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AACR-Ocular Melanoma Foundation Research Partnership Makes Impact on Ocular/Uveal Melanoma

Ocular/uveal melanoma is the most common primary cancer affecting the eye. The partnership of AACR with the Ocular Melanoma Foundation (OMF) reflects the commitment of both organizations to support the next generation of cancer researchers studying ocular melanoma and to make a difference in the lives of ocular melanoma patients.

Researchers supported by the AACR-OMF partnership have made progress in identifying new treatment strategies for ocular/uveal melanoma.

  • 2014 AACR-OMF Fellow Alexander N. Shoushtari, MD conducted a Phase II clinical trial comparing single agent MEK inhibitor trametinib versus the combination of trametinib and an Akt inhibitor in metastatic uveal melanoma patients (NCT01979523). Although the clinical trial results were not promising, analyses of the samples collected may help in the development of future treatment strategies.

    Moving forward from the grant, Dr. Shoushthari continues to conduct clinical trials, including an ongoing clinical trial testing an immunotherapy approach in metastatic uveal melanoma (NCT03070392). As reported during the 2021 AACR Annual Meeting, the Phase 3 trial showed that the bispecific antibody IMCgp100 (tebentafusp) significantly improved overall survival in patients with metastatic uveal melanoma.
  • 2016 AACR-OMF Fellow Jessica Teh, PhD explored the potential of combining MEK inhibitor with CDK4/6 inhibitors in uveal melanoma. She reported that adding a third inhibitor of OxPhos can increase the efficacy of the MEK and CDK 4/6 inhibitor combination.
  • 2017 AACR-OMF Fellow Vivian Chua, PhD, explored why uveal melanoma patients did not respond to the BET inhibitor PLX51107 in the Phase Ib/IIa clinical trial NCT02683395.  She and her laboratory found that this resistance may be explained, at least in part, due to the presence of a protein called fibroblast growth factor 2 (FGF2). With the support of her grant, Dr. Chua found that uveal melanoma cells can be made more susceptible to BET inhibitors by treating cells with an FGFR inhibitor that blocks the receptor for FGF2.