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To evaluate loss of imprinting (LOI) and expression of theIGF2gene in matched esophageal normal and adenocarcinoma tissues, we studied a prospective cohort of 77 patients who underwent esophageal resection between 1998 and 2003.IGF2imprinting status was determined by reverse transcription–polymerase chain reaction (PCR) following ApaI digestion, and quantitative PCR was used to evaluateIGF2expression, which was correlated with clinicopathologic findings, disease-free and overall survival. In total, 32% (14/44) of informative tissues showed loss ofIGF2imprinting, with a strong correlation between the tumor and normal esophageal epithelia (Kappa = 0.89,P &lt; 0.01). Normal epithelia with LOI had increased expression ofIGF2[median: 2.91, 95% confidence interval (CI): 0.93–5.06] compared with imprinted normal epithelia (median: 1.13, 95% CI: 0.85–1.39) (P = 0.03). In contrast, tumors with LOI had significantly reducedIGF2expression (median: 1.87, 95% CI: 0.53–5.21) compared with normally imprinted tumors (median: 6.79, 95% CI: 3.39–15.89) (P = 0.016). Patients below the age of 65 years with normally imprinted tumors had significantly reduced 5 year disease-free survival (DFS) (24%) compared with patients whose tumors had LOI forIGF2(55%) (P = 0.03). Cox regression analysis showed thatIGF2overexpression was associated with significantly reduced disease-free survival (P = 0.04). We conclude that in a subgroup of younger patients, loss ofIGF2imprinting was associated with improved outcome following esophageal resection. Expression ofIGF2in esophageal adenocarcinoma and normal esophageal epithelia depended on imprinting status and tissue type, suggesting novel molecular regulatory mechanisms in esophageal tumorigenesis.

Loss of imprinting of the insulin-like growth factor II ( IGF2 ) gene in esophageal normal and adenocarcinoma tissues