[Regulation of the cell cycle and the development of cancer: therapeutic prospects].
Several genetic alterations occur during the transformation process from normal to tumor cells, that involve the loss of fidelity of processes as replication, reparation, and segregation of the genomic material. Although normal cells have defense mechanisms against cancer progression, in tumor cells different escape pathways are activated leading to tumor progression. Recent advances have permitted cancer research to focus on the identification of some of its etiological factors. The knowledge of cell cycle reveals a precise mechanism achieved by the coordinated interactions and functions of cyclin-dependent kinases, control checkpoint, and repair pathways. Furthermore, it has been demonstrated that this coordinated function can be abrogated by specific genetic changes. These findings suggest that the molecular mechanisms responsible for cellular transformation may help to identify potential targets to improve cancer therapies.
Peralta-Zaragoza
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Centro de Investigación sobre Enfermedades Infecciosas, Instituto Nacional de Salud Pública, México.
Bahena-Román
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M
Díaz-Benítez
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CE
Madrid-Marina
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V
D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use; D002453:Cell Cycle / Q000187:drug effects / Q000502:physiology; D002471:Cell Transformation, Neoplastic / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D016161:Genes, Retinoblastoma / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control; D009374:Neoplasms, Experimental / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control; D014158:Transcription, Genetic / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
D000970:Antineoplastic Agents; D016159:Tumor Suppressor Protein p53