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Megakaryocyte Polyploidization in Acute Leukaemia and Preleukaemia
Author(s) -
Queisser W.,
Queisser U.,
Ansmann M.,
Brunner G.,
Hoelzer D.,
Heimpel H.
Publication year - 1974
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1974.tb06661.x
Subject(s) - megakaryocyte , labelling , megakaryocytopoiesis , ploidy , thymidine , platelet , biology , pathology , in vitro , andrology , microbiology and biotechnology , immunology , medicine , genetics , haematopoiesis , biochemistry , stem cell , gene
S ummary . Megakaryocyte polyploidy was studied in six cases of preleukaemic acute leukaemia (PL), and in acute leukaemia (AL), five cases in the overt phase and three during complete remission. The megakaryocyte polyploidization was determined cytophotometrically and in some cases also by in vitro labelling with tritiated thymidine ( 3 H‐TdR). The results obtained in PL and untreated AL. demonstrate an impairment of the 3 H‐TdR labelling index and altered megakaryocyte polyploidy such as decrease of the maximum polyploidization capacity (five cases), evidence of diploid megakaryocytes (two cases) and of hyperploid megakaryocytes (six cases). These disturbances reflected the cytological abnormalities (microkaryo‐cytes, polykaryocytes) observed in most of the cases studied. In contrast, in cases studied during complete remission of AL. a normal labelling index and polyploidy composition was observed, suggesting that the polyploidization disturbances are reversible. A strict correlation of the polyploidization defect and the platelet production could not be established from the patients investigated.