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Address correspondence to Jing Liu, M.D., Ph.D., Department of Pathology and Laboratory Medicine, University of Texas Health Science Center at Houston Medical School, 6431 Fannin Street, MSB 2.260A, Houston, Texas, USA; tel 713 500 5327; fax 713 500 0695; e-mail jing.liu.1{at}uth.tmc.edu.
The mammalian target of rapamycin (mTOR) signaling pathway was studied using immunohistochemical stains on paraffin-embedded tumor tissue from two patients with anaplastic thyroid carcinoma (ATC) and on paraffin-embedded normal thyroid tissue from 23 control patients. Immunoreactivities of p-mTOR, p-Akt, p-p70S6K, and PLD1 were observed in both of the ATCs, with nuclear translocation of p-mTOR, p-Akt, and p-p70S6K. Increased expression of Ki-67, Skp2, and cyclin D1, decreased expression of p27kip1, and increased mitotic index (MI) were noted in the ATCs in comparison with those of normal thyroid tissue. The results provide evidence of (a) constitutive activation of the mTOR pathway, (b) mTORC2 activation, suggested by the nuclear translocation of p-mTOR, and (c) enhanced cell cycle progression in ATCs. These preliminary findings warrant future studies in a large series of patients with ATC to evaluate a possible molecular basis for treating chemoradioresistant ATC.
Keywords: morphoproteomics, anaplastic thyroid carcinoma, mTOR pathway
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