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.
Original language | English (US) |
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Pages (from-to) | 1469-1472 |
Number of pages | 4 |
Journal | Leukemia Research |
Volume | 29 |
Issue number | 12 |
DOIs | |
State | Published - Dec 2005 |
Keywords
- Blast crisis
- CML
- LEDGF
- NUP98
ASJC Scopus subject areas
- Hematology
- Oncology
- Cancer Research