Recently the role of the microenvironment has become a target of intense study both to understand the evolution of malignancy as well as discover potential therapeutic strategies to it. While highly heterogeneous, the innate immune cells of the microenvironment are driving most of the initial suppression of anti-tumor responses and hence targeting them has become a priority. In particular the role of myeloid-derived suppressor cells, and the main receptor for immature myeloid cells CD33, have become the focus of the newest therapeutic development. In particular, targeting of the suppressive microenvironment has the potential to either prevent the evolution of malignancy by restarting anti-tumor immunity or facilitate/enhance the work of immunotherapeutic strategies that are hindered by the immunosuppressive microenvironment.
Therefore, a better understanding of the innate suppressive microenvironment will be critical to the development of MDSC-targeting or anti-immunosuppressive therapeutics that can restore anti-tumor immunity. Therefore, the aim of this special Research Topic will be to focus on recent advances on the understanding of the suppressive microenvironment with a focus on MDSC, suppressive signaling pathways and their potential to affect anti-tumor immunity. It will also extend this area into development and/or mechanistic understanding of novel therapeutic development aimed at immune-suppression as new potential stand-alone or combinatorial treatments with standard of care.
Potential areas to cover are (not exclusive):
• Identification of targetable pathways that drive or are driven by MDSC (e.g. JAK/STAT3, PERK/IRE1).
• Combinatorial therapeutic strategies targeting MDSC (e.g. 5-fluorouracil, gemcitabine) to overcome non-response to standard of care therapy.
• Mechanistic studies on MDSC targeted therapeutic strategies.
• Off-target effects of MDSC-targeted therapeutics in cancer.
• Interaction between MDSC and other immune cells (e.g. macrophages, dendritic cells) in the microenvironment.
Note: Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
Recently the role of the microenvironment has become a target of intense study both to understand the evolution of malignancy as well as discover potential therapeutic strategies to it. While highly heterogeneous, the innate immune cells of the microenvironment are driving most of the initial suppression of anti-tumor responses and hence targeting them has become a priority. In particular the role of myeloid-derived suppressor cells, and the main receptor for immature myeloid cells CD33, have become the focus of the newest therapeutic development. In particular, targeting of the suppressive microenvironment has the potential to either prevent the evolution of malignancy by restarting anti-tumor immunity or facilitate/enhance the work of immunotherapeutic strategies that are hindered by the immunosuppressive microenvironment.
Therefore, a better understanding of the innate suppressive microenvironment will be critical to the development of MDSC-targeting or anti-immunosuppressive therapeutics that can restore anti-tumor immunity. Therefore, the aim of this special Research Topic will be to focus on recent advances on the understanding of the suppressive microenvironment with a focus on MDSC, suppressive signaling pathways and their potential to affect anti-tumor immunity. It will also extend this area into development and/or mechanistic understanding of novel therapeutic development aimed at immune-suppression as new potential stand-alone or combinatorial treatments with standard of care.
Potential areas to cover are (not exclusive):
• Identification of targetable pathways that drive or are driven by MDSC (e.g. JAK/STAT3, PERK/IRE1).
• Combinatorial therapeutic strategies targeting MDSC (e.g. 5-fluorouracil, gemcitabine) to overcome non-response to standard of care therapy.
• Mechanistic studies on MDSC targeted therapeutic strategies.
• Off-target effects of MDSC-targeted therapeutics in cancer.
• Interaction between MDSC and other immune cells (e.g. macrophages, dendritic cells) in the microenvironment.
Note: Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
