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Table of Contents

Breaking Insights

Reviews

Priority Report

Genome and Epigenome

  • Genome and Epigenome | AuthorChoice
    Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors
    Pauline J. Beckmann, Jon D. Larson, Alex T. Larsson, Jason P. Ostergaard, Sandra Wagner, Eric P. Rahrmann, Ghaidan A. Shamsan, George M. Otto, Rory L. Williams, Jun Wang, Catherine Lee, Barbara R. Tschida, Paramita Das, Adrian M. Dubuc, Branden S. Moriarity, Daniel Picard, Xiaochong Wu, Fausto J. Rodriguez, Quincy Rosemarie, Ryan D. Krebs, Amy M. Molan, Addison M. Demer, Michelle M. Frees, Anthony E. Rizzardi, Stephen C. Schmechel, Charles G. Eberhart, Robert B. Jenkins, Robert J. Wechsler-Reya, David J. Odde, Annie Huang, Michael D. Taylor, Aaron L. Sarver and David A. Largaespada
    Cancer Res March 1 2019 79 (5) 905-917; DOI:10.1158/0008-5472.CAN-18-1261

    A transposon-induced mouse model identifies several novel genetic drivers and potential therapeutic targets in medulloblastoma and CNS-PNET.

  • Genome and Epigenome
    Acetylation of CCAR2 Establishes a BET/BRD9 Acetyl Switch in Response to Combined Deacetylase and Bromodomain Inhibition
    Praveen Rajendran, Gavin Johnson, Li Li, Ying-Shiuan Chen, Mohaiza Dashwood, Nhung Nguyen, Ahmet Ulusan, Furkan Ertem, Mutian Zhang, Jia Li, Deqiang Sun, Yun Huang, Shan Wang, Hon-Chiu Leung, David Lieberman, Laura Beaver, Emily Ho, Mark Bedford, Kyle Chang, Eduardo Vilar and Roderick Dashwood
    Cancer Res March 1 2019 79 (5) 918-927; DOI:10.1158/0008-5472.CAN-18-2003

    These results highlight the competition that exists among the “readers” of acetylated histone and nonhistone proteins and provide a mechanistic basis for potential new therapeutic avenues involving epigenetic combination treatments.

Molecular Cell Biology

  • Molecular Cell Biology
    PRL-3 Promotes Ubiquitination and Degradation of AURKA and Colorectal Cancer Progression via Dephosphorylation of FZR1
    Cheng Zhang, Like Qu, Shenyi Lian, Lin Meng, Li Min, Jiafei Liu, Qian Song, Lin Shen and Chengchao Shou
    Cancer Res March 1 2019 79 (5) 928-940; DOI:10.1158/0008-5472.CAN-18-0520

    Dephosphorylation of FZR1 by PRL-3 facilitates the activity of APC/CFZR1 by destabilizing AURKA, thus influencing aggressive characteristics and overall progression of colorectal cancer.

  • Molecular Cell Biology
    miR-192-5p Silencing by Genetic Aberrations Is a Key Event in Hepatocellular Carcinomas with Cancer Stem Cell Features
    Yuanzhuo Gu, Xiyang Wei, Yulin Sun, Hongjun Gao, Xin Zheng, Linda L. Wong, Ling Jin, Niya Liu, Brenda Hernandez, Karolina Peplowska, Xiaohang Zhao, Qi-Min Zhan, Xin-Hua Feng, Zhao-You Tang and Junfang Ji
    Cancer Res March 1 2019 79 (5) 941-953; DOI:10.1158/0008-5472.CAN-18-1675

    miR-192-5p and its regulatory pathway is significantly abolished in multiple groups of HCC expressing high levels of CSC markers, which may represent a key event for hepatic carcinogenesis.

  • Molecular Cell Biology
    Pleiotropic Effects of PPARD Accelerate Colorectal Tumorigenesis, Progression, and Invasion
    Yi Liu, Yasunori Deguchi, Rui Tian, Daoyan Wei, Ling Wu, Weidong Chen, Weiguo Xu, Min Xu, Fuyao Liu, Shen Gao, Jonathan C. Jaoude, Sarah P. Chrieki, Micheline J. Moussalli, Mihai Gagea, Jeffrey Morris, Russell R. Broaddus, Xiangsheng Zuo and Imad Shureiqi
    Cancer Res March 1 2019 79 (5) 954-969; DOI:10.1158/0008-5472.CAN-18-1790

    These findings address long-standing, important, and unresolved questions related to the potential role of PPARD in APC mutation-dependent colorectal tumorigenesis by showing PPARD activation enhances APC mutation-dependent tumorigenesis.

Tumor Biology and Immunology

  • Tumor Biology and Immunology
    Frizzled-7 Is Required for Wnt Signaling in Gastric Tumors with and Without Apc Mutations
    Dustin J. Flanagan, Nick Barker, Natasha S. Di Costanzo, Elizabeth A. Mason, Austin Gurney, Valerie S. Meniel, Sarah Koushyar, Chloe R. Austin, Matthias Ernst, Helen B. Pearson, Alex Boussioutas, Hans Clevers, Toby J. Phesse and Elizabeth Vincan
    Cancer Res March 1 2019 79 (5) 970-981; DOI:10.1158/0008-5472.CAN-18-2095

    The Wnt receptor Fzd7 plays an essential role in gastric tumorigenesis irrespective of Apc mutation status, therefore targeting Wnt/Fzd7 may be of therapeutic benefit to patients with gastric cancer.

Translational Science

  • The WNT10B Network Is Associated with Survival and Metastases in Chemoresistant Triple-Negative Breast Cancer
    Translational Science
    The WNT10B Network Is Associated with Survival and Metastases in Chemoresistant Triple-Negative Breast Cancer
    Ikbale El Ayachi, Iram Fatima, Peter Wend, Jackelyn A. Alva-Ornelas, Stephanie Runke, William L. Kuenzinger, Julio Silva, Wendy Silva, Joseph K. Gray, Stephan Lehr, Hilaire C. Barch, Raisa I. Krutilina, Andrew C. White, Robert Cardiff, Lisa D. Yee, Lily Yang, Ruth M. O'Regan, William E. Lowry, Tiffany N. Seagroves, Victoria Seewaldt, Susan A. Krum and Gustavo A. Miranda-Carboni
    Cancer Res March 1 2019 79 (5) 982-993; DOI:10.1158/0008-5472.CAN-18-1069

    These findings reveal targeting the WNT signaling pathway as a potential therapeutic strategy in triple-negative breast cancer.

  • Translational Science
    Enhancer Domains in Gastrointestinal Stromal Tumor Regulate KIT Expression and Are Targetable by BET Bromodomain Inhibition
    Matthew L. Hemming, Matthew A. Lawlor, Jessica L. Andersen, Timothy Hagan, Otari Chipashvili, Thomas G. Scott, Chandrajit P. Raut, Ewa Sicinska, Scott A. Armstrong, George D. Demetri and James E. Bradner
    Cancer Res March 1 2019 79 (5) 994-1009; DOI:10.1158/0008-5472.CAN-18-1888

    Expression and activity of mutant KIT is essential for driving the majority of GIST neoplasms, which can be therapeutically targeted using BET bromodomain inhibitors.

Resource Report

  • Resource Report
    esiCancer: Evolutionary In Silico Cancer Simulator
    Darlan Conterno Minussi, Bernardo Henz, Mariana dos Santos Oliveira, Eduardo C. Filippi-Chiela, Manuel M. Oliveira and Guido Lenz
    Cancer Res March 1 2019 79 (5) 1010-1013; DOI:10.1158/0008-5472.CAN-17-3924

    This study provides a customizable and hands-on simulation tool to model the effect of diverse types of genomic alterations on the fate of tumor cells.

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