Cellular kinetic differences between Hodgkin's and anaplastic large cell lymphomas: Relation to the expression of p34cdc2 and cyclin B‐1

Our study was designed to compare cellular kinetic parameters of classical Hodgkin's disease (HD) with those of anaplastic large cell lymphomas (ALCL‐C, common type; and ALCL‐HL, Hodgkin's like), with a particular focus on the G2/M transition. These disorders share some phenotypic properties, e.g., CD30 positivity of putative neoplastic cells. The percentages of cells expressing p34cdc2 (p34) and cyclin B‐1 (cyclin‐B), which form a complex (maturation/mitosis promoting factor, MPF) regulating the G2‐M phases of the cell cycle, were also registered. Highly significant differences between HD and ALCL‐C were recognized: a) in HD, evidence for abortive mitosis (i.e., difficulty to proceed beyond the metaphase stage) and consequent multinucleation and/or deletion of CD30+ cells was prominent, in contrast to ALCL‐C. This was associated with a markedly lower fraction of large atypical cells (LAC) expressing cyclin‐B in the cytoplasm and the nucleus (C + N) in HD than in ALCL‐C; b) the extent of multinucleation of CD30+ cells in HD, but not in ALCL‐C, was correlated with the %p34+ LAC; c) the proportions of LAC expressing p34 and/or cyclin‐B (C) were positively related to the percentages of cyclin‐B (C + N)+ LAC in ALCL‐C but not in HD; d) in HD, in contrast to ALCL‐C, the size of the fraction of cyclin‐B (C + N)+ LAC did not correlate with the ana/telophase indices (ATI, reflecting successful completion of mitosis) and the magnitude of cell loss; e) in ALCL‐C, the percentages of p34+ LAC were positively correlated with ATI or the degree of CD30+ cell deletion, but inversely in HD. With regard to all parameters mentioned above, ALCL‐HL tended to take an intermediate position between HD and ALCL‐C, but sided more with the latter. In conclusion, our present results suggest a derangement of MPF kinetics and functions that is more profound in HD than in ALCL‐C. Int. J. Cancer 77:408–414, 1998. © 1998 Wiley‐Liss, Inc.