Early in vivo changes of the transcriptome in Philadelphia chromosome-positive CD34+ cells from patients with chronic myelogenous leukaemia following imatinib therapy.

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

Who cites it

18 citing papers in PubMed.

1. Loss of G0/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolism.Clinical and translational medicine · 2022
   Article
2. Leonurine-Repressed miR-18a-5p/SOCS5/JAK2/STAT3 Axis Activity Disrupts CML malignancy.Frontiers in pharmacology · 2021
   Article
3. The lysophospholipase D enzyme Gdpd3 is required to maintain chronic myelogenous leukaemia stem cells.Nature communications · 2020
   Article
4. Stem cell persistence in CML is mediated by extrinsically activated JAK1-STAT3 signaling.Leukemia · 2019
   Article
5. Blood · 2018
   Article
6. Altered intracellular signaling by imatinib increases the anti-cancer effects of tyrosine kinase inhibitors in chronic myelogenous leukemia cells.Cancer science · 2018
   Article
7. Shift in energy metabolism caused by glucocorticoids enhances the effect of cytotoxic anti-cancer drugs against acute lymphoblastic leukemia cells.Oncotarget · 2017
   Article
8. Long-Term Exposure to Imatinib Mesylate Downregulates Hippo Pathway and Activates YAP in a Model of Chronic Myelogenous Leukemia.Stem cells and development · 2017
   Article
9. Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.Nature medicine · 2017
   Article
10. Inhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor-treated CML stem cells.Blood · 2016
    Article
11. Inverse regulation of bridging integrator 1 and BCR-ABL1 in chronic myeloid leukemia.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
12. Cks1 is a critical regulator of hematopoietic stem cell quiescence and cycling, operating upstream of Cdk inhibitors.Oncogene · 2015
    Article
13. Potential role of Notch signalling in CD34+ chronic myeloid leukaemia cells: cross-talk between Notch and BCR-ABL.PloS one · 2015
    Article
14. A therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid leukemia.Science translational medicine · 2014
    Article
15. The antiproliferative activity of kinase inhibitors in chronic myeloid leukemia cells is mediated by FOXO transcription factors.Stem cells (Dayton, Ohio) · 2014
    Article
16. STAP-2 interacts with and modulates BCR-ABL-mediated tumorigenesis.Oncogene · 2012
    Article
17. Antigens in chronic myeloid leukemia: implications for vaccine development.Cancer immunology, immunotherapy : CII · 2011
    Review
18. BCL6-mediated repression of p53 is critical for leukemia stem cell survival in chronic myeloid leukemia.The Journal of experimental medicine · 2011
    Article

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

Authors and funding

7 authors.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

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