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β decays of the heaviest N=Z−1 nuclei and proton instability of In97
Park, J.,Krü,cken, R.,Lubos, D.,Gernhä,user, R.,Lewitowicz, M.,Nishimura, S.,Ahn, D. S.,Baba, H.,Blank, B.,Blazhev, A.,Boutachkov, P.,Browne, F.,Č,eliković,, I.,de France, G.,Doornen American Physical Society 2018 Physical review. C Vol.97 No.5
Yu, Jun,Tao, Qian,Cheng, Yuen Y.,Lee, Kwan Y.,Ng, Simon S. M.,Cheung, Kin F.,Tian, Linwei,Rha, Sun Y.,Neumann, Ulf,Rö,cken, Christoph,Ebert, Matthias P. A.,Chan, Francis K. L.,Sung, Joseph J. Y. Wiley Subscription Services, Inc., A Wiley Company 2009 Cancer Vol.115 No.1
<P><B>Abstract</B></P><P><B>BACKGROUND:</B></P><P>Abnormal activation of the Wnt/β‐catenin signaling pathway is common and critical in the pathogenesis of digestive cancers. In this study, the authors investigated the promoter methylation of the dickkopf homolog 3 gene <I>Dkk‐3</I> in these cancers and its prognostic significance in gastric cancer.</P><P><B>METHODS:</B></P><P><I>Dkk‐3</I> methylation was assessed in 173 patients with gastric cancers (including 104 patients who were followed for up to 4090 days) and in 128 patients with colorectal cancer. Cell growth was evaluated by using a colony‐formation assay. For survival analyses, the authors used Kaplan‐Meier plots, the log‐rank test, and Cox proportional regression.</P><P><B>RESULTS:</B></P><P><I>Dkk‐3</I> was silenced or down‐regulated in 12 of 17 gastric cancer cell lines (70.6%) and in 3 of 9 colon cancer cell lines (33.3%). The loss of gene expression was associated with promoter methylation, which could be restored by demethylating agents. Ectopic expression of <I>Dkk‐3</I> suppressed colony formation. Moreover, methylation of <I>Dkk‐3</I> was detected in 117 of 173 primary gastric tumors (67.6%) and in 67 of 128 colorectal tumors (52.3%). The clinical significance and the prognostic value of <I>Dkk‐3</I> methylation also were examined in 104 gastric cancers and in 84 colorectal cancers. Multivariate analysis indicated that <I>Dkk‐3</I> methylation was associated significantly and independently with poor disease survival (relative risk, 2.534; 95% confidence interval, 1.54–4.17; <I>P</I> = .002) in gastric cancer, but not in colorectal cancer. Kaplan‐Meier survival curves revealed that patients who had <I>Dkk‐3</I> methylated gastric cancers had a significantly shorter survival (median, 0.76 years) compared with patients who did not have <I>Dkk‐3</I> methylation (median, 2.68 years; <I>P</I> < .0001; log‐rank test).</P><P><B>CONCLUSIONS:</B></P><P>Epigenetic silencing of the <I>Dkk‐3</I> gene by promoter methylation was a common event in gastric cancer and was associated with a poor outcome in such patients. Cancer 2009. © 2008 American Cancer Society.</P>