Ineffectiveness of the presence of H-ras/p53 combination of mutations in squamous cell carcinoma cells to induce a conversion of a nontumorigenic to a tumorigenic phenotype.

摘要: Human tumor cells have properties in vitro or surrogate hosts that are distinct from those of normal cells, such as immortality, anchorage independence, and formation nude mice. However, different individual tumors may exhibit some, but not all these features. In previous years, human cell lines derived tissue types been studied to determine molecular changes associated with the listed above tumorigenicity present study, seven were characterized for p53 ras mutations occur SCC phenotypes This investigation was designed examine whether co-occurrence mutated lead a malignant stage progression process. None contained recognized "hot spots" suppressor gene, four had nonsense/splice mutation codon 126 12 H-ras gene. The remaining three intron 5, 193, missense 126, respectively. Four nontumorigenic; two nonsense p53-126 ras; one at no fourth only 193. Two nontumorigenic converted after treatment methyl methanesulfonate N-methyl-N'-nitro-N-nitrosoguanidine apparent additional either Our analysis revealed there high frequency genetic diversity both H-ras. There also lack causal relationship presence cells' ability potential