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The stem cell factor receptor/c-Kit as a drug target in cancer
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Ludwig Institute for Cancer Research.
Experimental Clinical Chemistry, Dept. of Laboratory Medicine, Lund University, Malmö University Hospital, SE-205 02 Malmö, Sweden.
2006 (English)In: Current Cancer Drug Targets, ISSN 1568-0096, Vol. 6, no 1, 65-75 p.Article in journal (Refereed) Published
Abstract [en]

Tyrosine phosphorylation has a key role in intracellular signaling. Inappropriate proliferation and survival cues in tumor cells often occur as a consequence of unregulated tyrosine kinase activity. Much of the current development of anti-cancer therapies tries to target causative proteins in a specific manner to minimize side-effects. One attractive group of target proteins is the kinases. c-Kit is a receptor tyrosine kinase that normally controls the function of primitive hematopoietic cells, melanocytes and germ cells. It has become clear that uncontrolled activity of c-Kit contributes to formation of an array of human tumors. The unregulated activity of c-Kit may be due to overexpression, autocrine loops or mutational activation. This makes c-Kit an excellent target for cancer therapies in these tumors. In this review we will highlight the current knowledge on the signal transduction molecules and pathways activated by c-Kit under normal conditions and in cancer cells, and the role of aberrant c-Kit signaling in cancer progression. Recent advances in the development of specific inhibitors interfering with these signal transduction pathways will be discussed.

Place, publisher, year, edition, pages
2006. Vol. 6, no 1, 65-75 p.
Keyword [en]
Stem cell factor, c-Kit, receptor tyrosine kinase, signal transduction, transformation, cancer, leukemia
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-76065PubMedID: 16475976OAI: oai:DiVA.org:uu-76065DiVA: diva2:103976
Available from: 2006-02-23 Created: 2006-02-23 Last updated: 2012-02-29Bibliographically approved

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