Fax: (011) 985-108015
Gene amplification and protein overexpression of EGFR and ERBB2 in sinonasal squamous cell carcinoma†
Article first published online: 25 AUG 2011
Copyright © 2011 American Cancer Society
Volume 118, Issue 7, pages 1818–1826, 1 April 2012
How to Cite
López, F., Llorente, J. L., Oviedo, C. M., Vivanco, B., Álvarez Marcos, C., García-Inclán, C., Scola, B. and Hermsen, M. A. (2012), Gene amplification and protein overexpression of EGFR and ERBB2 in sinonasal squamous cell carcinoma. Cancer, 118: 1818–1826. doi: 10.1002/cncr.26451
We thank Sira Potes for the mutation analysis and Eva Allonca for the immunohistochemical experiments.
- Issue published online: 19 MAR 2012
- Article first published online: 25 AUG 2011
- Manuscript Revised: 20 JUN 2011
- Manuscript Accepted: 20 JUN 2011
- Manuscript Received: 6 MAY 2011
- maxillary sinus;
- ethmoid sinus;
- squamous cell carcinoma;
Sinonasal squamous cell carcinomas (SNSCCs) are rare tumors with no etiologic link to tobacco or alcohol, as opposed to other squamous cell carcinomas of the head and neck. Despite improvements in the field of surgery and radiotherapy, patients with these tumors still face a very unfavorable prognosis, partly because of their localization in a complex anatomic area, which has special relevance for surgery and postoperative treatment. Therefore, there is a need for new therapeutic possibilities for patients with these tumors.
Gene copy numbers of epidermal growth factor receptor (EGFR) and v-erb-b2 erythroblastic leukemia viral oncogene homolog 2 (ERBB2) were analyzed by fluorescence in situ hybridization and multiplex ligand-dependent probe amplification, and protein expression was evaluated by immunohistochemistry in 54 SNSCC specimens. The results were correlated with clinicopathologic and follow-up data.
EGFR gene copy number increases were observed in 20 of 45 tumors (44%), and 21 of 54 tumors (39%) had EGFR protein overexpression. Eight of 38 tumors (21%) had ERBB2 copy number increases, and 4 of 54 tumors (7%) exhibited elevated protein expression levels. Both copy number increases and protein overexpression of EGFR and ERBB2 were mutually exclusive. v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations were absent in 37 tumors that were analyzed.
A substantial proportion of SNSCCs carried alterations in EGFR or ERBB2. Together with the absence of KRAS mutations, these findings indicate that therapies targeting these molecules may be promising additions to the therapeutic options for patients with SNSCC. Cancer 2012;. © 2011 American Cancer Society.