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Histone methylation in pancreatic cancer and its clinical implications
- Source :
- World Journal of Gastroenterology
- Publication Year :
- 2021
- Publisher :
- Baishideng Publishing Group Inc., 2021.
-
Abstract
- Pancreatic cancer (PC) is an aggressive human cancer. Appropriate methods for the diagnosis and treatment of PC have not been found at the genetic level, thus making epigenetics a promising research path in studies of PC. Histone methylation is one of the most complicated types of epigenetic modifications and has proved crucial in the development of PC. Histone methylation is a reversible process regulated by readers, writers, and erasers. Some writers and erasers can be recognized as potential biomarkers and candidate therapeutic targets in PC because of their unusual expression in PC cells compared with normal pancreatic cells. Based on the impact that writers have on the development of PC, some inhibitors of writers have been developed. However, few inhibitors of erasers have been developed and put to clinical use. Meanwhile, there is not enough research on the reader domains. Therefore, the study of erasers and readers is still a promising area. This review focuses on the regulatory mechanism of histone methylation, and the diagnosis and chemotherapy of PC based on it. The future of epigenetic modification in PC research is also discussed.
- Subjects :
- Review
Methylation
Epigenesis, Genetic
Histones
Pancreatic cancer
Histone methylation
medicine
Humans
Epigenetics
biology
Mechanism (biology)
business.industry
Gastroenterology
General Medicine
medicine.disease
Clinical application
Demethylation
Pancreatic Neoplasms
Histone
Potential biomarkers
biology.protein
Cancer research
Histone modification
business
Protein Processing, Post-Translational
Human cancer
Subjects
Details
- ISSN :
- 10079327
- Volume :
- 27
- Database :
- OpenAIRE
- Journal :
- World Journal of Gastroenterology
- Accession number :
- edsair.doi.dedup.....ae220ceb6a3a84cde43b96e27325a2a3
- Full Text :
- https://doi.org/10.3748/wjg.v27.i36.6004