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Sivesh Kamarajah,Francesco Giovinazzo,Keith J. Roberts,Pankaj Punia,Robert P. Sutcliffe,Ravi Marudanayagam,Nikolaos Chatzizacharias,John Isaac,Darius F. Mirza,Paolo Muiesan,Bobby VM Dasari 한국간담췌외과학회 2020 Annals of hepato-biliary-pancreatic surgery Vol.24 No.1
Backgrounds/Aims: Approximately 60-80% of patients with intrahepatic cholangiocarcinoma (iCCA) are not suitable for surgical resection due to advanced disease at presentation. This review assesses the role of surgical resection followed by down staging treatment in the management of patients with locally advanced iCCA. Methods: A systematic review and pooled analysis were performed of the relevant published studies published between January 2000-December 2018. The primary outcome measure was overall survival. Secondary outcome measures were rates of clinical benefit, margin-negative (R0) resections, overall and surgery-specific complications, and post-operative mortality. Results: Eighteen cohort studies with 1880 patients were included in the review. The median overall survival in all patients was 14 months (range, 7-18 months). Patients undergoing resection following down staging had significantly longer survival than those who did not (median: 29 vs. 12 months, p<0.001). The Clinical Benefit Rate with this strategy (complete response+partial response+stable disease) was 64% (244/383), ranging from 33-90%. Thirty-eight percent of the patients underwent resections with a 60% R0 resection rate and 6% postoperative mortality. Conclusions: Although the evidence to support the benefits of NAT for iCCA is limited, the review supports the use of down staging treatment and also surgical resection in the cohort with response to NAT in order to improve long-term survival in patients with locally advanced iCCA.
Protein Microarray Characterization of the <i>S</i> -Nitrosoproteome
Lee, Yun-Il,Giovinazzo, Daniel,Kang, Ho Chul,Lee, Yunjong,Jeong, Jun Seop,Doulias, Paschalis-Thomas,Xie, Zhi,Hu, Jianfei,Ghasemi, Mehdi,Ischiropoulos, Harry,Qian, Jiang,Zhu, Heng,Blackshaw, Seth,Dawso The American Society for Biochemistry and Molecula 2014 Molecular and Cellular Proteomics Vol.13 No.1
<P>Nitric oxide (NO) mediates a substantial part of its physiologic functions via <I>S</I>-nitrosylation, however the cellular substrates for NO-mediated <I>S</I>-nitrosylation are largely unknown. Here we describe the <I>S</I>-nitrosoproteome using a high-density protein microarray chip containing 16,368 unique human proteins. We identified 834 potentially <I>S</I>-nitrosylated human proteins. Using a unique and highly specific labeling and affinity capture of <I>S</I>-nitrosylated proteins, 138 cysteine residues on 131 peptides in 95 proteins were determined, defining critical sites of NO's actions. Of these cysteine residues 113 are novel sites of <I>S</I>-nitrosylation. A consensus sequence motif from these 834 proteins for <I>S</I>-nitrosylation was identified, suggesting that the residues flanking the <I>S</I>-nitrosylated cysteine are likely to be the critical determinant of whether the cysteine is <I>S</I>-nitrosylated. We identify eight ubiquitin E3 ligases, RNF10, RNF11, RNF41, RNF141, RNF181, RNF208, WWP2, and UBE3A, whose activities are modulated by <I>S</I>-nitrosylation, providing a unique regulatory mechanism of the ubiquitin proteasome system. These results define a new and extensive set of proteins that are susceptible to NO regulation via <I>S</I>-nitrosylation. Similar approaches could be used to identify other post-translational modification proteomes.</P>