PURPOSE: To evaluate and distinguish malignant and nonmalignant pleural effusions utilizing surface marker analysis by flow cytometry and assessing tumor forming efficiency by subcutaneous injection into SCID/NOD/IL2Rgamma-mice.
METHODS: Samples of pleural effusions from nonmalignant causes: congestive heart failure, liver disease and renal disease and from malignant causes: lung, breast, ovarian, uterine, rectal carcinomas excluding mesothelioma and lymphoma were evaluated with surface marker analysis by flow cytometry. The tumor containing effusions were subcutaneously injected into SCID/NOD/IL2Rgamma-mice for assessment of tumorigenicity. CD45+ cells were excluded by surface staining and determined percentage positivity for EMT markers with 5% as the threshold.
RESULTS: Tumor forming efficiency in the study mice was limited, with only 50% of the malignant samples achieving tumor growth in the injected mice. There were no measureable growths recorded from those injected with nonmalignant cells. There is a drastic enrichment of EpCAM + population in the xenograft. The HLA+/CD45- cells in the xenograft are almost all EpCAM+ cells indicating that EpCAM+ cells have tumorigenic potential.The majority of malignant samples displayed a more epitheilial phenotype than a mesenchymal phenotype. EpCAM is the most specific marker for malignancy compared to E-cad and CEA cells.
CONCLUSION: Cellular analysis distinguishing a specific cellular marker that contributes to tumorigenicity seen in malignant effusions is identifiable as EpCAM. EpCAM is a more specific marker for malignancy than E-cad and CEA.
CLINICAL IMPLICATIONS: Cellular analysis of pleural effusions by surface marker analysis by flow cytometry identifying EpCAM may be another more specific measure to distinguish malignant from nonmalignant effusion. It appears to have a distinct role in tumorigenicity.
DISCLOSURE: Carla Lamb, No Financial Disclosure Information; No Product/Research Disclosure Information