Multicenter prospective study of angiogenesis polymorphism validation in HCC patients treated with sorafenib. An INNOVATE study protocol

Tumori. 2018 Dec;104(6):476-479. doi: 10.5301/tj.5000704. Epub 2018 May 9.

Abstract

Introduction: Although sorafenib is the upfront standard of care for advanced hepatocellular carcinoma (HCC), molecular predictors of efficacy have not been identified yet. In the ALICE-1 study, rs2010963 of VEGF-A and VEGF-C proved to be independent predictive factors for progression-free survival (PFS) and overall survival (OS) in multivariate analysis. The ALICE-1 study results were confirmed in the ALICE-2 study, in which VEGF and VEGFR SNPs were analyzed. In the ePHAS study we analyzed the SNPs of eNOS. In univariate analysis, patients homozygous for an eNOS haplotype (HT1: T-4b at eNOS-786/eNOS VNTR) had significantly shorter median PFS and OS than those with other haplotypes. These data were confirmed in the validation set.

Methods: This nonpharmacological, interventional, prospective multicenter study aims to determine whether eNOS, HIF-1, VEGF, Ang2 and VEGFR polymorphisms play a role in predicting the objective response rate, PFS, and OS of advanced HCC patients treated with sorafenib. The study will involve 160 advanced HCC patients with Child-Pugh class A disease. The primary aim is to validate the prognostic or predictive roles of eNOS, Ang2, HIF-1, VEGF and VEGFR polymorphisms in relation to the clinical outcome (PFS) of HCC patients treated with sorafenib.

Conclusions: Overall, our data may suggest that polymorphism analysis of the VEGF, VEGFR-2, HIF and eNOS genes can identify HCC patients who are more likely to benefit from sorafenib.

Keywords: Biomarkers; Hepatocellular carcinoma; Sorafenib; Trial; VEGF; eNOS.

Publication types

  • Multicenter Study

MeSH terms

  • Adolescent
  • Angiopoietin-2 / genetics
  • Antineoplastic Agents / therapeutic use
  • Carcinoma, Hepatocellular / drug therapy*
  • Carcinoma, Hepatocellular / genetics*
  • Disease-Free Survival
  • Female
  • Humans
  • Hypoxia-Inducible Factor 1 / genetics
  • Liver Neoplasms / drug therapy*
  • Liver Neoplasms / genetics*
  • Male
  • Neovascularization, Pathologic / genetics*
  • Nitric Oxide Synthase Type III / genetics
  • Polymorphism, Single Nucleotide / genetics*
  • Prospective Studies
  • Receptors, Vascular Endothelial Growth Factor / genetics
  • Sorafenib / therapeutic use*
  • Vascular Endothelial Growth Factor A

Substances

  • Angiopoietin-2
  • Antineoplastic Agents
  • Hypoxia-Inducible Factor 1
  • Vascular Endothelial Growth Factor A
  • Sorafenib
  • Nitric Oxide Synthase Type III
  • Receptors, Vascular Endothelial Growth Factor