Abstract 961P
Background
Galectin-3 plays critical roles in the adhesion, proliferation, and differentiation of tumor cells. Recent data has suggested that galectin-3 plays a role in the development of hepatocellular carcinoma (HCC), however, its prognostic value has not been validated. The aim of our study was to evaluate the clinical and prognostic value of galectin-3 in HCC patients.
Methods
We prospectively enrolled and collected clinicopathologic data and serum samples from 767 HCC patients between 2001 and 2014 at The University of Texas MD Anderson Cancer Center. The cut-off value for low versus high galectin-3 levels was established using ROC curve analysis. The Kaplan-Meier method was used to estimate overall survival (OS) distributions.
Results
The median OS in this cohort was 14.2 months (95% confidence interval [CI]: 12, 16.1 months). OS was significantly associated with clinicopathologic features, including tumor-node-metastasis (TNM) staging (p<0.001), Child-Pugh Score (CPS) (p<0.001), cirrhosis (p<0.001), metastasis (p<0.001), and alpha-fetoprotein (AFP) level (p<0.001). At the time of analysis, the one-year OS rate was 45% (95% CI: 0.4, 0.51) among patients with high galectin-3 levels, and 59% (95% CI: 0.54, 0.63) among patients with low galectin-3 levels. OS was significantly inferior in patients with high galectin-3 levels compared to patients with lower galectin-3 levels (median OS: 10.12 vs 16.49 months; p=0.0022). Higher galectin-3 levels were significantly associated with a higher risk of death (HR =1.29, 95% CI: 1.1, 1.53). Comparison between low (n = 464 patients) and high (n = 302 patients) galectin-3 levels showed that mean serum galectin-3 levels were significantly higher in HCC patients with HCV (p=0.0001), viral-induced hepatitis (p=0.0002), higher Child-Pugh Score (CPS) (p=0.0009), and higher Cancer of the Liver Italian Program (CLIP) score (p=0.0015).
Conclusions
In conclusion, our study shows that serum galectin-3 level is a valid prognostic biomarker candidate and a potential target for therapy in HCC.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
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