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Role of c‐kit receptor tyrosine kinase in the development, survival and neoplastic transformation of mast cells
Author(s) -
Tsujimura Tohru
Publication year - 1996
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.1996.tb03571.x
Subject(s) - mast cell , receptor tyrosine kinase , biology , stem cell factor , proto oncogene proteins c kit , cancer research , receptor , interleukin 33 , tyrosine kinase , neoplastic transformation , microbiology and biotechnology , stem cell , immunology , cytokine , gene , carcinogenesis , interleukin , progenitor cell , genetics
The c‐kit gene is allelic with the dominant spotting ( W ) locus on mouse chromosome 5 and encodes a receptor tyrosine kinase. The llgand for c‐klt receptor is stem cell factor (SCF), which is the principal growth factor for mast cells. The loss‐of‐function mutations of c‐kit receptor affect the development of mast cells, thereby resulting in a depletion of mast cells. The abundant expression of c‐ktt receptor is indispensable for the survival of mast cells. In addition, the galn‐of‐function mutations of c‐kit receptor were found in several tumor mast cell lines. When these galn‐of‐function mutations were introduced to cells of murine interleukin (IL)‐3‐dependent cell lines, the expression of c‐kit receptor with constitutive tyrosine kinase activity not only abrogated the IL‐3 requirement of the cells, but also caused them to become tumorlgenic in nude athymic mice. The gain‐of‐function mutations of c‐kit receptor appear to result in the malignant transformation of mast cells. Taken together, the signals from the c‐ktt receptor are essential for the development, survival, and malignant transformation of mast cells.