作者: Laura Attardi , Harold E. Varmus , Lucy A. Godley , Daniel Medina , Tyler Jacks
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摘要: Loss or mutation of p53 may have multiple biological and genetic effects that result in accelerated tumor progression. some tumors has been correlated with a marked decrease cell apoptosis. loss also accelerate growth through an increase proliferation rates. To examine the on progression controlled experimental context, we previously crossed p53-deficient mice to mammary tumor-susceptible Wnt-1 transgenic (TG) mice. The resulting female TG offspring this cross all developed tumors, regardless status (p53+/+, p53+/-, p53-/-). However, p53-/- much sooner than their p53+/+ counterparts. In report, demonstrate average rates missing (p53-/-) losing (p53+/- heterozygosity) are compared both wild-type alleles (p53+/+). This rate appears be due primarily increases proliferation. Tumor apoptotic levels were modest not measurably different presence absence p53. These results differ substantially from other mouse models which was closely attenuated Thus, mechanisms by influences differ, depending tissue type and/or oncogenic pathways involved.