0001). This hot spot is associated with aflatoxin B1, developed in non-cirrhotic(P=0. 01) tumors. IRF2 mutations were found exclusively in HBV-related HCC(P=0. 03). Regarding the transcriptome groups(G1-G6), HBV-related HCC were more frequently classified in G1-G3(57%,

p=0. 001). Overall, in the G1-G2, we observed a majority of young patients(age<60years, p=0. 003) and the Selleckchem RG 7204 presence of IRF2 mutations (P=0. 006). In the G2-G3, tumors were poorly differentiated(Edmondson III-IV, p=0. 001) with a higher rate of early recurrence(<24months, P=0. 01). G2-G3 was strongly associated with TP53 mutations (P=0. 0009), especially R249S (P= 0. 003). In the G1-G3 groups, tumors were larger(diameter>55 mm, P=0. 006) with both Axin1(P=0. 03) and HBx(P=0. 001) inactivating mutations. G5-G6 constitutes a homogeneous group of HCC, composed by elder patients(≥60 years P=0. 0007), strongly linked to CTNNB1 mutations(P<0. 0001). In general, G4-G6 was characterized by small tumors(<55mm, P=0. 006) and was associated with other cofactors (Alcohol/HCV/NASH, P=0. 04). In addition, all the HCC classified in G1-G3 were characterized by overexpression of several genes

involved in cell cycle and of genes encoding oncofoetal proteins such as EPCAM, KRT19, AFP and CCNB1(P<0. 001), while HCC in G5-G6 were characterised by the over expression of β-caten in-target genes: GLUL, TBX3, and RHBG(P<0. 001). Conclusion: The TP53 pathway is the most altered in HBV-related HCC. Transcriptomic classification shows a predominance distribution in G1-G3. The cofactors p38 MAPK phosphorylation are most frequently found in G4-G6. Inactivating mutations of HBx were associated with G1-G3. Disclosures: Jessica Zucman-Rossi – Consulting: pfizer; Grant/Research Support: Integragen; Speaking and Teaching: bayer, lilly The following people have nothing to disclose: Qian Cao, Giuliana Amaddeo, Yannick Ladeiro, Sandrine Imbeaud Purpose: The prognosis of patients with hepatocellular carcinoma (HCC) remains poor, particularly in patients with tumor thrombi

in the major trunk of portal vein, even after curative resection of the selleck products tumor. We have reported clinical efficiency of interferon (IFN)-based therapy for advanced HCC. However, prediction of the response to the therapy remains unsatisfactory. Accordingly, it is necessary to find novel biological markers that can accurately predict the clinical response to the therapy. Recently, some investigators have reported a correlation between microRNAs (miRNAs) expression and chemoresistance in several types of cancers. In the present study, we identified miRNAs that govern the chemoresistance to the therapy in HCC. Methods: In the first experimental step, we focused on miR-21 which is one of the most common miRNAs related to chemoresistance.