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C‐abl and bcr are rearranged in a Ph1‐negative CML patient.
Author(s) -
Bartram C.R.,
Kleihauer E.,
Klein A.,
Grosveld G.,
Teyssier J.R.,
Heisterkamp N.,
Groffen J.
Publication year - 1985
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1985.tb03683.x
Subject(s) - biology , cancer research , genetics
Chromosomal analysis of a patient with chronic myelocytic leukemia (CML) revealed a translocation (9;12) (q34;q21) without a detectable Philadelphia chromosome (Ph1). Using molecular approaches we demonstrate (i) a rearrangement within the CML breakpoint cluster region (bcr) on chromosome 22, and (ii) a joint translocation of bcr and c‐abl oncogene sequences to the derivative chromosome 12. These observations support the view that sequences residing on both chromosome 9 (c‐abl) and 22 (bcr) are involved in the generation of CML and suggest that a subset of Ph1‐negative patients may in fact belong to the clinical entity of Ph1‐positive CML.