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Gwak, Geum-Youn,Yoon, Jung-Hwan,Kim, Kang Mo,Lee, Hyo-Suk,Chung, Jin Wook,Gores, Gregory J. Elsevier 2005 Journal of hepatology Vol.42 No.3
<P><B>Background/Aims</B></P><P>In a hypoxic state, a glycolytic system is operating as a salvage pathway of generating ATP, and hexokinase II, the first enzyme in this system, might be over-expressed in hepatocellular carcinomas (HCCs). This study was to evaluate if hexokinase II is participating in HCC cell survival in a hypoxic state, and to analyze the mechanism of cell death caused by hexokinase II-specific inhibition.</P><P><B>Methods</B></P><P>Human hepatoma cell lines were grown either in a normoxic or hypoxic condition. Hexokinase II and hypoxia-inducible factor-1α (HIF-1α) expression were evaluated using immunoblot techniques. Cell growth was assessed using the MTS assay. Apoptotic signaling cascades were explored by immunoblot analysis.</P><P><B>Results</B></P><P>Hypoxia stimulated HCC cellular growth through HIF-1α-dependent induction of hexokinase II expression. The hexokinase II-specific inhibitor, 3-bromopyruvate, significantly suppressed cellular growth in a hypoxic state compared to cells in a normoxic condition. This suppression was due to the induction of apoptosis through activating mitochondrial apoptotic signaling cascades.</P><P><B>Conclusions</B></P><P>This study demonstrates that hypoxia stimulates HCC cellular growth through hexokinase II induction, and its inhibition induces apoptotic cell death. Therefore, hexokinase II induction may participate in HCC progression and the blockage of this enzyme may therapeutically be efficacious in human HCCs.</P>
Model to estimate survival in ambulatory patients with hepatocellular carcinoma
Yang, Ju Dong,Kim, W. Ray,Park, Kyung Woo,Chaiteerakij, Roongruedee,Kim, Bohyun,Sanderson, Schuyler O.,Larson, Joseph J.,Pedersen, Rachel A.,Therneau, Terry M.,Gores, Gregory J.,Roberts, Lewis R.,Park Wiley Subscription Services, Inc., A Wiley Company 2012 Hepatology Vol.56 No.2
<P><B>Abstract</B></P><P>Survival of patients with hepatocellular carcinoma (HCC) is determined by the extent of the tumor and the underlying liver function. We aimed to develop a survival model for HCC based on objective parameters including the Model for Endstage Liver Disease (MELD) as a gauge of liver dysfunction. This analysis is based on 477 patients with HCC seen at Mayo Clinic Rochester between 1994 and 2008 (derivation cohort) and 904 patients at the Korean National Cancer Center between 2000 and 2003 (validation cohort). Multivariate proportional hazards models and corresponding risk score were created based on baseline demographic, clinical, and tumor characteristics. Internal and external validation of the model was performed. Discrimination and calibration of this new model were compared against existing models including Barcelona Clinic Liver Cancer (BCLC), Cancer of the Liver Italian Program (CLIP), and Japan Integrated Staging (JIS) scores. The majority of the patients had viral hepatitis as the underlying liver disease (100% in the derivation cohort and 85% in the validation cohort). The survival model incorporated MELD, age, number of tumor nodules, size of the largest nodule, vascular invasion, metastasis, serum albumin, and alpha‐fetoprotein. In cross‐validation, the coefficients remained largely unchanged between iterations. Observed survival in the validation cohort matched closely with what was predicted by the model. The concordance (c)‐statistic for this model (0.77) was superior to that for BCLC (0.71), CLIP (0.70), or JIS (0.70). The score was able to further classify patient survival within each stage of the BCLC classification. <I>Conclusion</I>: A new model to predict survival of HCC patients based on objective parameters provides refined prognostication and supplements the BCLC classification. (H<SMALL>EPATOLOGY</SMALL> 2012)</P>