It is worth noting that HBV reactivation occurred after achieving

It is worth noting that HBV reactivation occurred after achieving MMR in the first case (Figure (Figure1A)1A) and after CCyR in the second case (Figure (Figure1B),1B), GNF-5? a similar condition as that in the report of Ikeda et al[7]. In the study of Mohamad et al[23], CML patients who were in complete molecular or cytogentic response after IM treatment restored function of plasmacytoid dendritic cells, which are crucial effectors in innate immunity. Therefore, the finding of hepatic flare after complete molecular or cytogenetic responses in the first two cases may provide evidence to support the hypothesis of immune-restoration stage of HBV reactivation. Furthermore, in the third case of our study, the hepatic flare occurred 5 mo before achieving CCyR (Figure (Figure1C).1C).

This finding suggests that nilotinib treatment might provoke a different pathway other than that of IM to achieve immune restoration. Further studies may be needed to explain this observation. An important issue that should be addressed is the preemptive therapy with nucleoside/nucleotide analogues (NAs) in patients undergoing TKI therapy. Although preemptive treatment with NAs before immunosuppressive chemotherapy is recommended in European Association for the Study of the Liver Clinical Practice guidelines[24], there is no recommendation on whether NAs should be given in patients undergoing TKI therapy due to lack of prospective studies. In conclusion, this case report highlights the importance that HBV reactivation may occur in hematologic patients undergoing TKI therapy.

Once HBV reactivation is suspected during TKI treatment, early detection of HBV load and utilization of antiviral agent are suggested to achieve better clinical outcome. Footnotes P- Reviewer Piekarska A S- Editor Gou SX L- Editor A E- Editor Zhang DN
Long-term colonic inflammation promotes carcinogenesis and histological abnormalities of the liver, and colorectal tumours frequently arise in a background of dysplasia, a precursor of adenomas. Altered colonic microbiota with an increased proportion of bacteria with pro-inflammatory characteristics, have been implicated in neoplastic progression. The composition of the microbiota can be modified by dietary components such as probiotics, polyphenols and dietary fibres. In the present study, the influence of probiotics in combination with blueberry husks on colorectal carcinogenesis and subsequent liver damage was evaluated.

Colorectal tumours were induced in rats by cyclic treatment with dextran sulphate sodium (DSS). Blueberry husks and a mixture of three probiotic strains (Bifidobacterium infantis DSM 15159, Lactobacillus gasseri, DSM 16737 and Lactobacillus plantarum DSM 15313) supplemented a basic diet fortified with oats. The condition of the rats was monitored using a disease activity index Anacetrapib (DAI).

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