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

✍ Scribed by Lorenzo Leoncini; Tiziana Megha; Stefano Lazzi; Cristiana Bellan; Pietro Luzi; Piero Tosi; Gabriele Cevenini; Paolo Barbini; Stefano Ascani; Aspasia Briskomatis; Stefano Pileri; Rainer Kraft; Jean A. Laissue; Hans Cottier

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: French
• Weight: 289 KB
• Volume: 77
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/(sici)1097-0215(19980729)77:3<408::aid-ijc17>3.0.co;2-3

✦ Synopsis

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 G 2 /M transition. These disorders share some phenotypic properties, e.g., CD30 positivity of putative neoplastic cells. The percentages of cells expressing p34 cdc2 (p34) and cyclin B-1 (cyclin-B), which form a complex (maturation/mitosis promoting factor, MPF) regulating the G 2 -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.