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Impaired access of lymphocytes to neoplastic prostate tissue is associated with neoangiogenesis in the tumour site

机译:淋巴细胞进入赘生性前列腺组织的障碍与肿瘤部位的新生血管生成有关

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摘要

Recent reports demonstrated that neovasculature of certain murine tumours inhibits migration of lymphocytes to malignant tissues. We examined the possible existence of this phenomenon in human prostate adenocarcinoma by relating extent, patterns and composition of leucocyte infiltrates in adenocarinoma specimens (N=28) to microvessel density and percentages of these vessels expressing adhesion molecules CD54, CD106 and CD62E. Specimens of nodular hyperplasia (N=30) were used as a control for nonmalignant prostate. Increased microvessel density was detected in foci of adenocarcinoma, as compared with adjacent benign areas (P=0.004) or hyperplastic specimens (P=0.001). Only CD54 was detected on prostate vasculature; percentages of CD54-expressing vessels in adenocarcinoma lesions and adjacent areas were higher than in hyperplasia (P=0.041 and P=0.014, respectively). Infiltrating leucocytes were either scattered diffusely in tissue or organised into clusters mainly composed of CD4-positive lymphocytes; smaller percentage of tissue was occupied by clustered infiltrates in adenocarcinoma foci (mean=0.7; median=0; range=0–5) than in adjacent tissue (mean=2.5; median=1; range=0–15; P=.021) and hyperplasia (mean=1.9; median=2; range=0–5; P=.006). In adenocarcinoma foci, microvessel density tended to negatively correlate with percentage of tissue occupied by an overall leucocyte infiltrate (mean=8.6; median=7.5; range=30) and negatively correlated with percentage of tissue occupied by clustered infiltrate (P=0.045). Percentage of CD54-expressing vessels positively correlated with percentage of tissue occupied by an overall (mean=12; median=10; range=30; P=0.01) and clustered (P=0.023) infiltrate in hyperplasia, whereas in carcinoma-adjacent benign areas, correlation was detected only for clustered infiltrates (P=0.02). The results indicate that impaired access of lymphocytes to malignant lesions is associated with increased numbers of newly formed blood vessels, whereas vascular CD54 likely contributes to extravasation of lymphocytes only in benign prostate tissue.
机译:最近的报道表明某些鼠类肿瘤的新脉管系统抑制淋巴细胞向恶性组织的迁移。我们通过将腺癌标本(N = 28)中白细胞浸润的程度,模式和组成与微血管密度和表达粘附分子CD54,CD106和CD62E的这些血管的百分比相关联,检查了该现象在人前列腺腺癌中的可能存在。结节性增生(N = 30)的样本用作非恶性前列腺的对照。与邻近的良性区域(P = 0.004)或增生标本(P = 0.001)相比,在腺癌灶中检测到微血管密度增加。在前列腺脉管系统上仅检测到CD54。腺癌病变和邻近区域中表达CD54的血管百分率高于增生组织(分别为P = 0.041和P = 0.014)。浸润性白细胞要么散布在组织中,要么组织成主要由CD4阳性淋巴细胞组成的簇。腺癌灶中的聚集浸润液占组织的百分比(平均值= 0.7;中位数= 0;范围= 0-5)比相邻组织中的百分比低(平均值= 2.5;中位数= 1;范围= 0-15; P = .021 )和增生(平均值= 1.9;中位数= 2;范围= 0-5; P = .006)。在腺癌病灶中,微血管密度往往与白细胞浸润占总组织的百分比呈负相关(平均值= 8.6;中位数= 7.5;范围= 30),而与聚集浸润占组织的百分比成负相关(P = 0.045)。在增生组织中,表达CD54的血管百分比与整体(平均= 12;中位数= 10;范围= 30; P = 0.01)和成簇(P = 0.023)浸润的组织所占百分比呈正相关,而在癌旁良性组织中浸润地区,相关性仅检测到群集浸润(P = 0.02)。结果表明,淋巴细胞进入恶性病变的障碍与新形成血管的数量增加有关,而血管CD54可能仅在良性前列腺组织中有助于淋巴细胞外渗。

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