Frequency of major molecular responses to imatinib or interferon alfa plus cytarabine in newly diagnosed chronic myeloid leukemia.
By T. Hughes, J. Kaeda, S. Branford, Z. Rudzki, Andreas Hochhaus, M. Hensley, I. Gathmann, A. Bolton, Iris van Hoomissen, J. Goldman and 1 more. New England Journal of Medicine, 2003
1,294 citations recorded by the source corpus.
Subfields: Hematology, Plant Science, Rheumatology
View Paper: https://www.semanticscholar.org/paper/996f490f19c49771bbe44cd78aee416b17cffbf2
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Citations in the corpus
- Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. (2011, background): “Those whose disease is undetectable by RT-PCR usually experience recurrence of active leukemia when imatinib therapy is discontinued (4, 5), which indicates that leukemic cells persist in most patients even when the disease burden is reduced below detectable limits.”
- Mechanisms of Disease: oncogene addiction—a rationale for molecular targeting in cancer therapy (2006, neutral): “BCR/ABL Chronic myeloid leukemiaa Imatinib Monotherapy Hughes et al. (2003)31”
- Tumour-initiating cells: challenges and opportunities for anticancer drug discovery (2009, background): “As a result, imatinib eliminates proliferating, committed leukaemia progenitors, but not primitive, quiescent tumour-initiating cells, and most patients are still positive for the fusion gene transcripts after treatmen”
- Chemotherapy and the war on cancer (2005, background): “However, BCR–ABL translocation can still be detected by PCR analysis in cells of most patient”
- Chronic Myeloid Leukemia (2007, positive): “Increasing levels of BCR-ABL1 transcripts are predictive of loss of response if levels rise more than 0.5 log over two serial samples 13,14 .”