Hepatocellular carcinoma (HCC) has been known as one of the most lethal human malignancies, due to the difficulty of early detection, chemoresistance, and radioresistance, and is characterized by active angiogenesis and metastasis, which account for rapid recurrence and poor survival. Its development has been closely associated with multiple risk factors, including hepatitis B and C virus infection, alcohol consumption, obesity, and diet contamination. Genetic alterations and genomic instability, probably resulted from unrepaired DNA lesions, are increasingly recognized as a common feature of human HCC. Dysregulation of DNA damage repair and signaling to cell cycle checkpoints, known as the DNA damage response (DDR), is associated with a predisposition to cancer and affects responses to DNA-damaging anticancer therapy. It has been demonstrated that various HCC-associated risk factors are able to promote DNA damages, formation of DNA adducts, and chromosomal aberrations. Hence, alterations in the DDR pathways may accumulate these lesions to trigger hepatocarcinogenesis and also to facilitate advanced HCC progression. This review collects some of the most known information about the link between HCC-associated risk factors and DDR pathways in HCC. Hopefully, the review will remind the researchers and clinicians of further characterizing and validating the roles of these DDR pathways in HCC.

In this study, we try to compare the benefit of laparoscopic versus open operative procedures.Patients and Methods. One hundred and sixteen patients underwent laparoscopic liver resection (LR) and another 208 patients went for open liver resection (OR) for hepatocellular carcinoma (HCC). Patients' selection for open or laparoscopic approach was not randomized.Results. The CLIP score for LR and OR was 0.59 ± 0.75 and 0.86 ± 1.04, respectively, (). The operation time was 156.3 ± 308.2 and 190.9 ± 79.2 min for LR and OR groups, respectively. The necessity for blood transfusion was found in 8 patients (6.9%) and 106 patients (50.9%) for LR and OR groups. Patients resumed full diet on the 2nd and 3rd postoperative day, and the average length of hospital stay was 6 days and 12 days for LR and OR groups. The complication rate and mortality rate were 0% and 6.0%, 2.9% and 30.2% for LR and OR groups, respectively. The 1-yr, 3-yr, and 5-yr survival rate was 87.0%, 70.4%, 62.2% and 83.2%, 76.0%, 71.8% for LR and OR group, respectively, of non-significant difference. From these results, HCC patients accepted laparoscopic or open approach were of no significant differences between their survival rates.

The risk factors for hepatocellular carcinoma (HCC) development have been established, and include chronic hepatitis B and C, heavy alcohol consumption, and aflatoxins. In fact, 5%-30% of patients with HCC still lack a readily identifiable risk factor. It has been reported that the majority of ‘‘cryptogenic’’ HCC may be attributed to nonalcoholic fatty liver disease, the hepatic presentation of the metabolic syndrome (MS). Obesity is associated with the development of the MS. Recently, adipose tissue has been considered as an endocrine organ because of its capacity to secrete a variety of cytokines, which are collectively known as the adipokines. Leptin, the product of the obese gene, is mainly produced by adipose tissue. Since leptin was first characterized in 1994, accumulated literature has demonstrated the involvement of this adipokine in several areas of human physiology. After binding to its receptor, leptin initiates a cascade of signaling events and subsequent cellular effects. In addition to being the regulatory mediator of energy homeostasis, several in vitro studies have demonstrated the fibrogenic role of leptin in the liver. Furthermore, the deregulated expression of leptin and its receptor have been demonstrated to be associated with a variety of metabolic disorders as well as human cancers. Most importantly, direct evidence supporting the inhibitory and/or activating role of leptin in the process of carcinogenesis and progression of human HCC has been accumulating rapidly. This review aims to provide important insights into the potential mechanisms of leptin in the development of HCC. Hopefully, further investigations will shed light on a new therapeutic target in HCC.