Cell-Free DNA Methylation as Blood-Based Biomarkers for Pancreatic Adenocarcinoma—A Literature Update

Henriksen, Stine Dam; Thorlacius-Ussing, Ole

doi:10.3390/epigenomes5020008

Cited by 14 publications

(7 citation statements)

References 45 publications

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“…There are several studies on cell-free DNA methylation analysis using plasma or serum as an analyte to diagnose or monitor pancreatic cancer (reviewed in [ 26 ]). In one study, methylation-specific PCR targeting 8 loci of blood-derived DNA in 95 patients with PDAC yielded only moderate accuracy with a sensitivity of 76% at 83% specificity [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Liquid biopsy, using a novel DNA methylation signature, distinguishes pancreatic adenocarcinoma from benign pancreatic disease

et al. 2022

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We tested the ability of a novel DNA methylation biomarker set to distinguish metastatic pancreatic cancer cases from benign pancreatic cyst patients and to monitor tumor dynamics using quantitative DNA methylation analysis of cell-free DNA (cfDNA) from blood samples. The biomarkers were able to distinguish malignant cases from benign disease with high sensitivity and specificity (AUC = 0.999). Furthermore, the biomarkers detected a consistent decline in tumor-derived cfDNA in samples from patients undergoing chemotherapy. The study indicates that our liquid biopsy assay could be useful for management of pancreatic cancer patients.

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Section: Discussionmentioning

confidence: 99%

Liquid biopsy, using a novel DNA methylation signature, distinguishes pancreatic adenocarcinoma from benign pancreatic disease

et al. 2022

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“…Adding another diagnostic modality (CA19-9 levels, KRAS mutation status etc.) to the assessment of cfDNA methylation can improve accuracy [ 90 , 92 , 93 ]. Evaluating CA 19-9 levels together with the methylation status of RUNX3 in cfDNA was able to increase sensitivity to detect PDAC from 50.9% ( RUNX3 DNA methylation alone) to 85.5% [ 92 ].…”

Section: Diagnostic Utility Of Epigenetic Modifications In Pdacmentioning

confidence: 99%

Epigenetics in Pancreatic Ductal Adenocarcinoma: Impact on Biology and Utilization in Diagnostics and Treatment

Elrakaybi

Ruess

Lübbert

et al. 2022

Cancers

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies with high potential of metastases and therapeutic resistance. Although genetic mutations drive PDAC initiation, they alone do not explain its aggressive nature. Epigenetic mechanisms, including aberrant DNA methylation and histone modifications, significantly contribute to inter- and intratumoral heterogeneity, disease progression and metastasis. Thus, increased understanding of the epigenetic landscape in PDAC could offer new potential biomarkers and tailored therapeutic approaches. In this review, we shed light on the role of epigenetic modifications in PDAC biology and on the potential clinical applications of epigenetic biomarkers in liquid biopsy. In addition, we provide an overview of clinical trials assessing epigenetically targeted treatments alone or in combination with other anticancer therapies to improve outcomes of patients with PDAC.

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“…Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant tumors with high mortality and tens of thousands of newly diagnosed cases are reported by global statistics [1,2]. Worldwide, the widespread application of screening has reduced the global morbidity and mortality associated with PDAC [3]. Although great progress have done in PDAC treatment, the 5-year survivals are still fabulously less than 6% [4,5].…”

Section: Introductionmentioning

confidence: 99%

m6A-modified circRNA MYO1C participates in the tumor immune surveillance of pancreatic ductal adenocarcinoma through m6A/PD-L1 manner

et al. 2023

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Emerging evidence indicates the critical roles of N6-methyladenosine (m6A) modification in human cancers. Herein, our work reported that a novel m6A-modified circRNA from the MYO1C gene, circMYO1C, upregulated in the pancreatic ductal adenocarcinoma (PDAC). Our findings demonstrated that circMYO1C is highly expressed in PDAC tissues. Functionally, circMYO1C promoted the proliferation and migration of PDAC cells in vitro and its silencing reduced the tumor growth in vivo. Mechanistically, circMYO1C cyclization was mediated by m6A methyltransferase METTL3. Moreover, methylated RNA immunoprecipitation sequencing (MeRIP-seq) unveiled the remarkable m6A modification on PD-L1 mRNA. Moreover, circMYO1C targeted the m6A site of PD-L1 mRNA to enhance its stability by cooperating with IGF2BP2, thereby accelerating PDAC immune escape. In conclusion, these findings highlight the oncogenic role of METTL3-induced circMYO1C in PDAC tumorigenesis via an m6A-dependent manner, inspiring a novel strategy to explore PDAC epigenetic therapy.

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Cell-Free DNA Methylation as Blood-Based Biomarkers for Pancreatic Adenocarcinoma—A Literature Update

Cited by 14 publications

References 45 publications

Liquid biopsy, using a novel DNA methylation signature, distinguishes pancreatic adenocarcinoma from benign pancreatic disease

Liquid biopsy, using a novel DNA methylation signature, distinguishes pancreatic adenocarcinoma from benign pancreatic disease

Epigenetics in Pancreatic Ductal Adenocarcinoma: Impact on Biology and Utilization in Diagnostics and Treatment

m6A-modified circRNA MYO1C participates in the tumor immune surveillance of pancreatic ductal adenocarcinoma through m6A/PD-L1 manner

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