Evaluation of KRAS mutations, angiogenic biomarkers, and DCE-MRI in patients with advanced non-small-cell lung cancer receiving sorafenib

Clin Cancer Res. 2011 Mar 1;17(5):1190-9. doi: 10.1158/1078-0432.CCR-10-2331. Epub 2011 Jan 11.

Abstract

Purpose: Sorafenib, a multikinase inhibitor targeting Raf and VEGFR, has shown activity in unselected patients with non-small-cell lung cancer (NSCLC). At present there are no validated biomarkers indicative of sorafenib activity.

Experimental design: Patients received sorafenib 400 mg BID daily to determine activity and tolerability and to measure its biological effects. KRAS mutation status (N = 34), angiogenesis markers (VEGF, bFGF, FLT-1, PLGF-1) and imaging with DCE-MRI (dynamic contrast enhanced MRI) to determine early changes in tumor vascular characteristics were evaluated. Three parameters K(trans), K(ep), and V(e) were measured by DCE-MRI at baseline and day 14 of cycle 1. Cytokine analysis was done on days 0, 14, 28, and 54.

Results: Thirty-seven patients with previously treated stage IV NSCLC were enrolled in this single-center phase II trial. In 34 evaluable patients, 2 had partial responses and 20 had stable disease for 3 to 17 months, a disease control rate of 65%. The median progression-free survival (PFS) was 3.4 months, and median overall survival (OS) was 11.6 months. Toxicity was consistent with the known side effects of sorafenib. KRAS (32%) and EGFR mutations (22%) showed no correlation with response, PFS, or OS. K(ep), was significant in predicting an improvement in OS (P = 0.035) and PFS (P = 0.029). Cytokine analysis demonstrated an improved OS for bFGF day 0 (<6 vs. >6 pg/mL; P = 0.042), whereas a PFS benefit was seen with bFGF at day 28 (<6 vs. >6; P = 0.028).

Conclusions: KRAS and EGFR mutational status showed no correlation with response, PFS, or OS. Radiologic and cytokine changes may act as biomarkers indicative of early angiogenesis inhibition.

Publication types

  • Clinical Trial, Phase II
  • Randomized Controlled Trial
  • Research Support, N.I.H., Intramural

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Angiogenesis Inhibitors
  • Antineoplastic Agents / therapeutic use*
  • Benzenesulfonates / therapeutic use*
  • Biomarkers, Tumor*
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Cytokines / analysis
  • Cytokines / metabolism
  • Disease-Free Survival
  • Drug-Related Side Effects and Adverse Reactions
  • ErbB Receptors / genetics
  • Female
  • Genes, ras*
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics
  • Lung Neoplasms / pathology
  • Magnetic Resonance Angiography
  • Male
  • Middle Aged
  • Mutation
  • Neovascularization, Pathologic
  • Niacinamide / analogs & derivatives
  • Phenylurea Compounds
  • Prognosis
  • Protein Kinase Inhibitors / therapeutic use
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins B-raf / genetics
  • Proto-Oncogene Proteins p21(ras)
  • Pyridines / therapeutic use*
  • Sorafenib
  • ras Proteins / genetics*

Substances

  • Angiogenesis Inhibitors
  • Antineoplastic Agents
  • Benzenesulfonates
  • Biomarkers, Tumor
  • Cytokines
  • KRAS protein, human
  • Phenylurea Compounds
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins
  • Pyridines
  • Niacinamide
  • Sorafenib
  • EGFR protein, human
  • ErbB Receptors
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins