SAN FRANCISCO—Endothelial nitric oxide synthase (eNOS) VNTR and eNOS -786 could determine outcomes in patients with advanced hepatocellular carcinoma treated with the tyrosine kinase inhibitor, sorafenib, a study (Abstract 230) presented this week at the 2015 Gastrointestinal Cancers Symposium has shown.
Cancer cells are known to adapt to hypoxic microenvironments by activating various molecules, such as eNOS. Sorafenib inhibits eNOS activity, thereby decreasing nitric oxide production and ultimately inhibiting tumor angiogenesis, tumor invasion, and metastasis.
For this study, researchers sought to investigate the effect of eNOS polymorphisms on clinical outcomes in patients with hepatocellular carcinoma treated with sorafenib.
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Researchers identified 54 patients treated with sorafenib for hepatocellular carcinoma between 2004 and 2014 and analyzed three eNOS polymorphisms (eNOS +894 G/T, eNOS VNTR 27bp 4a/b, eNOS -786 C/T) from peripheral blood samples or FFPE tumor tissues.
Results showed that patients with the ENOS VNTR b allele had increased overall survival compared with those that did not (4aa = 5.7 months, 4ab = 13.9 months, 4bb = 23.6 months; P = 0.016).
Patients with the eNOS -786 T allele also had significantly long overall survival compared to those who did not (P = 0.031). The researchers note that eNOS polymorphisms did not correlate with progression-free survival (P = 0.494).
Reference
- Gardini AC, Marisi G, Scarpi E, et al. eNOS polymorphisms in relation to outcome in advanced HCC patients receiving sorafenib. J Clin Oncol. 2015;33:(suppl 3; abstr 230).
