Molecular targeting in the treatment of either advanced or metastatic bladder cancer or both according to the signalling pathways.
OBJECTIVE
An estimated 300,000 new cases of bladder cancer worldwide are diagnosed annually. Although new cytotoxic chemotherapeutic agents for either advanced or metastatic bladder cancer or both are used, no improvement in survival has been observed. Indeed, the 5-year survival rate of metastatic bladder cancer is very low (6%). The target-directed approach is an attractive challenge for treating specific genetic alterations involved in progression and metastasis development. This article aims to describe the new targeted therapies available to cure advanced cancer or metastatic bladder cancer or both according to the signalling pathways potentially involved.


RESULTS
The rapidly expanding understanding of the pathogenesis of bladder cancer at the molecular level has led to the identification of signalling pathways involved in this disease and provided molecular targets for new biological agents directed against tumorigenesis and progression. The recent results of clinical trials have not only highlighted the need to select patients who could benefit from such a therapy but also the fact that oncology has completely entered into a new era.


CONCLUSIONS
Toxic chemotherapeutic agents are slowly being supplemented by a new generation of drugs that recognize specific targets in or on cancer cells. Recent technological advances in pharmacogenomics and proteomics have led to an improvement in identifying biomarkers predictive of response and thereby to identify patients who would be more likely to respond to such a therapy. There is a real hope to improve both the efficiency and the tolerability of bladder cancer treatment.
Wallerand
Hervé
H
Department of Urology, Centre Hospitalo-Universitaire Pellegrin-Tripode, Victor Segalen School of Medicine, France. herve.wallerand@chu-bordeaux.fr
Reiter
Robert R
RR
Ravaud
Alain
A
D000970:Antineoplastic Agents / Q000008:administration & dosage*; D002453:Cell Cycle / Q000187:drug effects; D019175:DNA Methylation; D016503:Drug Delivery Systems; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000378:metabolism; D016161:Genes, Retinoblastoma; D015316:Genetic Therapy; D006801:Humans; D009389:Neovascularization, Pathologic / Q000188:drug therapy; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000235:genetics; D001749:Urinary Bladder Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism
D000970:Antineoplastic Agents; D066246:ErbB Receptors; D019869:Phosphatidylinositol 3-Kinases; D019253:Proto-Oncogene Proteins c-bcl-2; D018719:Erb-b2 Receptor Tyrosine Kinases; D016159:Tumor Suppressor Protein p53; C512478:EGFR protein, human; C508053:ERBB2 protein, human