AIM:To examine the epidemiological data,hematological safety and treatment responses of peginterferonalpha 2a plus ribavirin therapy for hepatitis ***:Between March 2008 and February 2011,196 hepatitis C virus(HCV)gen...
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AIM:To examine the epidemiological data,hematological safety and treatment responses of peginterferonalpha 2a plus ribavirin therapy for hepatitis ***:Between March 2008 and February 2011,196 hepatitis C virus(HCV)genotype 1 infected Japanese(127 treatment-naive and 69 treatment-experienced patients)patients treated with peginterferonalpha 2a plus ribavirin were *** examined the epidemiological data and treatment responses were retrospectively analyzed in terms of hematological *** RNA was measured by the COBAS TaqMan HCV ***:Overall sustained virological response(SVR)rates of treatment-naive and treatment-experienced patients were 56% and 39%,*** logistic regression analysis showed that SVR was attained independently of early virological response in both treatment-naive and treatment-experienced *** rates did not differ between the pretreatment hemoglobin < 13 g/dL and ≥ 13 g/dL ***,in treatment-naive patients,the SVR rate of the pretreatment platelet count < 130000/μL group was significantly lower than that of the pretreatment platelet count ≥ 130000/μL ***:Attention should be paid to potential thrombocytopenia in the treatment of chronic hepatitis C patients.
In small cell lung cancer cells, various autocrine stimuli lead to the parallel activation of Gq/11 and G12/13 proteins. The contribution of the Gq/11-PLC-β cascade to the mitogenic effects in SCLC cells is well esta...
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In small cell lung cancer cells, various autocrine stimuli lead to the parallel activation of Gq/11 and G12/13 proteins. The contribution of the Gq/11-PLC-β cascade to the mitogenic effects in SCLC cells is well established, but the relevance of G12/13 signaling is less explored. While in prostate and breast cancer, G12/13 activation has been shown previously to promote invasiveness without being involved in cellular proliferation, previous data from our group indicate anti-proliferative effects of G12/13 knockdown in small cell lung cancer (SCLC) cells. To further investigate the role of G12/13-dependent signaling in lung tumor cells, we employed shRNA-mediated targeting of Gα12, Gα13, or both, in SCLC and NSCLC cell lines. Lentiviral expression of shRNAs resulted in specific Gα12 and Gα13 knockdown. Of note, upon single knockdown of one family member, no counter-upregulation of the other one was observed. Interestingly, inhibition of proliferation was cell line dependent. In cell lines where knock-down led to antiproliferation, single knockdown of either Gα12 or Gα13 was sufficient to impair proliferation and double knockdown of Gα12 and Gα13 tended not to further increase anti-proliferative effects. Likewise, when single knockdown was insufficient for an inhibition of proliferation, no effects were observed in double knockdowns. Taken together, these findings indicate that both Gα12 and Gα13 affect cellular proliferation individually and interference with one family member is sufficient for anti-tumor effects.
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