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Wando Mount Pleasant Library
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Village Library
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St. Paul's/Hollywood Library
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Signal transducer and activator of transcription proteins: regulators of myeloid-derived suppressor cell-mediated immunosuppression in cancer.
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- Author(s): Ko, Hyun-Jeong; Kim, Yeon-Jeong
- Source:
Archives of Pharmacal Research; Nov2016, Vol. 39 Issue 11, p1597-1608, 12p - Source:
- Additional Information
- Abstract: The success of cancer immunotherapy in patients depends on overcoming immunosuppressive mechanisms in addition to stimulating effective anticancer immune responses. Myeloid-derived suppressor cells (MDSCs) inhibit a spectrum of immune responses, including adaptive immune responses and innate immune responses at the tumor site. MDSCs have been targeted to overcome immunosuppression either by reducing their numbers or downregulating their immunosuppressive activities. Although signal transducer and activator of transcription (STAT) proteins are recognized as signaling and transcription factors induced by cytokines in normal cells, they also have roles in cancer and cancer-related cells, as well as MDSC differentiation and function. In in vitro and in vivo studies, including studies on humans, selective STAT3 inhibitors such as Stattic and S3I-201 have demonstrated potential in regulating MDSC-mediated immunosuppression. Thus, STAT pathways represent a promising target in cancer immunotherapy. Herein, we review the roles of STAT signaling in MDSC biology, and the clinical potential of STAT inhibitors in regulating tumor-associated immunosuppression mediated by MDSCs. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Archives of Pharmacal Research is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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