Medical Journals

Akt in Thyroid Tumorigenesis and Progression.

Authors:
  • Shinohara Motoo
  • Chung Yun Jae
  • Saji Motoyasu
  • Ringel Matthew D

From: Divisions of Endocrinology and Oncology, The Ohio State University College of Medicine, 1581 Dodd Drive, Columbus, OH 43210, USA.

Endocrinology

  • Publish Date: Mar 2007
  • ISSN: 0013-7227
  • Volume: 148
  • Issue: 3
  • Pages: 942-7
  • Medium: Print
  • Language: English
  • Citation (JAMA): Shinohara Motoo, Chung Yun Jae, Saji Motoyasu, et al. Akt in Thyroid Tumorigenesis and Progression.. Endocrinology Mar 2007;148:942-7

Abstract

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.

Mesh Headings (Keywords): Animals, Carcinoma, Papillary, Carcinoma, Papillary, Follicular, Disease Progression, Humans, Models, Biological, Oncogene Protein v-akt, Signal Transduction, Thyroid Neoplasms


Check for Full Text / PubMed Unique Identifier (PMID): 16946008


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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