In the last few decades, immunotherapy has emerged as the fourth pillar of hematologic malignancy therapy. One of the most effective immunotherapies is immune checkpoint blockade by immune checkpoint inhibitors (ICIs), such as programmed death receptor-1 (PD-1), cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) inhibitors. Early-phase clinical trial results have demonstrated the remarkable effectiveness of ICIs in specific lymphoma subtypes, including classical Hodgkin lymphoma and primary mediastinal B-cell lymphoma. Unfortunately, ICIs has relatively disappointing effect in follicular lymphoma, diffuse large B-cell lymphoma and acute myeloid leukemia (AML), indicating that cell-intrinsic and –extrinsic primary or acquired resistant mechanisms exist. Studies focus on identifying biomarkers to predict the efficacy of ICIs, seeking for other immune checkpoints (ICs) or small molecular inhibitors with less adverse events and toxicities, exploring for the cellular and molecular mechanisms of immune cell exhaustion will be appreciated in the future.
Early studies on the efficacy of ICIs suggest that immune cells, PD-L1 expression, neoantigens, and genetic and epigenetic signatures can predict the response to immune checkpoint blockade and immune-related adverse events, however, contradictory conclusions are obvious, hence continually explore the highly reliable predictive biomarkers are still needed which will facilitate patient selection and decision-making related to immune checkpoint inhibitor-based therapies for leukemia and lymphoma patients.
Except for the classical ICIs which targeted on T cells, newly discovered ICPs showing encouraging efficacy in cancer immunotherapy, for example, CD47-SIRPa signal inhibition with anti-CD47 which can enable phagocytosis of tumor by macrophages and stimulating the anti-tumor T cell response. In addition, CD161-CLEC2D pathways which have recently been reported as a potential target for immunotherapy of diffuse gliomas and other human cancers. Based on the above encouraging results, seeking for other ICPs and small molecular inhibitors will continually be an appreciable work.
Previous researches have demonstrated several cell-intrinsic and -extrinsic factors lead to primary or acquired immune therapy resistance, for instance, transcription regulators, metabolic and epigenetic factors impact T cell exhaustion, immune suppressive soluble mediators and tumor metabolites in immune microenvironment. Therefore, exploring the cell-intrinsic and -extrinsic mechanisms of immune cell dysfunction in the course of immunotherapy may help to identify biological targets to conquer resistance to immunotherapy.
In this Research Topic, we welcome authors to submit Reviews, Mini-Reviews, Original Research, Perspective, and Clinical Trial articles focusing on, but not limited to, the following subtopics:
1. Cellular and molecular biomarkers which could predict the outcome of immune check-points blockers in treating leukemia and lymphoma.
2. Newly discovered immune check-points (ICPs) and their ligands or small molecular inhibitors for treatment of leukemia and lymphoma.
3. Cell-intrinsic (e.g., transcription regulators, metabolic and epigenetic factors) and -extrinsic (e.g., immunosuppressive microenvironment) factors leading to immune cell dysfunction before and after ICPs therapy.
Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in Frontiers in Oncology.
In the last few decades, immunotherapy has emerged as the fourth pillar of hematologic malignancy therapy. One of the most effective immunotherapies is immune checkpoint blockade by immune checkpoint inhibitors (ICIs), such as programmed death receptor-1 (PD-1), cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) inhibitors. Early-phase clinical trial results have demonstrated the remarkable effectiveness of ICIs in specific lymphoma subtypes, including classical Hodgkin lymphoma and primary mediastinal B-cell lymphoma. Unfortunately, ICIs has relatively disappointing effect in follicular lymphoma, diffuse large B-cell lymphoma and acute myeloid leukemia (AML), indicating that cell-intrinsic and –extrinsic primary or acquired resistant mechanisms exist. Studies focus on identifying biomarkers to predict the efficacy of ICIs, seeking for other immune checkpoints (ICs) or small molecular inhibitors with less adverse events and toxicities, exploring for the cellular and molecular mechanisms of immune cell exhaustion will be appreciated in the future.
Early studies on the efficacy of ICIs suggest that immune cells, PD-L1 expression, neoantigens, and genetic and epigenetic signatures can predict the response to immune checkpoint blockade and immune-related adverse events, however, contradictory conclusions are obvious, hence continually explore the highly reliable predictive biomarkers are still needed which will facilitate patient selection and decision-making related to immune checkpoint inhibitor-based therapies for leukemia and lymphoma patients.
Except for the classical ICIs which targeted on T cells, newly discovered ICPs showing encouraging efficacy in cancer immunotherapy, for example, CD47-SIRPa signal inhibition with anti-CD47 which can enable phagocytosis of tumor by macrophages and stimulating the anti-tumor T cell response. In addition, CD161-CLEC2D pathways which have recently been reported as a potential target for immunotherapy of diffuse gliomas and other human cancers. Based on the above encouraging results, seeking for other ICPs and small molecular inhibitors will continually be an appreciable work.
Previous researches have demonstrated several cell-intrinsic and -extrinsic factors lead to primary or acquired immune therapy resistance, for instance, transcription regulators, metabolic and epigenetic factors impact T cell exhaustion, immune suppressive soluble mediators and tumor metabolites in immune microenvironment. Therefore, exploring the cell-intrinsic and -extrinsic mechanisms of immune cell dysfunction in the course of immunotherapy may help to identify biological targets to conquer resistance to immunotherapy.
In this Research Topic, we welcome authors to submit Reviews, Mini-Reviews, Original Research, Perspective, and Clinical Trial articles focusing on, but not limited to, the following subtopics:
1. Cellular and molecular biomarkers which could predict the outcome of immune check-points blockers in treating leukemia and lymphoma.
2. Newly discovered immune check-points (ICPs) and their ligands or small molecular inhibitors for treatment of leukemia and lymphoma.
3. Cell-intrinsic (e.g., transcription regulators, metabolic and epigenetic factors) and -extrinsic (e.g., immunosuppressive microenvironment) factors leading to immune cell dysfunction before and after ICPs therapy.
Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in Frontiers in Oncology.
