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

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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.