Carcinogenesis is the final result of a gradual reconfiguration of a variety of circuits of signaling pathways and the accumulation of multiple mutations in signaling components associated with enhanced cell proliferation and reduced apoptosis. Cancer arises from different combinations of activated oncogenes, inactivated suppressor genes and the emergence of anti-apoptotic mechanisms. Most human cancer cells accumulate genetic changes rapidly and become genetically unstable. Genetic instability is enhanced when changes in DNA alter the epigenetic control mechanisms. Normal cell proliferation is regulated by a plurality of positive and negative signaling pathways. The positive signals are provided by the proto-oncogenes, and the inhibitory signals from the promoters of tumor and anti-apoptotic signaling pathways. The mutations in proto-oncogenes convert these genes into constitutively activated oncogenes and lead to the continuous stimulation of the cell cycle. To contribute a tumor suppressor gene in carcinogenesis it must lose its activity, in contrast to oncogenes, inducing cancer formation.
Cancer cells have an active role in supporting the adjacent stromal cells when creating a tumor. One mechanism for this process is the effective blood flow through neo-angiogenesis. In this way, the proliferating tumor cells depend on the specific stromal cells leading to the simultaneous growth of the tumor and the stroma. Epigenetic mechanisms such as methylation of DNA, modifications of histones and action of small RNAs are associated with tumorigenicity, as the modified genetic material may alter normal to cancer cells.
Cancer is organized in a hierarchical manner, with rare stem cancer cells, which have the potential of self-renewal, remaining at the top of the hierarchy and being responsible for the maintenance of tumor cells. On the other hand environmental factors, such as chemicals, ultraviolet radiation, X-rays, and oncogenic DNA or RNA-viruses accelerate the appearance of most cancers.