About this Research Topic
PD-1 axis inhibitors are a group of immune checkpoint inhibitors (ICIs) that block the PD-1/PD-L1 interaction to reinstate immune recognition. The tumor microenvironment (TME) is complex and ever-changing and can affect response to anticancer therapies, including PD-1 axis inhibitors. Despite the established efficacy of PD-1 axis inhibitors, not all patients respond to treatment, and some will develop resistance. Therefore, it is essential to understand the factors that contribute to primary or secondary treatment resistance to develop new approaches and ultimately improve patient outcomes.
This Research Topic aims to explore different aspects of the TME that contribute to response/resistance to PD-1 axis inhibitors, including:
1) Understanding resistance mechanisms: Gaining a better understanding of the mechanisms behind immunotherapy resistance is crucial in developing effective strategies to overcome it. This involves studying the cellular interactions and molecular alterations within the TME that contribute to immunosuppression.
2) Combinatorial strategies: Rational and synergistic combination therapies can be designed to lower the risk of resistance and prolong the benefits of immunotherapy. This may involve combining ICIs or adding different treatment modalities such as chemotherapy or local therapies.
3) Enhancing immune response: Strategies that aim to enhance the immune response of T and NK cells have shown promise in overcoming immunotherapy resistance. This can be achieved through various approaches, such as targeting immunosuppressive factors in the TME.
4) Targeting specific mechanisms: Identifying specific mechanisms of resistance, such as inactivation of antigen presentation, can help develop tailored therapies to overcome resistance.
We are interested in Original Research, Systematic Review, Methods, Review/Mini Review, Clinical Trial, Case Report, Brief Research Report, Study Protocol, and Technology and Code articles focusing on, but not limited to, the following areas:
• Various cellular and molecular alterations within the TME that contribute to immunotherapy resistance, particularly the resistance mechanisms that are currently being targeted by novel therapeutic strategies. This can include intrinsic mechanisms (e.g., cell signaling, immune recognition, gene expression), extrinsic mechanisms (e.g., T cell activation, neo-angiogenesis), and specific pathways or molecules that play a role in immunotherapy resistance.
• Preclinical and clinical treatment approaches that have shown promise in lowering the risk of resistance and prolonging the benefits of immunotherapy
• Combination therapies that aim to overcome immunotherapy resistance
• The emerging role of antibody-drug conjugates (ADCs) in shaping the immune microenvironment and increasing treatment efficacy of ICIs
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
This Research Topic aims to explore different aspects of the TME that contribute to response/resistance to PD-1 axis inhibitors, including:
1) Understanding resistance mechanisms: Gaining a better understanding of the mechanisms behind immunotherapy resistance is crucial in developing effective strategies to overcome it. This involves studying the cellular interactions and molecular alterations within the TME that contribute to immunosuppression.
2) Combinatorial strategies: Rational and synergistic combination therapies can be designed to lower the risk of resistance and prolong the benefits of immunotherapy. This may involve combining ICIs or adding different treatment modalities such as chemotherapy or local therapies.
3) Enhancing immune response: Strategies that aim to enhance the immune response of T and NK cells have shown promise in overcoming immunotherapy resistance. This can be achieved through various approaches, such as targeting immunosuppressive factors in the TME.
4) Targeting specific mechanisms: Identifying specific mechanisms of resistance, such as inactivation of antigen presentation, can help develop tailored therapies to overcome resistance.
We are interested in Original Research, Systematic Review, Methods, Review/Mini Review, Clinical Trial, Case Report, Brief Research Report, Study Protocol, and Technology and Code articles focusing on, but not limited to, the following areas:
• Various cellular and molecular alterations within the TME that contribute to immunotherapy resistance, particularly the resistance mechanisms that are currently being targeted by novel therapeutic strategies. This can include intrinsic mechanisms (e.g., cell signaling, immune recognition, gene expression), extrinsic mechanisms (e.g., T cell activation, neo-angiogenesis), and specific pathways or molecules that play a role in immunotherapy resistance.
• Preclinical and clinical treatment approaches that have shown promise in lowering the risk of resistance and prolonging the benefits of immunotherapy
• Combination therapies that aim to overcome immunotherapy resistance
• The emerging role of antibody-drug conjugates (ADCs) in shaping the immune microenvironment and increasing treatment efficacy of ICIs
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
Keywords: PD-1 inhibitor, Tumor microenvironment, immunotherapy response, resistance to PD-1 inhibitor, PD-1/PD-L1 blockade, cancer immunotherapy, T cells, NK cells, immunotherapy resistance
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
