The tumor microenvironment (TME) of solid tumors consists of various cell types embedded in a complex connective tissue matrix. Tissue-specific and recruited cells in the TME include cancer cells, immune cells, stromal cells, and endothelial cells. Increasing evidence indicates that the interplay among the TME components is the major cause of tumor heterogeneity and, hence, resistance to current cancer therapy.
Despite the rapid progress of the research on TME in the past decades, there are still many mechanisms to be investigated about the function and impact of the TME components on tumor progression and heterogeneity. A better mechanistic understanding of fundamental processes within the TME of solid tumors (e.g., epithelial-to-mesenchymal transition, inflammation, hypoxia, cell plasticity, cancer cell fusion, vascularization, cancer-associated fibroblasts, and ECM remodeling) may allow the development of therapeutic strategies targeting the TME to reduce tumor heterogeneity and increase the chance for therapy success. Therefore, researchers are working to develop improved preclinical models that better recapitulate the pathophysiology of solid tumors and technologies that allow identifying the cellular and molecular phenotypes involved in tumor heterogeneity and drug resistance. Current emerging technologies to address the complex role of the TME in tumor heterogeneity and drug resistance include, but are not limited to, in vitro and in vivo preclinical models such as 3-dimensional heterocellular spheroids, organoids, and humanized mouse models as well as methods of analysis such as genomic characterization, single-cell RNA sequencing, methylome, digital spatial transcriptomics and highly multiplexed spatial phenotyping.
This Research Topic aims to provide insights into the most recent developments in the field of tumor heterogeneity. We welcome Original Research, Brief Research Report, Method, Opinion, Review, Mini-review, Perspective, and Study Protocol articles covering the advances and challenges in understanding the influence of the TME on tumor heterogeneity and TME-related resistance to current therapies, with a particular focus on the progress in preclinical models and technologies to address these challenges and design eventually new therapies
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.
The tumor microenvironment (TME) of solid tumors consists of various cell types embedded in a complex connective tissue matrix. Tissue-specific and recruited cells in the TME include cancer cells, immune cells, stromal cells, and endothelial cells. Increasing evidence indicates that the interplay among the TME components is the major cause of tumor heterogeneity and, hence, resistance to current cancer therapy.
Despite the rapid progress of the research on TME in the past decades, there are still many mechanisms to be investigated about the function and impact of the TME components on tumor progression and heterogeneity. A better mechanistic understanding of fundamental processes within the TME of solid tumors (e.g., epithelial-to-mesenchymal transition, inflammation, hypoxia, cell plasticity, cancer cell fusion, vascularization, cancer-associated fibroblasts, and ECM remodeling) may allow the development of therapeutic strategies targeting the TME to reduce tumor heterogeneity and increase the chance for therapy success. Therefore, researchers are working to develop improved preclinical models that better recapitulate the pathophysiology of solid tumors and technologies that allow identifying the cellular and molecular phenotypes involved in tumor heterogeneity and drug resistance. Current emerging technologies to address the complex role of the TME in tumor heterogeneity and drug resistance include, but are not limited to, in vitro and in vivo preclinical models such as 3-dimensional heterocellular spheroids, organoids, and humanized mouse models as well as methods of analysis such as genomic characterization, single-cell RNA sequencing, methylome, digital spatial transcriptomics and highly multiplexed spatial phenotyping.
This Research Topic aims to provide insights into the most recent developments in the field of tumor heterogeneity. We welcome Original Research, Brief Research Report, Method, Opinion, Review, Mini-review, Perspective, and Study Protocol articles covering the advances and challenges in understanding the influence of the TME on tumor heterogeneity and TME-related resistance to current therapies, with a particular focus on the progress in preclinical models and technologies to address these challenges and design eventually new therapies
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.
