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Epigenetics and pancreatic cancer: pathophysiology and novel treatment aspects
Daniel Neureiter1, Tarkan Jäger1, Matthias Ocker1
1Daniel Neureiter, Institute of Pathology, Paracelsus Medical University/Salzburger Landeskliniken (SALK), 5020 Salzburg, Austria.
Abstract:
An improvement in pancreatic cancer treatment represents an urgent medical goal. Late diagnosis and high intrinsic resistance to conventional chemotherapy has led to a dismal overall prognosis that has remained unchanged during the past decades. Increasing knowledge about the molecular pathogenesis of the disease has shown that genetic alterations, such as mutations of K-ras, and especially epigenetic dysregulation of tumor-associated genes, such as silencing of the tumor suppressor p16(ink4a), are hallmarks of pancreatic cancer. Here, we describe genes that are commonly affected by epigenetic dysregulation in pancreatic cancer via DNA methylation, histone acetylation or miRNA (microRNA) expression, and review the implications on pancreatic cancer biology such as epithelial-mesenchymal transition, morphological pattern formation, or cancer stem cell regulation during carcinogenesis from PanIN (pancreatic intraepithelial lesions) to invasive cancer and resistance development. Epigenetic drugs, such as DNA methyltransferases or histone deactylase inhibitors, have shown promising preclinical results in pancreatic cancer and are currently in early phases of clinical development. Combinations of epigenetic drugs with established cytotoxic drugs or targeted therapies are promising approaches to improve the poor response and survival rate of pancreatic cancer patients.
Insights
Pancreatic cancer treatment needs improvement due to late diagnosis and chemoresistance. Epigenetic dysregulation plays a key role, and epigenetic drugs show promise for better patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Pancreatic cancer has a poor prognosis due to late diagnosis and chemotherapy resistance.
- Genetic alterations and epigenetic dysregulation are key features of pancreatic cancer.
- Specific epigenetic changes include DNA methylation, histone acetylation, and microRNA expression affecting tumor suppressor genes like p16(ink4a).
Purpose of the Study:
- To review genes commonly affected by epigenetic dysregulation in pancreatic cancer.
- To discuss the implications of epigenetic changes on pancreatic cancer biology, including carcinogenesis and resistance.
- To explore the potential of epigenetic drugs in improving treatment outcomes.
Main Methods:
- Review of literature on epigenetic dysregulation in pancreatic cancer.
- Analysis of molecular mechanisms including DNA methylation, histone acetylation, and microRNA expression.
- Examination of the role of epigenetic alterations in epithelial-mesenchymal transition, cancer stem cell regulation, and drug resistance.
Main Results:
- Epigenetic dysregulation impacts key pathways in pancreatic cancer development and progression.
- Specific epigenetic modifications are linked to epithelial-mesenchymal transition, cancer stem cell regulation, and resistance to therapy.
- Preclinical studies of epigenetic drugs demonstrate promising results.
Conclusions:
- Epigenetic alterations are crucial in pancreatic cancer pathogenesis and progression.
- Epigenetic drugs, including DNA methyltransferase and histone deacetylase inhibitors, offer potential therapeutic strategies.
- Combination therapies involving epigenetic drugs with conventional treatments may improve patient survival rates.
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