Dysregulation of the phosphatidylinositol 3-kinase pathway in thyroid neoplasia.
The phosphatidylinositol 3-kinase (PI3K) signaling pathway is an important regulator of many cellular events, including apoptosis, proliferation, and motility. Enhanced activation of this pathway can occur through several mechanisms, such as inactivation of its negative regulator, phosphatase and tensin homolog deleted on chromosome ten (PTEN), and activating mutations and gene amplification of the gene encoding the catalytic subunit of PI3K (PIK3CA). These genetic abnormalities have been particularly associated with follicular thyroid neoplasia and anaplastic thyroid cancer, suggesting an important role for PI3K signaling in these disorders. In this article, the role of PI3K pathway activation in thyroid cancer is discussed, with a focus on recent advances.
Paes
John E
JE
Division of Endocrinology, The Ohio State University Medical Center, The Ohio State University, 1581 Dodd Drive, 4th Floor, McCampbell Hall, Columbus, OH 43210, USA.
Ringel
Matthew D
MD
D002277:Carcinoma / Q000235:genetics* / Q000628:therapy; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008954:Models, Biological; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000502:physiology; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D015398:Signal Transduction / Q000235:genetics*; D013964:Thyroid Neoplasms / Q000235:genetics* / Q000628:therapy
D019869:Phosphatidylinositol 3-Kinases; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human