MMI-166 is a third-generation selective matrix metalloproteinase (MMP) inhibitor that prevents tumor invasion and metastasis by downregulating the activity of MMP-2 and MMP-9. However, MMI-166's effect in pancreatic cancer cells has not been widely studied. Initially, we treated SW1990, human pancreatic cancer cells, with 0, 50 or 100 μg/ml of MMI-166 for 24 h. Apoptosis in the cells was then observed by inverted fluorescence microscope and flow cytometry; the apoptosis rate was dependent on MMI-166 concentration. We then injected nude mice with SW1990 cells. Volume of the resulting xenograft tumors in nude mice treated with MMI-166 was far less than that of the control group, whereas their apoptotic index was much greater. Expression of MMP-2, MMP-9, c-myc and survivin were markedly lower in tumors from the treated mice than in the control group. In cell experiments, MMP-2 and MMP-9 activities were downregulated by MMI-166 compared with controls, as were both mRNA and protein levels of MMP-2, MMP-9 and c-myc, although survivin expression did not differ. These results show that MMI-166 can induce apoptosis of pancreatic cancer cells in vitro and in vivo. The mechanism may be related to downregulation of c-myc by MMI-166.

The frequency of oropharyngeal excreters of the Epstein-Barr virus among patients with nasopharyngeal carcinoma in Hong Kong was compared with those of healthy adults in Hong Kong and California. 6 (3%) of 177 patients, 11 (12%) of 92 Hong Kong residents, and 20 (15%) of 132 Californians were excreters. The virus was detected in the nasopharyngeal secretion of only 1 of 67 patients and in 2 of 73 healthy adults. No convincing evidence for neutralizing antibody in the throat wash and nasopharyngeal secretions of the patients could be obtained. Epstein-Barr viral gene sequencing could not be detected in the throat washes from 27 patients with nasopharyngeal carcinoma, 8 patients with infectious mononucleosis, and 15 healthy adults and in the nasopharyngeal secretions of 35 patients and 17 controls. We conclude that patients with nasopharyngeal carcinoma are no more likely to be oropharyngeal or nasopharyngeal excreters of the Epstein-Barr virus than healthy adults. One possible explanation for this unexpected finding is that the virus infections in nasopharyngeal carcinoma cells are predominantly nonproductive.