Patients with inoperable HCC had higher levels of serum HGF than the healthy controls, and serum HGF was negatively correlated with the survival time. Serum HGF levels of 1.0 ng/ml or more in HCC patients are suggestive of a grave prognosis, indicating that HGF plays important and active roles in the disease progression. The detailed mechanisms need to be further investigated.

Biliary atresia (BA) is a neonatal obliterative cholangiopathy of unknown etiology. Despite the Kasai procedure, hepatic fibrosis and portal hypertension (PH) still occur. Interleukin-8 (IL-8) is an important mediator of inflammation and immune response in human disease. The objective of this study was to investigate the potential role of IL-8 in the pathogenesis of the progressive, sclerosing, inflammatory process and fibrosis in BA. A total of 60 pediatric patients with BA and 15 healthy children were evaluated. The mean ages of BA patients and controls were 6.3 +/- 0.6 and 6.7 +/- 1.1 years, respectively. The patients were classified into two groups according to their clinical outcomes: patients with jaundice (total bilirubin +/- 25.5 micromol/l) and patients without jaundice (total bilirubin < 25.5 micromol/l). The IL-8 levels in serum samples were determined by commercially available enzyme-linked immunosorbent assay. Serum IL-8 levels were higher in the BA patients than in healthy children (236.2 +/- 60.1 vs. 34.5 +/- 12.1 pg/ml, P < 0.001). Patients with jaundice had lower levels of albumin but had greater levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gamma glutamyl transpeptidase compared with patients without jaundice. Serum IL-8 levels in the jaundice group were significantly higher than in those without jaundice (516.5 +/- 130.0 vs. 49.3 +/- 10.4 pg/ml, P < 0.0005). Furthermore, patients with PH had higher IL-8 levels than those without PH (378.1 +/- 102.2 vs. 106.6 +/- 48.4 pg/ml, P < 0.005). In the jaundice-free group, IL-8 levels were elevated in patients with PH compared with those without PH (79.0 +/- 17.4 vs. 19.7 +/- 5.8 pg/ml, P < 0.005). The present study demonstrated elevation of serum IL-8 levels in children with BA. Serum IL-8 levels were also higher in patients with jaundice compared with patients without jaundice. These findings suggest that IL-8 may play a significant role in the pathogenesis of BA.

No abstract

Survivin is an inhibitor of apoptosis protein that inhibits caspase 3 function. While cytoplasmic survivin suppresses apoptosis, nuclear survivin regulates cell division. Little is known about the subcellular localization of survivin in oral carcinogenesis. This study examined the subcellular distribution of these 2 proteins in oral squamous cell carcinoma (OSCC) and premalignant lesions including oral leukoplakia (OL) with and without dysplasia. Expression of survivin and caspase 3 were immunohistochemically analyzed in 114 samples including OSCC, OL with and without dysplasia, and normal oral mucosa (NM). Cytoplasmic and nuclear positive cells were counted separately. The results were presented as the frequency of positive cases. The positive expression rates of cytoplasmic and nuclear survivin in OSCC were significantly higher than in NM, OL with and without dysplasia. NM showed a low rate of cytoplasmic survivin expression compared to OL with and without dysplasia. The numbers of cytoplasmic and nuclear expression of caspase 3 in OSCC were significantly higher than that of NM, OL with and without dysplasia. In conclusion, the overexpression of cytoplasmic survivin in OSCC and premalignant lesions suggest that suppression of apoptosis by survivin occurs at early and late stages of oral carcinogenesis. The elevated expression of nuclear survivin and caspase 3 in OSCC indicate that at the late stage survivin increases cell proliferation whereas caspase 3 promotes apoptosis.

The association between XPNPEP1 rs17095355 polymorphism and BA has been demonstrated, particularly with the T allele. We hypothesize that the XPNPEP1 rs17095355 polymorphism confers increased susceptibility to the disease.