Response: too much BCR-ABL to live on, but too little BCR-ABL to die on?
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[1] F. Guilhot,et al. BCR-ABL expression in leukemic progenitors and primitive stem cells of patients with chronic myeloid leukemia. , 2012, Blood.
[2] A. Neubauer,et al. Low BCR-ABL expression levels in hematopoietic precursor cells enable persistence of chronic myeloid leukemia under imatinib. , 2012, Blood.
[3] R. Bhatia,et al. Persistence of leukemia stem cells in chronic myelogenous leukemia patients in prolonged remission with imatinib treatment. , 2011, Blood.
[4] A. Bennaceur-Griscelli,et al. Leukemic stem cell persistence in chronic myeloid leukemia patients with sustained undetectable molecular residual disease. , 2011, Blood.
[5] B. Druker,et al. Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. , 2011, The Journal of clinical investigation.
[6] Youngho Seo,et al. Selective activation of p53-mediated tumour suppression in high-grade tumours , 2010, Nature.
[7] Philippe Rousselot,et al. Discontinuation of imatinib in patients with chronic myeloid leukaemia who have maintained complete molecular remission for at least 2 years: the prospective, multicentre Stop Imatinib (STIM) trial. , 2010, The Lancet. Oncology.
[8] G. Evan,et al. Distinct thresholds govern Myc's biological output in vivo. , 2008, Cancer cell.
[9] M. Deininger,et al. Can we afford to let sleeping dogs lie? , 2005, Blood.
[10] X. H. Wang,et al. Variable transcription of BCR-ABL by Ph+ cells arising from hematopoietic progenitors in chronic myeloid leukemia. , 1994, Blood.
[11] B. Zehnbauer,et al. BCR-ABL gene rearrangement and expression of primitive hematopoietic progenitors in chronic myeloid leukemia. , 1993, Blood.