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Biology of CML stem cells: the basis for clinical heterogeneity?

Abstract

Although chronic myeloid leukemia (CML) is now defined on the basis of the presence of the BCR-ABL1 fusion gene, which may or may not be the initial genetic event that triggers the inappropriate expansion of the myeloid cell mass, CML, similar to other leukemias, is in fact clinically heterogeneous. The biological basis for this heterogeneity is unknown. Here, we summarize some of the data illustrating this heterogeneity and speculate about possible mechanisms that may cause it. It could, for example, be intrinsic in the leukemia stem cell or could be related to some aspect of the patient's response to the leukemia.

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Correspondence to J M Goldman.

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Competing interests

JMG and DM received financial support from Novartis and Bristol-Myers Squibb. JMG has also received consulting fees from Ariad Pharmaceuticals and lecture fees from Amgen Inc. MG and AB have no relevant financial support to disclose.

Additional information

This article was published as part of a supplement that was supported by Novartis, MSD Italia, Roche, Celgene, GlaxoSmithKline, Sanofi, Gilead, Adienne, Italfarmaco, Pierre Fabre Pharmaceuticals with an unrestricted educational contribution to AREO—Associazione Ricerche Emato-Oncologiche (Genoa) and AMS—Associazione Malattie del Sangue (Milan) for the purpose of advancing research in acute and chronic leukemia.

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Goldman, J., Gordon, M., Bazeos, A. et al. Biology of CML stem cells: the basis for clinical heterogeneity?. Leukemia Suppl 1 (Suppl 2), S43–S45 (2012). https://doi.org/10.1038/leusup.2012.23

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