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This version published online on August 31, 2006
Endocrinology, doi:10.1210/en.2006-0937
A more recent version of this article appeared on March 1, 2007
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Submitted on July 13, 2006
Accepted on August 21, 2006

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, OH

* To whom correspondence should be addressed. E-mail: matthew.ringel{at}osumc.edu.

AKT (protein kinase b, PKB) is a central signaling molecule in the phosphatidyl inositol 3-kinase (PI3K) 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. PI3K 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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