Intracellular signal transduction pathway proteins as targets for cancer therapy Review uri icon

Overview

MeSH Major

  • Antineoplastic Agents
  • Biomarkers, Tumor
  • Enzyme Inhibitors
  • Neoplasms
  • Signal Transduction

abstract

  • Circulating cytokines, hormones, and growth factors control all aspects of cell proliferation, differentiation, angiogenesis, apoptosis, and senescence. These chemical signals are propagated from the cell surface to intracellular processes via sequential kinase signaling, arranged in modules that exhibit redundancy and cross talk. This signal transduction system comprising growth factors, transmembrane receptor proteins, and cytoplasmic secondary messengers is often exploited to optimize tumor growth and metastasis in malignancies. Thus, it represents an attractive target for cancer therapy. This review will summarize current knowledge of selected intracellular signaling networks and their role in cancer therapy. The focus will be on pathways for which inhibitory agents are currently undergoing clinical testing. Original data for inclusion in this review were identified through a MEDLINE search of the literature. All papers from 1966 through March 2005 were identified by the following search terms: "signal transduction," "intracellular signaling," "kinases," "proliferation," "growth factors," and "cancer therapy." All original research and review papers related to the role of intracellular signaling in oncogenesis and therapeutic interventions relating to abnormal cell signaling were identified. This search was supplemented by a manual search of the Proceedings of the Annual Meetings of the American Association for Cancer Research, American Society of Clinical Oncology, and the American Association for Cancer Research (AARC)--European Organisation for Research and Treatment of Cancer (EORTC)--National Cancer Institute (NCI) Symposium on New Anticancer Drugs.

publication date

  • December 2005

Research

keywords

  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1200/JCO.2005.23.648

PubMed ID

  • 15983388

Additional Document Info

start page

  • 5386

end page

  • 403

volume

  • 23

number

  • 23