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BCR‐ABL‐positive progenitors in chronic myeloid leukaemia patients in complete cytogenetic remission after treatment with interferon‐α
Author(s) -
Reiter Andreas,
Marley Stephen B.,
Hochhaus Andreas,
Sohal Jastinder,
Raanani Pia,
Hehlmann RÜdiger,
Gordon Myrtle Y.,
Goldman John M.,
Cross Nicholas C. P.
Publication year - 1998
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 - 10.1046/j.1365-2141.1998.00905.x
Subject(s) - clone (java method) , clonogenic assay , breakpoint cluster region , interferon , myeloid , minimal residual disease , immunology , cytogenetics , peripheral blood mononuclear cell , bone marrow , biology , philadelphia chromosome , interferon alfa , alpha interferon , progenitor cell , medicine , cancer research , stem cell , chromosomal translocation , chromosome , receptor , cell , genetics , dna , gene , in vitro
To determine the source of residual disease detected in patients with chronic myeloid leukaemia (CML) in complete cytogenetic remission ( n = 8) after treatment with interferon‐α (IFN‐α), we have tested CFU‐GM colonies grown from bone marrow mononuclear cells or from plastic‐adherent (PΔ) cells for BCR‐ABL mRNA using a nested multiplex RT‐PCR. We compared our results with those obtained by analysis of colonies from newly diagnosed patients ( n = 4) and patients achieving no cytogenetic response ( n = 1) or incomplete cytogenetic response to treatment with IFN‐α ( n = 5). A total of 1239 informative colonies were analysed. A small proportion of BCR‐ABL‐positive colonies was detected in all eight patients in complete cytogenetic remission, suggesting the persistence of leukaemia that could potentially lead to relapse. The overall proportion of BCR‐ABL‐positive colonies in patients achieving a cytogenetic response to IFN‐α correlated with the levels of BCR‐ABL transcripts detected in the peripheral blood by competitive RT‐PCR ( P = 0.004). We conclude that residual disease detected in the peripheral blood of complete cytogenetic responders to IFN‐α is at least partly derived from clonogenic myeloid cells. It is probable that the leukaemia clone in CML is only very rarely or never entirely eradicated by treatment with IFN‐α.