Epidermal growth factor receptor (EGFR) promoter methylation may be responsible for the loss of EGFR expression in neoplastic cells. The primary aim of our study was to verify a possible correlation between EGFR gene promoter methylation and clinical outcome in metastatic colorectal cancer patients receiving chemotherapy with irinotecan and cetuximab.Colorectal samples from patients treated with irinotecan-cetuximab were analysed for EGFR promoter methylation and EGFR immunohistochemistry.Fifty-two patients were analysed. Thirty patients (58\%) showed EGFR promoter hypermethylation. In EGFR promoter methylated and EGFR promoter unmethylated patients, we observed a partial response in 3 (10\%) and 13 (59\%) patients, respectively (P=0.03), progressive disease was obtained in 19 (63\%) and 2 (9\%) patients, respectively, with EGFR promoter methylated and EGFR promoter unmethylated tumours (P=0.0001). Median progression-free survival was 2.4 months in patients showing EGFR promoter methylated tumours and 7.4 months for those who had EGFR promoter unmethylated tumours (P<0.0001; Figure 1). Median overall survival was 6.1 months in patients showing EGFR promoter methylated tumours and 17.8 months for those who had EGFR promoter unmethylated tumours (P<0.0001; Figure 2).EGFR promoter hypermethylation, after confirmation in larger data set, may represent a valuable asset in further studies investigating EGFR as a therapeutic target in colorectal cancer.

Epidermal growth factor receptor (EGFR) gene promoter methylation and cetuximab treatment in colorectal cancer patients / Scartozzi, M.; Bearzi, I.; Mandolesi, A.; Giampieri, R.; Faloppi, L.; Galizia, E.; Loupakis, F.; Zaniboni, A.; Zorzi, F.; Biscotti, T.; Labianca, R.; Falcone, A.; Cascinu, Stefano. - In: BRITISH JOURNAL OF CANCER. - ISSN 0007-0920. - 104:(2011), pp. 1786-1790. [10.1038/bjc.2011.161]

Epidermal growth factor receptor (EGFR) gene promoter methylation and cetuximab treatment in colorectal cancer patients.

CASCINU, Stefano
2011-01-01

Abstract

Epidermal growth factor receptor (EGFR) promoter methylation may be responsible for the loss of EGFR expression in neoplastic cells. The primary aim of our study was to verify a possible correlation between EGFR gene promoter methylation and clinical outcome in metastatic colorectal cancer patients receiving chemotherapy with irinotecan and cetuximab.Colorectal samples from patients treated with irinotecan-cetuximab were analysed for EGFR promoter methylation and EGFR immunohistochemistry.Fifty-two patients were analysed. Thirty patients (58\%) showed EGFR promoter hypermethylation. In EGFR promoter methylated and EGFR promoter unmethylated patients, we observed a partial response in 3 (10\%) and 13 (59\%) patients, respectively (P=0.03), progressive disease was obtained in 19 (63\%) and 2 (9\%) patients, respectively, with EGFR promoter methylated and EGFR promoter unmethylated tumours (P=0.0001). Median progression-free survival was 2.4 months in patients showing EGFR promoter methylated tumours and 7.4 months for those who had EGFR promoter unmethylated tumours (P<0.0001; Figure 1). Median overall survival was 6.1 months in patients showing EGFR promoter methylated tumours and 17.8 months for those who had EGFR promoter unmethylated tumours (P<0.0001; Figure 2).EGFR promoter hypermethylation, after confirmation in larger data set, may represent a valuable asset in further studies investigating EGFR as a therapeutic target in colorectal cancer.
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Epidermal growth factor receptor (EGFR) gene promoter methylation and cetuximab treatment in colorectal cancer patients / Scartozzi, M.; Bearzi, I.; Mandolesi, A.; Giampieri, R.; Faloppi, L.; Galizia, E.; Loupakis, F.; Zaniboni, A.; Zorzi, F.; Biscotti, T.; Labianca, R.; Falcone, A.; Cascinu, Stefano. - In: BRITISH JOURNAL OF CANCER. - ISSN 0007-0920. - 104:(2011), pp. 1786-1790. [10.1038/bjc.2011.161]
Scartozzi, M.; Bearzi, I.; Mandolesi, A.; Giampieri, R.; Faloppi, L.; Galizia, E.; Loupakis, F.; Zaniboni, A.; Zorzi, F.; Biscotti, T.; Labianca, R.; Falcone, A.; Cascinu, Stefano
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1079104
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