Δευτέρα, 14 Ιανουαρίου 2019

Cancer Cell

  1. Previews

    1. Hijacking EMT: Better Fat Than Dead

      Pages 1-2
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      Potential for cancers to form metastases requires cell dissemination utilizing epithelial-to-mesenchymal transition (EMT) program. In this issue of Cancer Cell, Ishay-Ronen et al. show that plasticity intrinsic to the EMT program can be exploited to divert cancer cells into becoming post-mitotic adipocytes, thus preventing formation of metastases.

    2. Tumor Extracellular Vesicles Impede Interferon Alert Responses

      Pages 3-5
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      Tumor-derived extracellular vesicles promote metastasis by inducing functional changes in cells at pre-metastatic sites conducive for tumor cell colonization. In this issue of Cancer Cell, Ortiz and colleagues show that type I interferon regulates extracellular vesicle uptake and that modulating this pathway holds promise for treating metastasis.

    3. The Deadly Bite of STAT3

      Pages 5-7
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      The Tasmanian devils' facial tumor disease (DFTD) is a transmissible cancer that spreads by biting and threatens extinction of this marsupial. In this issue of Cancer Cell, Kosack et al. describe how overexpression of ERBB and uncontrolled activation of STAT3 drive DFTD growth and immune evasion.

    4. Tails of a Super Histone

      Pages 7-9
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      Diffuse intrinsic brain stem gliomas (DIPGs) with characteristic K27M mutation of H3.3 are lethal and poorly understood childhood cancers. In this issue of Cancer Cell, Larson et al. exploit a unique murine DIPG model with inducible, endogenous K27M expression to reveal insights into mechanisms of K27M-mediated transformation in DIPG.

  2. Perspective

    1. The Roles of Initiating Truncal Mutations in Human Cancers: The Order of Mutations and Tumor Cell Type Matters

      Pages 10-15
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      We propose that initiating truncal mutations plays a special role in tumor formation by both enhancing the survival of the initiating cancer cell and by selecting for secondary mutations that contribute to tumor progression, and that these mutations often act in a tissue-preferred fashion. Here, we explain why inherited mutations often have different tissue specificities compared with spontaneous mutations in the same gene. Initiating truncal mutations make excellent neo-antigens for immunotherapy, and understanding why one mutation selects for a second mutation in a particular tissue type could one day aid in the design of gene-targeted combination therapies.

  3. Articles

    1. Gain Fat—Lose Metastasis: Converting Invasive Breast Cancer Cells into Adipocytes Inhibits Cancer Metastasis

      Pages 17-32.e6
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    2. An Interferon-Driven Oxysterol-Based Defense against Tumor-Derived Extracellular Vesicles

      Pages 33-45.e6
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    3. p62/SQSTM1 Fuels Melanoma Progression by Opposing mRNA Decay of a Selective Set of Pro-metastatic Factors

      Pages 46-63.e10
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    4. Tinagl1 Suppresses Triple-Negative Breast Cancer Progression and Metastasis by Simultaneously Inhibiting Integrin/FAK and EGFR Signaling

      Pages 64-80.e7
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    5. Hyper-Editing of Cell-Cycle Regulatory and Tumor Suppressor RNA Promotes Malignant Progenitor Propagation

      Pages 81-94.e7
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    6. Comprehensive Analysis of Chromatin States in Atypical Teratoid/Rhabdoid Tumor Identifies Diverging Roles for SWI/SNF and Polycomb in Gene Regulation

      Pages 95-110.e8
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      Summary

      Biallelic inactivation of SMARCB1, encoding a member of the SWI/SNF chromatin remodeling complex, is the hallmark genetic aberration of atypical teratoid rhabdoid tumors (ATRT). Here, we report how loss of SMARCB1 affects the epigenome in these tumors. Using chromatin immunoprecipitation sequencing (ChIP-seq) on primary tumors for a series of active and repressive histone marks, we identified the chromatin states differentially represented in ATRTs compared with other brain tumors and non-neoplastic brain. Re-expression of SMARCB1 in ATRT cell lines enabled confirmation of our genome-wide findings for the chromatin states. Additional generation of ChIP-seq data for SWI/SNF and Polycomb group proteins and the transcriptional repressor protein REST determined differential dependencies of SWI/SNF and Polycomb complexes in regulation of diverse gene sets in ATRTs.

    7. Proteogenomic Characterization of Human Early-Onset Gastric Cancer

      Pages 111-124.e10
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    8. The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease

      Pages 125-139.e9
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    9. Histone H3.3 K27M Accelerates Spontaneous Brainstem Glioma and Drives Restricted Changes in Bivalent Gene Expression

      Pages 140-155.e7
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  4. Correction

    1. CARM1 Is Essential for Myeloid Leukemogenesis but Dispensable for Normal Hematopoiesis

      Page 156
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