Summary Elucidation of the basic genetic changes of human hepatocellular carcinoma is important for the understanding and treatment of this cancer. We used microsatellite polymorphism markers to study 30 cases of hepatocellular carcinoma (34 tumours) on all human chromosomes. DNA from 34 pairs of hepatocellular carcinomas and corresponding non-tumour parts was prepared. Loss of heterozygosity (LOH) and microsatellite instability on 23 chromosomes were investigated by 231 sets of microsatellite markers. More than 20% LOH was shown for loci on 16q (47.1%), 13q (32.4%), 17p (32.4%), 5q (26.5%), 11p (23.5%) and 9p (20.6%). The commonly affected regions were mapped to 16q12.1, 16q12.2, 16q24, 13q12.1-32, 17p13, 5q32, 5q34, 5q3, 11p15, 11q23-24 and 9p21. Hepatitis B virus carriers had a significantly higher frequency of LOH on chromosomes 5q, 11p and 16q. Furthermore, larger tumour size tended to have higher frequency of LOH at D16S409 locus (16q12.1). Microsatellte instability was only found in 12 of 231 markers and the frequency is very low. These data suggest that the chromosomes 16q, 13q, 17p, 5q, 11p and 9p might participate in hepatocarcinogenesis. However, microsatellite instability might play little role in the development of this cancer in Taiwan.

In countries with low and moderate incidence of tuberculosis (TB), the disease tends to concentrate in specific high-risk populations such as people with diabetes mellitus (DM). We review the updated evidence on the association between 1) DM and active TB, and 2) DM and latent tuberculous infection (LTBI), and 3) we summarize the findings on the population-level impact of DM on TB epidemiology, with particular focus on low- and moderate-incidence settings. We conducted an updated review of studies on DM and active TB, and found 11 more cohort studies published after the previous systematic review from 2008. The updated pooled relative risk (RR) (2.03, 95%CI 1.62-2.55) of all the studies was substantially lower than the three-fold risk increase in the previous review. Substantial heterogeneity of RR across studies was found. Possible reasons for such heterogeneity include different levels of residual confounding, the effect of modification by age, and different levels of glycemic control in the population. In a recently published systematic review on DM and LTBI, one cohort study and 12 cross-sectional studies were identified. The results from cross-sectional studies suggest a significant but modestly increased risk of LTBI among patients with DM (pooled odds ratio 1.18, 95%CI 1.06-1.30). We reviewed evidence on the population-level impact of DM on TB epidemiology in studies using population-attributable fraction analysis and infectious disease modelling. Those studies revealed that DM accounted for a substantial TB burden in low- and moderate-incidence countries. Finally, we discussed the complex association of obesity, DM and TB risk and the impact of the global obesity pandemic on TB epidemiology.

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