Additional Supporting Information may be found in the online version of this article.

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“Hepatocellular carcinoma (HCC) is a common, treatment-resistant malignancy with a complex molecular pathogenesis. Statins are a widely used class of cholesterol-lowering drugs with potential anticancer activity. We reviewed the evidence for a role of statins in primary and secondary chemoprevention of HCC and slowing the course of otherwise EMD 1214063 incurable primary or recurrent disease. A literature search (key words: Statins, hepatocellular carcinoma) conducted to this end, retrieved 119 references. Here we summarize the history, mechanism of action and cardiovascular use of statins and highlight that statins can affect several pathways implicated in the development of HCC. In vitro and animal studies provide strong evidence for a favorable effect of statins on HCC. However, evidence in humans is conflicting. We discuss in full detail the methodological strengths and pitfalls of published data including three cohort studies suggesting that the use Crizotinib order of statins may protect from the development of HCC and of a single trial reporting increased survival in those with advanced HCC randomized to receive statins.

A remarkably hepato-safe class of drugs acting on both hepatocyte and endothelial cells, statins also have potentially beneficial effects in lowering portal hypertension. In conclusion, there is strong experimental evidence that statins are beneficial in chemopreventing and slowing the growth of HCC. However, randomized controlled trials are necessary in order to investigate the role of statins in the chemoprevention of HCC and in slowing the course of otherwise incurable disease in humans. Hepatocellular carcinoma (HCC) is one of the most lethal cancers, and affects many of the world’s populations. Various etiologies have been linked to HCC development, the most prominent of which include hemochromatosis, chronic viral hepatitis due to either B or C infection, excess alcohol consumption and aflatoxin-B1-contaminated food.[1] Virtually all cirrhosis-inducing

conditions can cause HCC, pointing to important interactions with selleck chemicals the host micro-environment.[2] Moreover, the number of multifocal disease stemming from non-cirrhotic disease[3] may be expected to increase as a result of the “explosion” of nonalcoholic fatty liver disease (NAFLD) worldwide and of failure to offer surveillance to patients with clinically occult chronic liver disease developed in the setting of the metabolic syndrome. The presently available therapeutic weaponry, which includes radical and palliative options,[4] is not applicable to all patients. Therapeutic failures may result from diagnostic delays, particularly in those with underlying non-cirrhotic liver disease, or recurrent HCC in those with poor liver function.