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    Cyclooxygenase-dependent tumor growth through evasion of immunity.

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    Authors
    Zelenay, Santiago
    van der Veen, A
    Böttcher, J
    Snelgrove, K
    Rogers, N
    Acton, S
    Chakravarty, P
    Girotti, Maria Romina
    Marais, Richard
    Quezada, S
    Sahai, E
    Reis E Sousa, C
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    Affiliation
    Immunobiology Laboratory, The Francis Crick Institute, Lincoln's Inn Fields Laboratory, 44 Lincoln's Inn Fields, London WC2A 3LY, UK
    Issue Date
    2015-09-10
    
    Metadata
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    Abstract
    The mechanisms by which melanoma and other cancer cells evade anti-tumor immunity remain incompletely understood. Here, we show that the growth of tumors formed by mutant Braf(V600E) mouse melanoma cells in an immunocompetent host requires their production of prostaglandin E2, which suppresses immunity and fuels tumor-promoting inflammation. Genetic ablation of cyclooxygenases (COX) or prostaglandin E synthases in Braf(V600E) mouse melanoma cells, as well as in Nras(G12D) melanoma or in breast or colorectal cancer cells, renders them susceptible to immune control and provokes a shift in the tumor inflammatory profile toward classic anti-cancer immune pathways. This mouse COX-dependent inflammatory signature is remarkably conserved in human cutaneous melanoma biopsies, arguing for COX activity as a driver of immune suppression across species. Pre-clinical data demonstrate that inhibition of COX synergizes with anti-PD-1 blockade in inducing eradication of tumors, implying that COX inhibitors could be useful adjuvants for immune-based therapies in cancer patients.
    Citation
    Cyclooxygenase-dependent tumor growth through evasion of immunity. 2015, 162 (6):1257-70 Cell
    Journal
    Cell
    URI
    http://hdl.handle.net/10541/581091
    DOI
    10.1016/j.cell.2015.08.015
    PubMed ID
    26343581
    Type
    Article
    Language
    en
    ISSN
    1097-4172
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.cell.2015.08.015
    Scopus Count
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    All Paterson Institute for Cancer Research

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