Pathophysiology of lymphatic stomata in the pathogenesis of cancerous pleural effusion and mechanisms of anchorage-independent growth of cancer

分析了癌症的尸检病例，以阐明人类癌性胸腔积液的机制。卡方检验显示，癌性胸腔积液的胸膜播散/浸润、肺门淋巴结转移、肺韧带淋巴孔转移、静脉角淋巴结转移率均显著高于非癌性胸腔积液;然而，多元Logistic回归分析表明，在这些变量中，只有肺韧带淋巴孔转移是癌性胸膜炎的独立预测因素，积液未经治疗的癌性胸腔积液患者中，原发灶与肺韧带淋巴孔转移灶的癌细胞Ki-67和凋亡指数差异无统计学意义;然而，VEGF-C免疫组织化学显示，与原发病灶相比，在淋巴孔转移病灶处的表达水平可能增加，E-cadherin免疫组化结果显示，与原发灶相比，转移灶的淋巴孔表达水平可能降低。这些结果提出了一种可能性，即癌细胞转移到淋巴孔在癌性胸腔积液的发病机制中发挥作用。

Autopsy cases with carcinomas were analyzed in order to elucidate mechanisms of cancerous pleural effusion in humans. Chi-square test demonstrated that the frequencies of dissemination/invasion onto the pleura, pulmonary hilar lymph node metastasis, metastasis to the lymphatic stomata on the pulmonary ligament, and venous angle lymph node metastasis in cases with cancerous pleural effusion were all significantly higher than those in cases without cancerous pleural effusion; however, multiple logistic regression analysis demonstrated that among these variables, only the metastasis to the lymphatic stomata on the pulmonary ligament was a significantly independent predictive factor for cancerous pleural effusion. Among untreated cases with cancerous pleural effusion, Ki-67 and apoptosis indexes of cancer cells were not significantly different between primary lesions and metastatic lesions to the lymphatic stomata on the pulmonary ligament; however, VEGF-C immunohistochemistry demonstrated a potentially increased expression levels at the metastatic lesions to the lymphatic stomata compared with the primary lesions, and E-cadherin immunohistochemistry demonstrated a potentially decreased expression levels at the metastatic lesions to the lymphatic stomata compared with the primary lesions. These results raise a possibility that cancer metastasis to the lymphatic stomata plays a role in the pathogenesis of cancerous pleural effusion.