Naumann Carsten Maik, Al-Najar Amr, Alkatout Ibrahim, Hegele Axel, Korda Joanna Beate, Bolenz Christian, Kalthoff Holger, Sipos Bence, Juenemann Klaus-Peter, van der Horst Christof
Department of Urology and Paediatric Urology, University Hospitsl Schleswig Holstein, Campus Kiel, Kiel, Germany.
BJU Int. 2009 Jun;103(12):1655-9; discussion 1659. doi: 10.1111/j.1464-410X.2009.08365.x. Epub 2009 Feb 10.
To examine the potential effect of tumour-induced lymphangiogenesis in squamous cell carcinoma of the penis as a possible mechanism responsible for lymphatic spread.
Specimens from 65 patients with invasive tumours (31 with and 34 without metastases) were evaluated for lymphatic vessel density (LVD) by the 'hot-spot' method as the density of lymphatic endothelium hyaluronan receptor (LYVE-1)-positive lymphatic vessels per unit area of tissue. LVD was examined in peritumoral, intratumoral and normal tissue areas. The LVD of each tumour in these locations was calculated as the mean of the three highest lymph vessel counts in three to five hot-spots. The nodal status was based on histopathological examination or an uneventful follow-up of >or=2 years.
In all patients the mean (SD) peritumoral LVD of 8.05 (3.14)/0.75 mm(2) was significantly higher than for intratumoral and normal tissue, of 4.67 (2.58) and 5.20 (1.87), respectively (P < 0.001). The slightly lower intratumoral LVD than in normal tissue was not significant. The peritumoral LVD was 8.07 (3.29) in metastatic and 8.03 (3.03) in non-metastatic carcinomas. The intratumoral LVD was 5.13 (3.01) in node-positive carcinomas and 4.28 (2.15) in tumours with no lymphatic node metastasis (LNM). Comparing tumours with and without LNM, there was no statistically significant difference between intra- and peritumoral LVD.
Increased LVD does not significantly affect the lymphatic spread in penile carcinomas, indicating that there must be alternative mechanisms that selectively enable tumour cells to invade lymph vessels and to metastasize into the lymph nodes.
研究阴茎鳞状细胞癌中肿瘤诱导的淋巴管生成的潜在作用，作为淋巴转移可能的机制。
采用“热点”法评估65例浸润性肿瘤患者（31例有转移，34例无转移）标本的淋巴管密度（LVD），即每单位组织面积中淋巴管内皮透明质酸受体（LYVE-1）阳性淋巴管的密度。在肿瘤周围、肿瘤内和正常组织区域检测LVD。每个肿瘤在这些部位的LVD计算为三到五个热点中三个最高淋巴管计数的平均值。淋巴结状态基于组织病理学检查或≥2年的无异常随访。
所有患者肿瘤周围LVD的平均值（标准差）为8.05（3.14）/0.75mm²，显著高于肿瘤内和正常组织，分别为4.67（2.58）和5.20（1.87）（P<0.001）。肿瘤内LVD略低于正常组织，但差异无统计学意义。转移性癌的肿瘤周围LVD为8.07（3.29），非转移性癌为8.03（3.03）。淋巴结阳性癌的肿瘤内LVD为5.13（3.01），无淋巴结转移（LNM）的肿瘤为4.28（2.15）。比较有无LNM的肿瘤，肿瘤内和肿瘤周围LVD之间无统计学显著差异。
LVD增加对阴茎癌的淋巴转移无显著影响，表明必定存在其他机制，使肿瘤细胞能够选择性地侵入淋巴管并转移至淋巴结。
