Training
B.S.: Pennsylvania State University, Microbiology 1992
Ph.D.: Duke University Medical Center, Pharmacology, 1997
Postdoctoral Fellow: Lineberger Comprehensive Cancer Center, University of North Carolina

Research Interests

My laboratory is interested in identifying novel oncogenes that contribute to the formation and progression of cancer.  The model disease that we have primarily utilized is acute myeloid leukemia (AML).  We utilize a retroviral-based cDNA expression library system, coupled with functional assays to identify transforming sequences expressed in AML patients.  While cytogenetic analyses have lead to the identification of a large number of mutations (e.g. chromosomal translocations) involved in leukemogenesis, more subtle mutations such as point mutations or small deletions can not be identified by this technique.  Thus, functional assays, such as the ones we employ, are required to identify these subtle genetic changes.  Therefore, we have utilized the leukemic cells of patients with cytogenetically normal AML as sources of genetic material to identify mutations that play a role in myeloid leukemogenesis.  Through this work, we have identified a number of functionally diverse transforming genes.  These include a transcription factor, a G-protein coupled receptor, and a novel mutation in the TrkA nerve growth factor receptor tyrosine kinase.  Our identification of a mutation in TrkA in a patient with AML is the first implication of TrkA playing a role in human leukemogenesis.  This mutation was a small deletion in the coding sequence that would not have been detected by cytogenetic analyses.
            Currently, we are utilizing novel functional genetic screens to identify additional oncogenes in AML.  These studies have uncovered unique cell signaling properties of different cytokine receptors.  We are currently analyzing the properties of these proteins to determine their potential roles in leukemogenesis.

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This search will be conducted at the US National Library of Medicine (NLM) and PubMed.

Selected Publications
Reuther GW, Lambert QT, Rebhun JF, Caligiuri MA, Quilliam LA, and Der CJ. (2002) RasGRP4 is a novel ras activator isolated from acute myeloid leukemia. J Biol Chem 277(34), 30508-14.

Reuther GW, Lambert QT, Booden MA, Wennerberg K, Becknell B, Marcucci G, Sondek J, Caligiuri MA, and Der CJ (2001). LARG, a Dbl family protein found mutated in leukemia, causes transformation by activation of RhoA. J Biol Chem. 276(29), 27145-51.

Reuther GW, Lambert QT, Caligiuri MA, and Der CJ (2000). Identification and Characterization of an Activating TrkA Deletion Mutation in Acute Myeloid Leukemia. Mol Cell Biol. 20(23), 8655-66.

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Cancer Biology Ph.D. Program
H. Lee Moffitt Cancer Center, MRC-4 East
12902 Magnolia Drive
Tampa, Florida 33612
Phone: 813-745-6876
E-mail: CancerPHD@moffitt.org
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