NUP98-LEDGF fusion and t(9;11) in transformed chronic myeloid leukemia

Francis H. Grand, Prasad Koduru, Nicholas C P Cross, Steven L. Allen

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


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 languageEnglish (US)
Pages (from-to)1469-1472
Number of pages4
JournalLeukemia Research
Issue number12
StatePublished - Dec 2005


  • Blast crisis
  • CML
  • NUP98

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research


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