Serial EUS-Guided FNA for the Surveillance of Pancreatic Cysts: A Study of Long-Term Performance of Tumor Markers.
KRAS mutations in pancreatic cysts can frequently change over time, with age being a predictor of these changes.
Where it sits
this study against the rest of the pancragen (kedw) corpusSummary and findings
This study examined the performance of DNA markers and changes in KRAS mutations in mucinous pancreatic cysts over time. A total of 933 pancreatic cyst fluid samples were collected from patients undergoing EUS-FNA, with a median follow-up of 30 months. The study found that KRAS mutations can frequently change during long-term surveillance.
Abstract
<h4>Background and aim</h4>The natural history of KRAS mutations in mucinous pancreatic cysts (MPCs) over time remains to be fully understood. The aim of this study was to examine the performance of DNA markers and assess changes of KRAS mutations over time.<h4>Methods</h4>Patients who underwent EUS-FNA of pancreatic cysts with at least two separate molecular analysis results were included in the study. We assessed the baseline patient and cyst characteristics, and DNA fluid analysis. The presence of either a KRAS mutation, or a CEA > 192 ng/ml was used as the diagnostic standard for mucinous cysts when surgical pathology was not available.<h4>Results</h4>A total of 933 pancreatic cyst fluid samples were collected, including 117 with ≥ 2 FNAs. Examinations were performed over a median of 30 months (range 1-115 months). Forty-three (36%) had a mutant KRAS on the index analysis out of which 26 had a change in their KRAS status to the wild-type. Eighty-one (64%) had a wild-type KRAS on the index analysis out of which 18 had change in their KRAS status to mutant type. There was no significant difference in the index cyst characteristics, presence of symptoms, or main duct involvement based on KRAS status change. Increasing age was associated with a changing KRAS mutation status (p = 0.023).<h4>Conclusion</h4>KRAS mutations gain and loss in pancreatic cyst fluid appears to occur frequently during long-term surveillance of MPCs. Age appears to be the only predictor for KRAS change over time.
Background
This paper addresses the natural history of KRAS mutations in mucinous pancreatic cysts (MPCs), which is not fully understood. Prior research has indicated that KRAS mutations may play a role in the diagnosis and management of pancreatic cysts. Understanding the dynamics of these mutations over time is crucial for improving surveillance strategies.
Methods
The study included patients who underwent EUS-FNA of pancreatic cysts and had at least two separate molecular analysis results. A total of 933 pancreatic cyst fluid samples were collected, with 117 samples having two or more FNAs. The primary outcome was the change in KRAS mutation status over a median follow-up of 30 months.
Results
Out of 933 samples, 43 (36%) had a mutant KRAS on the index analysis, and 26 of these changed to wild-type. Conversely, 81 (64%) had a wild-type KRAS on the index analysis, with 18 changing to mutant type. The study reported a p-value of 0.023 for the association between increasing age and changing KRAS mutation status.
Interpretation
The findings suggest that KRAS mutations can frequently change during long-term surveillance of MPCs, which aligns with some previous literature indicating variability in mutation status. However, the clinical significance of these changes remains uncertain, particularly given the lack of significant differences in cyst characteristics based on KRAS status change. Limitations such as the observational design and reliance on molecular analysis without surgical confirmation may confound the conclusions.
Key findings
- 933 pancreatic cyst fluid samples collected, n=117 with ≥2 FNAs.
- 43 (36%) had a mutant KRAS on the index analysis.
- 26 had a change in their KRAS status to wild-type.
- 81 (64%) had a wild-type KRAS on the index analysis.
- 18 had a change in their KRAS status to mutant type.
- Increasing age was associated with a changing KRAS mutation status (p=0.023).
Limitations
- observational study design
- reliance on molecular analysis without surgical pathology
- median follow-up of 30 months may not capture long-term trends
- n=933 samples but only n=117 with ≥2 FNAs