Clinical & Translational Oncology

, Volume 8, Issue 4, pp 231–241

Molecular alterations in the pathogenesis of endometrial adenocarcinoma. Therapeutic implications

Educational Series Blue Series

DOI: 10.1007/BF02664933

Cite this article as:
Cerezo, L., Cárdenes, H. & Michael, H. Clin Transl Oncol (2006) 8: 231. doi:10.1007/BF02664933


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.

Key words

endometrial cancer molecular markers genetic alterations new targets 

Copyright information

© FESEO 2006

Authors and Affiliations

  • Laura Cerezo
    • 1
  • Higinia Cárdenes
    • 2
  • Helen Michael
    • 3
  1. 1.Radiation Oncology Service. La Princesa University HospitalAutonoma UniversityMadridSpain
  2. 2.Department of Radiation OncologyIndiana University School of MedicineIndianapolis. EE.UU.
  3. 3.Department of PathologyIndiana University School of MedicineIndianapolis. EE.UU.

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