期刊
CANCER GENETICS
卷 205, 期 12, 页码 630-635出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cancergen.2012.10.005
关键词
EGFR; fluorescence in situ hybridization; gene copy number; colorectal cancer
资金
- Lega Tumori (Reggio Emilia branch)
- Fondazione Lodini of Reggio Emilia
- Emilia Romagna Region [RicOncol RF-EMR-2006-361866]
Adenomas are the easily identifiable precursors of the vast majority of colorectal cancers. Some of their morphological features, such as dysplasia, are predictive of their biological evolution toward adenocarcinomas. A large body of evidence has demonstrated that the epidermal growth factor receptor (EGFR) signaling pathway is commonly activated in colorectal cancer and EGFR-target therapies have improved the outcome for colorectal cancer patients. Nevertheless, the mechanisms underlying the role of EGFR in the adenoma-carcinoma sequence are not entirely clear. We retrospectively analyzed EGFR gene copy number by fluorescence in situ hybridization (FISH) in paraffin-embedded tissue from 215 patients recruited through a prospective colorectal cancer screening procedure and undergoing surgical colectomy. We observed that in human colorectal carcinogenesis, EGFR copy number increases progressively, from adenomas with high-grade dysplasia to locally advanced adenocarcinomas, through early invasive adenocarcinomas, suggesting that deregulation of EGFR may correlate with the malignant progression.
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