Tumor microenvironment (TME) is a heterogeneous, dynamic, well-organized complex tissue system, supported by cellular and molecular players that directly influence tumor immune responses, which in turn determines whether a primary tumor is eradicated, metastasizes, or establishes dormant micro-metastases. TME also impacts on response or resistance to therapy. It has become evident that tumor colonization of secondary sites is preceded by changes in target tissues. Different TME immunophenotypes can either instigate or restrain the establishment of premetastatic niches in different affected organs. These complex processes involve signaling among cells present in the TME and systemically, which causes leukocytes immunomodulation at distant sites. The TME different populations generate and respond to biochemical signals as inflammatory mediators, metabolites, and extracellular vesicles. These elements display paracrine and endocrine signaling. In addition, the microbiota and its products have been shown to play important roles in tumor progression and response to treatment.
TME resident macrophages, dendritic cells, eosinophils, mast cells, NK cells, neutrophils, and T cell subsets, with distinct immunophenotypes, have been implicated in the promotion or inhibition of metastatic progression in different tumor types, both mouse and human cancers. It is clear now that myeloid derived suppressor cells, regulatory or Th2 and Th17 T lymphocytes, macrophages and neutrophils are important for metastasis establishment. This Research Topic focuses on the impact of TME on leukocyte populations, on its ability to promote secondary sites colonization, and on the overall role of TME in disease progression and response to therapy.
We welcome submissions of Original Research, Review, Mini Review, Methods and Perspectives articles focusing on the following sub-topics:
1. Immunophenotypes in the primary TME, the metastatic organ microenvironment, or pre-metastatic niche, and the mechanisms that regulate tumor invasion, colonization, and maintenance.
2. Tumor cell mutations (genetic and/or epigenetic events) that lead to different immunophenotypes in the primary TME.
3. Local or systemic microbiome in the regulation of immunophenotypes in the primary or secondary TME.
4. Prognostic targeting of tumor immunophenotypes in the prevention of tumor metastasis in preclinical models and clinical settings.
5. Therapeutic targeting of tumor immunophenotypes in the prevention and treatment of tumor metastasis in preclinical models and clinical settings.
6. Heterogeneity of TME immunophenotypes, both from primary or secondary TME, by high throughput multi-omics analyses, at the single cell and/or spatial levels.
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 and will not be accepted as part of this Research Topic.
Tumor microenvironment (TME) is a heterogeneous, dynamic, well-organized complex tissue system, supported by cellular and molecular players that directly influence tumor immune responses, which in turn determines whether a primary tumor is eradicated, metastasizes, or establishes dormant micro-metastases. TME also impacts on response or resistance to therapy. It has become evident that tumor colonization of secondary sites is preceded by changes in target tissues. Different TME immunophenotypes can either instigate or restrain the establishment of premetastatic niches in different affected organs. These complex processes involve signaling among cells present in the TME and systemically, which causes leukocytes immunomodulation at distant sites. The TME different populations generate and respond to biochemical signals as inflammatory mediators, metabolites, and extracellular vesicles. These elements display paracrine and endocrine signaling. In addition, the microbiota and its products have been shown to play important roles in tumor progression and response to treatment.
TME resident macrophages, dendritic cells, eosinophils, mast cells, NK cells, neutrophils, and T cell subsets, with distinct immunophenotypes, have been implicated in the promotion or inhibition of metastatic progression in different tumor types, both mouse and human cancers. It is clear now that myeloid derived suppressor cells, regulatory or Th2 and Th17 T lymphocytes, macrophages and neutrophils are important for metastasis establishment. This Research Topic focuses on the impact of TME on leukocyte populations, on its ability to promote secondary sites colonization, and on the overall role of TME in disease progression and response to therapy.
We welcome submissions of Original Research, Review, Mini Review, Methods and Perspectives articles focusing on the following sub-topics:
1. Immunophenotypes in the primary TME, the metastatic organ microenvironment, or pre-metastatic niche, and the mechanisms that regulate tumor invasion, colonization, and maintenance.
2. Tumor cell mutations (genetic and/or epigenetic events) that lead to different immunophenotypes in the primary TME.
3. Local or systemic microbiome in the regulation of immunophenotypes in the primary or secondary TME.
4. Prognostic targeting of tumor immunophenotypes in the prevention of tumor metastasis in preclinical models and clinical settings.
5. Therapeutic targeting of tumor immunophenotypes in the prevention and treatment of tumor metastasis in preclinical models and clinical settings.
6. Heterogeneity of TME immunophenotypes, both from primary or secondary TME, by high throughput multi-omics analyses, at the single cell and/or spatial levels.
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 and will not be accepted as part of this Research Topic.