Molecular alterations in the pathogenesis of endometrial adenocarcinoma. Therapeutic implications

RESUMEN

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ABSTRACT

Molecular genetic evidence indicates that endometrialcarcinoma likely develops as the result of a multistepprocess of oncogene activation and tumor suppressorgene inactivation. These molecular alterations appearto be specific for Type I (endometrioid) and Type II(non endometrioid) cancers. Type I cancers are characterizedby mutation of PTEN, KRAS2, defects in DNAmismatch repair, as evidenced by the microsatelliteinstability phenotype, and a near diploid karyotype.Type II cancers often contain mutations of TP53 andHer-2/neu and are usually nondiploid. The clinicalvalue of many of these molecular markers is now beingtested and it may help to refine diagnosis and establishan accurate prognosis. Furthermore, some ofthese tumor biomarkers constitute the targets foremerging therapies. Transtuzumab against Her-2/neuand bevacizumab against VEGF overexpressing carcinomasare among the promising novel treatments.Additional translational research is needed to identifymolecular and genetic alterations with potential fortherapeutic interventions: