Sunitinib in urothelial cancer: clinical, pharmacokinetic, and immunohistochemical study of predictors of response

Eur Urol. 2011 Aug;60(2):344-9. doi: 10.1016/j.eururo.2011.05.034. Epub 2011 May 25.

Abstract

Background: Sunitinib has activity in patients with metastatic urothelial cancer (UC), but most patients do not respond.

Objective: To identify predictors of response to sunitinib.

Design, setting, and participants: Seventy-seven patients with advanced UC received sunitinib on one of two schedules at a single institution. Blood pressure (BP), immunohistochemistry (IHC), and pharmacokinetic (PK) results were correlated with response to sunitinib.

Measurements: BP was assessed on day 1 and 28 of each cycle and on day 14 of cycle 1. IHC was performed on 55 samples from 38 cases using mammalian target of rapamycin and hypoxia-inducible factor (HIF) pathway marker antibodies. Blood samples for PK analysis were collected from 15 patients at three time points. Response was assessed using Response Evaluation Criteria in Solid Tumors criteria.

Results and limitations: Sunitinib-induced hypertension predicted improved response when hypertension was categorized as a discrete (p = 0.02) or continuous variable (p = 0.005 [systolic BP] and p = 0.007 [diastolic BP]). The odds ratio of response was 12.5 (95% confidence interval, 1.95-246.8) for grade 3/4 hypertension compared with grade 0. Response was associated with low HIF-1α expression in primary (p = 0.07) tissue. A nonstatistically significant trend was seen for an association between greater drug concentration and best response. A correlation between expression markers within the same pathways was identified, phosphorylated-4EBP1 and phosphorylated-S6 (p = 6.5 × 10(-9)), and vascular endothelial growth factor receptor 2 and HIF-1α (p = 0.008). Results are limited by small numbers.

Conclusions: Clinical and molecular biomarkers of response to sunitinib may have clinical relevance and require prospective validation. There is an urgent need for predictive biomarkers to guide the management of UC.

MeSH terms

  • Adaptor Proteins, Signal Transducing / analysis
  • Angiogenesis Inhibitors / administration & dosage
  • Angiogenesis Inhibitors / adverse effects
  • Angiogenesis Inhibitors / pharmacokinetics*
  • Biomarkers, Tumor / analysis
  • Biomarkers, Tumor / antagonists & inhibitors*
  • Blood Pressure / drug effects
  • Carcinoma, Transitional Cell / chemistry
  • Carcinoma, Transitional Cell / drug therapy*
  • Carcinoma, Transitional Cell / pathology
  • Cell Cycle Proteins
  • Drug Administration Schedule
  • Humans
  • Hypertension / chemically induced
  • Hypoxia-Inducible Factor 1, alpha Subunit / analysis
  • Immunohistochemistry*
  • Indoles / administration & dosage
  • Indoles / adverse effects
  • Indoles / pharmacokinetics*
  • Logistic Models
  • New York City
  • Phosphoproteins / analysis
  • Phosphorylation
  • Pyrroles / administration & dosage
  • Pyrroles / adverse effects
  • Pyrroles / pharmacokinetics*
  • Retrospective Studies
  • Risk Assessment
  • Risk Factors
  • Sunitinib
  • TOR Serine-Threonine Kinases / analysis
  • Tissue Array Analysis
  • Treatment Outcome
  • Urologic Neoplasms / chemistry
  • Urologic Neoplasms / drug therapy*
  • Urologic Neoplasms / pathology
  • Urothelium / chemistry
  • Urothelium / drug effects*
  • Urothelium / pathology
  • Vascular Endothelial Growth Factor Receptor-2 / analysis
  • Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors*

Substances

  • Adaptor Proteins, Signal Transducing
  • Angiogenesis Inhibitors
  • Biomarkers, Tumor
  • Cell Cycle Proteins
  • EIF4EBP1 protein, human
  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Indoles
  • Phosphoproteins
  • Pyrroles
  • MTOR protein, human
  • Vascular Endothelial Growth Factor Receptor-2
  • TOR Serine-Threonine Kinases
  • Sunitinib