Resistance to angiogenesis inhibitors in renal cell carcinoma

Ila Tamaskar, Jaspreet Dhillon, Roberto Pili

Research output: Contribution to journalArticle

25 Scopus citations

Abstract

Antiangiogenic drugs are now available for treatment of renal cell carcinoma and are utilized sequentially to prolong clinical benefit in patients with recurrent disease. These antiangiogenic agents are disease stabilizing in most cases, and resistance eventually develops over time. Because different combinations and sequences are tested in clinical trials, resistance patterns and mechanisms should be investigated. Much effort has been devoted to understanding the biology and elucidating the pathways and additional targets during tumorigenesis and metastasis. Resistance appears to be either primary nonresponsiveness, or it is acquired over time and related to various evasive/escape mechanisms that the tumor develops in response to therapy. Primary resistance is less common, but may be due to an intrinsic redundancy of available angiogenic signals for the tumor, causing unresponsiveness to vascular endothelial growth factor (VEGF)-targeted therapies. During acquired resistance, tumors may activate an "angiogenic switch," which leads to either upregulation of the existing VEGF pathway or recruitment of alternative factors responsible for tumor revascularization. Rationally designed preclinical and clinical trials will shed additional light on our understanding of the potential mechanisms of resistance to antiangiogenic drugs.

Original languageEnglish (US)
Pages (from-to)101-110
Number of pages10
JournalClinical Advances in Hematology and Oncology
Volume9
Issue number2
StatePublished - Feb 1 2011

    Fingerprint

Keywords

  • Antiangiogenesis
  • Renal cell carcinoma
  • Resistance
  • VEGF

ASJC Scopus subject areas

  • Hematology
  • Oncology

Cite this