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Interphase cytogenetics and competitive RT‐PCR for residual disease monitoring in patients with chronic myeloid leukaemia during interferon‐α therapy
Author(s) -
Tchirkov Andrei,
Giollant Michel,
Tavernier FranÇoise,
BrianÇon Georges,
Tournilhac Olivier,
Kwiatkowski Fabrice,
Philippe Pierre,
Choufi Bachra,
DemÉocq FranÇois,
Travade Philippe,
Malet Paul
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.1365-2141.1998.00717.x
Subject(s) - fluorescence in situ hybridization , cytogenetics , metaphase , alpha interferon , minimal residual disease , interferon alfa , biology , clone (java method) , interphase , bone marrow , immunology , microbiology and biotechnology , interferon , medicine , chromosome , genetics , gene
There is a need for fast and sensitive methods to evaluate the response of patients with chronic myeloid leukaemia (CML) to interferon‐α (IFN‐α) therapy to complement cytogenetic analysis of Philadelphia (Ph) chromosome‐positive metaphases. We have used interphase FISH (fluorescence in situ hybridization) and competitive RT‐PCR (reverse transcriptase‐polymerase chain reaction) techniques for detection of BCR‐ABL‐positive cells to measure suppression of leukaemic clone in a series of 51 follow‐up samples from 24 CML patients undergoing IFN‐α treatment. Interphase FISH analysis of the malignant clone in bone marrow using BCR and ABL probes was found to be highly correlated to conventional G‐banding metaphase examination ( r = 0.98). RT‐PCR quantification of BCR‐ABL mRNA transcripts in blood also showed a high degree of concordance with the proportion of Ph‐positive metaphases ( r = 0.93). In addition, the degree of cytogenetic response did not influence the equivalence between karyotype analysis and molecular methods. We concluded that interphase FISH and competitive RT‐PCR provide reliable information on residual tumour burden and response to IFN‐α in CML patients. These molecular methods may significantly improve the efficiency of residual disease monitoring during IFN‐α therapy of CML.