The most important result obtained in the work is that DNase I decreased the level of B-subfamily repeats having homology to human ALU repeats, known as markers of carcinogenesis, to the level of healthy animals.
It is also demonstrated that horizontal cancer progression mediated by circulating DNA occurs via its uptake by recipient cells in an in vivo model where immunocompetent rats subjected to colon carcinogenesis with 1,2-dimethylhydrazine had increased rate of colonic tumors when injected in the dorsum with human SW480 colon carcinoma cells as a source of circulating oncogenic DNA, which could be offset by treating these animals with DNAse I and proteases.
Different groups have shown that: 1) the global structure of the albumin and AFP genes does not change during the course of development and hepatic carcinogenesis; 2) modifications at the level of the methylation of certain specific cytosines could be associated with the variations in the transcription of these genes; 3) global or local (hypersensitive sites with DNase I) changes of chromatin conformation could be correlated to the potential or the overt activity of the transcription of these genes.