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- W3201715601 abstract "Breast cancer is one of the top-ranked cancers for incidence and mortality worldwide. The biggest challenges in breast cancer treatment are metastasis and drug resistance, for which work on molecular evaluation, mechanism studies, and screening of therapeutic targets is ongoing. Factors that lead to inflammatory infiltration and immune system suppression in the tumor microenvironment are potential therapeutic targets. Interleukin-1 is known as a proinflammatory and immunostimulatory cytokine, which plays important roles in inflammatory diseases. Recent studies have shown that interleukin-1 cytokines drive the formation and maintenance of an inflammatory/immunosuppressive microenvironment through complex intercellular signal crosstalk and tight intracellular signal transduction, which were found to be potentially involved in the mechanism of metastasis and drug resistance of breast cancer. Some preclinical and clinical treatments or interventions to block the interleukin-1/interleukin-1 receptor system and its up- and downstream signaling cascades have also been proven effective. This study provides an overview of IL-1-mediated signal communication in breast cancer and discusses the potential of IL-1 as a therapeutic target especially for metastatic breast cancer and combination therapy and current problems, aiming at enlightening new ideas in the study of inflammatory cytokines and immune networks in the tumor microenvironment." @default.
- W3201715601 created "2021-10-11" @default.
- W3201715601 creator A5037908114 @default.
- W3201715601 creator A5037959245 @default.
- W3201715601 creator A5047264496 @default.
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- W3201715601 creator A5062977227 @default.
- W3201715601 creator A5067485668 @default.
- W3201715601 creator A5086241180 @default.
- W3201715601 creator A5089882787 @default.
- W3201715601 date "2021-09-23" @default.
- W3201715601 modified "2023-10-16" @default.
- W3201715601 title "Key Factor Regulating Inflammatory Microenvironment, Metastasis, and Resistance in Breast Cancer: Interleukin-1 Signaling" @default.
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