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... read moreassociated 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
Maffini, Maricel, Ana M. Soto, Carlos Sonnenschein, Nikoletta
Papadopoulos, and Theoharis C. Theoharides. "Lack of c-kit receptor promotes mammary
tumors in N-nitrosomethylurea-treated Ws/Ws rats." Cancer Cell International 8, no. 1
(12, 2008): 1-7.