Cancer, nowadays, con be considered as genetic-component pathology characterized by a rapid cellular growth. The cells of our body receive signals indicating them when to grow and multiply and when to stop the growth. In cancer these cells, due to an alteration in the genetic heritage, don’t respond to the control signals and they keep growing and multiplying irregularly spreading in different part of the body. The event that determinates the alteration of the gene functions is called mutation. When a gene is mutated due to biological, chemical, physical causes, the infor- mation reaching the cell will be improper for its function. The majority of tumors are sporadic, the alterations of DNA develop casually in the somatic cells, the ones constituting every organ and system in our organism. These mutations are originated in the DNA of a restricted number of cells and give rise to the genetic defect that will propagate in the descending cells and, accumulating in a specific organ, will replace initially the healthy tissue and then will spread to far (metastasis ) or near organs.
DNA methylation is a post-replicative process. The exemption of the modifications regarding the DNA methylation is basically determined during development. DNA methylation is therefore one of the mechanisms related with cell differentiation through inhibition of gene expression at the transcriptional level and is essential for the normal development of mammals; it is associated with genomic imprinting, transcriptional inactivation of the X chromosome and aging, and has a role in the development of pathological events, such as cancer-genesis. DNA methylation is an epigenetic post-synthetic modification that, with the transfer of a methyl group from S- adenosylmetionina C atom in position 5 of the cytosine ring, introduces 5mC as the new base in the DNA .
The CpG islands contain CpG dinucleotides at a frequency mathematically predetermined. The CpG islands are about 30,000 generally located 5 'end of the promoter region of housekeeping genes, sometimes overlapping the region coding for a variable extension (usually the first exon). The frequency of the presence the CpG dinucleotides in the genome is less than expected, except for the regions of CpG islands. This is the result of an evolutionary mechanism linked to the pres- ence of a spontaneous deaminase activity in the nucleus. This enzymatic reaction transforms the methylated cytosine in thymine and the non-methylated C in Uracil. Following controls and repair mechanisms recognize the Uracil base as extraneous DNA and therefore they replace it, this sub- stitution does not occur for Thymine, common base in the DNA. The most CpG are no methylated in a normal cell, regardless of the state of the transcriptional gene, while during cancer develop- ment the CpGs outside of CpG islands become hypomethylated, and CpG islands in the promoter region of tumor suppressor genes become hypermethylated. This hypermethylation is associated with chromatin condensation and loss of transcription. The recent data indicate that genetic and epigenetic events interact to help the progressive development of the cancers .
