作者: T. D. Tlsty , B. H. Margolin , K. Lum
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摘要: Abstract It has been hypothesized that genomic fluidity is an important component of tumorigenesis. Previous studies described the relationship between tumorigenicity and one marker for fluidity, gene amplification. In this report, these are extended with rat liver epithelial cell lines to show that: (i) amplification in cells arises a spontaneous fashion population (i.e., variants detected not preexisting population), (ii) rate (mutation), as measured by Luria-Delbruck fluctuation analysis, significantly lower nontumorigenic than tumorigenic cells. The was estimated using Po method means. encoding multifunctional protein CAD (containing enzymatic activities carbamoyl-phosphate synthase, aspartate transcarbamylase, dihydroorotase) highly greater cells, reaching almost 1 x 10(-4) events per generation. mutagenic event high compared point mutations usually reported mammalian its potential contribution process will be discussed.