@entity1860 ( @entity1860 ) progresses through three distinct clinical stages: chronic phase, accelerated phase, and @entity9638 . The progression to accelerated phase and @entity9638 is driven by activation of oncogenes, inactivation of @entity5 suppressor genes, and/or amplification of the @entity1861 fusion gene, which causes the chronic phase of the disease. The cell of origin of @entity9638 is a subject of speculation. Here, I develop a simple mathematical model of @entity1860 to investigate whether blasts arise from leukemic stem cells or more differentiated leukemic cells. I use data of @entity1 treated with @entity2213 and previous agents to estimate the effects of therapy on the rate of progression. @entity2213 reduces the progression rate 10-fold as compared with previous (ineffective) therapies. If blasts were produced by leukemic stem cells, there would be no difference in the rate of progression between @entity1 treated with @entity2213 and previous therapies, because @entity2213 seems to be incapable of depleting leukemic stem cells. @entity2213 does, however, deplete leukemic progenitors. Therefore, @entity1860 blasts are likely to arise from leukemic progenitors. Disclosure of potential conflicts of interest is found at the end of this article.

XXXX @entity9638 arises from progenitors.

@entity1 :: ('9606', 'Species') :: ['patients'] @entity1861 :: ('25', 'Gene') :: ['BCR-ABL'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor'] @entity9638 :: ('MESH:D001752', 'Disease') :: ['blast crisis'] @entity1860 :: ('MESH:D015464', 'Disease') :: ['CML', 'Chronic myeloid leukemia', 'CML blast crisis'] @entity2213 :: ('MESH:C097613', 'Chemical') :: ['imatinib', 'Imatinib']
@entity1860 :: (MESH:D015464,Disease) :: ['Chronic myeloid leukemia']
