32P - Prognostic impact of KRAS mutation in cell-free DNA in patients with pancreatic cancer

Date 11 September 2017
Event ESMO 2017 Congress
Session Poster display session
Topics Pancreatic Cancer
Translational Research
Presenter Min Kyeong Kim
Citation Annals of Oncology (2017) 28 (suppl_5): v1-v21. 10.1093/annonc/mdx361
Authors M.K. Kim1, S.M. Woo2, B. Park3, K. Yoon4, Y.H. Kim5, J. Joo3, S.J. Park2, S. Kong6
  • 1Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, 10408 - Goyang/KR
  • 2Center For Liver Cancer, National Cancer Center, 10408 - Goyang/KR
  • 3Biometric Research Branch, National Cancer Center, 10408 - Goyang/KR
  • 4College Of Veterinary Medicine, Konkuk University, 05029 - Seoul/KR
  • 5Molecular Imaging & Therapy Branch, National Cancer Center, 10408 - Goyang/KR
  • 67center For Hematologic Malignancy, National Cancer Center, 10408 - Goyang/KR

Abstract

Background

Cell-free DNA (cfDNA) has been known to be released from tumor cells and evaluated potential biomarkers for therapeutic responses. However, the role of cfDNA in pancreatic cancer has not been well studied. Here we selected KRAS mutation which has been known common over 95% of pancreatic ductal adenocarcinoma (PDA) and evaluated applicability as a prognostic marker through the quantitative analysis of cfDNA and KRAS mutation in the patients with PDA.

Methods

Total of 106 PDA patients were enrolled in the study. The concentration and fraction of KRAS mutation were measured by KRAS screening multiplex droplet digital PCR kit (Biorad, USA) in plasma samples.

Results

KRAS mutation was detected in 97.4% of tissue samples and the correlation with cfDNA was 0.561 with 80.5% positivity. KRAS mutation concentration and fractional abundance showed the association with poor survival in both PFS (P

Conclusions

This study represents that KRAS mutation concentration and fractional abundance in cfDNA could be prognostic marker in pancreatic cancer especially in resectable group.

Clinical trial identification

Legal entity responsible for the study

Sun-Young Kong

Funding

This work was supported by grants from the National Cancer Center of Korea (NCC-1510203).

Disclosure

All authors have declared no conflicts of interest.