Expressions of cyclin E, A, and B1 in Hodgkin and Reed-Sternberg cells: Not suppressed by cyclin-dependent kinase inhibitor p21 expression

p21 Is involved in the control of the mammalian cell cycle through the bind ing and inhibition of cyclin-dependent kinases. The cyclins are dependent o n the phases of the cell cycle, and divided into two classes: mitotic cycli ns (A, B1, B2) and G1 cyclins (C, D1, D2, D3, E). The product of the p21 ge ne is a potent downstream effector of the p53 tumor-suppressor gene functio n. The Hodgkin and Reed-Sternberg (H & RS) cells in Hodgkin's disease are r eported to frequently express p53, p21, and nuclear proliferative activity (Ki-67). To clarify the relationship of p21, p53 and cyclins, we performed the immunohistochemistry of p53, p21, Ki-67, cyclin D1, cyclin E, cyclin A and cyclin Bt, using 11 cases with Hodgkin's disease. In addition, we perfo rmed p53 gene sequencing of exon 5-8, and in situ hybridization of Epstein- Barr virus (EBV) EBER-1 region, whose products have reported to induce the expression of cyclin D. In this study, in all cases, Ki-67 was expressed in almost all H & RS cells, and p53 and p21 were expressed in H & RS cells. N o p53 gene mutations were detected in any case, and p53 protein overexpress ion did not correlate with p53 gene mutations. The number of p21-positive H & RS cells was significantly related with that of the p53-positive cells. The cyclins E, A, B1 and D1 were also expressed in H & RS cells. Unexpected ly, the expression of the cyclins was not suppressed by p21 and p53 express ion. In addition, the existence of EBV was not related to the expression of cyclins. It is considered that H & RS cells are, indeed, in cell cycle and commonly express the cell cyclins, and that the cell cycle of H & RS cells may not be specifically fixed in the G1, S, G2 or M phases.