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The crosstalk between autophagy and myeloid-derived suppressor cell responses in cancer
Nie, Jia; Wang, Di; Li, MingJian.
Affiliation
  • Nie, Jia; Chengdu University of Traditional Chinese Medicine. School of Ethnic Medicine. Chengdu. China
  • Wang, Di; Chengdu University of Traditional Chinese Medicine. School of Pharmacy. Chengdu. China
  • Li, MingJian; Chengdu University of Traditional Chinese Medicine. College of Medical Technology. Chengdu. China
Clin. transl. oncol. (Print) ; 25(10): 2832-2840, oct. 2023. ilus
Article in En | IBECS | ID: ibc-225063
Responsible library: ES1.1
Localization: ES15.1 - BNCS
ABSTRACT
The development of cancers is aided by the accumulation of myeloid-derived suppressor cells (MDSCs) within tumors, which are highly effective at suppressing anti-tumor immune responses. Direct cell-to-cell interaction and the production of immunosuppressive mediators have both been proposed as pathways for MDSC-mediated suppression of anti-tumor immune responses. The majority of current cancer treatments focus on altering the development and activity of MDSCs so that they have more of an immunogenic character. Autophagy is a catabolic system that contributes to the breakdown of damaged intracellular material and the recycling of metabolites. However, depending on the stage of tumor growth, autophagy can play both a prophylactic and a therapeutic function in carcinogenesis. However, several indirect lines of research have indicated that autophagy is a significant regulator of MDSC activity. The purpose of this work was to outline the interactions between MDSC and autophagy in cancer (AU)
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Collection: 06-national / ES Database: IBECS Main subject: Autophagy / Myeloid-Derived Suppressor Cells / Neoplasms Limits: Humans Language: En Journal: Clin. transl. oncol. (Print) Year: 2023 Document type: Article
Search on Google
Collection: 06-national / ES Database: IBECS Main subject: Autophagy / Myeloid-Derived Suppressor Cells / Neoplasms Limits: Humans Language: En Journal: Clin. transl. oncol. (Print) Year: 2023 Document type: Article