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Phenotypic conversion of acute leukaemia from T‐lymphoblastic to myeloblastic induced by therapy with 2′‐deoxycoformycin
Author(s) -
Murphy S. B.,
Stass S.,
Kalwinsky D.,
Rivera G.
Publication year - 1983
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.1365-2141.1983.tb01249.x
Subject(s) - calla , deoxycoformycin , terminal deoxynucleotidyl transferase , adenosine deaminase , myeloid , cancer research , immunology , progenitor cell , myeloperoxidase , biology , microbiology and biotechnology , chemistry , medicine , stem cell , adenosine , antibody , immunohistochemistry , monoclonal antibody , tunel assay , inflammation
S ummary . A 6‐year‐old boy with T‐cell acute lymphoblastic leukaemia (ALL) in relapse was treated with the adenosine deaminase inhibitor, 2′‐deoxycoformycin (DCF). Remarkably, his residual leukaemia underwent an abrupt phenotypic shift, coincident with a massive anti‐leukaemic effect of DCF. Both at diagnosis and prior to therapy with DCF, blast cells had typical lymphoblastic morphology and T‐cell characteristics (terminal transferase +, T‐antigen +, Ia –, cALLa –, myeloperoxidase –, and high in adenosine deaminase content). After four courses of DCF by constant infusion, the blast cells were myeloid in appearance and reactivity to a variety of tests (terminal transferase –, myeloperoxidase +, Sudan black B +, esterase +, My‐1 +). We hypothesize that DCF therapy created a selection pressure, blocking pathways of T‐cell differentiation and proliferation, permitting the emergence of a newly dominant myeloid subclone of a multipotential leukaemic cell progenitor with the innate capacity for both T‐lymphocytic and myeloid differentiation.