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Molecular alterations in MAPK/ERK, β-Catenin/Wnt, and PI3K/mTOR pathways in adenomatoid odontogenic tumor

Jintana Pankam1, Puangwan Lapthanasupkul2, Nakarin Kitkumthorn3,4

  • 1Mahidol University, Faculty of Dentistry, Bangkok, Thailand.

Journal of Applied Oral Science : Revista FOB
|June 24, 2026
PubMed
Abstract

Insights

KRAS mutations and p-ERK1/2 expression suggest the MAPK/ERK pathway is involved in adenomatoid odontogenic tumor (AOT) development. PI3K/mTOR pathway activation may occur independently of PIK3CA mutations in AOT.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pathology

Background:

  • Adenomatoid odontogenic tumor (AOT) tumorigenesis may involve the MAPK/ERK pathway.
  • Limited research exists on other oncogenic signaling pathways in AOT.

Purpose of the Study:

  • Investigate gene mutations (KRAS, CTNNB1, PIK3CA) and protein expressions (p-ERK1/2, β-catenin, p-mTOR) in AOT.
  • Examine associations between gene mutations and protein expression in AOT.

Main Methods:

  • DNA extraction and sequencing of KRAS, CTNNB1, and PIK3CA genes from AOT tissues.
  • Immunohistochemistry to assess p-ERK1/2, β-catenin, and p-mTOR protein expression.
  • Analysis of mutations in specific codons and exons of targeted genes.

Main Results:

  • KRAS mutations (G12R, G12V) found in 37.5% of AOT cases.
  • CTNNB1 mutation (T42I) in 16.7%; no PIK3CA mutations detected.
  • Moderate p-ERK1/2 and p-mTOR expression; β-catenin accumulation in 87.5% (membranous/cytoplasmic).

Conclusions:

  • KRAS mutations and p-ERK1/2 support MAPK/ERK signaling in AOT pathogenesis.
  • PI3K/mTOR pathway activation may be mutation-independent in AOT.
  • Lack of nuclear β-catenin suggests limited canonical Wnt signaling contribution to AOT tumorigenesis.

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