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Acute Myeloid Leukaemia with Monosomy‐7 Follows Acute Lymphoblastic Leukaemia
Author(s) -
Walker Lorna M. Secker,
Sandler R. M.
Publication year - 1978
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.1365-2141.1978.tb01055.x
Subject(s) - pancytopenia , medicine , monosomy , bone marrow , myeloid , chromosome 7 (human) , myeloid leukaemia , neoplasm , karyotype , malignant histiocytosis , pathology , immunology , chromosome , biology , genetics , gene , histiocyte
A case report of an 8‐year‐old girl who developed acute myeloid leukaemia (AML) following the successful treatment of acute lymphoblastic leukaemia (ALL) is presented. Haematological and cytochemical evidence for the two types of leukaemia is given. This is reinforced by the cytogenetic findings. After 2 years' treatment for ALL the patient became pancytopenic and marrow depression continued even when all treatment was stopped. Marrow cells monosomic for chromosome‐7 (45 XX ‐7) were first seen 2 months before the onset of progressive pancytopenia when blood parameters were normal. Both during the pre‐leukaemic and frankly leukaemic stages of the myeloid neoplasm, cells with monosomy‐7 constituted the dominant cell line in the marrow. This suggests that in this case the preceding pancytopenia was part of the malignant change and that the chromosomal change was one of the earliest events in the neoplastic process. Other reports of AML following cytotoxic therapy for treatment of malignant diseases as well as for non‐malignant conditions are briefly reviewed and the neoplastic mechanisms under these conditions are discussed. There is some evidence that in the case reported here genetic factors may have been at least as important as environmental conditions in triggering off the second malignant change.

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