Immunohistochemical detection of retroviral-P15E-related material in carcinomas of the head and neck.

As has been reported previously, head and neck carcinomas produce low molecular weight factors (H/N ca LMWFs); a molecular weight less than 25000 daltons is capable of inhibiting the chemotaxis of mononuclear phagocytes. The effect of the factors could be neutralized by antibodies to P15E, one of the structural envelope proteins of Murine Leukemia Viruses (MuLV). This indicates that these low molecular weight factors derived from the tumors are related to P15E. In this study, 35 biopsy specimens of head and neck carcinomas were subjected to an indirect immunoperoxidase assay, in order for P15E-like material to be detected morphologically. All head and neck carcinomas gave positive results. Sixty-three percent of other carcinomas (used as controls) were positive as well. P15E-like material was also expressed in epithelia-overlaying inflammatory responses. Healthy epithelia were not positive. This report thus supports the view that P15E-like molecules can be easily detected in cancerous disease--not only by way of biologic isolation, but also by use of immunohistochemical techniques. Since the factor is not specific for the malignant state, it cannot be used as a tumor marker. Possibly involved in the pathogenesis of cancerous disease, its relationship to growth factors, oncogenes, and the immune system needs further clarification.

Influence of oral 15(R)-15-methyl prostaglandin E2 on human gastric mucosa. A light microscopic, cell kinetic, and ultrastructural study.

Histomorphometric, electron microscopic, and cell kinetic studies of gastric mucosa were performed in 12 healthy men treated with 100 micrograms of 15(R)-15-methyl prostaglandin E2 (PGE2) orally q.i.d. for 2 mo followed by 2 mo of placebo. Results were compared with 13 control subjects receiving placebo for 4 mo. After PGE2 administration, total antral mucosal thickness and antral and corpus foveolar thicknesses increased 36%, 44%, and 51%, respectively, over baseline values. The total number and height of the foveolar cells also increased. These morphologic changes reversed completely within 2 mo of stopping PGE2 therapy. After PGE2 administration, no evidence of mucosal inflammation or atypia was observed, nor was there any evidence of ultrastructural changes in the overall appearance of the parietal and gastrin cells. The increased thickness of the gastric mucosa could not be explained by alteration of the proliferative activity, as the labeling index and localization of the proliferative compartment remained unchanged after PGE2 therapy. Presumably PGE2 retards senescence and exfoliation of epithelial cells, which explains the foveolar expansion in the presence of unaltered proliferation.