[LAK sensitivity of human pancreas carcinoma cell lines]

Surface intercellular adhesion molecule-1 (ICAM-1) on pancreas carcinoma cell has been shown to be critical in lymphokine-activated killer (LAK) cytotoxicity. However, whether or not ICAM-1 itself is a target structure of LAK cells remains unclear. In this study, original pancreas carcinoma cell lines, PCI-6, 10, 19, 24, 35, and 43, were established from surgically resected or biopsied cancer tissues. These cell lines all generated tumor nodules upon subcutaneous injection into nude mice, and morphology of the nodules all closely resembled original pancreas cancer. When the cell lines were cultivated in collagen gel, spheroid formation was exclusively seen in cell lines of moderately differentiated tubular adenocarcinoma in original tumor sites. In the two cell lines derived with poorly differentiated adenocarcinoma, no three dimensional structures were generated in the gel. These PCI cells were natural killer (NK)-resistant, but were all LAK-sensitive. Blocking experiments confirmed the importance of ICAM-1 on PCI and lymphocyte function-associated antigen-1 (LFA-1) on LAK cells. LAK sensitivity expressed by percent cytotoxicity was not correlated with the surface ICAM-1 expression on individual PCI lines. Moreover, a LAK-resistant variant of PCI-24, designated PCI-24R, which was obtained by repeated co-cultivation of LAK with PCI-24, did not change surface ICAM-1 molecule expression and its function. These combined data indicate that the pancreas carcinoma cell lines remain original biologic properties, and that, although ICAM-1 serves as an important adhesion molecule in interaction with LAK, the adhesion molecule itself does not function as a target structure in LAK cytotoxicity.