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Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
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HRAS mutations in epithelial-myoepithelial carcinoma
Simion I Chiosea1, Megan Miller, Raja R Seethala
1Department of Pathology and Laboratory Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
Head and Neck Pathology
|November 27, 2013
Summary
Epithelial-myoepithelial carcinomas (EMCa) with Harvey rat sarcoma viral oncogene homolog (HRAS) codon 61 mutations were identified in 26.7% of cases. These mutations were observed in classic and variant EMCa subtypes, but not high-grade tumors.
Area of Science:
- Oncology
- Molecular Pathology
- Head and Neck Cancer Research
Background:
- Epithelial-myoepithelial carcinomas (EMCa) are rare salivary gland tumors with an incompletely understood molecular basis.
- Recent studies suggest a potential link between HRAS mutations and EMCa development.
Purpose of the Study:
- To investigate the frequency and spectrum of HRAS codon 61 mutations in a cohort of EMCa.
- To correlate HRAS mutation status with clinicopathologic features and patient outcomes.
Main Methods:
- Fifteen EMCa cases were analyzed for HRAS exon 3, codon 61 mutations using molecular testing.
- Clinicopathologic parameters including age, gender, tumor site, histology, recurrence, and metastasis were recorded.
Main Results:
- HRAS codon 61 mutations (p.Q61R and p.Q61K) were detected in 4 out of 15 (26.7%) tested EMCa cases.
- Mutations were found in classic EMCa and variant morphologies (oncocytic, myoepithelial overgrowth), with one case showing mutation in primary and recurrent tumors.
- High-grade EMCa and EMCa arising from pleomorphic adenoma lacked HRAS codon 61 mutations.
Conclusions:
- HRAS codon 61 mutations are present in a subset of epithelial-myoepithelial carcinomas.
- The presence of these mutations does not appear to correlate with significant differences in age, gender, or clinical outcome in this small cohort.
- Further research with larger cohorts is needed to fully elucidate the role of HRAS mutations in EMCa pathogenesis and prognosis.
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