Cancer arises from a stepwise accumulation of genetic changes through expansion of the malignant cell clones in the population of pre-malignant cells undergoing the Darwinian selection process. In other words, cancer is an outcome of continuous and random acquisition of the changes in the genomes of individual cells. These modifications gradually and progressively change the phenotype of the normal cell making it more malignant through a loss of an overall stability of genome. To gain the comprehension of the mechanisms underlying tumor development, a number of high-throughput expression studies have been performed. The objective of the current study is to use publicly available datasets in order to analyze the most general features of the malignant cell, thus, investigating molecular phenomena common for all tumor cells, with no regard to the characteristics related to tumor’s tissue of origin. Thus, we analyzed and compared the transcript diversity patterns in tumor and normal cells, studied an expression of the genes located adjacent to the telomeres and provided an evidence for the hypothesis that tumor state behaves as stable “attractor” state. An intermediate regulatory framework hypothesis implying a set of local ‘vantage points’ genes that control the transcription of all other genes in a semi-democratic fashion has been endorsed.