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

为阐明人类癌性胸腔积液的发病机制，对癌性胸腔积液的尸检病例进行了分析。卡方检验显示，癌性胸腔积液组胸膜转移/侵袭、肺门淋巴结转移、肺韧带淋巴孔转移、静脉角淋巴结转移均显著高于非癌性胸腔积液组，但多因素Logistic回归分析显示，在这些变量中，只有肺韧带淋巴孔转移是癌性胸腔积液的独立预测因素。在未经治疗的癌性胸腔积液患者中，原发灶和肺韧带淋巴孔转移灶之间癌细胞的Ki-67和细胞凋亡指数无显著差异，但VEGF-C免疫组织化学显示转移灶淋巴孔的表达水平较原发灶增强，E-钙粘素免疫组织化学显示淋巴孔转移灶与原发灶相比表达水平降低。这些结果提出了一种可能性，即癌转移到淋巴孔在癌性胸腔积液的发病机制中起作用。

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.