Molecular alterations in the pathogenesis of endometrial adenocarcinoma. Therapeutic implications

Laura Cerezo, Higinia Cárdenes, Helen Michael

Research output: Contribution to journalArticle

16 Scopus citations


Molecular genetic evidence indicates that endometrial carcinoma likely develops as the result of a multistep process of oncogene activation and tumor suppressor gene inactivation. These molecular alterations appear to be specific for Type I (endometrioid) and Type II (non endometrioid) cancers. Type I cancers are characterized by mutation of PTEN, KRAS2, defects in DNA mismatch repair, as evidenced by the microsatellite instability phenotype, and a near diploid karyotype. Type II cancers often contain mutations of TP53 and Her-2/neu and are usually nondiploid. The clinical value of many of these molecular markers is now being tested and it may help to refine diagnosis and establish an accurate prognosis. Furthermore, some of these tumor biomarkers constitute the targets for emerging therapies. Transtuzumab against Her-2/neu and bevacizumab against VEGF overexpressing carcinomas are among the promising novel treatments. Additional translational research is needed to identify molecular and genetic alterations with potential for therapeutic interventions.

Original languageEnglish (US)
Pages (from-to)231-241
Number of pages11
JournalClinical and Translational Oncology
Issue number4
StatePublished - Dec 1 2006


  • Endometrial cancer
  • Genetic alterations
  • Molecular markers
  • New targets

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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