We examined the expression of intercellular--adhesion molecule-I (ICAM-I, CD54) in 6 surgically removed pancreatic tumors and 8 pancreatic tumor cell lines. Immunohistochemistry revealed a varying percentage of ICAM-I-positive pancreas tumor cells, while normal pancreatic tissue (except for slight reactivity of endothelial cells) was not stained. The presence of the ICAM-I molecule on the cell surface and the expression of ICAM-I mRNA were investigated for 8 different pancreatic tumor cell lines. Three of these (Capan-I, Capan-2, QGP-I) expressed ICAM-I constitutively. In 4 of the ICAM-I-negative pancreas cancer cell lines, it was possible to induce a remarkable expression of ICAM-I by incubating the cells in the presence of inflammatory cytokines, whereas one cell line, 818-4, remained ICAM-I-negative. The responsiveness to either IFN-gamma, TNF-alpha, or IL-I beta treatment was shown to vary from cell line to cell line, indicating complex mechanisms that regulate the expression of ICAM-I at both, the transcriptional and the post-transcriptional level. Interestingly, ICAM-I is shed by pancreatic tumor cells, since soluble sICAM-I was detected in the cell-culture supernatants. In comparison with normal sera, the mean level of sICAM-I in sera of patients with pancreas carcinoma is elevated 2-fold.