Wróel Tomasz, Mazur Grzegorz, Dziegiel Piotr, Jeleń Michał, Szuba Andrzej, Kuliczkowski Kazimierz, Zabel Maciej
Department of Haematology, Blood Neoplasms and Bone Marrow Transplantation, Medical University, Wrocław, Poland.
Folia Histochem Cytobiol. 2006;44(1):43-7.
Lymphatic vasculature in solid tumors may serve as the pathway for metastatic spread of the cancer to the regional lymph nodes and to distant organs. Controversy still exists whether tumors metastasize through existing lymphatics or through newly formed vessels (lymphangiogenesis). The role of lymphangiogenesis in lymphoma spread and proliferation is not clearly established. VEGF-C is the most potent inducer of lymphangiogenesis. LYVE-1 was shown to be a specific marker for lymphatic vessels in normal and tumor tissue. The aim of the present study was the evaluation of lymph node LYVE-1-positive lymphatic sinus density (LSD) and VEGF-C expression in patients with non-Hodgkin's lymphoma (nHL) and in reactive lymph nodes. Sixty paraffin-embedded lymph nodes from newly diagnosed patients with B-cell nHL were evaluated. Twelve lymph node biopsy specimens from adult patients with reactive lymphonodulitis were used as controls. Sections of lymph nodes were stained immunohistochemically for LYVE-1 and VEGF-C. VEGF-C expression in lymph nodes of nHL patients was low and not significantly different from that in the control (p = 0.6). Moreover, VEGF-C expression did not differ significantly between aggressive and indolent lymphomas (p = 0.53). Similarly we did not find differences in LSD in aggressive nHL and in indolent nHL (p=0.49). The mean LSD in reactive lymph nodes was higher than in nHL (p = 0.03). Only in 2 out of 12 reactive lymph nodes LYVE-1-positive vessels were absent. In all groups we demonstrated a strong positive correlation between VEGF-C and LYVE-1-expression (p = 0.0001). Higher LSD in reactive lymph nodes as compared to those of nHL patients suggests that lymphoma proliferation leads to the destruction of the existing lymphatics rather than to lymphangiogenesis within lymph nodes. NHL are not associated with increased expression of VEGF-C nor increased LYVE-1-positive lymphatic sinuses density within lymph nodes.
实体瘤中的淋巴管系统可能是癌症转移至区域淋巴结和远处器官的途径。肿瘤是通过现有的淋巴管还是通过新形成的血管（淋巴管生成）发生转移，目前仍存在争议。淋巴管生成在淋巴瘤扩散和增殖中的作用尚未明确。血管内皮生长因子C（VEGF-C）是淋巴管生成最有效的诱导剂。淋巴细胞抗原6E（LYVE-1）被证明是正常组织和肿瘤组织中淋巴管的特异性标志物。本研究的目的是评估非霍奇金淋巴瘤（nHL）患者和反应性淋巴结中淋巴结LYVE-1阳性淋巴窦密度（LSD）及VEGF-C的表达情况。对60例新诊断的B细胞nHL患者石蜡包埋的淋巴结进行了评估。选取12例成年反应性淋巴细胞炎患者的淋巴结活检标本作为对照。淋巴结切片进行LYVE-1和VEGF-C免疫组织化学染色。nHL患者淋巴结中VEGF-C的表达较低，与对照组无显著差异（p = 0.6）。此外，侵袭性淋巴瘤和惰性淋巴瘤之间VEGF-C的表达也无显著差异（p = 0.53）。同样，侵袭性nHL和惰性nHL的LSD也没有差异（p = 0.49）。反应性淋巴结的平均LSD高于nHL（p = 0.03）。12例反应性淋巴结中只有2例没有LYVE-1阳性血管。在所有组中，我们均证实VEGF-C与LYVE-1表达之间存在强正相关（p = 0.0001）。与nHL患者相比，反应性淋巴结中较高的LSD表明淋巴瘤增殖导致现有淋巴管的破坏，而非淋巴结内的淋巴管生成。nHL与淋巴结内VEGF-C表达增加或LYVE-1阳性淋巴窦密度增加无关。
