Kucera E, Hejda V, Dankovcik R, Valha P, Dudas M, Feyereisl J
Institute for the Care of Mother and Child, Prague, Czech Republic.
Eur J Gynaecol Oncol. 2011;32(2):182-4.
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.
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.
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.
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.
我们这项回顾性研究的目的是评估子宫切除标本中子宫腺肌病病灶的病理变化,并指出子宫肌层内子宫腺肌病病灶可能的致癌机制。
对临床资料进行回顾性分析;2003年至2008年期间,我们科室对219例诊断为早期子宫内膜癌的患者进行了手术。所有病例均采用标准分期手术,所有子宫切除标本随后进行常规分析。
在219例子宫切除标本中,88例发现有子宫腺肌病,而这219例中有205例患有子宫内膜样腺癌,10例患有透明细胞癌,4例患有乳头状浆液性癌。在这些亚组中,205例子宫内膜样腺癌标本中有87例(42.4%)记录有子宫腺肌病,10例透明细胞癌标本中有1例(2.2%)记录有子宫腺肌病,均发现于在位子宫内膜。子宫腺肌病中所有恶性变化病例(n = 6)均仅与共存的子宫内膜样腺癌同时存在:子宫腺肌病中的腺癌5例为高分化或中分化,仅1例为低分化。子宫腺肌病中肿瘤的分化与在位子宫内膜癌的分化有50%的相关性。在所有癌症阳性的子宫腺肌病病灶中同时发现了良性腺体增生或非典型复杂增生(ACH)等增生性变化。
子宫内膜癌患者中6.8%存在子宫腺肌病的恶性变化。所有子宫腺肌病恶性阳性病例均与在位子宫内膜的子宫内膜样腺癌相关。有趣的是,在所有这些病例中,同时也发现了不同阶段的增生性变化。这一观察结果表明,子宫腺肌病的致癌途径与已知的雌激素反应性I型子宫内膜癌相似。