<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rizzo, Toni</style></author></authors><secondary-authors><author><style face="normal" font="default" size="100%">Llovet, Josep M.</style></author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Limited Progress in the Treatment of HCC</style></title><secondary-title><style face="normal" font="default" size="100%">MD Conference Express</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014-10-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">24-26</style></pages><abstract><style  face="normal" font="default" size="100%">The main risk factors for hepatocellular carcinoma (HCC) are hepatitis C virus, hepatitis B virus, and alcohol consumption, which can lead to cirrhosis, genomic instability, and progression to HCC. This process involves a cycle of regeneration and necrosis that induces release of cytokines, proangiogenic factors, and profibrotic factors. Fibrosis and increased cell proliferation can result in formation of a dysplastic nodule, marked genomic instability, loss of p53, and development of HCC [Farazi PA, DePinho RA. Nat Rev Cancer. 2006].</style></abstract><number><style face="normal" font="default" size="100%">22</style></number><volume><style face="normal" font="default" size="100%">14</style></volume></record></records></xml>