Cyclooxygenase-2 promotes angiogenesis in pTa/T1 urothelial bladder carcinoma but does not predict recurrence

Cyclooxygenase-2 promotes angiogenesis in pTa/T1 urothelial bladder carcinoma but does not predict recurrence
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DOI:
10.1046/j.1464-410x.2003.04345.x
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发表时间:
2003-09-01
期刊:
影响因子:
4.5
通讯作者:
Huland, H
Huland, H
中科院分区:
医学2区
文献类型:
--
作者:
Friedrich, MG;Toma, MI;Huland, H

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为了研究环氧合酶-2 (COX-2) 对膀胱非肌层浸润性尿路上皮癌患者微血管密度 (MVD) 和临床预后的影响,因为 COX-2 表达在上皮性肿瘤中显着较高,并且越来越多的证据表明 COX-2 可能有助于肿瘤新生血管形成。我们评估了 110 名接受经尿道切除原发性 pTa/pT1 膀胱癌 (pTa、 84;pT1,26;1 级,22;2 级,81;7)。使用针对 COX-2、CD34(内皮细胞)和 CD105(增殖血管)的抗体对石蜡切片进行免疫组织化学评估。 COX-2 表达通过染色细胞数(阴性、+、++)和按每视野血管计算的 MVD 进行量化。在 110 个肿瘤中,45 个(41%)没有 COX-2 免疫染色,40 个肿瘤有微弱染色,至少有分离的阳性细胞(+),25 个肿瘤有 ++ 染色。 COX-2 阳性肿瘤的增殖血管的血管化明显增强。在 COX-2 阴性肿瘤中,通过 CD34 免疫染色鉴定,MVD 为 22.1,增殖血管 (CD105) 的 MVD 为 3.4,而 COX-2 阳性肿瘤的 MVD 分别为 18.3 (CD34) 和 5.8 (CD105)。 91 名患者获得了完整的随访数据;平均随访 25 个月后,18 名患者 (20%) 出现肿瘤复发。 COX-2阳性患者(19%,25.6个月)和阴性患者(21%,25.2个月)之间的复发率或无病生存率没​​有显着差异。这些结果证实了COX-2参与膀胱癌的血管生成,因为COX-2促进肿瘤区域的血管增殖,并表明COX-2抑制药物在预防和治疗浅表性膀胱癌中的有用性。
To investigate the effect of cyclooxygenase-2 (COX-2) on microvessel density (MVD) and on the clinical prognosis in patients with non-muscle invasive urothelial carcinoma of the bladder, as COX-2 expression is significantly greater in epithelial tumours and there is increasing evidence that COX-2 might contribute to tumour neovascularization.We assessed tumour samples from 110 patients undergoing transurethral resection for primary pTa/pT1 bladder carcinoma (pTa, 84; pT1, 26; grade 1, 22; grade 2, 81; grade 3, seven). Paraffin sections were assessed immunohistochemically using antibodies against COX-2, CD34 ( endothelial cells) and CD105 ( proliferating vessels). COX-2 expression was quantified by the number of stained cells ( negative, +, ++) and the MVD calculated as vessels per field.Of the 110 tumours, 45 (41%) had no immunostaining for COX-2, 40 had faint staining with at least isolated positive cells ( +) and 25 stained ++. COX-2 positive tumours had significantly greater vascularization for proliferating vessels. In COX-2 negative tumours the MVD was 22.1, identified by CD34 immunostaining, and 3.4 for proliferating vessels ( CD105), whereas COX-2 positive tumours had a MVD of 18.3 ( CD34), and of 5.8, respectively ( CD105). Complete follow-up data were available in 91 patients; after a mean follow-up of 25 months, 18 (20%) had tumour recurrences. There was no significant difference in the recurrence rates or disease-free survival between COX-2-positive (19%, 25.6 months) or - negative patients (21%, 25.2 months).These results confirm the involvement of COX-2 in angiogenesis in bladder cancer, as COX-2 promoted blood vessel proliferation in the tumour zone, and indicate the usefulness of COX-2-inhibiting drugs in preventing and treating superficial bladder cancer.