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AIM:To investigate the polymorphic simple sequencerepeat in intron 1 of the epidermal growth factor receptorgene(EGFR)(CA-SSRⅠ),which is known to affect theefficiency of gene transcription as a putative target of themismatch repair(MMR)machinery in colorectal tumors.METHODS:The CA-SSRⅠgenotype was analyzed ina total of 86 primary colorectal tumors,selected upontheir microsatellite instability(MSI)status[42 with highfrequency MSI(MSI-H)and 44 microsatellite stable(MSS)]and their respective normal tissue.The effect of the CA-SSRⅠgenotype on the expression of the EGFR gene wasevaluated in 18 specimens using quantitative real-timereverse transcription PCR and immunohistochemistry.RESULTS:Mutations in CA-SSRⅠwere detected in 86%(36 of 42)of MSI-H colorectal tumors and 0%(0 of 44)ofMSS tumors,indicating the EGFR gene as a novel putativespecific target of the defective MMR system(P<0.001).Impaired expression of EGFR was detected in most ofthe colorectal tumors analyzed[6/12(50%)at the mRNAlevel and 15/18(83%)at the peptide level].However,noassociation was apparent between EGFR expression andCA-SSRⅠstatus in tumors or normal tissues.CONCLUSION:Our results suggest that CA-SSRⅠsequence does not contribute to the regulation of EGFRtranscription in colon,and should thus not be consideredas a promising predictive marker for response to EGFRinhibitors in patients with colorectal cancer.
AIM: To investigate the polymorphic simple sequence repeat in intron 1 of the epidermal growth factor receptor gene (EGFR) (CA-SSRI), which is known to affect the efficiency of gene transcription as a putative target of themismatch repair (MMR) machinery in colorectal tumors. METHODS: The CA-SSRI genotype was analyzed in total of 86 primary colorectal tumors, selected upontheir microsatellite instability (MSI) status [42 with high frequency MSI (MSI-H) and 44 microsatellite stable (MSS)] and their respective normal tissues. of the CA-SSRI genotype on the expression of the EGFR gene wasevaluated in 18 specimens using quantitative real-time reverse transcription PCR and immunohistochemistry .RESULTS: Mutations in CA-SSRI detected in 86% (36 of 42) of MSI-H colorectal tumors and 0 (0 of 44) of MSS tumors, indicating the EGFR gene as a novel putative specific target of the defective MMR system (P <0.001). Impressive expression of EGFR was detected in the most of the colorectal salient analyzed [6/12 (50%) at the However, the mRNA level and 15/18 (83%) at the peptide level] .However, noassociation was apparent between EGFR expression and CA-SSRIstatus in tumors or normal tissues. CONCLUSION: Our results suggest that CA-SSRIsequence doesnt contribute to the regulation of EGFR transcription in colon, and should not be considered as a promising predictive marker for response to EGFR inhibitors in patients with colorectal cancer.