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Endocrinology Vol. 148, No. 3 942-947
Copyright © 2007 by The Endocrine Society

AKT in Thyroid Tumorigenesis and Progression

Motoo Shinohara, Yun Jae Chung, Motoyasu Saji and Matthew D. Ringel

Divisions of Endocrinology and Oncology and Thyroid Cancer Unit, Department of Internal Medicine, The Ohio State University College of Medicine and Arthur G. James Comprehensive Cancer Center, Columbus, Ohio 43210

Address all correspondence and requests for reprints to: Matthew D. Ringel, M.D., Associate Professor of Medicine, Divisions of Endocrinology and Oncology, The Ohio State University College of Medicine, 445D McCampbell Hall, 1581 Dodd Drive, Columbus, Ohio 43210. E-mail: matthew.ringel{at}osumc.edu.

AKT (protein kinase B) is a central signaling molecule in the phosphatidyl inositol 3-kinase pathway that is frequently activated in human cancer. AKT activation regulates energy metabolism, apoptosis, proliferation, and migration in many cell systems. In thyroid cancer, AKT activation is involved in tumorigenesis, particularly in both inherited and sporadic forms of follicular thyroid cancer. Phosphatidyl inositol 3-kinase and AKT signaling also appear to play an important role in progression of both papillary and follicular cancers. In this review, the role of AKT in thyroid cancer development and progression are discussed with a focus on areas of current debate in the literature.




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Copyright © 2007 by The Endocrine Society