed in normal cells in response to many stresses as well as in cancer, and they mediate pro-survival responses. Dr. Andrew S. Kraft and
Dr. Michael B. Lilly have collaborated on PIM1 studies for many years, and each has independently identified small molecule inhibitors of the kinase.  

Recently, Dr. Bo Cen and Dr. Charles D. Smith have worked with Dr. Kraft on preclinical inhibitor studies, leading to collaborative interactions with other Developmental Cancer Therapeutics Program members, Dr. Lilly and Dr. Campbell McInnes, and with investigators at other NCI Cancer Centers (UCLA, UC Irvine, University of Colorado, Harvard). Dr. Kraft’s lead compound, SMI-4a, a novel benzylidene-thiazolidine-2, 4-dione pan-PIM inhibitor, kills a wide range of myeloid and lymphoid cell lines.  Precursor T-cell lymphoblastic leukemia/lymphoma (pre-T-LBL/T-ALL) is especially sensitive, both in culture and xenograft models. (MORE)

 

 
 
 

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