title: Cellular kinetic differences between Hodgkin's and anaplastic large cell lymphomas: relation to the expression of p34cdc2 and cyclin B-1.
abstract: 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.
authors.affiliation: Institute of Pathologic Anatomy and Histology, University of Siena, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Leoncini
authors.forename: T
authors.initials: T
authors.lastname: Megha
authors.forename: S
authors.initials: S
authors.lastname: Lazzi
authors.forename: C
authors.initials: C
authors.lastname: Bellan
authors.forename: P
authors.initials: P
authors.lastname: Luzi
authors.forename: P
authors.initials: P
authors.lastname: Tosi
authors.forename: G
authors.initials: G
authors.lastname: Cevenini
authors.forename: P
authors.initials: P
authors.lastname: Barbini
authors.forename: S
authors.initials: S
authors.lastname: Ascani
authors.forename: A
authors.initials: A
authors.lastname: Briskomatis
authors.forename: S
authors.initials: S
authors.lastname: Pileri
authors.forename: R
authors.initials: R
authors.lastname: Kraft
authors.forename: J A
authors.initials: JA
authors.lastname: Laissue
authors.forename: H
authors.initials: H
authors.lastname: Cottier
mesh_terms: D016203:CDC2 Protein Kinase / Q000096:biosynthesis*; D002453:Cell Cycle; D019926:Cyclin B / Q000096:biosynthesis*; D056744:Cyclin B1; D004249:DNA Damage; D006689:Hodgkin Disease / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D017730:Ki-1 Antigen / Q000032:analysis; D007700:Kinetics; D008198:Lymph Nodes / Q000378:metabolism / Q000473:pathology; D016403:Lymphoma, Large B-Cell, Diffuse / Q000378:metabolism / Q000473:pathology*; D008938:Mitosis; D008940:Mitotic Index
chemical_list: C534699:CCNB1 protein, human; D019926:Cyclin B; D056744:Cyclin B1; D017730:Ki-1 Antigen; D016203:CDC2 Protein Kinase