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Annotation: CELLULAR CHANGES IN CHRONIC MYELOID LEUKAEMIA
Author(s) -
Pedersen Bent,
Hayhoe F. G. J.
Publication year - 1971
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.1365-2141.1971.tb03436.x
Subject(s) - chronic myeloid leukaemia , clone (java method) , chromosome , philadelphia chromosome , blast crisis , alkaline phosphatase , karyotype , myeloid , medicine , immunology , gene , chromosomal translocation , biology , cancer research , genetics , enzyme , biochemistry
Since the original observation by Wachstein (1946), numerous investigations have demonstrated that the vast majority of patients with chronic myeloid leukaemia have very low alkaline‐phosphatase activities in their polymorphonuclear leucocytes. The observation of a high leucocyte alkaline‐phosphatase (LAP) activity in Down's syndrome (Alter et al, 1962), where the karyotype contains an extra G chromosome, and the fact that patients with chronic myeloid leukaemia (CML) have a partially deleted G chromosome, the so‐called Philadelphia chromosome (Ph 1 ), at one time led to the hypothesis that a specific gene regulating LAP activity was present in a G chromosome, possibly no. 21 (Alter et al, 1963). The fact that LAP activity increases during successful treatment of CML and even returns to the normal range in a few cases (Hayhoe & Quaglino, 1958; Xefteris et al, 1961; Linke & Löffler, 1963; Elves et al 1963) might be explained if a non‐leukaemic clone of cells were activated under treatment. The bone marrow remains, however, entirely Ph 1 ‐positive in remission (Tough et al, 1963). Moreover, the observation by Hammouda et al (1964) of persisting Ph 1 ‐positivity in patients with high LAP activity in blast crisis of CML was incompatible with the existence of a simple causal relationship between the Ph 1 deletion and depression of LAP activity.