![]() The methylation frequency of each gene is presented in Table 2. The hypermethylation profile for each patient is illustrated on the heat map plot in Additional file 6. In addition, the correlation between level of cell-free DNA and number of hypermethylated genes was statistically significant with a Kendall’s τ of 0.34 (Additional file 5). Patients with pancreatic adenocarcinoma had a significant higher median level of cell-free DNA (11.60 ng/ml (range 0.60–957.17)) compared to control group 1 with 6.17 ng/ml (range 1.06–48.43), control group 2 with 2.18 ng/ml (0.11–115.44) and 4.09 ng/ml (range 0.65–62.42) for control group 3 (Additional file 4). The aim of this study was to test (by methylation-specific polymerase chain reaction (PCR)) cell-free DNA promoter hypermethylation of a panel of 28 genes as a blood-based diagnostic marker for pancreatic adenocarcinoma, including clinical relevant control groups of patients with benign pancreatic disease. When developing and testing a biomarker for pancreatic cancer, inclusion of relevant control groups with benign pancreatic disease is very important to enable differentiation of pancreatic cancer-specific hypermethylation and hypermethylation related to pancreatic disease in general. None of the previously examined genes have the potential to serve as an individual diagnostic marker. However, the studies had difficulties in differentiating between malignant and benign pancreatic disease. These data have shown a significant difference in DNA hypermethylation between patients with pancreatic cancer and healthy controls. Thus far, only a few studies with small numbers of patients have evaluated cell-free DNA hypermethylation as a blood-based marker for pancreatic cancer, testing the methylation status of only a single gene or small gene panel. DNA hypermethylation can be detected in cell-free DNA in plasma and serum and is potentially tumour specific and useable as blood-based diagnostic markers for pancreatic cancer. Ĭancer cells may release cell-free DNA into the blood. Hypermethylation in the promoter region results in gene silencing, which may be associated with cancer formation. DNA hypermethylation is an epigenetic phenomenon, where a methyl (CH3) residue is added to cytosines preceding guanosines (CpGs). Epigenetic modifications change the DNA conformation and therefore the gene expression. Epigenetic modifications occur at a genomic level, which does not change the DNA sequence. It would be a major advance for the patients if a blood-based diagnostic marker was available.ĭuring the development of pancreatic cancer, genetic and epigenetic changes take place. Moreover, 10% of the population lack the ability to produce CA-19-9, making its utility less apparent. The only useful biomarker is CA-19-9, which is unspecific as patients with chronic pancreatitis and particularly benign biliary obstruction tend to express high levels of CA-19-9. However, the differentiation between malignant and benign pancreatic disease can be difficult, and even surgery may be needed to establish a definite diagnosis. Often, several complex or invasive techniques such as PET scan (positron emission tomography), CT scan (computed tomography), endoscopic or laparoscopic ultrasound and ERCP (endoscopic retrograde cholangiopancreatography) are needed for the diagnosis and many patients also need a histological evaluation. This is mainly due to lacking or non-specific symptoms, which are also related to chronic pancreatitis, an essential differential diagnosis and a known risk factor for pancreatic cancer. ![]() Difficulties in detecting the disease at an early stage results in high mortality. ![]() Despite surgery, 50% of patients experience recurrence. Unfortunately, only 10–20% of patients receive treatment with the intend to cure. The only curative treatment is complete tumour resection. Pancreatic cancer is the fourth leading cause of cancer death in the world, with a 5-year survival rate of approximately 5–7%.
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