Conclusion: our study confirms that male patients with type 2 diabetes mellitus have a significantly increased risk of HCC independently of other cofactor such as HBV, HCV and alcoholic abuse. DM2 is a pre-existing disease in most HCC patients and suggests that insulin and sulphonylurea treatments in DM2 are associated with an increased risk of HCC development, while metformin may have a protective effect. Background & Aims: Over the last few years, techniques that allow systematic analysis of chromosome aberrations at a genome-wide level were applied to HCC. The purpose of this study is to apply gene loss expression profiling in the attempt to discover new related genomic regions not revealed by LOH or CGH, and search the new tumor suppression genes for HCC. Methods: Primary HCC and corresponding non-tumor liver tissues were obtained from surgery. Serologically, 13 cases were with hepatitis B virus infection and 12 cases were with hepatitis C virus infection. Four non-viral infected tissues from four patients receiving surgical resection for hepatic adenoma or focal nodular hyperplasia.Affymetrix GeneChip, U133A, was used to compare the loss and gained gene expression in liver needle biopsy samples (n=54). Results: After adjusting by chromosome arm length, 16p, 17p, 19p, 19q and 22q showed higher gene loss-expression ratio (>= 10 loss / cM) in the comparison between normal samples and tumor samples; 1q, 2p and 4q showed higher gene loss-expression ratio in the comparison between tumor and non-tumor tissues. More than 50 genes showed different loss expression level in this study. For example, CD10 was loss expression in all non-tumor samples comparing to four normal samples. Ficolin 3 and ficolin 2 were loss expression in HCC samples with HBV infection and with HCV infection, respectively. Conclusion: Our results revealed the potential tumor suppression genes and the genomic region they harbored. Further study is needed to validate the observation. Background/Aims: Hepatocellular carcinoma is common malignancy in human, accounting for 1 million deaths in the world annually. Caspase 8, as an initiator caspase, is involved in the induction of apoptosis. Survivin, a novel inhibitor of apoptosis is related to the ability to inhibit caspases and involved in critical steps of onset and progression of HCC with unfavorable prognosis. Methods: To explore the possibility that the epigenetic alteration of caspase 8 and survivin genes is implicated in the development and progression of HCC, promoter methylation of two genes was analyzed in 73 cases of primary HCC by methylation specific PCR. The relationship between immunohistochemical expression of gene products and proliferative/apoptotic indices, and clinicopathologic parameters was also investigated. Results: The methylation of caspase 8 (34.2%, 25/73) and survivin (32.9%, 24/73) demonstrated a negative correlation with immunohistochemical expression of capsase 8 (47.9%, 35/73) and survivin (43.8%, 32/73) (p=0.042 and p=0.001 respectively). Methylation of caspase 8 and immunohistochemical expression of its gene product was significantly correlated with apoptosis (p=0.026 and p=0.032). Survivin nuclear immunoreativity revealed significantly correlated with proliferative activity of tumor cells (p=0.001). By survivial analysis, the negative caspase 8 expression and positive survivin expression showed worse prognosis in HCC, that was statistically insignificant (p>0.05).