Synchronous endometrioid carcinomas of the uterine corpus and ovary: Alterations in the β-catenin (CTNNB1) pathway are associated with independent primary tumors and favorable prognosis

Julie A. Irving, Lluis Catasús, Alberto Gallardo, Elena Bussaglia, Marisa Romero, Xavier Matias-Guiu, Jaime Prat

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    Abstract

    Diagnosis of synchronous endometrioid carcinomas of the uterine corpus and ovary as either separate independent primary or as metastatic tumors requires careful consideration of a number of gross and histological features. Although such assessment is often sufficient, recent evidence has suggested that molecular analysis may facilitate the diagnosis in problematic cases. Furthermore, as independent synchronous tumors limited to the uterus and ovary are generally associated with favorable outcome, determination of genetic alterations associated with this group of neoplasms may indicate molecular markers of less aggressive behavior. We examined 12 cases of synchronous carcinomas of the uterus and ovary, correlating conventional gross and histological parameters with molecular genetic alterations common to single endometrioid carcinomas occurring in these sites. We identified a frequency of molecular alterations in both independent and metastatic tumors, including microsatellite instability (uterine tumors, 50% and 67%, respectively; ovarian tumors, 33% and 67%) and PTEN mutations (uterine tumors, 38% and 100%; ovarian tumors, 33% and 83%) that is higher than that observed in single sporadic tumors. Loss of heterozygosity for chromosome 17p and 10q was also frequently observed. Nuclear immunoreactivities for β-catenin and CTNNB1 mutations were restricted to independent uterine and ovarian tumors and were absent in all of the metastatic tumors, providing direct evidence for a divergence of molecular oncogenetic mechanisms in the subset of synchronous endometrioid carcinomas. Furthermore, our data show that molecular genetic classification of synchronous independent versus metastatic tumors based on β-catenin expression/mutation correlates with clinical outcome. © 2005 Elsevier Inc. All rights reserved.
    Original languageEnglish
    Pages (from-to)605-619
    JournalHuman Pathology
    Volume36
    DOIs
    Publication statusPublished - 1 Jun 2005

    Keywords

    • Endometrial carcinoma
    • Microsatellite instability
    • Ovarian carcinoma
    • PTEN
    • Synchronous
    • β-Catenin

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