About this Research Topic
During normal hematopoietic cell development, epigenetic regulation of transcriptional programs leads to self-renewal and lineage differentiation of these cell lines. Disruption of the components of the epigenome, which is a combination of DNA methylation and histone modification can lead to clonal hematopoiesis and development and progression of myeloid neoplasms. Myeloid neoplasms comprise a group of diverse neoplasms ranging from myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap and acute myeloid leukemia affecting the elderly population. Recent advancements in next generation sequencing platforms have enabled us to decipher these aberrancies in DNA methylation pathways particularly affecting myeloid neoplasms. Studies of these epigenetic pathways not only helped us know the pathogenesis of these myeloid neoplasms but also helped identify therapeutic targets and mechanisms of residual/relapsed disease. However, despite recent advancements in the molecular sequencing, epigenetic therapies thus far have failed to show curative benefit to these malignancies and tumor heterogeneity and mechanisms of resistance and clonal evolution are the major concerns leading to an altered oncogenic environment causing dysregulation of promoters and enhancers leading to enhancement of oncogene expression and failure of suppression of tumor suppressor genes.
This research topic will aim to associate the latest research findings, hypothesis, and experimental approaches that explain the mechanisms underlying epigenetic regulation of transcriptional programs in the development of myeloid neoplasms. This will provide insights into how DNA methylation and histone modification can lead to clonal hematopoiesis and development and progression of myeloid neoplasms, how mutations associated with these neoplasms drive their tumorigenesis and how mutational heterogeneity and evolution can lead to the mechanisms of resistance. Our final aim will be to decipher how these epigenetic studies can be utilized for more efficient management of these diverse landscape of myeloid malignancies.
We invite researchers to submit manuscripts addressing the following themes:
1. Epigenetic dysregulation in myeloid neoplasms: This will include mutations in DNA methylation pathways including cytosine modifications, formation of complex genomic rearrangements, posttranslational histone modifications including acetylation, methylation, phosphorylation and ubiquitylation and telomere silencing.
2. Genomic alterations in myeloid neoplasms: different mutations and genomic rearrangements affecting myeloid neoplasms, the mutations and rearrangements that drive tumorigenesis, and the effect of genome instability on tumor heterogeneity and clonal evolution.
3. Further management and Clinical Applications: Investigate different therapeutic approaches by targeting epigenetic dysregulation, such as hypomethylating agents, histone deacetylases (HDACs) etc. and explore personalized medicine options. We welcome original research articles, case reports, reviews, mini-reviews, perspectives, and methodological papers that contribute to a deeper understanding of epigenetic dysregulation in myeloid malignancies. Animal models, clinical trials and articles bridging the gap from "bench to bedside" are particularly welcomed.
This research topic will aim to associate the latest research findings, hypothesis, and experimental approaches that explain the mechanisms underlying epigenetic regulation of transcriptional programs in the development of myeloid neoplasms. This will provide insights into how DNA methylation and histone modification can lead to clonal hematopoiesis and development and progression of myeloid neoplasms, how mutations associated with these neoplasms drive their tumorigenesis and how mutational heterogeneity and evolution can lead to the mechanisms of resistance. Our final aim will be to decipher how these epigenetic studies can be utilized for more efficient management of these diverse landscape of myeloid malignancies.
We invite researchers to submit manuscripts addressing the following themes:
1. Epigenetic dysregulation in myeloid neoplasms: This will include mutations in DNA methylation pathways including cytosine modifications, formation of complex genomic rearrangements, posttranslational histone modifications including acetylation, methylation, phosphorylation and ubiquitylation and telomere silencing.
2. Genomic alterations in myeloid neoplasms: different mutations and genomic rearrangements affecting myeloid neoplasms, the mutations and rearrangements that drive tumorigenesis, and the effect of genome instability on tumor heterogeneity and clonal evolution.
3. Further management and Clinical Applications: Investigate different therapeutic approaches by targeting epigenetic dysregulation, such as hypomethylating agents, histone deacetylases (HDACs) etc. and explore personalized medicine options. We welcome original research articles, case reports, reviews, mini-reviews, perspectives, and methodological papers that contribute to a deeper understanding of epigenetic dysregulation in myeloid malignancies. Animal models, clinical trials and articles bridging the gap from "bench to bedside" are particularly welcomed.
Keywords: Hematopoeitic stem cell, epigenome, myeloid neoplasms, DNA methylation pathway, histone modification, nucleosome, gene expression, mutations, methylome, gene rearranegments, epigenetic modifiers
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
