Molecular basis for the treatment of renal cell carcinoma

Clin Transl Oncol. 2010 Jan;12(1):15-21. doi: 10.1007/s12094-010-0461-4.

Abstract

Renal cell carcinoma (RCC) is a heterogeneous malignancy whose incidence rate has notably increased in recent years without any evident reason. Traditionally, RCC has been resistant to classic treatments (chemotherapy, radiotherapy and hormonal therapy), with only a small percentage of patients benefiting from cytokine therapy. Different hereditary syndromes have been associated with RCC, Von Hippel Lindau (VHL) being the most important syndrome. Understanding key molecular pathways implicated in the tumorigenesis of RCC has crystallised in the development of more effective therapies. Specifically, drugs targeting VEGF (bevacizumab, sunitinib, sorafenib, axitinib, pazopanib) and PI3K-mTOR (temsirolimus and everolimus) have become the cornerstone of renal cancer treatment.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / administration & dosage
  • Carcinoma, Renal Cell / drug therapy
  • Carcinoma, Renal Cell / etiology
  • Carcinoma, Renal Cell / genetics*
  • Drug Delivery Systems
  • Genetic Predisposition to Disease
  • Humans
  • Intracellular Signaling Peptides and Proteins / genetics
  • Kidney Neoplasms / drug therapy
  • Kidney Neoplasms / etiology
  • Kidney Neoplasms / genetics*
  • Protein Serine-Threonine Kinases / genetics
  • Signal Transduction / genetics
  • Syndrome
  • TOR Serine-Threonine Kinases
  • Vascular Endothelial Growth Factor A / genetics

Substances

  • Antineoplastic Agents
  • Intracellular Signaling Peptides and Proteins
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • MTOR protein, human
  • Protein Serine-Threonine Kinases
  • TOR Serine-Threonine Kinases