UNSCHEDULED EXPRESSION OF CYCLIN-B1 AND CYCLIN-E IN SEVERAL LEUKEMIC AND SOLID TUMOR-CELL LINES

Normal, nontumorous cells express cyclin proteins in an orderly, sched uled fashion, at a given phase of the cell cycle. Thus, cyclin B1 is s ynthesized during G(2) and abruptly degraded during mitosis. The onset of cyclin E synthesis takes place in mid-G(1), its maximal expression is at the time of cell entrance to S, and its degradation occurs duri ng cell progression through S phase. In the present study, multiparame ter flow cytometry was used to correlate expression of cyclin B1 or cy clin E with cell cycle position (estimated by cellular DNA content) in normal human proliferating lymphocytes as well as in T-cell MOLT-4 le ukemia; promyelocytic HL-60 leukemia; histiocytic U937 lymphoma; MCF-7 , T-47D, and Hs 587T breast carcinoma; Cole 320DM colon carcinoma; and the T-24 transitional cell carcinoma cell line. The scheduled express ion of both cyclins, namely of cyclin B1 restricted to G(2) + M cells and of cyclin E restricted to late G(1) and early S cells, was observe d only in normal lymphocytes and MOLT-4 cells. The cells of HL-60, U93 7, T-47D, and Hs 587T lines expressed both cyclins in an unscheduled ( ''ectopic'') fashion, i.e., unrelated to cell cycle position. Cole 320 DM cells showed unscheduled expression of cyclin E (i.e., during G(2)) but expression of cyclin B1 in this line was generally restricted to G(2) + M cells. There were relatively few (10-12%) cells in MCF-7 and T-24 cell lines that expressed cyclin B1 or E in an unscheduled manner . It may be expected that the unscheduled expression of cyclins in tum or cells may lead to a loss of the regulatory mechanisms of cell cycle progression and that such feature of the tumor may be of prognostic v alue. There is a need, therefore, to conduct similar studies in primar y tumor cells.