Artikel
Galectin-1 expression in human glioblastoma specimens with regard to clinical outcome
Suche in Medline nach
Autoren
Veröffentlicht: | 18. Juni 2018 |
---|
Gliederung
Text
Objective: Galectin-1 (Gal-1) is a small protein that plays important roles in inflammatory response, tumor development, and in tumor progression. It is known that Gal-1 is overexpressed in GBM cell lines and could influence chemo- and immunotherapy resistance. This study was conducted to investigate Gal-1 expression in human methylated and unmethylated GBM specimens and to determine the influence of Gal-1 overexpression on overall survival (OS) and progression-free survival (PFS).
Methods: In 31 glioblastoma patients Gal-1 expression was determined by performing quantitative real-time PCR (qPCR). Median Gal-1 expression in qPCR was 2.18 (IQR: 0.71 – 8.10). Gal-1 expression below the median was defined as low Gal-1 expression (LGE). Gal-1 expression ≥2.18 was defined as high Gal-1 expression (HGE). Groups were compared by using the Mann-Whitney U test. The influence of Gal-1 expression on PFS and OS was analyzed by the Kaplan-Meier method and the log-rank test.
Results: Median patients' age was 58 (IQR: 52-67) years. Median overall survival (OS) was 308 (IQR: 161 - 499) days and median PFS was 166 (IQR: 114 - 216) days. MGMT-methylation was positive in 18 patients (58.1%) and negative in 13 patients (41.9%). No statistically significant difference (p=0.394) in median Gal-1 expression between methylated (1.89; IQR: 1.16 - 9.88) and umethylated (3.27; IQR: 0.35 - 7.39) patients was found.
Survival analysis showed that HGE was associated with a shorter progression free survival compared to patients with LGE (163 vs. 266 days; p=0.041). No statistically significant effect on OS for patients with HGE compared to patients with LGE was observed (313 vs. 470 days; p=0.243).
Conclusion: Gal-1 overexpression seems to be associated with a shorter PFS in patients with GBM, independent of MGMT methylation. Gal-1 could be a target of anti-proliferative therapies in human GBM.