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Neumann et al. J Cancer Metastasis Treat 2018;4:13                  Journal of Cancer
               DOI: 10.20517/2394-4722.2017.60                           Metastasis and Treatment




               Commentary                                                                    Open Access


               Targeting adenosine receptor 2B in triple negative
               breast cancer

               Carola A. Neumann , Kevin Levine , Steffi Oesterreich 1,2
                                1,2
                                             1,2
               1 Department of Pharmacology & Chemical Biology, University of Pittsburgh Medical Center Hillman Cancer Center, Womens Cancer
               Research
               Center, Magee Womens Research Institute, Pittsburgh, PA 15213, USA.
               2 Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15261, USA.

               Correspondence to: Dr. Carola A. Neumann, Department of Pharmacology & Chemical Biology, University of Pittsburgh Medical
               Center Hillman Cancer Center, Womens Cancer Research Center, Magee Womens Research Institute, 204 Craft Ave, Pittsburgh, PA
               15213, USA. E-mail: neumannc@upmc.edu
               How to cite this article: Neumann CA, Levine K, Oesterreich S. Targeting adenosine receptor 2B in triple negative breast cancer. J
               Cancer Metastasis Treat 2018;4:13. http://dx.doi.org/10.20517/2394-4722.2017.60

               Received: 26 Oct 2017    First Decision: 29 Dec 2017    Revised: 8 Mar 2018    Accepted: 8 Mar 2018    Published: 15 Mar 2018

               Science Editor: William P. Schiemann    Copy Editor: Jun-Yao Li    Production Editor: Huan-Liang Wu


               In the review “Role of adenosine in tumor progression: focus on A2B receptor as potential therapeutic
               target”, Sorrentino and Morello make a compelling case for considering adenosine 2B receptor (A2BR) as a
               target in cancer therapy (J Cancer Metastasis Treat 2017;3:127-38). A large body of evidence has accumulated
               suggesting A2BR to play an active role in tumor immune suppression and metastasis. Thus, this commentary
               will discuss the intriguing possibility of targeting A2BR in specific breast cancers that express high levels of
               A2BR and attract infiltrating immune cells.


               TRIPLE NEGATIVE BREAST CANCER IS SUSCEPTIVE TO IMMUNE MODULATION
               Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer that disproportionally affects
                                                                              [1,2]
               younger women and those of African origins, compared with Caucasians . TNBC is devoid of the three
               receptors that classify and define most mammary cancers: estrogen receptor (ER), progesterone receptor (PR)
                                                               [3]
               and human epidermal growth factor receptor 2 (HER2) . The lack of these receptors reduces the efficacy
               of targeted therapies for this cancer type, limiting treatment options to chemotherapeutic agents, ionizing
               radiation and surgery. TNBC patients are therefore in dire need for novel targeted therapies.

               Breast cancer has long been thought of as a non-immunogenic malignancy. However, a growing body of
               evidence suggests that this is not the case for all breast cancers. Tumor-infiltrating lymphocytes (TILs) are
               the most widely studied immune cells and include T cells and B cells. TILs are part of a larger category of
               infiltrating immune cells that include natural killer (NK) cells, macrophages, neutrophils, dendritic cells,

                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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