[Introduction to cancer molecular genetics. Genetic mechanisms of neoplasms] [Spanish]

Neoplasms are generally acquired genetically based processes that take place in multiple stages to achieve the capacity to metastasize. On most occasions, the morphological expression and genetic alterations underlying this evolutionary process are unknown, although certain "rules" general obtained in the study of tumors of certain sites (eg, colon) are applicable to most of neoplasms.
Cell neoplasms are diseases that affect basic processes that regulate replication and cell death (including the call immortality), cellular differentiation and motility, ability to induce neovascularization, as well as the maintenance of genomic integrity. All tumors have more than one abnormality in each of these basic aspects, in which more sequence alterations that is the sum of them in the same direction determines the appearance of the malignancy. Regulatory genes of these cellular functions are multiple and redundant, but can be classified into three main groups: oncogenes (tumor-inducing), tumor suppressor genes (tumor inhibitors) and genetic repair genes (responsible for maintaining the integrity of the genome).
The basic genetic mechanisms that have been described above responsible for alterations occur are equally varied and good activation of the tumor-inducing mechanisms lock mechanisms well inhibitors neoplasms or both aspects simultaneously. Defects in DNA repair contribute to a more rapid progression of the disease. Such mechanisms can be summarized as: changes in the genetic dose (gain / loss), gene fusion / rearrangements, injuries microsatellite mutations / nucleotide polymorphisms isolated, modifications of gene expression, epigenetic modifications, alterations and reactivation of mitochondrial genetic telomerase. In hereditary cancer syndromes, the initial genetic alteration appears in germline and normally it is a localized mutation in a tumor suppressor gene (except in the case of multiple endocrine neoplasia syndrome type 2 is an oncogene).