Molecular alterations in the pathogenesis of endometrial adenocarcinoma. Therapeutic implications

被引：44

作者：

Cerezo L. ^{[1
]}

Cárdenes H. ^{[2
]}

Michael H. ^{[3
]}

机构：

[1] Radiation Oncology Service, La Princesa University Hospital, Autonoma University, 28006 Madrid

[2] Department of Radiation Oncology, Indiana University School of Medicine, Indianapolis, IN

[3] Department of Pathology, Indiana University School of Medicine, Indianapolis, IN

来源：

Clinical & Translational Oncology | 2006年 / 8卷 / 4期

关键词：

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

D O I：

10.1007/BF02664933

中图分类号：

学科分类号：

摘要：

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. © FESEO 2006.

引用

页码：231 / 241

页数：10

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