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Research Note: Stem Cell Factor & Mast Cell Tumors

Clinician's Brief (Capsule)

Oncology

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April 2014

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Tyrosine kinase inhibitors (TKIs) work by inhibiting the KIT receptor. Two TKIs (ie, toceranib phosphate, masitinib mesylate) have been used for treatment of canine mast cell tumors (MCTs), achieving ~50% response in trials. Because of their mechanism of action, KIT activation should be necessary in tumors sensitive to these drugs; however, KIT mutations have been reported in ≤20% of MCTs, including those in trials. Mutation-independent KIT activation must therefore occur in at least some MCTs. Stem cell factor (SCF) is an important ligand for the KIT receptor that promotes mast cell migration, proliferation, and survival. SCF has been shown to stimulate mast cell tumorigenesis in an autocrine or paracrine fashion in vitro.

The purpose of this study was to determine the association of SCF expression with clinical MCTs. SCF was quantified in MCT specimens from canine patients and SCF expression during active cell growth was confirmed. Approximately 40% of cells expressed SCF, as compared with 0% of murine stromal cell controls. Canine MCTs express SCF especially in the growth phase, which may promote mast cell expansion in an autocrine or paracrine fashion, independent of whether a KIT mutation is present. TKIs can thus be rationally used for canine MCTs, even those lacking a KIT mutation. For the ~50% of MCTs unresponsive to TKIs, other unknown mutations or autocrine or paracrine actions of other cytokines may play a role.

Source

Production of stem cell factor in canine mast cell tumors. Amagai Y, Tanaka A, Jung K, et al. RES VET SCI 96:124-126, 2014.

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