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Epidermal growth factor receptor and K-RAS status in two cohorts of squamous cell carcinomas

Nancy Van Damme UGent, Philippe Deron UGent, Nadine Van Roy UGent, Pieter Demetter, Alain Bols, Jo Van Dorpe UGent, Filip Baert, Jean-Luc Van Laethem, Franki Speleman UGent and Patrick Pauwels UGent, et al. (2010) BMC CANCER. 10.
abstract
Background: With the availability of effective anti-EGFR therapies for various solid malignancies, such as non-cell small lung cancer, colorectal cancer and squamous cell carcinoma of the head and neck, the knowledge of EGFR and K-RAS status becomes clinically important. The aim of this study was to analyse EGFR expression, EGFR gene copy number and EGFR and K-RAS mutations in two cohorts of squamous cell carcinomas, specifically anal canal and tonsil carcinomas. Methods: Formalin fixed, paraffin-embedded tissues from anal and tonsil carcinoma were used. EGFR protein expression and EGFR gene copy number were analysed by means of immunohistochemistry and fluorescence in situ hybridisation. The somatic status of the EGFR gene was investigated by PCR using primers specific for exons 18 through 21. For the K-RAS gene, PCR was performed using exon 2 specific primers. Results: EGFR immunoreactivity was present in 36/43 (83.7%) of anal canal and in 20/24 (83.3%) of tonsil squamous cell carcinomas. EGFR amplification was absent in anal canal tumours (0/23), but could be identified in 4 of 24 tonsil tumours. From 38 anal canal specimens, 26 specimens were successfully analysed for exon 18, 30 for exon 19, 34 for exon 20 and 30 for exon 21. No EGFR mutations were found in the investigated samples. Thirty samples were sequenced for K-RAS exon 2 and no mutation was identified. From 24 tonsil specimens, 22 were successfully analysed for exon 18 and all 24 specimens for exon 19, 20 and 21. No EGFR mutations were found. Twenty-two samples were sequenced for K-RAS exon 2 and one mutation c. 53C > A was identified. Conclusion: EGFR mutations were absent from squamous cell carcinoma of the anus and tonsils, but EGFR protein expression was detected in the majority of the cases. EGFR amplification was seen in tonsil but not in anal canal carcinomas. In our investigated panel, only one mutation in the K-RAS gene of a tonsil squamous cell carcinoma was identified. This indicates that EGFR and K-RAS mutation analysis is not useful as a screening test for sensitivity to anti-EGFR therapy in anal canal and tonsil squamous cell carcinoma.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
EGFR KINASE DOMAIN, LUNG-CANCER, METASTATIC COLORECTAL-CANCER, HUMAN-PAPILLOMAVIRUS, GENE-MUTATIONS, NECK-CANCER, ACTIVATING MUTATIONS, COPY NUMBER, ANAL CANCER, HEAD
journal title
BMC CANCER
BMC Cancer
volume
10
article_number
189
pages
9 pages
Web of Science type
Article
Web of Science id
000279772300002
JCR category
ONCOLOGY
JCR impact factor
3.153 (2010)
JCR rank
66/181 (2010)
JCR quartile
2 (2010)
ISSN
1471-2407
DOI
10.1186/1471-2407-10-189
language
English
UGent publication?
yes
classification
A1
copyright statement
I have retained and own the full copyright for this publication
id
1014105
handle
http://hdl.handle.net/1854/LU-1014105
date created
2010-07-23 12:29:36
date last changed
2015-04-27 12:52:24
@article{1014105,
  abstract     = {Background: With the availability of effective anti-EGFR therapies for various solid malignancies, such as non-cell small lung cancer, colorectal cancer and squamous cell carcinoma of the head and neck, the knowledge of EGFR and K-RAS status becomes clinically important. The aim of this study was to analyse EGFR expression, EGFR gene copy number and EGFR and K-RAS mutations in two cohorts of squamous cell carcinomas, specifically anal canal and tonsil carcinomas.

Methods: Formalin fixed, paraffin-embedded tissues from anal and tonsil carcinoma were used. EGFR protein expression and EGFR gene copy number were analysed by means of immunohistochemistry and fluorescence in situ hybridisation. The somatic status of the EGFR gene was investigated by PCR using primers specific for exons 18 through 21. For the K-RAS gene, PCR was performed using exon 2 specific primers.

Results: EGFR immunoreactivity was present in 36/43 (83.7\%) of anal canal and in 20/24 (83.3\%) of tonsil squamous cell carcinomas. EGFR amplification was absent in anal canal tumours (0/23), but could be identified in 4 of 24 tonsil tumours.

From 38 anal canal specimens, 26 specimens were successfully analysed for exon 18, 30 for exon 19, 34 for exon 20 and 30 for exon 21. No EGFR mutations were found in the investigated samples. Thirty samples were sequenced for K-RAS exon 2 and no mutation was identified. From 24 tonsil specimens, 22 were successfully analysed for exon 18 and all 24 specimens for exon 19, 20 and 21. No EGFR mutations were found. Twenty-two samples were sequenced for K-RAS exon 2 and one mutation c. 53C {\textrangle} A was identified.

Conclusion: EGFR mutations were absent from squamous cell carcinoma of the anus and tonsils, but EGFR protein expression was detected in the majority of the cases. EGFR amplification was seen in tonsil but not in anal canal carcinomas. In our investigated panel, only one mutation in the K-RAS gene of a tonsil squamous cell carcinoma was identified. This indicates that EGFR and K-RAS mutation analysis is not useful as a screening test for sensitivity to anti-EGFR therapy in anal canal and tonsil squamous cell carcinoma.},
  articleno    = {189},
  author       = {Van Damme, Nancy and Deron, Philippe and Van Roy, Nadine and Demetter, Pieter and Bols, Alain and Van Dorpe, Jo and Baert, Filip and Van Laethem, Jean-Luc and Speleman, Franki and Pauwels, Patrick and Peeters, Marc},
  issn         = {1471-2407},
  journal      = {BMC CANCER},
  keyword      = {EGFR KINASE DOMAIN,LUNG-CANCER,METASTATIC COLORECTAL-CANCER,HUMAN-PAPILLOMAVIRUS,GENE-MUTATIONS,NECK-CANCER,ACTIVATING MUTATIONS,COPY NUMBER,ANAL CANCER,HEAD},
  language     = {eng},
  pages        = {9},
  title        = {Epidermal growth factor receptor and K-RAS status in two cohorts of squamous cell carcinomas},
  url          = {http://dx.doi.org/10.1186/1471-2407-10-189},
  volume       = {10},
  year         = {2010},
}

Chicago
Van Damme, Nancy, Philippe Deron, Nadine Van Roy, Pieter Demetter, Alain Bols, Jo Van Dorpe, Filip Baert, et al. 2010. “Epidermal Growth Factor Receptor and K-RAS Status in Two Cohorts of Squamous Cell Carcinomas.” Bmc Cancer 10.
APA
Van Damme, Nancy, Deron, P., Van Roy, N., Demetter, P., Bols, A., Van Dorpe, J., Baert, F., et al. (2010). Epidermal growth factor receptor and K-RAS status in two cohorts of squamous cell carcinomas. BMC CANCER, 10.
Vancouver
1.
Van Damme N, Deron P, Van Roy N, Demetter P, Bols A, Van Dorpe J, et al. Epidermal growth factor receptor and K-RAS status in two cohorts of squamous cell carcinomas. BMC CANCER. 2010;10.
MLA
Van Damme, Nancy, Philippe Deron, Nadine Van Roy, et al. “Epidermal Growth Factor Receptor and K-RAS Status in Two Cohorts of Squamous Cell Carcinomas.” BMC CANCER 10 (2010): n. pag. Print.