Epigenetic Modifications for Cancer Therapy

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Epigenomics".

Deadline for manuscript submissions: closed (25 May 2024) | Viewed by 553

Special Issue Editor


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Guest Editor
Biochemistry & Molecular Biology Department, Medical University of South Carolina, Charleston, SC 29425, USA
Interests: post-translational modifications; cancer; DNA methylation; cell signaling pathway

Special Issue Information

Dear Colleagues,

Cancer, a consequence of accumulative genetic mutations and epigenetic alterations, remains a formidable global human health threat due to its incurable nature. Over the past two decades, our understanding of mechanisms and roles of epigenetics in cancer initiation, progression, and metastasis has significantly expanded. Epigenetics, including DNA and RNA methylation, histone post-translational modifications, chromatin remodelers, and non-coding RNA regulation, play critical roles in many various cancer types by regulating the expression and activity of many oncogenes and tumor suppressors without DNA sequence alteration. Given the importance of epigenetic modifications in cancers, epigenetic therapy has become an attractive strategy. While DNA methyltransferase inhibitors and histone deacetylase inhibitors have been approved by the FDA for cancer treatment, numerous other epi-drugs, such as chromatin-remodeling factors, are currently undergoing clinical trials. However, challenges persist with side effects and resistance in the application of epi-drugs for cancer treatment. Epigenetic modifications in metabolism reprogramming, cancer immunology, and tumor microenvironment are being currently researched. Discovering novel epi-drugs with specificity and safety and exploring combinations with other anti-cancer therapies including tumor metabolism control, targeted therapy, and immunotherapy, emerge as a pivotal frontier in epigenetics.

The Special Issue aims to focus on the latest advancements in the field of novel epigenetic therapies and epigenetic modifications for cancer, especially in metabolic reprogramming and the immune system. This Special Issue also seeks to explore further possibilities for epigenetic therapy in cancers. We invite submissions of original research articles, reviews, and perspectives on all relevant topics. Studies that include novel epi-drugs, new epigenetic modifications and mechanisms, and epigenetic-related combination therapies will be prioritized.

Dr. Shasha Yin
Guest Editor

Manuscript Submission Information

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Keywords

  • cancer
  • epigenetics
  • DNA methylation
  • RNA methylation
  • histone modifications
  • non-coding RNAs
  • chromatin remodelers
  • regulator of epigenetics
  • epigenetics in metabolic reprogramming
  • epi-drugs

Published Papers (1 paper)

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Review

32 pages, 5113 KiB  
Review
Pediatric Hemispheric High-Grade Gliomas and H3.3-G34 Mutation: A Review of the Literature on Biological Features and New Therapeutic Strategies
by Marta Bonada, Matilde Pittarello, Emerson De Fazio, Alessandro Gans, Paolo Alimonti, Hasan Slika, Federico Legnani, Francesco Di Meco and Betty Tyler
Genes 2024, 15(8), 1038; https://doi.org/10.3390/genes15081038 - 6 Aug 2024
Viewed by 292
Abstract
Pediatric high-grade glioma (pHGG) encompasses a wide range of gliomas with different genomic, epigenomic, and transcriptomic features. Almost 50% of pHGGs present a mutation in genes coding for histone 3, including the subtype harboring the H3.3-G34 mutation. In this context, histone mutations are [...] Read more.
Pediatric high-grade glioma (pHGG) encompasses a wide range of gliomas with different genomic, epigenomic, and transcriptomic features. Almost 50% of pHGGs present a mutation in genes coding for histone 3, including the subtype harboring the H3.3-G34 mutation. In this context, histone mutations are frequently associated with mutations in TP53 and ATRX, along with PDGFRA and NOTCH2NL amplifications. Moreover, the H3.3-G34 histone mutation induces epigenetic changes in immune-related genes and exerts modulatory functions on the microenvironment. Also, the functionality of the blood–brain barrier (BBB) has an impact on treatment response. The prognosis remains poor with conventional treatments, thus eliciting the investigation of additional and alternative therapies. Promising molecular targets include PDGFRA amplification, BRAF mutation, EGFR amplification, NF1 loss, and IDH mutation. Considering that pHGGs harboring the H3.3-G34R mutation appear to be more susceptible to immunotherapies (ITs), different options have been recently explored, including immune checkpoint inhibitors, antibody mediated IT, and Car-T cells. This review aims to summarize the knowledge concerning cancer biology and cancer-immune cell interaction in this set of pediatric gliomas, with a focus on possible therapeutic options. Full article
(This article belongs to the Special Issue Epigenetic Modifications for Cancer Therapy)
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