dysregulated expression of tensin 2 and components of the pi3 kinase/akt signaling pathway in human thyroid carcinoma

Background: the phosphatidylinositol 3-kinase/akt signaling pathway is recognizedas a key driver of cancer cell survival and proliferation, and is often contingent uponan impairment of expression/function of the pten tumor suppressor, a negativeregulator of this pathway. in addition, the cytoskeletal signaling protein tensin 2 hasalso been implicated as a negative regulator of this pathway. however, the pi3kpathway remains to be fully characterized in clinical thyroid carcinomas. the aim ofthis study is to determine the expression of components of the pi3k pathway inneoplastic and normal tissue sections obtained from patients with thyroid carcinoma.methods: tissues from 58 cases with thyroid carcinoma underwent immunohistochemistryfor activated akt (phosphorylated akt, pakt), tensin 2 and pten.results: a total of 100% of thyroid cancerous tissues were positive for paktstaining compared to 67.9% of normal tissues. in contrast, 46.8% of cancer tissues werepositive for tensin 2 compared to 61.7% of normal tissues. for pten, 82.8% ofcancerous tissues and 67.2% of normal tissues stained positive for this protein. therewere no associations between the expression levels of the molecules with the patients’clinicopathological characteristics.conclusion:we have found evidence for an enhanced activation of the pi3k/aktsignaling pathway in clinical thyroid carcinoma tissues. this can be coupled withconcomitant downregulation of tensin 2. further work is required to determine therelative significance of pten expression versus its activity in thyroid carcinoma in orderto determine its role in the observed increased akt activity.