Fas ligand expression in esophageal carcinomas and their lymph node metastases
Adenocarcinoma; Immunohistochemistry; Metastasis; Squamous cell carcinoma
BACKGROUND. Although esophageal adenocarcinomas (FADCA) have been shown to have substantially reduced or absent Fas expression, the status of Fas ligand (FasL) in these tumors, especially adenocarcinomas, is largely unknown. METHODS. Using immunohistochemistry, the authors investigated FasL expression in sections of formalin fixed, paraffin embedded tissue from 13 EADCA. They also studied sections of 15 esophageal squamous cell carcinomas (ESCCA) and of lymph node metastases from 7 EADCA and 4 ESCCA. The percentage of FasL positive cells in each tumor was recorded. FasL expression in EADCA was compared with that in ESCCA and with lymph node status. Statistical analysis was performed using the Fisher exact test. RESULTS. No specific staining pattern was seen in adenocarcinomas. In ESCCA, FasL was often located in the cells at the periphery of tumor nests. All (100%) of EADCA showed FasL expression in greater than 25% of the cancer cells, and all were associated with lymph node metastasis. Fifty-three percent of ESCCA showed FasL expression in greater than 25% of the cancer cells and 33% had lymph node metastasis. Expression of FasL in greater than 25% of tumor cells was associated with a significantly higher incidence of lymph node metastasis (P=0.001). All lymph node metastases from esophageal carcinomas showed FasL immunoreactivity in greater than 50% of the metastatic tumor cells. Conclusions. FasL expression in greater than 25% of cancer cells correlates with a high incidence of lymph node metastasis in esophageal carcinomas. All cancer metastases in lymph nodes express FasL in >50% of the cells. These findings indicate that FasL plays an important role in the immune evasion and metastasis of esophageal carcinomas.
Younes, M., Schwartz, M., Ertan, A., Finnie, D., & Younes, A. (2000). Fas ligand expression in esophageal carcinomas and their lymph node metastases. Cancer, 88 (3). http://dx.doi.org/10.1002/(SICI)1097-0142(20000201)88:3<524::AID-CNCR5>3.0.CO;2-U