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Detection of the BCR‐ABL gene by reverse transcription/polymerase chain reaction and fluorescence in situ hybridization in a patient with Philadelphia chromosome negative acute lymphoblastic leukaemia
Author(s) -
RHEE F. VAN,
KASPRZYK A.,
JAMIL A.,
DICKINSON H.,
LIN F.,
CROSS N. C. P.,
GALVIN M. C.,
GOLDMAN I J. M.,
SECKERWALKER L. M.
Publication year - 1995
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.1365-2141.1995.tb03408.x
Subject(s) - fluorescence in situ hybridization , philadelphia chromosome , abl , breakpoint cluster region , biology , microbiology and biotechnology , cancer research , bone marrow , in situ hybridization , acute lymphocytic leukemia , cosmid , chromosome , gene , leukemia , chromosomal translocation , immunology , genetics , gene expression , lymphoblastic leukemia , receptor , tyrosine kinase
The Philadelphia (Ph) chromosome is detected in leukaemia cells in approximately 20% of adults with acute lymphoblastic leukaemia (ALL). When treated with chemotherapy alone, Ph‐positive ALL has a poor prognosis, and patients may benefit from bone marrow transplantation in first remission. Here we report a patient with chromosomally normal bone marrow, in all 60 cells analysed, who was found to have the p210‐type BCR‐ABL chimaeric transcript by RT/PCR. Fluorescence in situ hybridization was labelled cosmid probes for BCR and ABL showed the presence of BCR‐ABL juxtaposition on a normal chromosome 22 in leukaemia cell metaphases. We conclude that molecular and cytogenetic methods should be used in conjunction to detect the BCR‐ABL gene rearrangement in ALL.