Histological features pertinent to local tumour progression in Barrett's adenocarcinoma.

Sections from 18 resected esophagi having a Barrett's adenocarcinoma were reviewed. Particular attention was paid to the neoplastic glands at the tumour-host tissue interphase (T/HI). In 3 (17%) of the 18 adenocarcinomas, the glands at the T/HI displayed a thinner layer of tumour cells. In 13 (72%) of the 18 adenocarcinomas, the glands at the T/HI showed a partial loss of tumour cells; that phenomenon was denominated glandular pore formation. The thinner epithelium appears to be a stage preceding the focal destruction of the tumour cells leading to pore formation. Through those glandular pores, cell-free mucin, inflammatory cells or necrotic elements were released into the surrounding host tissues. It is conceivable that those non-neoplastic "pseudopodial" forerunners, rich in proteolytic enzymes, encourage the disintegration of the surrounding host tissues. From the tip of the glandular pores malignant cells will grow around the secreted products to restore glandular continuity. The remodelling of the glands will guarantee a stepwise but everlasting tumour progression deeper into the host. The remaining 2 (11%) of the 18 Barrett's adenocarcinomas were of signet ring cell type. The presence of cell-free mucin "lakes" within the tissues of the host in signet ring cell Barrett's adenocarcinomas suggest a similar mechanism of tumour progression.