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Table of Contents

In This Issue

  • In This Issue
    In This Issue
    Cancer Discov February 1 2019 9 (2) 151-154; DOI:10.1158/2159-8290.CD-ITI9-2

In the Spotlight

Review

Research Briefs

  • Research Briefs | AuthorChoice
    EGFR and MET Amplifications Determine Response to HER2 Inhibition in ERBB2-Amplified Esophagogastric Cancer
    Francisco Sanchez-Vega, Jaclyn F. Hechtman, Pau Castel, Geoffrey Y. Ku, Yaelle Tuvy, Helen Won, Christopher J. Fong, Nancy Bouvier, Gouri J. Nanjangud, Joanne Soong, Efsevia Vakiani, Mark Schattner, David P. Kelsen, Robert A. Lefkowitz, Karen Brown, Mario E. Lacouture, Marinela Capanu, Marissa Mattar, Besnik Qeriqi, Fabiola Cecchi, Yuan Tian, Todd Hembrough, Rebecca J. Nagy, Richard B. Lanman, Steven M. Larson, Neeta Pandit-Taskar, Heiko Schöder, Christine A. Iacobuzio-Donahue, David H. Ilson, Wolfgang A. Weber, Michael F. Berger, Elisa de Stanchina, Barry S. Taylor, Jason S. Lewis, David B. Solit, Jorge A. Carrasquillo, Maurizio Scaltriti, Nikolaus Schultz and Yelena Y. Janjigian
    Cancer Discov February 1 2019 9 (2) 199-209; DOI:10.1158/2159-8290.CD-18-0598

    Coamplification of EGFR and ERBB2 is associated with afatinib response in patients with trastuzumab-refractory esophagogastric cancer, whereas selection for MET amplification or loss of EGFR amplification is associated with resistance.

  • Research Briefs | AuthorChoice
    BRCA Reversion Mutations in Circulating Tumor DNA Predict Primary and Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma
    Kevin K. Lin, Maria I. Harrell, Amit M. Oza, Ana Oaknin, Isabelle Ray-Coquard, Anna V. Tinker, Elena Helman, Marc R. Radke, Carmen Say, Lan-Thanh Vo, Elaina Mann, Jeffrey D. Isaacson, Lara Maloney, David M. O'Malley, Setsuko K. Chambers, Scott H. Kaufmann, Clare L. Scott, Gottfried E. Konecny, Robert L. Coleman, James X. Sun, Heidi Giordano, James D. Brenton, Thomas C. Harding, Iain A. McNeish and Elizabeth M. Swisher
    Cancer Discov February 1 2019 9 (2) 210-219; DOI:10.1158/2159-8290.CD-18-0715

    Analysis of cfDNA from 112 patients with high-grade ovarian carcinoma showed that BRCA reversion mutations may be associated with reduced clinical benefit from the PARP inhibitor rucaparib.

  • Research Briefs | AuthorChoice
    PPT1 Promotes Tumor Growth and Is the Molecular Target of Chloroquine Derivatives in Cancer
    Vito W. Rebecca, Michael C. Nicastri, Colin Fennelly, Cynthia I. Chude, Julie S. Barber-Rotenberg, Amruta Ronghe, Quentin McAfee, Noel P. McLaughlin, Gao Zhang, Aaron R. Goldman, Rani Ojha, Shengfu Piao, Estela Noguera-Ortega, Alessandra Martorella, Gretchen M. Alicea, Jennifer J. Lee, Lynn M. Schuchter, Xiaowei Xu, Meenhard Herlyn, Ronen Marmorstein, Phyllis A. Gimotty, David W. Speicher, Jeffrey D. Winkler and Ravi K. Amaravadi
    Cancer Discov February 1 2019 9 (2) 220-229; DOI:10.1158/2159-8290.CD-18-0706

    Chloroquine derivatives exert their antiautophagic and antitumor effects by binding palmitoyl-protein thioesterase 1 (PPT1) and inhibiting its enzymatic activity.

Research Articles

  • Research Articles
    Cells Lacking the RB1 Tumor Suppressor Gene Are Hyperdependent on Aurora B Kinase for Survival
    Matthew G. Oser, Raquel Fonseca, Abhishek A. Chakraborty, Rachel Brough, Alexander Spektor, Rebecca B. Jennings, Abdallah Flaifel, Jesse S. Novak, Aditi Gulati, Elizabeth Buss, Scott T. Younger, Samuel K. McBrayer, Glenn S. Cowley, Dennis M. Bonal, Quang-De Nguyen, Laura Brulle-Soumare, Paula Taylor, Stefano Cairo, Colm J. Ryan, Elizabeth J. Pease, Kim Maratea, Jon Travers, David E. Root, Sabina Signoretti, David Pellman, Susan Ashton, Christopher J. Lord, Simon T. Barry and William G. Kaelin Jr
    Cancer Discov February 1 2019 9 (2) 230-247; DOI:10.1158/2159-8290.CD-18-0389

    A CRISPR/Cas9 screen identifi es a synthetic lethal relationship between RB1 and AURKB loss in SCLC cells.

  • Research Articles | AuthorChoice
    Aurora A Kinase Inhibition Is Synthetic Lethal with Loss of the RB1 Tumor Suppressor Gene
    Xueqian Gong, Jian Du, Stephen H. Parsons, Farhana F. Merzoug, Yue Webster, Philip W. Iversen, Li-Chun Chio, Robert D. Van Horn, Xi Lin, Wayne Blosser, Bomie Han, Shaoling Jin, Sufang Yao, Huimin Bian, Chris Ficklin, Li Fan, Avnish Kapoor, Stephen Antonysamy, Ann M. Mc Nulty, Karen Froning, Danalyn Manglicmot, Anna Pustilnik, Kenneth Weichert, Stephen R. Wasserman, Michele Dowless, Carlos Marugán, Carmen Baquero, María José Lallena, Scott W. Eastman, Yu-Hua Hui, Matthew Z. Dieter, Thompson Doman, Shaoyou Chu, Hui-Rong Qian, Xiang S. Ye, David A. Barda, Gregory D. Plowman, Christoph Reinhard, Robert M. Campbell, James R. Henry and Sean G. Buchanan
    Cancer Discov February 1 2019 9 (2) 248-263; DOI:10.1158/2159-8290.CD-18-0469

    A screen of cell-cycle inhibitors reveals that RB1-mutant cancer cells are selectively dependent on Aurora kinase A.

  • Research Articles
    EIF1AX and RAS Mutations Cooperate to Drive Thyroid Tumorigenesis through ATF4 and c-MYC
    Gnana P. Krishnamoorthy, Natalie R. Davidson, Steven D. Leach, Zhen Zhao, Scott W. Lowe, Gina Lee, Iňigo Landa, James Nagarajah, Mahesh Saqcena, Kamini Singh, Hans-Guido Wendel, Snjezana Dogan, Prasanna P. Tamarapu, John Blenis, Ronald A. Ghossein, Jeffrey A. Knauf, Gunnar Rätsch and James A. Fagin
    Cancer Discov February 1 2019 9 (2) 264-281; DOI:10.1158/2159-8290.CD-18-0606

    The EIF1AX-A113spl mutation results in an alternatively spliced transcript that cooperates with RAS mutations to stabilize MYC, activate mTOR, and promote tumorigenesis.

  • Research Articles | AuthorChoice
    IL1-Induced JAK/STAT Signaling Is Antagonized by TGFβ to Shape CAF Heterogeneity in Pancreatic Ductal Adenocarcinoma
    Giulia Biffi, Tobiloba E. Oni, Benjamin Spielman, Yuan Hao, Ela Elyada, Youngkyu Park, Jonathan Preall and David A. Tuveson
    Cancer Discov February 1 2019 9 (2) 282-301; DOI:10.1158/2159-8290.CD-18-0710

    TGFβ antagonizes IL1-driven JAK/STAT activation, which induces an inflammatory pancreatic ductal adenocarcinoma cancer-associated fi broblast (CAF) phenotype, to promote CAF heterogeneity.

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