007) and a nonsignificant trend toward less portal inflammation (P = 0.06). No such associations

were noted among HCV genotype 2-infected patients. In contrast, Grs8099917 carriage in HCV genotype 2 was associated with less steatosis (P = 0.044). It should be noted that patients infected with HCV genotype 2 were older than those infected with HCV genotype 3 (mean age, 47.2 versus 39.8 years; P < 0.0001), as well as fewer in number (n = 98 versus 241). These results confirm and extend the findings of Bochud et al. and indicate that Grs8099917 and Trs12979860 carriage is associated with milder liver histopathology, especially in patients infected with HCV genotype 3, and that IL28B polymorphisms may differentially regulate the natural course of infection across HCV genotypes. Karolina Rembeck M.D.*, Johan Westin M.D., Ph.D.*, Magnus Lindh M.D., Ph.D.*, Kristoffer Hellstrand M.D., Ph.D.*, Gunnar www.selleckchem.com/products/BIBW2992.html Norkrans , M.D., Ph.D.*, Martin Laging M.D., Ph.D.*, * Department of Infectious Diseases/Virology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden. “
“We read in HEPATOLOGY a very interesting and valuable article1 MI-503 concentration suggesting that the simultaneous targeting of

epidermal growth factor receptor (ErbB1) and human epidermal growth factor receptor 2 (ErbB2) could potentially be a selective strategy for cholangiocarcinoma therapy. Reading this article and considering our own study on the treatment of tuclazepam cholangiocarcinoma with a combinative strategy involving tamoxifen and other chemotherapeutic drugs, we see indications that the use of tamoxifen for cholangiocarcinoma prevention and treatment will become more popular. Tamoxifen is a classic drug for estrogen receptor–positive primary breast cancer that is positive for ErbB1 and/or ErbB2,2 and the same mechanism could be indicated for the treatment of cholangiocarcinoma. We have also performed some experiments with this strategy (as mentioned later), and now we

think that the expression levels of ErbB1, ErbB2, or both could be markers for the effects of tamoxifen. To find new ways of using chemotherapeutics for human cholangiocarcinoma, we have been paying attention to the growth-inhibition effects of tamoxifen in combination chemotherapeutics. Some of our pilot studies have shown that tamoxifen can lead to increased cell damage by competing with other chemotherapeutic molecules for binding sites on P-glycoprotein and by limiting the extracellular transport of drugs from the human cholangiocarcinoma cell line QBC939.3, 4 Because cholangiocarcinoma cells gradually develop resistance to conventional chemotherapeutic drugs, we have selected tamoxifen as a sensitizer that competes with chemotherapeutic drugs as the P-glycoprotein substrate for the P-glycoprotein binding site and enhances the drug concentration and effects of chemotherapy.3 To further our study, we have established a human, multidrug-resistant cholangiocarcinoma cell line (QBC939/ADM).