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Annals of Oncology Advance Access originally published online on March 8, 2006
Annals of Oncology 2006 17(6):962-967; doi:10.1093/annonc/mdl037
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© 2006 European Society for Medical Oncology

EGFR in colorectal cancer: more than a simple receptor

M. Francoual1, M.-C. Etienne-Grimaldi1, J.-L. Formento1, D. Benchimol2, A. Bourgeon2, M. Chazal3, C. Letoublon4, T. André5, N. Gilly6, J.-R. Delpero7, P. Lasser8, J.-P. Spano9 and G. Milano1,*

1 Centre Antoine-Lacassagne, Nice; 2 Hôpital l'Archet, Nice; 3 Centre Médical Valbrise, Nice; 4 CHU de Grenoble, Grenoble; 5 Hôpital Tenon, Paris; 6 Centre Hospitalier Lyon-Sud, Pierre-Bénite; 7 Institut Paoli-Calmettes, Marseille; 8 Institut Gustave Roussy, Villejuif; 9 GH Pitié-Salpétrière, Paris, France

* Correspondence to: Dr G. Milano, Oncopharmacology Unit, Centre Antoine Lacassagne, 33, Avenue de Valombrose, 06189 Nice Cedex 2, France. Tel: +33. (4).92.03.15.53; Fax: +33. (4).93.81.71.31; E-mail: gerard.milano{at}nice.fnclcc.fr

Background: Advances in the understanding of tumor biology have led to the development of targeted therapies allowing progress in colorectal cancer treatment. One of the most promising targets is the epidermal growth factor receptor (EGFR).

Method: The presence and distribution of high- and low-affinity EGFR was investigated retrospectively in a group of 82 colorectal cancer samples (43 normal colon–colon cancer paired samples) using a specific ligand binding assay (Scatchard Analysis).

Findings: A large majority of tumor samples exhibited one class of high-affinity binding sites (78%). Eighteen cases (22%) exhibited both high- and low-affinity binding sites. A wide interpatient variability was observed for the site number, with physiologically-relevant high-affinity sites ranging from 7 to 310 fmol/mg protein in tumors and from 6 to 313 fmol/mg protein in normal mucosa. A significant positive correlation was demonstrated between tumor and normal mucosa for the high-affinity Kd values and for the number of high-affinity sites, suggesting a common regulation for both tumor and normal tissue.

Interpretation: These observations (i) could explain recently-reported clinically-active EGFR targeting in colorectal tumors apparently negative for EGFR, and (ii) may offer a plausible explanation for the link observed between toxicity in normal tissue (cutaneous rash) and clinical outcome of patients treated with anti-EGFR drugs. Present data extends our understanding of EGFR identity in colorectal cancer which could be useful in reconsidering the predictive tools for the identification of tumors putatively responsive to EGFR targeted therapy.

Key words: colorectal cancer, EGFR, epidermal growth factor receptor


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