Background: Follicular cell-derived thyroid carcinomas harboring RET/PTC oncoproteins are immunostimulatory and highly curable, despite activating RAS/BRAF/MEK/ERK and PI3K/AKT. Results: RET/PTC oncoproteins associate with TRAFs to mediate cytokine production but not transformation.
Conclusion:The RET/PTC-TRAF pathway is functionally separable from the RET/PTC-induced MEK/ERK and PI3K/AKT pathways. Significance: Understanding RET/PTC-mediated immunostimulation could provide new strategies for treating more aggressive forms of thyroid carcinoma.
Cancer immunotherapy continues to be a viable potential therapy for many tumor types, however, discovering the existence of and breaking tolerance to tumor specific antigens remains a challenge. In our strategy we will take advantage of a common theme of all cancer cell types - the constitutive activation of signal transduction members that promote cell survival and proliferation. Post-translational modification of tyrosine, serine, and threonine via the addition of a phosphate group can both activate signal transduction pathways and generate the production of “neophosphoantigens”. Here we use both sodium vanadate and a model fusion oncogene, RET/PTC, to transform fibroblasts and examine the immunoreactivity of phosphoantigens derived from class I and class II.
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