Detection of Eukaryotic Microorganisms in Pancreatic Cancer Patients with 18S rRNA Gene–Based Digital PCR
Project no. 32247 · Status: Kapanmış · 2024
Summary
<p class="ql-align-justify"><span style="color: black;">Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies due to late diagnosis, limited therapeutic options, and high recurrence rates. The majority of patients are diagnosed at advanced stages, with restricted eligibility for surgical resection and a high risk of postoperative recurrence and metastasis. Therefore, there is an urgent need to identify novel mechanisms and biomarkers that influence tumor biology in order to improve early detection, prognostic assessment, and therapeutic response in PDAC. In recent years, increasing evidence has suggested that microbial components may play a significant role in pancreatic cancer development, postoperative complications, and treatment efficacy, with both bacterial and eukaryotic microorganisms influencing inflammation, immune responses, and the tumor microenvironment.</span></p><p class="ql-align-justify"><span style="color: black;">In this study, the presence and abundance of eukaryotic microorganisms potentially involved in PDAC pathogenesis were investigated using a digital PCR (dPCR)–based approach. Tissue samples obtained from patients with PDAC and distal cholangiocarcinoma (DCC), as well as saliva samples from these patients and from healthy controls, were analyzed for the 18S rRNA gene region. As part of this study, a dPCR assay enabling quantitative detection of the 18S rRNA gene in clinical samples was validated for the first time.</span></p><p class="ql-align-justify"><span style="color: black;">The results demonstrated no statistically significant difference in 18S rRNA gene copy numbers between PDAC and DCC tissue samples. However, higher 18S rRNA levels were consistently observed in PDAC tissues compared with DCC. Similarly, no statistically significant differences were detected among PDAC, DCC, and healthy control groups in saliva samples, although PDAC patients exhibited the highest median 18S rRNA levels, whereas healthy controls showed the lowest. Considering the anatomical connection of the pancreas to the gastrointestinal tract via the pancreatic duct, these findings suggest that oral eukaryotic microbial signals may partially reflect intrapancreatic dysbiosis, although salivary microbial burden alone may be insufficient as a standalone biomarker.</span></p><p class="ql-align-justify"><span style="color: black;">In conclusion, our findings support the concept that pancreatic cancer–associated microbiota is shaped by complex microbial interactions and global dysbiosis rather than by a single causative microorganism. Moreover, the 18S rRNA–based dPCR approach emerges as a promising and cost-effective tool for evaluating overall eukaryotic microbial burden in pancreatic cancer research.</span></p>