132P - Biomarker analysis using circulating tumor DNA in patients treated with sorafenib for advanced hepatocellular carcinoma

Date 11 September 2017
Event ESMO 2017 Congress
Session Poster display session
Topics Anti-Cancer Agents & Biologic Therapy
Cancer in Adolescents
Hepatobiliary Cancers
Translational Research
Presenter Sook Ryun Park
Citation Annals of Oncology (2017) 28 (suppl_5): v22-v42. 10.1093/annonc/mdx363
Authors S.R. Park1, C.R. Oh2, S. Kong3, M.K. Kim4, K. Yoon5, E. Cho6, J. Jang6, J. Lee6, B. Ryoo7
  • 1Department Of Oncology, Asan Medical Center, University of Ulsan College of Medicine, 05505 - Seoul/KR
  • 2Department Of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 138-736 - Seoul/KR
  • 3Department Of Laboratory Medicine, Hospital, National Cancer Center, 10408 - Goyang/KR
  • 4Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, 10408 - Goyang/KR
  • 5College Of Veterinary Medicine, Konkuk University, 05029 - Seoul/KR
  • 6Genome Research Center, Green Cross Genome, Yongin/KR
  • 7Department Of Oncology, Asan Medical Center, University of Ulsan College of Medicine, 138-736 - Seoul/KR

Abstract

Background

We aimed to investigate potential biomarkers in patients treated with sorafenib for advanced hepatocellular carcinoma (HCC) using circulating tumour DNA (ctDNA).

Methods

155 patients who had started sorafenib between March 2014 and November 2016 were identified from a prospective biomarker cohort of Asan Medical Center, Korea. We quantified the concentration of ctDNA extracted from blood samples of each patient collected before sorafenib treatment and measured the copy numbers of vascular endothelial growth factor-A (VEGFA) in ctDNA. We also applied low depth whole genome sequencing from ctDNA to find copy number aberrations in HCC and employed Q-score, defined as a standard deviation regarding Z-scores of sequenced reads on each chromosome.

Results

Among 155 patients, 124 were finally included in the analysis. 82 patients achieved partial response, stable disease or non-CR/non-PD with sorafenib treatment (non-PD group) whereas 42 exhibited progressive disease (PD group). The PD group had significantly higher levels of ctDNA concentrations than the non-PD group (153.3 vs. 109.3 ng/mL; p = 0.038). Q-score of PD group was also higher than that of non-PD group but there was a borderline significant difference between two groups (6.10 vs. 3.80; p = 0.058). VEGFA copy number, which was available for only 41 patients, did not differ between PD (n = 16) and non-PD (n = 25) groups (2.56 vs. 2.48; p = 0.467). Divided into two groups based on the median value (119.7 ng/mL) of ctDNA concentrations, patients with high ctDNA had significantly shorter time to progression (TTP) (median, 2.3 vs. 4.1 months; p = 0.025) and overall survival (OS) (median, 4.5 vs. 14.8 months; p 

Conclusions

Our results showed that ctDNA level and copy number aberrations represented by Q-score could be potential prognostic biomarkers in HCC patients treated with sorafenib.

Clinical trial identification

Legal entity responsible for the study

Department of Oncology, Asan Medical Center, Seoul, Republic of Korea

Funding

None

Disclosure

All authors have declared no conflicts of interest.