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Epigenetic Controls for Gene Panels in Oncology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 May 2024) | Viewed by 1452

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Center of Tobacco Control Research, 5230 Odense, Denmark
Interests: cancer biology; urologic oncology; tumor markers
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Special Issue Information

Dear Colleagues,

In 2012, the Nobel prize in medicine was awarded to research on induced pluripotent stem cells (iPSC), which is important for regenerative medicine. The two gene panels generated were OCT4, SOX2, KLF4, and MYC (OSKM), and OCT4, SOX2, LIN28, and NANOG (OSLN). The gene panels are also found in the testicular cancer subtype embryonal carcinoma and in cancer stem cells. Their expression is governed by epigenetic mechanisms. Thus, a new point of view is the role of gene panels in oncology, being essential between different types of cancers. Gene panels may explain the development of cancers better than single genes do. A well-known example are the Vogelstein panels for colorectal cancer. Panels of genes may create blocks of RNA that may serve as new therapeutic targets. Many sources may lead to the understanding of gene panels in oncology. Gene panels may be sets of oncogenes and tumor suppressor genes or may work synergistically with known mutations, oncogenes and tumor suppressor genes. Therefore, the coming issue of the International Journal of Molecular Sciences welcomes experimental and clinical studies in oncology that advance the knowledge of the role of gene panels and epigenetic regulation of gene expression.

Dr. Finn Edler von Eyben
Guest Editor

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Published Papers (1 paper)

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Research

21 pages, 6342 KiB  
Article
Mechanism of Histone Arginine Methylation Dynamic Change in Cellular Stress
by Xiao-Guang Ren, Wei Li, Wen-Xuan Li and Wenqiang Yu
Int. J. Mol. Sci. 2024, 25(14), 7562; https://doi.org/10.3390/ijms25147562 - 10 Jul 2024
Viewed by 1218
Abstract
Histone arginine residue methylation is crucial for individual development and gene regulation. However, the dynamics of histone arginine methylation in response to cellular stress remains largely unexplored. In addition, the interplay and regulatory mechanisms between this and other histone modifications are important scientific [...] Read more.
Histone arginine residue methylation is crucial for individual development and gene regulation. However, the dynamics of histone arginine methylation in response to cellular stress remains largely unexplored. In addition, the interplay and regulatory mechanisms between this and other histone modifications are important scientific questions that require further investigation. This study aimed to investigate the changes in histone arginine methylation in response to DNA damage. We report a global decrease in histone H3R26 symmetric dimethylation (H3R26me2s) and hypoacetylation at the H3K27 site in response to DNA damage. Notably, H3R26me2s exhibits a distribution pattern similar to that of H3K27ac across the genome, both of which are antagonistic to H3K27me3. Additionally, histone deacetylase 1 (HDAC1) may be recruited to the H3R26me2s demethylation region to mediate H3K27 deacetylation. These findings suggest crosstalk between H3R26me2s and H3K27ac in regulating gene expression. Full article
(This article belongs to the Special Issue Epigenetic Controls for Gene Panels in Oncology)
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