Insulin-like growth factor I receptor b expression in XXXX .

@entity1 @entity157 @entity1561 @entity5
The insulinlike growth factor signaling axis (factors I and II and their receptor) has been implicated in hepatocarcinogenesis. Previous studies on insulinlike growth factor I receptor using resected @entity157 generated mixed results; however, the distribution and clinical significance of insulinlike growth factor I receptor b expression in @entity157 in the setting of liver transplantation have not been evaluated. Immunohistochemical staining for insulinlike growth factor I receptor b was performed in 72 liver explants from @entity1 with @entity157 undergoing liver transplantation. Expression of insulinlike growth factor I receptor b in hepatocytes was noted in 59.7% of @entity5 but only 6.9% of adjacent, nontumorous liver tissues (P < .001). Compared with subjects with @entity5 within Milan criteria, those who fell beyond had 3.1 times higher odds of having insulinlike growth factor I receptor b-positive @entity5 (95% confidence interval, 1.003-9.8). Poorly differentiated @entity157 had 10.3 times higher odds of insulinlike growth factor I receptor b positivity compared with well- or moderately differentiated @entity5 (95% confidence interval, 1.3-85.2). Subjects with @entity1561 were less likely to have insulinlike growth factor I receptor b-positive @entity5 (P = .015). Finally, higher arteriolar insulinlike growth factor I receptor b scores in the @entity5 and adjacent liver were significantly associated with insulinlike growth factor I receptor b expression in @entity5 cells (P = .015 and .043 for intratumoral and adjacent arterioles, respectively) in a subset of 26 randomly chosen @entity157 . Our results suggest that synchronized up-regulation of the insulinlike growth factor I receptor axis in @entity5 cells and intratumoral and adjacent arterioles could represent a mechanism of hepatocarcinogenesis and progression as manifest by poor differentiation and @entity5 beyond Milan criteria. Targeted therapies against insulinlike growth factor receptors may be justifiable in the treatment of @entity157 .
