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Cancer Research
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Table of Contents

Breaking Advances

  • Breaking Advances
    Highlights from Recent Cancer Literature
    Cancer Res January 15 2012 72 (2) 377-378;

Reviews

  • Reviews
    JNK-Induced Apoptosis, Compensatory Growth, and Cancer Stem Cells
    Fei Chen
    Cancer Res January 15 2012 72 (2) 379-386; DOI:10.1158/0008-5472.CAN-11-1982

  • Reviews
    Metastasis-Associated Protein 1/Nucleosome Remodeling and Histone Deacetylase Complex in Cancer
    Da-Qiang Li, Suresh B. Pakala, Sujit S. Nair, Jeyanthy Eswaran and Rakesh Kumar
    Cancer Res January 15 2012 72 (2) 387-394; DOI:10.1158/0008-5472.CAN-11-2345

Priority Reports

  • Priority Reports
    Stress-Regulated Transcription Factor ATF4 Promotes Neoplastic Transformation by Suppressing Expression of the INK4a/ARF Cell Senescence Factors
    Michiko Horiguchi, Satoru Koyanagi, Akinori Okamoto, Satoshi O. Suzuki, Naoya Matsunaga and Shigehiro Ohdo
    Cancer Res January 15 2012 72 (2) 395-401; DOI:10.1158/0008-5472.CAN-11-1891

    A gene overexpressed in many cancers that promotes cell survival in stressed tumor microenvironments is found to also exert a major role in suppressing a central pathway of cellular senescence.

  • Priority Reports
    Increased Survival of Glioblastoma Patients Who Respond to Antiangiogenic Therapy with Elevated Blood Perfusion
    A. Gregory Sorensen, Kyrre E. Emblem, Pavlina Polaskova, Dominique Jennings, Heisoog Kim, Marek Ancukiewicz, Meiyun Wang, Patrick Y. Wen, Percy Ivy, Tracy T. Batchelor and Rakesh K. Jain
    Cancer Res January 15 2012 72 (2) 402-407; DOI:10.1158/0008-5472.CAN-11-2464

    This seminal study provides direct clinical evidence that the survival of a cancer patient is prolonged by antiangiogenic therapy if the therapy achieves increased tumor blood perfusion, in support of the vascular normalization hypothesis for cancer treatment.

Clinical Studies

  • Clinical Studies
    Genetic Variants in Oxidative Stress–Related Genes Predict Chemoresistance in Primary Breast Cancer: A Prospective Observational Study and Validation
    Ke-Da Yu, A-Ji Huang, Lei Fan, Wen-Feng Li and Zhi-Ming Shao
    Cancer Res January 15 2012 72 (2) 408-419; DOI:10.1158/0008-5472.CAN-11-2998

    This study offers compelling evidence that genetic polymorphisms in oxidative stress–related genes in the host affect chemosensitivity, such that host gene status must be considered to optimize personalized chemotherapy beyond variations in simply the tumor cells themselves.

Microenvironment and Immunology

  • Microenvironment and Immunology
    Interleukin-10 Ablation Promotes Tumor Development, Growth, and Metastasis
    Takashi Tanikawa, Cailin Moira Wilke, Ilona Kryczek, Grace Y. Chen, John Kao, Gabriel Núñez and Weiping Zou
    Cancer Res January 15 2012 72 (2) 420-429; DOI:10.1158/0008-5472.CAN-10-4627

    This study of cancer susceptibility and progression in mice lacking IL-10 challenges the generally held view that this immune inhibitory cytokine supports cancer, instead offering powerful evidence that endogenous IL-10 actually suppresses cancer by impeding the development of 2 key cellular mechanisms of immune escape.

  • Microenvironment and Immunology
    Potent Induction of Tumor Immunity by Combining Tumor Cryoablation with Anti–CTLA-4 Therapy
    Rebecca Waitz, Stephen B. Solomon, Elena N. Petre, Anne E. Trumble, Marcella Fassò, Larry Norton and James P. Allison
    Cancer Res January 15 2012 72 (2) 430-439; DOI:10.1158/0008-5472.CAN-11-1782

    One use of the recently approved immune activating drug ipilumimab may be to enhance the benefits of tumor cryoablation, a simple older treatment strategy being explored anew in breast and prostate cancers, where it might be very effectively combined with immunotherapy to enhance cure rates in patients with localized tumors.

  • Microenvironment and Immunology
    Platelet-Derived MHC Class I Confers a Pseudonormal Phenotype to Cancer Cells That Subverts the Antitumor Reactivity of Natural Killer Immune Cells
    Theresa Placke, Melanie Örgel, Martin Schaller, Gundram Jung, Hans-Georg Rammensee, Hans-Georg Kopp and Helmut Rainer Salih
    Cancer Res January 15 2012 72 (2) 440-448; DOI:10.1158/0008-5472.CAN-11-1872

    This important paper elucidates a fascinating mechanism of immune escape from NK cells in which platelets function to shield cancer cells and promote their metastatic spread.

  • Microenvironment and Immunology
    Chromogranin A Regulates Tumor Self-Seeding and Dissemination
    Eleonora Dondossola, Luca Crippa, Barbara Colombo, Elisabetta Ferrero and Angelo Corti
    Cancer Res January 15 2012 72 (2) 449-459; DOI:10.1158/0008-5472.CAN-11-2944

    Findings define a role for a circulating regulator of multidirectional trafficking of tumor cells between tumors, blood, and normal tissues, with general implications for metastasis formation and tumor progression.

  • Microenvironment and Immunology
    Tumor Suppressive MicroRNAs miR-34a/c Control Cancer Cell Expression of ULBP2, a Stress-Induced Ligand of the Natural Killer Cell Receptor NKG2D
    Anja Heinemann, Fang Zhao, Sonali Pechlivanis, Jürgen Eberle, Alexander Steinle, Sven Diederichs, Dirk Schadendorf and Annette Paschen
    Cancer Res January 15 2012 72 (2) 460-471; DOI:10.1158/0008-5472.CAN-11-1977

    The perspective that tumor suppressor functions often manifest as immune responses against tumor cells is quickly widening with broader investigations in more valid immunocompetent models of cancer.

Molecular and Cellular Pathobiology

  • Molecular and Cellular Pathobiology
    Role of JNK in Mammary Gland Development and Breast Cancer
    Cristina Cellurale, Nomeda Girnius, Feng Jiang, Julie Cavanagh-Kyros, Shaolei Lu, David S. Garlick, Arthur M. Mercurio and Roger J. Davis
    Cancer Res January 15 2012 72 (2) 472-481; DOI:10.1158/0008-5472.CAN-11-1628

    This study offers in vivo evidence that the JNK stress kinases have a tumor suppressor function in the setting of mammary carcinogenesis, a role that likely extends to many other settings of epithelial carcinogenesis.

  • Molecular and Cellular Pathobiology
    Arsenic Trioxide Treatment Decreases the Oxygen Consumption Rate of Tumor Cells and Radiosensitizes Solid Tumors
    Caroline Diepart, Oussama Karroum, Julie Magat, Olivier Feron, Julien Verrax, Pedro Buc Calderon, Vincent Grégoire, Philippe Leveque, Julie Stockis, Nicolas Dauguet, Bénédicte F. Jordan and Bernard Gallez
    Cancer Res January 15 2012 72 (2) 482-490; DOI:10.1158/0008-5472.CAN-11-1755

    This study offers a sound preclinical rationale for immediate clinical repositioning of arsenic trioxide, an approved treatment for acute promyelocytic leukemias, as a radiosensitizer for any solid tumor.

  • Molecular and Cellular Pathobiology
    Functional Interaction between Responses to Lactic Acidosis and Hypoxia Regulates Genomic Transcriptional Outputs
    Xiaohu Tang, Joseph E. Lucas, Julia Ling-Yu Chen, Gregory LaMonte, Jianli Wu, Michael Changsheng Wang, Constantinos Koumenis and Jen-Tsan Chi
    Cancer Res January 15 2012 72 (2) 491-502; DOI:10.1158/0008-5472.CAN-11-2076

    This provocative study suggests that lactic acidosis occuring in the microenvironment of many solid tumors can abolish canonical responses to hypoxia, suggesting that many models used for development of cancer-selective therapeutics against tumor hypoxia may be deeply flawed.

Prevention and Epidemiology

  • Prevention and Epidemiology
    Circulating Insulin-Like Growth Factors and IGF-Binding Proteins in PSA-Detected Prostate Cancer: The Large Case–Control Study ProtecT
    Mari-Anne Rowlands, Jeff M.P. Holly, David Gunnell, Jenny Donovan, J. Athene Lane, Freddie Hamdy, David E. Neal, Steven Oliver, George Davey Smith and Richard M. Martin
    Cancer Res January 15 2012 72 (2) 503-515; DOI:10.1158/0008-5472.CAN-11-1601

    This large UK-based case–control study suggests potentially important associations of circulating IGF-II, IGFBP-2, and IGFBP-3 in prostate cancers that are detected by the PSA test.

Therapeutics, Targets, and Chemical Biology

  • Therapeutics, Targets, and Chemical Biology
    Regulation of Matrix Metalloproteinase Genes by E2F Transcription Factors: Rb–Raf-1 Interaction as a Novel Target for Metastatic Disease
    Jackie L. Johnson, Smitha Pillai, Danielle Pernazza, Saïd M. Sebti, Nicholas J. Lawrence and Srikumar P. Chellappan
    Cancer Res January 15 2012 72 (2) 516-526; DOI:10.1158/0008-5472.CAN-11-2647

    Matrix metalloproteases regulated by the Rb-E2F pathway may serve as its major connection to invasion and metastasis control, with implications for therapeutic intervention such as through targeting the Rb-Raf-1 interaction as illustrated in this study.

  • Therapeutics, Targets, and Chemical Biology | Free Article
    Androgen Deprivation Causes Epithelial–Mesenchymal Transition in the Prostate: Implications for Androgen-Deprivation Therapy
    Yuting Sun, Bu-Er Wang, Kevin G. Leong, Peng Yue, Li Li, Suchit Jhunjhunwala, Darrell Chen, Kyounghee Seo, Zora Modrusan, Wei-Qiang Gao, Jeffrey Settleman and Leisa Johnson
    Cancer Res January 15 2012 72 (2) 527-536; DOI:10.1158/0008-5472.CAN-11-3004

    Findings argue that androgen-deprivation therapy, used widely in prostate cancer treatment, can trigger epithelial-mesenchymal transition, a foreboding event that may detract from the response to other treatments.

Tumor and Stem Cell Biology

  • Tumor and Stem Cell Biology
    Hyaluronan Synthase HAS2 Promotes Tumor Progression in Bone by Stimulating the Interaction of Breast Cancer Stem–Like Cells with Macrophages and Stromal Cells
    Hiroshi Okuda, Aya Kobayashi, Bo Xia, Misako Watabe, Sudha K. Pai, Shigeru Hirota, Fei Xing, Wen Liu, Puspa R. Pandey, Koji Fukuda, Vishnu Modur, Arnab Ghosh, Andrew Wilber and Kounosuke Watabe
    Cancer Res January 15 2012 72 (2) 537-547; DOI:10.1158/0008-5472.CAN-11-1678

    Findings define a mechanism used by cancer stem cells to produce an extracellular matrix glycosaminoglycan that may help seed a metastatic niche in foreign organ microenvironments, with major implications for antimetastatic therapy.

  • Tumor and Stem Cell Biology
    Metastatic Progression with Resistance to Aromatase Inhibitors Is Driven by the Steroid Receptor Coactivator SRC-1
    Jean McBryan, Sarah M. Theissen, Christopher Byrne, Eamon Hughes, Sinead Cocchiglia, Stephen Sande, Jane O'Hara, Paul Tibbitts, Arnold D.K. Hill and Leonie S. Young
    Cancer Res January 15 2012 72 (2) 548-559; DOI:10.1158/0008-5472.CAN-11-2073

    This study reveals insights into the mechanism by which clinical resistance and metastatic progression occur with aromatase inhibitors, a first-line treatment for endocrine-sensitive breast cancers.

  • Tumor and Stem Cell Biology
    p53 Negatively Regulates Transcription of the Pyruvate Dehydrogenase Kinase Pdk2
    Tanupriya Contractor and Chris R. Harris
    Cancer Res January 15 2012 72 (2) 560-567; DOI:10.1158/0008-5472.CAN-11-1215

    This study reveals how p53 controls the Warburg effect, a universal property of cancer cells in which glycolysis is driven powerfully despite aerobic conditions that should otherwise favor oxidative phosphorylation.

Correction

  • Correction
    Correction: CD8+ T Cells Regulate Bone Tumor Burden Independent of Osteoclast Resorption
    Cancer Res January 15 2012 72 (2) 568-568; DOI:10.1158/0008-5472.CAN-11-3840

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Cancer Research: 72 (2)
January 2012
Volume 72, Issue 2
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Issue Highlights

  • Androgen Deprivation Causes Epithelial–Mesenchymal Transition in the Prostate: Implications for Androgen-Deprivation Therapy
  • Arsenic Trioxide Treatment Decreases the Oxygen Consumption Rate of Tumor Cells and Radiosensitizes Solid Tumors
  • Potent Induction of Tumor Immunity by Combining Tumor Cryoablation with Anti–CTLA-4 Therapy

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  • Tumor and Stem Cell Biology
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  • Metabolomic Gradients in Glioblastoma Models
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Cancer Research Online ISSN: 1538-7445
Cancer Research Print ISSN: 0008-5472
Journal of Cancer Research ISSN: 0099-7013
American Journal of Cancer ISSN: 0099-7374

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