Abstract
Receptor tyrosine kinases, such as c-Kit, are proteins whose function it is to transduce signals from the environment into the cell leading to complex behaviors such as proliferation, migration, survival and differentiation. Many of these behaviors are deregulated in cancer, which is characterized by uncontrolled proliferation, insensitivity
towards death stimuli, migration of tumor cells away from the primary tumor site and in some cases also block of
cellular differentiation leaving the cell in an immature proliferative state. To be able to target these processes it is vital to have a detailed understanding of the receptor function and the downstream pathways activated. In this article we will review the mechanisms by which c-Kit induces signal transduction as well as describing tumors in
which c-Kit function is perturbed.
towards death stimuli, migration of tumor cells away from the primary tumor site and in some cases also block of
cellular differentiation leaving the cell in an immature proliferative state. To be able to target these processes it is vital to have a detailed understanding of the receptor function and the downstream pathways activated. In this article we will review the mechanisms by which c-Kit induces signal transduction as well as describing tumors in
which c-Kit function is perturbed.
Original language | English |
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Pages (from-to) | 5-28 |
Journal | Cancer Therapy |
Volume | 3 |
Publication status | Published - 2005 |
Bibliographical note
The information about affiliations in this record was updated in December 2015.The record was previously connected to the following departments: Experimental Clinical Chemistry (013016010)
Subject classification (UKÄ)
- Medicinal Chemistry
Free keywords
- Fertility
- Phospholipase C-g
- PI3-kinase
- Ras/Erk pathway
- degradation
- Transcription factors
- Adapter proteins
- tyrosine kinases
- c-Kit signal transduction
- Dimerization
- Internalization
- cancer
- Protein tyrosine phosphatases
- Hematopoiesis
- Gastrointestinal tract
- Nervous system
- Mastocytosis
- Melanoma
- Small-cell lung cancer
- JAK/STAT pathway
- homeostasis
- Pigmentation