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Background  The  EGFR  3′ untranslated region (UTR) harbors a polyadenine repeat which is polymorphic (A13/A14) and undergoes somatic deletions in microsatellite instability (MSI) colorectal cancer (CRC). These mutations could be oncogenic in colorectal tissue since they were shown to result into increased EGFR mRNA stability in CRC cell lines.    Methods  First, we determined in a case control study including 429 CRC patients corresponding to different groups selected or not on age of tumor onset and/or familial history and/or MSI, whether or not, the germline  EGFR  A13/A14 polymorphism constitutes a genetic risk factor for CRC; second, we investigated the frequency of somatic mutations of this repeat in 179 CRC and their impact on EGFR expression.    Results  No statistically significant difference in allelic frequencies of the  EGFR  polyA repeat polymorphism was observed between CRC patients and controls. Somatic mutations affecting the  EGFR  3′UTR polyA tract were detected in 47/80 (58.8%) MSI CRC  versus  0/99 microsatellite stable (MSS) tumors. Comparative analysis in 21 CRC samples of EGFR expression, between tumor and non malignant tissues, using two independent methods showed that somatic mutations of the  EGFR  polyA repeat did not result into an EGFR mRNA increase.    Conclusion  Germline and somatic genetic variations occurring within the  EGFR  3′ UTR polyA tract have no impact on CRC genetic risk and EGFR expression, respectively. Genotyping of the  EGFR  polyA tract has no clinical utility to identify patients with a high risk for CRC or patients who could benefit from anti-EGFR antibodies.

Genetic variations of the A13/A14 repeat located within the EGFR3′ untranslated region have no oncogenic effect in patients with colorectal cancer