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Review
. 2023 Sep 15;15(9):1505-1519.
doi: 10.4251/wjgo.v15.i9.1505.

Deoxyribonucleic acid methylation driven aberrations in pancreatic cancer-related pathways

Akash Bararia  1 , Amlan Das  2 , Sangeeta Mitra  3 , Sudeep Banerjee  4 , Aniruddha Chatterjee  5   6 , Nilabja Sikdar  7
Affiliations
Review

Deoxyribonucleic acid methylation driven aberrations in pancreatic cancer-related pathways

Akash Bararia et al. World J Gastrointest Oncol. .

Abstract

Pancreatic cancer (PanCa) presents a catastrophic disease with poor overall survival at advanced stages, with immediate requirement of new and effective treatment options. Besides genetic mutations, epigenetic dysregulation of signaling pathway-associated enriched genes are considered as novel therapeutic target. Mechanisms beneath the deoxyribonucleic acid methylation and its utility in developing of epi-drugs in PanCa are under trails. Combinations of epigenetic medicines with conventional cytotoxic treatments or targeted therapy are promising options to improving the dismal response and survival rate of PanCa patients. Recent studies have identified potentially valid pathways that support the prediction that future PanCa clinical trials will include vigorous testing of epigenomic therapies. Epigenetics thus promises to generate a significant amount of new knowledge of biological and medical importance. Our review could identify various components of epigenetic mechanisms known to be involved in the initiation and development of pancreatic ductal adenocarcinoma and related precancerous lesions, and novel pharmacological strategies that target these components could potentially lead to breakthroughs. We aim to highlight the possibilities that exist and the potential therapeutic interventions.

Keywords: Methylation driven pathways; PanCa enriched methylated pathway; Pancreatic cancer methylation markers; Pre-cancer methylated pathways; Signaling pathway targeted therapy.

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Conflict of interest statement

Conflict-of-interest statement: All the authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Comprehensive visualization showcasing interaction between epigenetic pathways and probable drug treatments concerning pancreatic cancer. EGF: Epidermal growth factor; Ras/Raf/MEK/ERK: Rat sarcoma virus/Rapidly Accelerated Fibrosarcoma/Mitogen-activated protein kinase/extracellular-signal-regulated kinase; PI3K/AKT/mTOR: Phosphoinositide 3-kinases/Ak strain transforming/Mammalian target of rapamycin; Wnt: Wingless-related integration site; PDGF: Platelet-derived growth factor; SCF/c-Kit: Stem cell factor/receptor tyrosine kinase; ALK: Anaplastic lymphoma kinase; TGF-β: Transforming growth factor beta; HGF: Hepatocyte growth factor; JAK/STAT: Janus kinase/signal transducers and activators of transcription; BTK: Bruton tyrosine kinase; Src: Tyrosine-protein kinase (sarcoma); COX-2: Cyclooxygenase 2; NRF2: Nuclear factor erythroid 2–related factor 2; HIF-1: Hypoxia-inducible factor-1; PKCδ-PKD1: Protein Kinase Cδ-Polycystin 1, Transient Receptor Potential Channel Interacting; IGF: Insulin like growth factor; VEGF: Vascular endothelial growth factor.
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