Lack of c-kit receptor promotes mammary tumors in N-nitrosomethylurea-treated Ws/Ws rats |
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Authors: | Maricel V Maffini Ana M Soto Carlos Sonnenschein Nikoletta Papadopoulos Theoharis C Theoharides |
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Institution: | (1) Department of Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, USA;(2) Department of Pharmacology and Experimental Therapeutics, Biochemistry and Internal Medicine, Tufts University School of Medicine, and Tufts-New England Medical Center, Boston, USA |
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Abstract: | Background c-kit is expressed in various cell types during development and it has been linked to the promotion of cellular migration, proliferation
and/or survival of melanoblasts, hematopoietic progenitors and primordial germ cells. Several reports have proposed a role
for the c-kit gene on carcinogenesis. Gain-of-function mutations are associated with diseases such as mastocytosis and gastrointestinal
stromal tumors among others. However, very little is known about pathologies associated with loss-of-function mutations. Regarding
breast cancer, c-kit protein and mRNA are highly expressed in normal breast but their expression decreases or is absent in
the presence of breast cancer. We studied the role of c-kit in mammary carcinogenesis in the Ws/Ws rats carrying spontaneous lack-of-function mutation in the c-kit gene. Fifty day-old virgin female Ws/Ws rats and their wild type counterparts were injected with either 50 mg/kg body weight
of the chemical carcinogen N-nitrosomethylurea or with vehicle. The animals were followed-up for 6 months. Fisher 344 rats
were used as positive controls for tumor development. |
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