| Literature DB >> 15982735 |
Francis H Grand1, Prasad Koduru, Nicholas C P Cross, Steven L Allen.
Abstract
The molecular basis for disease progression in chronic myeloid leukaemia (CML) is poorly understood, but is believed to be a consequence of additional acquired genetic lesions. We describe here a case of CML who presented de novo in transformation with a t(9;11)(p21;p15) and NUP98-LEDGF fusion in addition to the t(9;22). The t(9;11) was present in only 2/45 (4%) of bone marrow metaphases, but 17/20 (85%) of metaphases from peripheral blood, suggesting an extramedullary or focal origin. This is the first description of NUP98-LEDGF in CML and strengthens the association between disease progression in and NUP98 abnormalities.Entities:
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Year: 2005 PMID： 15982735 DOI： 10.1016/j.leukres.2005.05.002
Source DB: PubMed Journal: Leuk Res ISSN： 0145-2126 Impact factor: 3.156