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Relation between Karyotype and Cytology in Chronic Myelogenous Leukaemia
Author(s) -
Pedersen Bent
Publication year - 1971
Publication title -
scandinavian journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0036-553X
DOI - 10.1111/j.1600-0609.1971.tb00904.x
Subject(s) - karyotype , supernumerary , biology , cytology , peripheral blood , small supernumerary marker chromosome , chromosome , centromere , pathology , immunology , genetics , anatomy , medicine , gene
Cytogenetic parameters in 56 blood cultures from 27 patients with Ph 1 ‐positive CML covering all stages of the disease were compared with the cytological character of the corresponding peripheral blood samples. The main observations were: (1) Increasing frequencies of hyperdiploid metaphases were associated with circulation of more granulocyte precursors, and the precursor cytology tended to become more primitive. (2) Pseudodiploid metaphases showed no such relation to the peripheral blood picture. (3) This difference between hyper‐ and pseudodiploid cells was apparently associated with the different ratios of missing/supernumerary chromosomes in these cells, but in addition a different Denver group composition of the supernumerary chromosomes appeared to be responsible. The pseudodiploid metaphases demonstrated significantly higher frequencies of additional small acrocentric chromosomes, whereas supernumerary C members characterized the hyperdiploid karyotypes. (4) The proportions of supernumerary chromosomes belonging to the C group were positively correlated to the frequencies of circulating nucleolated granulocyte precursors. The small acrocentric chromosomes, however, showed the reverse relation to the peripheral blood cytology. Between these cytogenetic and cytological parameters a close relationship apparently exists, which is explainable on the assumption that presence of excess numbers of certain chromosomes delays maturation of granulocyte precursors and leads to development of haematological relapse, ultimately blastic crisis. If this hypothesis is substantiated, it opens possibilities of improved therapeutical prospects by prevention of karyotype evolution.