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RISS 인기검색어
- 검색키워드
- 저자 : Chatila, Walid K. (검색결과 3 건)
- 무료
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Oncogenic Signaling Pathways in The Cancer Genome Atlas
Sanchez-Vega, Francisco,Mina, Marco,Armenia, Joshua,Chatila, Walid K.,Luna, Augustin,La, Konnor C.,Dimitriadoy, Sofia,Liu, David L.,Kantheti, Havish S.,Saghafinia, Sadegh,Chakravarty, Debyani,Daian, F Elsevier 2018 Cell Vol.173 No.2
<P><B>Summary</B></P> <P>Genetic alterations in signaling pathways that control cell-cycle progression, apoptosis, and cell growth are common hallmarks of cancer, but the extent, mechanisms, and co-occurrence of alterations in these pathways differ between individual tumors and tumor types. Using mutations, copy-number changes, mRNA expression, gene fusions and DNA methylation in 9,125 tumors profiled by The Cancer Genome Atlas (TCGA), we analyzed the mechanisms and patterns of somatic alterations in ten canonical pathways: cell cycle, Hippo, Myc, Notch, Nrf2, PI-3-Kinase/Akt, RTK-RAS, TGFβ signaling, p53 and β-catenin/Wnt. We charted the detailed landscape of pathway alterations in 33 cancer types, stratified into 64 subtypes, and identified patterns of co-occurrence and mutual exclusivity. Eighty-nine percent of tumors had at least one driver alteration in these pathways, and 57% percent of tumors had at least one alteration potentially targetable by currently available drugs. Thirty percent of tumors had multiple targetable alterations, indicating opportunities for combination therapy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Alteration map of 10 signaling pathways across 9,125 samples from 33 cancer types </LI> <LI> Reusable, curated pathway templates that include a catalogue of driver genes </LI> <LI> 57% of tumors have at least one potentially actionable alteration in these pathways </LI> <LI> Co-occurrence of actionable alterations suggests combination therapy opportunities </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Comparative Molecular Analysis of Gastrointestinal Adenocarcinomas
Liu, Yang,Sethi, Nilay S.,Hinoue, Toshinori,Schneider, Barbara G.,Cherniack, Andrew D.,Sanchez-Vega, Francisco,Seoane, Jose A.,Farshidfar, Farshad,Bowlby, Reanne,Islam, Mirazul,Kim, Jaegil,Chatila, Wa Elsevier 2018 Cancer cell Vol.33 No.4
<P><B>Summary</B></P> <P>We analyzed 921 adenocarcinomas of the esophagus, stomach, colon, and rectum to examine shared and distinguishing molecular characteristics of gastrointestinal tract adenocarcinomas (GIACs). Hypermutated tumors were distinct regardless of cancer type and comprised those enriched for insertions/deletions, representing microsatellite instability cases with epigenetic silencing of <I>MLH1</I> in the context of CpG island methylator phenotype, plus tumors with elevated single-nucleotide variants associated with mutations in <I>POLE</I>. Tumors with chromosomal instability were diverse, with gastroesophageal adenocarcinomas harboring fragmented genomes associated with genomic doubling and distinct mutational signatures. We identified a group of tumors in the colon and rectum lacking hypermutation and aneuploidy termed genome stable and enriched in DNA hypermethylation and mutations in <I>KRAS</I>, <I>SOX9</I>, and <I>PCBP1</I>.</P> <P><B>Highlights</B></P> <P> <UL> <LI> GI adenocarcinomas comprised five molecular subtypes: EBV, MSI, HM-SNV, CIN, and GS </LI> <LI> Hypermutated tumors had diverse immune features varying by tissue and subtype </LI> <LI> CIN tumors displayed more fragmented copy-number alterations in the upper GI tract </LI> <LI> Genome-stable CRC subtype was enriched for recurrent mutations in <I>SOX9</I> and <I>PCBP1</I> </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Evidence for a role of CaMKIV in the development of opioid analgesic tolerance
Ko, Shanelle W.,Jia, Yongheng,Xu, Hui,Yim, Se-Jeong,Jang, Dong-Hyuk,Lee, Yong-Seok,Zhao, Ming-Gao,Toyoda, Hiroki,Wu, Long-Jun,Chatila, Talal,Kaang, Bong-Kiun,Zhuo, Min Blackwell Publishing Ltd 2006 The European journal of neuroscience Vol.23 No.8
<P>Abstract</P><P>cAMP response-element binding protein (CREB), a transcription factor involved in learning, memory and drug addiction, is phosphorylated by calcium–calmodulin-dependent protein kinase IV (CaMKIV). Here, we show that CaMKIV-knockout (KO) mice developed less analgesic tolerance after chronic morphine administration with no alteration in physical dependence or acute morphine-induced analgesia. The increase in phosphorylated CREB expression observed in wild-type mice after chronic morphine was absent in CaMKIV-KO mice, while there was no difference in the expression or phosphorylation of the µ-opioid receptor between groups. Morphine-treated CaMKIV-KO mice showed less G-protein uncoupling from the µ-opioid receptor than did wild-type mice, while uncoupling was similar in control wild-type and KO mice. In addition, morphine reduced inhibitory transmission to a greater degree in CaMKIV-KO mice than in controls after chronic morphine exposure. Our results provide novel evidence for the role of CaMKIV in the development of opioid analgesic tolerance but not physical dependence.</P>
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