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Expression and alterations of the PTEN / AKT / mTOR pathway in ameloblastomas

M A Scheper1, R Chaisuparat, N G Nikitakis

  • 1Department of Diagnostic Sciences and Pathology, University of Maryland, Baltimore, MD 21201, USA. mscheper@umaryland.edu

Oral Diseases
|October 2, 2008
PubMed
Abstract

Insights

Loss of phosphatase and tensin homologue (PTEN) is frequent in ameloblastomas, leading to overactive PI3K/AKT/mTOR signaling. This pathway dysregulation drives uncontrolled cell proliferation and survival, impacting tumor development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ameloblastomas exhibit allelic loss of phosphatase and tensin homologue (PTEN).
  • PTEN loss activates the phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathway, upregulating mammalian-target of rapamycin (mTOR).
  • This aberrant signaling promotes uncontrolled cell proliferation, inhibits apoptosis, and deregulates the cell cycle.

Purpose of the Study:

  • To investigate the immunohistochemical expression of PTEN, AKT, and downstream signaling molecules in ameloblastomas.
  • To assess the role of the PI3K/AKT/mTOR pathway in ameloblastoma pathogenesis.

Main Methods:

  • Immunohistochemical analysis of 30 ameloblastomas and 5 dental follicles.
  • Assessed expression of total and phosphorylated PTEN and AKT.
  • Evaluated phosphorylated ribosomal-subunit-6 kinase (pS6K) as an indicator of mTOR activity and extracellular-signal-regulated kinase (ERK).

Main Results:

  • PTEN was absent in 33.3% and its active form in 83.3% of ameloblastomas.
  • High expression of active AKT forms (p-thr308 and p-ser473) was observed in 93.3% and 56.6% of tumors, respectively.
  • Activated mTOR signaling (pS6K) was detected in 86.7% of ameloblastomas, with ERK overexpression in 70.0%.

Conclusions:

  • Aberrant signaling in the PI3K/AKT/mTOR pathway is a common feature of ameloblastomas.
  • Immunohistochemical analysis of this pathway can aid in understanding ameloblastoma pathogenesis and aggressiveness.
  • Targeting the PI3K/AKT/mTOR pathway may offer therapeutic strategies for ameloblastomas.

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