Page 52 - Hormel Report 2021

James Robinson, Ph.D.
“My research centers on the molecular mechanisms
by which oncogenic signaling regulates tumorigenesis, with the eventual goal of developing or improving
therapeutic approaches for melanoma and glioma.”
James Robinson
52 | THE HORMEL INSTITUTE // UNIVERSITY OF MINNESOTA Cell Signaling and Tumorigenesis
SECTION LEADER / ASSISTANT PROFESSOR
Our research on the mechanisms and bio- markers of drug resistance in melanoma is funded by an American Cancer Society
Research Scholar Grant. To study melanoma, we have developed a novel transgenic brain metas- tasis model of melanoma. Using this model, we demonstrated that gain of function MEK mutants the de novo development of melanoma. We also adapted the model to permit the control of BRAF and MEK in the tumors to mimic pharmacological inhibition. Using this model we also investigated the role played by epigenetic regulation in resis- tance to therapy. This work has now been pub- lished and was presented at the 2019 Society for Melanoma Research 16th International Congress
of the Society for Melanoma Research Annual Meeting Salt Lake City, UT.
APC and CTNNB1 mutations occur in up to 15% and 23% of melanomas and there is a higher incidence of brain metastases in patients with CTNNB1 and APC mutations. We are currently investigating the role of APC and CTNNB1 muta- tions in melanoma. The outcome of our work on melanoma will be to increase the understanding of melanoma and to aid in the development of combination therapies and identify biomarkers that will assist in the identification of patients most likely to develop metastases and benefit from more aggressive therapy.