ANGIOGENESIS IN ENDOMETRIAL HYPERPLASIA AND STAGE-I ENDOMETRIAL CARCINOMA

ANGIOGENESIS IN ENDOMETRIAL HYPERPLASIA AND STAGE-I ENDOMETRIAL CARCINOMA
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DOI:
10.1016/0029-7844(95)00203-4
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发表时间:
1995-10-01
影响因子:
7.2
通讯作者:
GHEZZI, F
GHEZZI, F
中科院分区:
医学2区
文献类型:
--
作者:
ABULAFIA, O;TRIEST, WE;GHEZZI, F

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目的:评价子宫内膜增生症和I期子宫内膜癌的血管生成情况,并探讨血管生成与肿瘤分级和浸润深度的关系。方法:分析三组患者:因良性疾病接受子宫切除术的对照患者(n = 19)、子宫内膜增生症患者(n = 24)和I期子宫内膜癌患者(n = 34)。所有子宫切除标本均进行免疫组织化学染色,检测因子 VIII 相关抗原,作为血管内皮的敏感和特异性标记物。选择接近最深子宫肌层浸润的区域或子宫内膜增生程度最高且血管生成强度最高的区域。为每个载玻片选择三个视野(x 400),并计算平均微血管计数。统计分析包括 Mann-Whitney LI 检验或 Kruskal-Wallis 方差分析和 Dunn 事后程序,P < .05 被认为是显着的。结果:对照组与复杂子宫内膜增生组的微血管计数之间发现显着差异(中位数 21,范围 16-80,中位数 38,范围 20-130;P < .05)。复杂子宫内膜增生的微血管计数显着高于单纯增生(中位数 25,范围 16-42;P < .05),并且显着低于子宫内膜癌的微血管计数(中位数 77.5,范围 19-189;P < .05)。复杂增生中的微血管计数与非侵袭性 I 期子宫内膜癌没有显着差异(中位数 38,范围 20-130,中位数 44,范围 19-119;P = .5)。在 I 期子宫内膜癌病例中,有肌层浸润的标本中微血管数量高于无肌层浸润的标本(中位数 44,范围 19-119,中位数 83,范围 19-189;P < .01)。 2 级病例中的微血管数量高于 1 级 I 期子宫内膜癌病例(中位数 44 个,范围 19-98,中位数 96,范围 63-189;P < .001)。结论:复杂子宫内膜增生和子宫内膜癌具有血管生成性。此外,在 I 期子宫内膜癌中,更大的浸润深度和更高的肿瘤分级与血管生成强度直接相关。
Objective: To evaluate angiogenesis in endometrial hyperplasia and stage I endometrial carcinoma, and to investigate the relationship between angiogenesis and tumor grade and depth of invasion.Methods: Three groups of patients were analyzed: control patients who underwent hysterectomy for benign conditions (n = 19), patients with endometrial hyperplasia (n = 24), and patients with stage I endometrial carcinoma (n = 34). All hysterectomy specimens were stained immunohistochemically for factor VIII-related antigen as a sensitive and specific marker for vascular endothelium. Areas close to the deepest myometrial invasion or those with the highest grade of endometrial hyperplasia and the highest angiogenic intensity were selected. Three fields (x 400) were selected for each slide, and the mean microvessel count was calculated. Statistical analysis included Mann-Whitney LI test or Kruskal-Wallis analysis of variance and Dunn post hoc procedure, P < .05 was considered significant.Results: A significant difference was found between the microvessel count of controls versus the group with complex endometrial hyperplasia (median 21, range 16-80, versus median 38, range 20-130; P < .05). Microvessel counts of complex endometrial hyperplasia were significantly higher than those of simple hyperplasia (median 25, range 16-42; P < .05) and significantly lower than counts of endometrial carcinoma (median 77.5, range 19-189; P < .05). Microvessel counts in complex hyperplasia were not significantly different than those of noninvasive stage I endometrial carcinoma (median 38, range 20-130, versus median 44, range 19-119; P = .5). In cases of stage I endometrial carcinoma, a higher number of microvessels was noted in specimens with myometrial invasion than in those without myometrial invasion (median 44, range 19-119, versus median 83, range 19-189; P < .01). A higher number of microvessels was noted in cases with grade 2 than in those with grade 1, stage I endometrial carcinoma (median 44, range 19-98, versus median 96, range 63-189; P < .001).Conclusion: Complex endometrial hyperplasia and endometrial carcinoma are angiogenic Furthermore, in stage I endometrial carcinoma, greater depth of invasion and higher tumor grade are directly correlated with angiogenic intensity.