We also identified TGFβ2 as a good candidate biomarker for ICC prognosis. Importantly, osteopontin this website and TGFβ2 protein expression were the most correlated independent variables (Supporting Table 5). Accordingly, differences in OS (P = 0.06) and DFS (P = 0.008) could be also observed by combining the expression of TGFβ2 and osteopontin (Supporting Fig. 3). Identifying ICC with favorable or unfavorable prognoses might orientate the selection of the most appropriate treatment, including liver resection/transplantation, chemotherapy, and targeted therapy,

either alone or in combination. Although ICC is not currently a widely accepted indication for orthotopic liver transplantation (OLT), some studies suggest that OLT could be indicated for selected ICC patients, as suggested for hilar cholangiocarcinoma.[47] A combination of neoadjuvant RO4929097 concentration therapy followed by OLT in appropriately selected patients with unresectable ICC also demonstrated promising disease recurrence-free survival.[48] Given that the expression of osteopontin correlates with relevant clinical variables (OS, DFS, hilar lymph nodes, macrovascular invasion), we believe that patients with

low to absent expression may benefit from OLT. In conclusion, by using an unsupervised approach we showed a clear correlation between genomic changes in the stroma and the aggressiveness of ICC, and we identified osteopontin as a promising prognostic biomarker. In addition, these observations support the idea that targeting the tumor stroma may represent a valid and innovative therapeutic strategy in ICC. The authors thank the Plateforme Génomique Santé, the Centre de Ressources Biologiques Santé (Rennes), the

Liver Biobanks Network, and Pascale Bellaud from the H2P2 histopathological platform (Biosit, Rennes). C.C. thanks Dr. Wendy T. Watford from the University of Georgia click here for critically reviewing the article. Additional Supporting Information may be found in the online version of this article. “
“Background and Aim:  Aplasia ras homolog member I (ARHI) is a maternally imprinted tumor suppressor gene. ARHI protein is widely expressed in many types of human tissues; however, its expression is frequently reduced or absent in various tumors and plays a tumor suppressor role for in vitro study. In this study, we investigated the expression level of ARHI in gastric cancer in order to investigate the function of ARHI and signaling pathways that might be linked during gastric cancer development. Methods:  ARHI mRNA and protein expression levels were analyzed in primary gastric cancer tissues, adjacent noncancerous gastric tissues and gastric cancer cell lines using semi-quantitative polymerase chain reaction, western blotting and immunohistochemistry, respectively. Results:  Our results showed that both mRNA and protein expression levels of the ARHI gene were significantly downregulated (P < 0.