ABSTRACT
Objective To explore the distribution and characteristics of hepatitis B virus (HBV) genotype in the region in Guangxi with high incidence of primary liver cancer (PLC). Methods 103 pairs of samples from the sex- and age-matched members with HBsAg-positive from PLC-clustering families (the experimental group) and carcinoma-free families (control group) were collected. Nested polymerase chain reaction (PCR) and sequencing methods were applied for the analysis of HBV genotype. Results Four HBV genotypes: B, C, B/C and D, were detected, the percentages of them in the two groups were 31.1%, 63.1%, 1.9%, 1.9% and 30.1%, 55.3%, 6.8%, 2.9%, respectively, showed no significant differences (P > 0.05). HBeAg positive rates were significantly different between genotype C and B (P 0.05). Conclusions The main genotypes were types B and C besides a small number of combined genotypes B/C and D in the regions of Guangxi with a high incidence of PLC. There may be few relationships between HBV genotypes and the high incidence of PLC for familial clustering in Guangxi.
ABSTRACT
Objective To explore the relationship between mutations in basic core promoter (BCP) of hepatitis B virus (HBV) and familial clustering of hepatocellular carcinoma (HCC) in Guangxi. Methods 153 pairs of members with HBsAg-positive were selected and matched from HCC high-incidence families and carcinoma-free families in Guangxi. The BCP genes were amplified and sequenced. Results The hotspot sites of the previous five mutations in BCP were T1762, A1764, G1775, V1753, G1803. In univariant analysis, HBV DNA≥105 copies/mL, T1762, A1764 and V1753 mutations were associated with the HCC high-incidence (P <0.05). The multivariate logistic analysis showed that HBV DNA≥105 copies/mL and A1764 were independent risk factors for it. Conclusion HBV DNA level, the mutations in BCP showed correlations with familial clustering of HCC in Guangxi.
ABSTRACT
Objective To investigate the expression of signal transducer and activator of transcription 3 (STAT3) in colorectal car- cinoma tissues and adenomatous polyp tissues, and analyze the relationship between the expression of STAT3 and its clinicopathological pa- rameters in colorectal carcinoma tissues. Methods The protein expressions of STAT3 were detected in 40 colorectal carcinoma tissues, 30 adenomatons polyp tissues and 30 normal colorectal mucosa tissues by MaxVisionTM immunohistochemistry, and the relationship with clinical data were analyzed. Results The STAT3 protein was located mainly in cytoplasm. Positive expression rates of STAT3 protein in colorectal carcinoma tissues, adenomatous polyp tissues and normal colorectal mucosa tissues were 80.0%, 56.7% and 30.0%, respectively. The ex- pression of STAT3 protein in colorectal carcinoma tissues was higher than that in edenomatous polyp tissues (P<0.05 ). Compared with normal colorectal mucosa tissues, the positive expression rates and intensities of STAT3 protein in colorectal carcinoma tissues and adenoma- tous polyp tissues were significantly higher(P<0.05 ) . It was found that overexpreesion of STAT3 protein was related te differentiation, Dukes stage and lymph node metastasis in colorectal carcinoma ( P < 0. 05 ), and no significant differences were found between STAT3 pro- tein expression and other factors such as serosa invasion, distant metastasis , age and gender( P<0.05 ). Conclusions The overexpres- sion of STAT3 protein may play an important role in the genesis and progression of colorectal cancer. In adenomatous polyp tissues, STAT3- positive cells may be potential pre-cancerous cells. Detection of STA'r3 is helpful in accessing the malignant degree and the biological behav- ior of colorectal cancer.