The Use of Cell Markers in The Study of Human Hematopoietic Neoplasia

Raskind, Wendy H.; Fialkow, Philip J.

doi:10.1016/s0065-230x(08)60796-4

Cited by 97 publications

(33 citation statements)

References 186 publications

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“…Previous studies have shown that such cells represent a subset of the CD34 þ CD38 À population that have long-term repopulating ability 7,14,15 and likely overlap with the cells in which chronic phase CML originates in patients. 16 Interestingly, the relative numbers of cells belonging to the different lineages produced by the P210-transduced cells in vivo was clearly abnormal. B-lineage cell output was markedly reduced and this was frequently accompanied by a sustained enhancement of erythroid and megakaryocytic cell production.…”

Section: Discussionmentioning

confidence: 99%

BCR-ABL-transduced human cord blood cells produce abnormal populations in immunodeficient mice

et al. 2005

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In this study, we describe the successful use of a gene transfer approach to demonstrate the ability of forced BCR-ABL expression to deregulate the growth and differentiation of primitive naïve human hematopoietic cells after their transplantation into immunodeficient mice. Human CD34 þ cord blood cells were exposed to an MSCV retrovirus containing a BCR-ABL-IRES-GFP (P210) cassette and then injected immediately into sublethally irradiated nonobese diabetic-severe combined immunodeficiency (NOD/SCID) or NOD/SCID-b2microglobulin À/À mice. P210-and control-transduced (GFP þ ) human hematopoietic cells were produced in the bone marrow of the mice at similar levels until termination of the experiments 5-6 months later. However, the P210-transduced cells produced a markedly different spectrum of progeny, with an increased ratio of myeloid to B-lymphoid cells and a frequently prolonged increase in erythroid and megakaryocytic cells. After 5 months, several of the mice transplanted with P210-transduced cells developed an increased WBC count and/or splenomegaly due to an expansion of the human GFP þ population. These findings demonstrate that forced expression of BCR-ABL in primitive transplantable human hematopoietic cells is sufficient to cause a rapid and persistent deregulation of their growth and differentiation in vivo with occasional evidence after several months of progression to an early stage of disease.

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Section: Discussionmentioning

confidence: 99%

BCR-ABL-transduced human cord blood cells produce abnormal populations in immunodeficient mice

et al. 2005

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“…In all of these diseases, the bone marrow fibrosis is polyclonal in origin, suggesting that it is a reactive process stimulated by activity of an abnormal stem cell clone, e.g., PDGF production. 2,20,40,[42][43][44][45] With effective therapy, fibrosis may be reversible (e.g., interferon-␣ [IFN-␣] in hairy cell leukemia [HCL], IFN-␣ IFN/Gleevec in CML).…”

Section: Pathogenetic Featuresmentioning

confidence: 99%

Beyond chronic myelogenous leukemia

Cortés¹,

Kantarjian²

2004

Cancer

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The myeloproliferative disorders (MPDs) are chronic malignant conditions originating from the clonal expansion of a multipotential hematopoietic stem cell.These diseases include polycythemia vera (PV), essential thrombocythenia, atypical chronic myeloid leukemia, idiopathic hypereosinophilic syndrome (HES), ag- Insight into the molecular pathogenesis of MPDs will improve the definitions of different disease categories and suggests that signal transduction inhibition is likely to be an increasingly important treatment option in the future.

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“…2,3 The underlying hypothesis is that a lymphoid-determined progenitor cell undergoes neoplastic transformation. In contrast, chronic myeloid leukemia (CML), which is considered to originate from a pluripotent stem cell, 4,5 shows multilineage involvement.…”

Section: Introductionmentioning

confidence: 99%