Blood 2002,100(5):1628–1633.PubMedCrossRef Competing interests The authors declare that they have no competing interests.

Authors’ contributions ZXS, JML and AHW designed research; YYW, YY, ZZX, LZ, LW, LZ and YC performed research; AHW and YYW analyzed data; AHW wrote the paper, JH revised the paper. eFT-508 datasheet All authors read and approved the final manuscript.”
“Background Hepatocellular carninoma (HCC) is the fifth most common cancer in the world and the third most common cause of cancer mortality [1]. Hereditary hemochromatosis (HH) is an autosomal recessive genetic condition in which excess iron is absorbed by the intestine and deposited throughout the body [2]. If untreated, affected individuals may accumulate excess iron over the many years of their adult life, and this causes progressive tissue damage [3]. It has been reported that HH may result in many diseases, including liver disease (fibrosis, cirrhosis, and hepatocellular carcinoma). Some studies reported that liver disease was the most common cause of death of patients with HH [4, 5]. In 1996, Feder and colleagues [6] showed that homozygosity for mutation (C282Y,

G>A, rs1800562) in the HFE gene was responsible for the majority of cases of typical phenotypic HH. The frequency of the second variant (H63D, C>G, rs1799945) is also increased in HH patients, but its penetrance is low. From then on, HFE gene has been postulated as a candidate gene of HCC. Some studies [7–16] demonstrated that C282Y or H63D increased the risk of HCC,

while some [17–19] gave selleck products negative results. Some large scale cohort studies [20, 21] also showed that HFE gene mutation penetrance was low and did not increase the likelihood of death from any cause among the C282Y homozygotes compared with subjects who had no C282Y mutation. However, the estimates in these cohort studies were conservative Celecoxib in the sense that in the cohort study period, a proportion of HH patients had received phlebotomy treatment. As a result, the role of C282Y and H63D mutations in HCC occurrence still merits study. To clarify the relationship between HFE C282Y and H63D mutations and HCC, a meta-analysis was performed. Methods Study identification and selection Eligible studies were identified by searching the databases of PubMed and ISI Web of Knowledge for relevant reports published before May 2009. The search criteria “”c282y OR h63d”" and “”liver cancer OR hepatocellular carcinoma”" were used. We also searched reports and dissection databases published in the Chinese Biomedical database (CBM), China National Knowledge Infrastructure (CNKI), and Wan Fang (Chinese) database to collect articles of case-control studies or cohort studies on Akt inhibitor associations between HFE mutations and susceptibility to HCC before May 2009. The reference lists of the retrieved articles were also reviewed to identify additional articles missed by the above search.