About this Research Topic
Cancer immunotherapy has revolutionized cancer treatment by leveraging the immune system to target tumor cells. N6-methyladenosine (m6A) methylation, a prevalent mRNA modification, plays a crucial role in gene expression regulation and cancer immunity modulation. The tumor microenvironment (TME) significantly influences the success of these therapies, featuring a complex interaction of immune cells, stromal components, and signaling molecules that can either enhance or inhibit anti-tumor immunity.
A major challenge is the TME's promotion of immunosuppressive conditions, where myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs) dampen the immune response. These cells, along with immunosuppressive cytokines like TGF-β and IL-10, create barriers to effective T-cell infiltration and function. m6A methylation affects the differentiation and function of these immunosuppressive cells, impacting the immune landscape within tumors.
Recent advancements highlight the potential of targeting m6A regulatory proteins to improve immune cell activity. Inhibiting m6A demethylases or modulating m6A methyltransferases can change the expression of key immunoregulatory genes, potentially overcoming TME's immunosuppressive barriers. Identifying specific m6A-modified transcripts and associated proteins has also enabled the stratification of patients more likely to respond to immune checkpoint inhibitors.
The goal of this Research Topic is to advance our understanding of m6A methylation's role in modulating cancer immunity. We aim to identify and explore innovative strategies to target m6A regulatory pathways to overcome immunosuppressive barriers within the TME, thereby enhancing T-cell access and function. By fostering a comprehensive discussion on the manipulation of m6A methylation, we seek to accelerate the development of novel therapeutic approaches that can significantly improve patient outcomes across various cancer types.
We encourage the submission of manuscripts that explore, but are not limited to, the following areas:
1. Analysis of how m6A methylation influences the immunosuppressive nature of the tumor microenvironment (TME) at cellular and molecular levels.
2. Examination of how m6A methylation in stromal cells affects immune cell behavior and potential targeting strategies.
3. Studies on the role of m6A methylation in the efficacy and optimization of immune checkpoint inhibitors within the TME.
4. Approaches to enhance T-cell infiltration, survival, and anti-tumor activity by targeting m6A pathways.
5. Exploration of synergistic effects when combining m6A-targeted therapies with other treatments such as chemotherapy, radiation, or immunotherapy.
6. Identification and validation of m6A-related biomarkers for patient stratification and treatment response prediction.
7. Research on emerging immunotherapeutic agents, such as bispecific antibodies or CAR T-cells, and their interaction with m6A-modified targets.
8. Presentation of clinical trial outcomes focusing on m6A-targeted therapies and their impact on patient outcomes.
9. Strategies to induce immunogenic cell death through modulation of m6A methylation to enhance the immune response.
10. Utilization of various model systems to study the dynamics of m6A methylation in the TME and test new therapeutic hypotheses.
A major challenge is the TME's promotion of immunosuppressive conditions, where myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs) dampen the immune response. These cells, along with immunosuppressive cytokines like TGF-β and IL-10, create barriers to effective T-cell infiltration and function. m6A methylation affects the differentiation and function of these immunosuppressive cells, impacting the immune landscape within tumors.
Recent advancements highlight the potential of targeting m6A regulatory proteins to improve immune cell activity. Inhibiting m6A demethylases or modulating m6A methyltransferases can change the expression of key immunoregulatory genes, potentially overcoming TME's immunosuppressive barriers. Identifying specific m6A-modified transcripts and associated proteins has also enabled the stratification of patients more likely to respond to immune checkpoint inhibitors.
The goal of this Research Topic is to advance our understanding of m6A methylation's role in modulating cancer immunity. We aim to identify and explore innovative strategies to target m6A regulatory pathways to overcome immunosuppressive barriers within the TME, thereby enhancing T-cell access and function. By fostering a comprehensive discussion on the manipulation of m6A methylation, we seek to accelerate the development of novel therapeutic approaches that can significantly improve patient outcomes across various cancer types.
We encourage the submission of manuscripts that explore, but are not limited to, the following areas:
1. Analysis of how m6A methylation influences the immunosuppressive nature of the tumor microenvironment (TME) at cellular and molecular levels.
2. Examination of how m6A methylation in stromal cells affects immune cell behavior and potential targeting strategies.
3. Studies on the role of m6A methylation in the efficacy and optimization of immune checkpoint inhibitors within the TME.
4. Approaches to enhance T-cell infiltration, survival, and anti-tumor activity by targeting m6A pathways.
5. Exploration of synergistic effects when combining m6A-targeted therapies with other treatments such as chemotherapy, radiation, or immunotherapy.
6. Identification and validation of m6A-related biomarkers for patient stratification and treatment response prediction.
7. Research on emerging immunotherapeutic agents, such as bispecific antibodies or CAR T-cells, and their interaction with m6A-modified targets.
8. Presentation of clinical trial outcomes focusing on m6A-targeted therapies and their impact on patient outcomes.
9. Strategies to induce immunogenic cell death through modulation of m6A methylation to enhance the immune response.
10. Utilization of various model systems to study the dynamics of m6A methylation in the TME and test new therapeutic hypotheses.
Keywords: m6A Methylation, Cancer Immunotherapy
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