Tumor immune evasion is a major obstacle to designing effective anti-tumor therapeutic strategies. Great progress has been made in exploring how tumors evade destructive immunity.
Tumor immunity is affected by the complex composition of tumor, host, and environmental factors that influence the strength and timing of the anti-tumor response. Tumor immune landscapes vary markedly between and within cancer types. Increasing data indicate that genetic aberrations in tumor cells dictate the immune contexture of tumors. In addition, tumor-microenvironmental factors including macrophages, fibroblast ts, myeloid-derived suppressor cells (MDSC), regulatory T cells (Tregs) and secreted chemokines/cytokines, and host-related influences such as dysregulated systemic metabolic state and gut microbiota might also account for tumor immune evasion.
Inhibition of immune checkpoints, such as PD-1-PD-L1 and CTLA-4, is at the forefront of immunotherapy for multiple cancers. However, such immunotherapies frequently fail to control tumor progression in a large proportion of patients. Cancer cell-intrinsic and -extrinsic factors influencing tumor immunity were also involved in the failures often encountered during immune checkpoint blockade therapies. Although increasing progress has been made in understanding how tumors evade immunity, the detailed mechanisms and measures to counteract tumor escape are still limited.
The goal of this Research Topic is to provide a forum to advance research on the contribution of cancer cell-intrinsic and -extrinsic factors to tumor immune evasion as well as to explore potential ways to target these factors to reverse immunotherapy resistance or enhance immunotherapy efficacy.
In this Research Topic, we welcome the submissions of Original Research articles, Reviews, Mini Reviews, Methods, and Perspectives that address the roles of cancer cell-intrinsic and -extrinsic factors in tumor immune evasion and immunotherapy response. Some potential topics of interest include but are not limited to:
(1) Role of key oncogenes or tumor suppressor genes in modulating the tumor immune milieu.
(2) Relationship between tumor cell metabolism and tumor immunity.
(3) Role of tumor-microenvironmental factors including macrophages, fibroblasts, myeloid-derived suppressor cells, regulatory T cells, and secreted chemokines/cytokines in tumor evasion and immunotherapy.
(4) Relationship between stromal cell metabolism and tumor immunity.
(5) Interactions between tumor cells and stromal cells in the tumor microenvironment that regulate tumor immunity.
(6) Role of host-related influences including dysregulated systemic metabolic state and gut microbiota in tumor immunity and immunotherapy response.
(7) Therapeutic targeting tumor cell-intrinsic and -extrinsic factors to inhibit tumor evasion or enhance immunotherapy efficacy.
(8) New technologies and models to study the mechanism of tumor evasion.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Tumor immune evasion is a major obstacle to designing effective anti-tumor therapeutic strategies. Great progress has been made in exploring how tumors evade destructive immunity.
Tumor immunity is affected by the complex composition of tumor, host, and environmental factors that influence the strength and timing of the anti-tumor response. Tumor immune landscapes vary markedly between and within cancer types. Increasing data indicate that genetic aberrations in tumor cells dictate the immune contexture of tumors. In addition, tumor-microenvironmental factors including macrophages, fibroblast ts, myeloid-derived suppressor cells (MDSC), regulatory T cells (Tregs) and secreted chemokines/cytokines, and host-related influences such as dysregulated systemic metabolic state and gut microbiota might also account for tumor immune evasion.
Inhibition of immune checkpoints, such as PD-1-PD-L1 and CTLA-4, is at the forefront of immunotherapy for multiple cancers. However, such immunotherapies frequently fail to control tumor progression in a large proportion of patients. Cancer cell-intrinsic and -extrinsic factors influencing tumor immunity were also involved in the failures often encountered during immune checkpoint blockade therapies. Although increasing progress has been made in understanding how tumors evade immunity, the detailed mechanisms and measures to counteract tumor escape are still limited.
The goal of this Research Topic is to provide a forum to advance research on the contribution of cancer cell-intrinsic and -extrinsic factors to tumor immune evasion as well as to explore potential ways to target these factors to reverse immunotherapy resistance or enhance immunotherapy efficacy.
In this Research Topic, we welcome the submissions of Original Research articles, Reviews, Mini Reviews, Methods, and Perspectives that address the roles of cancer cell-intrinsic and -extrinsic factors in tumor immune evasion and immunotherapy response. Some potential topics of interest include but are not limited to:
(1) Role of key oncogenes or tumor suppressor genes in modulating the tumor immune milieu.
(2) Relationship between tumor cell metabolism and tumor immunity.
(3) Role of tumor-microenvironmental factors including macrophages, fibroblasts, myeloid-derived suppressor cells, regulatory T cells, and secreted chemokines/cytokines in tumor evasion and immunotherapy.
(4) Relationship between stromal cell metabolism and tumor immunity.
(5) Interactions between tumor cells and stromal cells in the tumor microenvironment that regulate tumor immunity.
(6) Role of host-related influences including dysregulated systemic metabolic state and gut microbiota in tumor immunity and immunotherapy response.
(7) Therapeutic targeting tumor cell-intrinsic and -extrinsic factors to inhibit tumor evasion or enhance immunotherapy efficacy.
(8) New technologies and models to study the mechanism of tumor evasion.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
