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Molecular confirmation of BCR‐ABL fusion in a chronic myeloid leukemia with a complex translocation involving chromosomes 9, 15, and 22
Author(s) -
Tharapel Sugandhi A.,
VnencakJones Cindy L.,
Whitlock James A.,
Jain Rajiv
Publication year - 1992
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.2870040412
Subject(s) - chromosomal translocation , breakpoint cluster region , complementary dna , myeloid leukemia , microbiology and biotechnology , abl , biology , fusion transcript , bone marrow , philadelphia chromosome , reverse transcriptase , chromosome 22 , rna , cancer research , genetics , gene , immunology , tyrosine kinase , receptor
We performed molecular studies to resolve the status of BCR and ABL in the bone marrow cells of a CML patient with a Ph chromosome resulting from a complex translocation involving chromosomes 9, 15, and 22. DNA digestion with Bam HL, Hindlll , and Bglll , followed by hybridization to a bcr ‐specific 32 P‐labeled probe, showed a rearranged banding pattern confirming the involvement of the bcr , locus in the translocation. Furthermore, total cellular RNA isolated from the marrow was subjected to reverse transcription into cDNA and amplified by PCR with primers specific for BCR‐ABL fusion cDNA. The amplified products obtained from this patient and from a CML patient with the standard t(9;22) were both of the expected length of approximately 317 bp.