Henson Donald Earl, Schwartz Arnold M, Tilara Amy, Grimley Philip M, Anderson William F
George Washington University Cancer Institute, Ross Hall, Room 502, 2300 Eye St, NW, Washington, DC 20037, USA.
Arch Pathol Lab Med. 2007 Sep;131(9):1337-42. doi: 10.5858/2007-131-1337-PAOPDA.
Population-based analysis of the histopathology of endometrioid adenocarcinoma of the endometrium and ovary combined with epidemiologic techniques offer a new approach to exploring the relationship of tumors that share a similar range of morphologic phenotypes.
To evaluate the contribution of the Surveillance, Epidemiology, and End Results database to our understanding of gynecologic pathology. Specifically, to test and compare whether the etiology/pathogenesis of ovarian endometrioid cancer is as dependent upon the reproductive environment as uterine endometrial carcinoma.
Graphic plots of the epidemiologic patterns were analyzed relating to incidence and age-specific rates of ovarian and uterine endometrioid carcinomas. The graphic analysis included evaluation of age frequency density plots and logarithmic plots (log-log) of age-specific incidence rates.
At all ages, uterine endometrioid carcinomas have higher incidence rates than their ovarian homologues. Up to the age of 50 years, the log-log plots of age-specific incidence rates for each of these tumors remain essentially parallel. In contrast, after age 50 (menopause), the incidence rates begin to diverge: the rates for uterine endometrial carcinomas continue to rise, whereas the rates for ovarian endometrioid carcinomas plateau. This divergence persists even when the age-specific incidence is stratified according to histologic grade. Interestingly, endometrial stromal sarcomas follow an incidence rate pattern nearly identical to that of ovarian endometrioid carcinomas.
The continuum of cellular and molecular events predisposing to gynecologic cancers of endometrioid phenotype apparently cease to operate in the ovary after menopause, but additional cellular and molecular events appear to occur in the ageing uterine endometrium.
结合流行病学技术对子宫内膜和卵巢子宫内膜样腺癌的组织病理学进行基于人群的分析,为探索具有相似形态学表型范围的肿瘤之间的关系提供了一种新方法。
评估监测、流行病学和最终结果数据库对我们理解妇科病理学的贡献。具体而言,测试并比较卵巢子宫内膜样癌的病因/发病机制是否与子宫内膜癌一样依赖于生殖环境。
分析了与卵巢和子宫子宫内膜样癌的发病率及年龄别发病率相关的流行病学模式的图表。图表分析包括对年龄频率密度图和年龄别发病率的对数图(对数-对数)的评估。
在所有年龄段,子宫内膜样癌的发病率均高于其卵巢同源肿瘤。在50岁之前,这些肿瘤各自的年龄别发病率对数-对数图基本保持平行。相比之下,50岁(绝经)之后,发病率开始出现差异:子宫内膜癌的发病率持续上升,而卵巢子宫内膜样癌的发病率趋于平稳。即使根据组织学分级对年龄别发病率进行分层,这种差异仍然存在。有趣的是,子宫内膜间质肉瘤的发病率模式与卵巢子宫内膜样癌几乎相同。
导致子宫内膜样表型妇科癌症的细胞和分子事件连续体在绝经后显然在卵巢中不再起作用,但在衰老的子宫内膜中似乎会发生额外的细胞和分子事件。