The relationship between epigenetic modifications and cancer is well established. DNA methylation and histone modifications are typical epigenetic modifications associated with cancer development and progression. Numerous tumor suppressor genes and oncogenes are associated with epigenetic modifications. Various epigenetic modifiers are currently used as anti-cancer treatments, and many of these drugs are undergoing clinical trials for multiple cancers. Dynamic control mechanisms involved in the regulation of gene expression are epigenetic modifications. In comparison to the DNA sequence, they differ not only between individuals but also between cell types of the same individual. Environmental factors, somatic mutations, and aging contribute to epigenomic changes over time, which may serve as early disease markers. In developmental biology and human disease, epigenetic mechanisms play a critical role. They function at the intersection of genetic and environmental factors to control, regulate, and propagate cellular responses, thereby significantly contributing to the diversity of cellular phenotypes. Consequently, they provide unique diagnostic and therapeutic opportunities and offer promising targets for precision medicine approaches, with applications in cancer treatment being of particular interest. Thus, epigenetic modifications are responsible for the critical cell differentiation in the tumor microenvironment (TME). TME refers to the ecological niche in which tumor cells interact with the host stroma, including diverse immune cells, endothelial cells, fibroblasts, tumor cells, and metabolites. It is now commonly recognized that TME significantly affects the effectiveness of anti-cancer drugs. Recent research has identified epigenetic dysregulation-induced TME reprogramming as a crucial factor in cancer progression. In addition, findings revealed a relationship between epigenetic repressive mechanisms and a "cold immunological" environment in tumors. In some preclinical and clinical trials, epigenetic modifiers were used to investigate immune targeting strategies.
This Research Topic aims to advance our insight into the interaction between epigenetic modifications and TME and identify potential prognostic markers and specific components influencing the efficacy of immunotherapy or other tumor therapies. We encourage the contribution of original research articles, reviews, and opinions on the following, but not limited to:
1. Exploration of the interaction between epigenetic modifications and TME
2. Determination of innovative predictive models based on epigenetic modifications and TME
3. Mechanism of epigenetic modifications in cancer immunotherapy and the related clinical research
4. Unique molecular landscapes in tumors based on epigenetic modifications
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 relationship between epigenetic modifications and cancer is well established. DNA methylation and histone modifications are typical epigenetic modifications associated with cancer development and progression. Numerous tumor suppressor genes and oncogenes are associated with epigenetic modifications. Various epigenetic modifiers are currently used as anti-cancer treatments, and many of these drugs are undergoing clinical trials for multiple cancers. Dynamic control mechanisms involved in the regulation of gene expression are epigenetic modifications. In comparison to the DNA sequence, they differ not only between individuals but also between cell types of the same individual. Environmental factors, somatic mutations, and aging contribute to epigenomic changes over time, which may serve as early disease markers. In developmental biology and human disease, epigenetic mechanisms play a critical role. They function at the intersection of genetic and environmental factors to control, regulate, and propagate cellular responses, thereby significantly contributing to the diversity of cellular phenotypes. Consequently, they provide unique diagnostic and therapeutic opportunities and offer promising targets for precision medicine approaches, with applications in cancer treatment being of particular interest. Thus, epigenetic modifications are responsible for the critical cell differentiation in the tumor microenvironment (TME). TME refers to the ecological niche in which tumor cells interact with the host stroma, including diverse immune cells, endothelial cells, fibroblasts, tumor cells, and metabolites. It is now commonly recognized that TME significantly affects the effectiveness of anti-cancer drugs. Recent research has identified epigenetic dysregulation-induced TME reprogramming as a crucial factor in cancer progression. In addition, findings revealed a relationship between epigenetic repressive mechanisms and a "cold immunological" environment in tumors. In some preclinical and clinical trials, epigenetic modifiers were used to investigate immune targeting strategies.
This Research Topic aims to advance our insight into the interaction between epigenetic modifications and TME and identify potential prognostic markers and specific components influencing the efficacy of immunotherapy or other tumor therapies. We encourage the contribution of original research articles, reviews, and opinions on the following, but not limited to:
1. Exploration of the interaction between epigenetic modifications and TME
2. Determination of innovative predictive models based on epigenetic modifications and TME
3. Mechanism of epigenetic modifications in cancer immunotherapy and the related clinical research
4. Unique molecular landscapes in tumors based on epigenetic modifications
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.