Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML.

By Catriona H. M. Jamieson, L. Ailles, S. Dylla, M. Muijtjens, Carol D. Jones, J. Zehnder, J. Gotlib, Kevin Li, M. Manz, A. Keating and 2 more. New England Journal of Medicine, 2004

1,581 citations recorded by the source corpus.

Subfields: Hematology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/8de4cee674fb63bfe7796ee3b9d5a8c54ae865b2

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Citations in the corpus

Cancer Stem Cells (CSCs) in Drug Resistance and their Therapeutic Implications in Cancer Treatment (2018, background): “For example, BCR-ABL fusion protein is present in hematopoietic stem cell- (HSC-) like CML cells but granulocyte-macrophage progenitors are found to be a candidate of the advanced-stage LSCs during blast crisis in blast-crisis CML by activating the self-renewal process via β-catenin pathway [47].”
Cancer stem cells: current status and evolving complexities. (2012, background): “In the transition to the blast cell crisis phase, the LSC appears to originate from the granulocyte-macrophage progenitor cell through the acquired activation of the Wnt pathway (Jamieson et al., 2004).”
Hematopoietic stem cell quiescence promotes error prone DNA repair and mutagenesis (2010, background): “As a consequence, mutations resulting in transformation of the MP compartment are unlikely to become established unless the cells gain substantial survival advantage(s) either by inheriting mutations from the HSC compartment (as observed with BCR/ABL1 during CML progression) (Jamieson et al., 2004) ”
Wnt/beta-catenin signaling in development and disease. (2006, positive): “Granulocyte-macrophage progenitors from Chronic Myelogenous Leukemia patients and blast crisis cells from patients resistant to therapy display active Wnt signaling as demonstrated by Tcf reporter activity and the accumulation of nuclear β-catenin (Jamieson et al., 2004).”
Colorectal Cancer Stem Cells Are Enriched in Xenogeneic Tumors Following Chemotherapy (2008, background): “Unlike in normal development, however, neoplastic progenitor cell populations can gain self-renewal capabilities, thereby also fulfilling the definition of a CSC [2, 3 ].”
Tumour stem cells and drug resistance (2005, neutral): “gov/cancertopics/pdq/treatment/CML">chronic myelogenous leukaemia (CML”
Preleukemic mutations in human acute myeloid leukemia affect epigenetic regulators and persist in remission (2014, background): “Additionally, in chronic myeloid leukemia, the breakpoint cluster region–Abelson tyrosine-protein kinase 1 (BCR-ABL) translocation occurs in HSCs, causing chronic disease, but subsequent progression to blast crisis involves mutation evolution at the level of granulocyte–macrophage progenitors (19, 2”
Stems cells and the pathways to aging and cancer. (2008, background): “The molecular mechanisms driving progression of human CML from its chronic phase through myeloid blast crisis have been extensively investigated, but only recently has the role of stem cell and progenitor cell biology been evaluated (Jamieson et al., 2004).”