A point mutation in the protein kinase C alpha (PKC alpha) gene has been discovered in a subpopulation of human pituitary tumors characterized by their invasive phenotype. Here we show that: (1) thyroid tumors can express the PKC alpha mutation detected in a subpopulation of follicular adenomas and carcinomas, and (2) mutated PKC alpha has modified enzymatic properties as compared to wild-type PKC alpha. It has lost its capacity to phosphorylate the S17R substrate and exhibits a higher sensitivity to degradation as compared to wild-type PKC alpha. In conclusion, the presence of the PKC alpha mutant in tumors other than pituitary tumors and the observation that the presence of the point mutation induces changes in PKC alpha properties suggest the involvement of this mutant in tumorigenesis.