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. 2011;32(2):182-4.

Malignant changes in adenomyosis in patients with endometrioid adenocarcinoma

Affiliations
  • PMID: 21614909

Malignant changes in adenomyosis in patients with endometrioid adenocarcinoma

E Kucera et al. Eur J Gynaecol Oncol. 2011.

Abstract

Objective: The aim of our retrospective study was to evaluate pathological changes in adenomyotic foci in hysterectomy specimens, and point out a possible mechanism of carcinogenesis in adenomyotic foci inside the myometrium.

Methods: Retrospective analysis of clinical data; 219 patients were operated at our departments from 2003-2008 with the diagnosis of early endometrial cancer. Standard staging operation was used in all cases and all hysterectomy specimens were afterwards routinely analyzed.

Results: Adenomyosis was found in 88 of a total of 219 hysterectomy specimens, while 205 of these 219 were affected by endometrioid adenocarcinoma, ten with clear cell carcinoma and four with papillary serous carcinoma. Within these subgroups adenomyosis was documented in 87 of 205 specimens with endometrioid adenocarcinoma (42.4%) and in one specimen of ten with clear cell carcinoma (2.2%), all found in the eutopic endometrium. All cases of malignant changes (n = 6) in adenomyosis were found exclusively with coexisting endometrioid adenocarcinoma: adenocarcinoma in adenomyosis was well or moderately differentiated in five cases, and poorly differentiated in just one case. Differentiation of the tumor in adenomyosis correlated with differentiation of the eutopic endometrial cancer in 50%. Hyperplastic changes like benign glandular hyperplasia, or atypical complex hyperplasia (ACH) were identified simultaneously in all cancer-positive adenomyotic foci.

Conclusion: Malignant changes in adenomyosis were present in 6.8% of patients with endometrial cancer. All malignancy-positive cases of adenomyosis were associated with endometrioid adenocarcinoma of the eutopic endometrium. Interestingly, in all these cases, different stages of hyperplastic changes were also simultaneously identified. This observation suggests a similar pathway of carcinogenesis in adenomyosis as is known in estrogen-responsive endometrial cancer type I.

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