Biological diversity and risk-adapted treatment of chronic lymphocytic leukemia

been hypothesized that interference with niche-induced quiescence, either by altered niche signaling or detachment from the niche, may result in increased cycling of cells that have the inherent machinery of self-renewal, thus poising these cells ready for the acquisition of somatic mutations and malignant transformation. Recently experimental evidence introduced the concept of niche-induced oncogenesis in the hematopoietic system, showing that specific genetic abnormalities in osteoprogenitor cells can induce myelodysplasia and acute myeloid leukemia in mice. 19 Whether leukemic transformation in this system was associated with impaired trafficking or aberrant localization of HSC in their niche remains to be determined. It is noteworthy, however, that aberrant localization of hematopoietic stem/progenitor cells in human disease is not unprecedented, as atypical localization of immature progenitors is a common finding in myelodysplastic syndromes. 20 Indeed, recent findings in mouse models warrant reconsideration of a possible involvement of the dynamic interaction between HSC and their niche in the pathogenesis of certain hematopoietic diseases, including bone marrow failure syndromes and myelodysplastic syndromes. Studies such as the one published by Staudt et al. in this issue of the Journal, identifying determinants of this interaction, will greatly facilitate such investigations.