Molecular evolution of chronic myeloid leukaemia

Pesach J. Shteper, Dina Ben-Yehuda*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Chronic myeloid leukaemia (CML) is a clonal disorder of the pluripotent haematopoietic stem cell. The typical triphasic course of CML starts with the premalignant chronic phase initiated by BCR-ABL hybrid oncogene formation. Secondary genetic and epigenetic aberrations accompany the progression to the accelerated phase and fatal blastic crisis. Properly timed bone marrow transplantation in eligible patients can result in durable remissions or cure. Both of these states are often accompanied by a long-term persistence of quiescent leukaemic cells. Accordingly, a 'functional cure' (i.e. turnout dormancy induction), rather than complete eradication of the malignant cells, is an adequate therapeutical goal. The level of the residual BCR-ABL-positive clones should be monitored and salvage treatment initiated whenever these quiescent leukaemic cells exit their dormant state.

Original languageAmerican English
Pages (from-to)313-322
Number of pages10
JournalSeminars in Cancer Biology
Issue number4
StatePublished - 2001
Externally publishedYes

Bibliographical note

Funding Information:
We are grateful to Dr Deborah Rund for her critical revision of the manuscript. Our work was supported by The Israel Science Foundation founded by The Israel Academy of Sciences and Humanities, and by The Gabrielle Rich Leukemia Research Foundation.


  • ABL
  • Chronic myeloid leukaemia
  • Dormancy
  • Methylation
  • Progression


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