Estimation and prediction of incidence, mortality and prevalence on liver cancer, in 2008,China / 中华流行病学杂志

Objective To estimate the incidence,mortality and 5-year prevalence rates of liver cancer in 2008,China.Methods Data from both 36 cancer registries and the Third National Death Survey in China (2004-2005) were used to estimate the incidence,mortality and 5-year prevalence of liver cancer in 2008 in the country by using the mathematical models to predict the liver cancer incidence and mortality in the next 20 years.Results In 2008,the incident cases of liver cancer was 402 208 ( 14.3％ of the total cancers) and the number of deaths from liver cancer was 372 079 ( 19.0％ of the total cancers).The incidence rate was 25.7/100 000,ranking the third among all cancers.The mortality rate was 23.7/100 000,ranking the second among all the cancers.The 5-year prevalence of liver cancer was 296 082 (6.4％ of the total cancers) with the proportion as 27.7/100 000,ranking the sixth among all the cancers.72.8％ of the liver cancer cases appeared in men and the sex ratio of male to female was 2.7:1.In terms of deaths due to liver cancer,74.3％ of them occurred in men,with sex ratio of male to female as 2.9:1.At any age group,the incidence and mortality of liver cancer among males were higher than those of females.Liver cancer happened more frequently among people older than 40 years of age,particularly among males.Data under our prediction showed that the incidence and mortality of liver cancer in China would gradually increase in the next 20 years.Conclusion Liver cancer is one of the most important public health issues in China.Both incidence and mortality of liver cancer have been increasing in China.The key populations for liver cancer prevention and control programs should be those who were older than 40-year-old,particularly on men.

Establishment of a syngeneic mouse model of liver tumor stably expressing hepatitis B virus antigens / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To establish a syngeneic mouse model of liver tumor stably expressing hepatitis B virus (HBV) antigens.</p><p><b>METHODS</b>Melanoma cell line B16 cells were transfected with pLXSN-2HBV. Cells (named B16/HBV) stably and persistently expressing HBV surface (HBsAg) and core (HBcAg) antigens were identified. The cells were injected into the hepatic subcapsular space of fifteen C57BL/6J mice. The mice were divided into 3 groups, receiving 100, 1000 or 5000 cells in a total volume of 5 µl per mouse, respectively, five mice in each group. Two weeks after the tumor cell inoculation, serum samples from the mice were collected weekly and the serum concentration of HBsAg and anti-HBs was quantified by ELISA. The tumor growth in the mouse liver was monitored by a high-resolution ultrasound system. Expression of HBsAg and HBcAg in the tumor tissues was determined by immunohistochemistry.</p><p><b>RESULTS</b>Liver tumors were formed in all the mice receiving 1000 and 5000 B16/HBV cells per mouse, and in 80% of the mice receiving 100 B16/HBV cells. HBsAg and anti-HBs were detectable in their sera from 2 weeks after tumor cell inoculation. The mice receiving 100 cells per mouse began to die 4 weeks, those receiving 1000 cells per mouse began to die 3 - 4 weeks and those receiving 5000 cells began to die 2 - 3 weeks after the cell inoculation. All the tumor cells expressed HBsAg and HBcAg.</p><p><b>CONCLUSIONS</b>The B16/HBV cells stably and persistently express HBV antigens both in vitro and in vivo. A mouse model of transplanted liver tumor stably expressing HBV antigens has been successfully established by inoculation of those cells into the hepatic subcapsular space.</p>

Progressive increase of serum circulating immune complexes and its significance in patients during the progression from chronic hepatitis B to hepatocellular carcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the significance of increasing circulating immune complex (CIC) in patients during the progression from chronic hepatitis B to hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>Serum levels of CIC from 20 hospitalized patients diagnosed by pathology with primary HCC, and 13 with hepatic hemangioma, and from 45 subjects with chronic HBV infection who finally developed into HCC (45 cases), and age- and gender-matched 45 subjects who kept the chronic HBV infection after consecutively followed up for 10 - 13 years by June of 2009 were quantified by ELISA. The serum levels of anti liver-kidney microsomal (anti LKM-1) antibodies were also measured by ELISA, and that of HBV-DNA were quantified by Taqman probe-based real time PCR in the followed up chronic HBV infection subjects. In the 45 chronic HBV subjects who finally developed into HCC and the 45 controls, serum samples were collected and determined at 3 time points: the baseline when the subjects were recruited, the middle point during the follow-up, and the end of follow-up.</p><p><b>RESULTS</b>The serum level of CIC was significantly higher in the 20 HCC patients than that in the 13 hemangioma cases (P < 0.001). When HCC was diagnosed, the CIC concentration was significantly higher than that in the baselines (P < 0.001) in the 45 chronic HBV subjects who finally developed into HCC after the consecutively follow-up for 5 - 13 years. Of them, 36 patients (80.0%) showed progressively increased CIC during the follow-up (P < 0.001). In the controls, the CIC levels were kept relatively stable during the follow-up. Among them, 17 patients (37.8%) showed CIC slightly increased (P = 0.046). Kaplan-Meier survival analysis indicated that elevated serum CIC during the follow-up increased cumulative HCC incidence (HR = 2.77, 95%CI 1.47 - 5.22). In addition, the serum levels of anti-LKM-1 and HBV-DNA were also significantly higher in the patients who finally progressed into HCC than that in the controls and maintained at a high level during the follow-up tested at all the 3 time points. Further analysis indicated that the serum level of CIC was correlated with that of serum HBV-DNA only when HCC was diagnosed (r = 0.344, P = 0.026).</p><p><b>CONCLUSION</b>Progressive increase of serum CIC level may be one of risk factors reflecting HCC development from chronic HBV infection.</p>