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Sequential therapy in renal cell carcinoma.

Abstract
Because of the recent approval of several drugs for the treatment of renal cell carcinoma (including sorafenib, sunitinib, temsirolimus, and, in Europe, bevacizumab plus interferon), the use of sequential therapy has become routine practice. There is now evidence that administering these targeted agents sequentially provides clinical benefit by inducing tumor shrinkage and prolonged progression-free survival (PFS) in a large number of patients. However, data regarding overall survival (OS) are still pending. By adding these drugs in an adequate order, one can expect an increase in overall PFS of up to 27 months and a subsequent improvement in the OS of patients with renal cell carcinoma. It has been recently reported that the OS of patients treated with sunitinib in the first-line setting was 26 months. Expecting a survival of 40 months does appear possible based on currently available data, although this assumption will have to be proven in the future.
AuthorsBernard Escudier, Marine Gross Goupil, Christophe Massard, Karim Fizazi
JournalCancer (Cancer) Vol. 115 Issue 10 Suppl Pg. 2321-6 (May 15 2009) ISSN: 0008-543X [Print] United States
PMID19402067 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Copyright(c) 2009 American Cancer Society.
Chemical References
  • Antineoplastic Agents
  • Cytokines
  • Multiprotein Complexes
  • Proteins
  • Transcription Factors
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Protein-Tyrosine Kinases
  • Mechanistic Target of Rapamycin Complex 1
  • TOR Serine-Threonine Kinases
Topics
  • Antineoplastic Agents (administration & dosage)
  • Carcinoma, Renal Cell (drug therapy, mortality)
  • Clinical Trials as Topic
  • Cytokines (administration & dosage)
  • Drug Delivery Systems
  • Humans
  • Kidney Neoplasms (drug therapy, mortality)
  • Mechanistic Target of Rapamycin Complex 1
  • Multiprotein Complexes
  • Protein-Tyrosine Kinases (antagonists & inhibitors)
  • Proteins
  • TOR Serine-Threonine Kinases
  • Transcription Factors (antagonists & inhibitors)
  • Vascular Endothelial Growth Factor A (antagonists & inhibitors)

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