ArticleBlood2011
Bcr-abl signals to desensitize chronic myeloid leukemia cells to IFNα via accelerating the degradation of its receptor.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Trial
- Targeting natural killer cells: from basic biology to clinical application in hematologic malignancies.Experimental hematology & oncology · 2024Review
- Malignant cell-specific pro-tumorigenic role of type I interferon receptor in breast cancers.Cancer biology & therapy · 2020Article
- Differential roles of STAT1 and STAT2 in the sensitivity of JAK2V617F- vs. BCR-ABL-positive cells to interferon alpha.Journal of hematology & oncology · 2019Article
- JAK2V617F but not CALR mutations confer increased molecular responses to interferon-α via JAK1/STAT1 activation.Leukemia · 2019Article
- Review
- Expression of the IFNAR1 chain of type 1 interferon receptor in benign cells protects against progression of acute leukemia.Leukemia & lymphoma · 2018Article
- Downregulation of the IFNAR1 chain of type 1 interferon receptor contributes to the maintenance of the haematopoietic stem cells.Cancer biology & therapy · 2017Article
- Anti-metastatic functions of type 1 interferons: Foundation for the adjuvant therapy of cancer.Cytokine · 2017Review
- Ubiquitin-dependent Turnover of Adenosine Deaminase Acting on RNA 1 (ADAR1) Is Required for Efficient Antiviral Activity of Type I Interferon.The Journal of biological chemistry · 2016Article
- Review
- Type I interferons in anticancer immunity.Nature reviews. Immunology · 2015Review
- Eliminative signaling by Janus kinases: role in the downregulation of associated receptors.Journal of cellular biochemistry · 2014Review
- Anti-tumorigenic effects of Type 1 interferon are subdued by integrated stress responses.Oncogene · 2013Article
- Hope and fear for interferon: the receptor-centric outlook on the future of interferon therapy.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013Review
- Review
- Ubiquitination-mediated regulation of interferon responses.Growth factors (Chur, Switzerland) · 2012Review
- Curing chronic myeloid leukemia.Current hematologic malignancy reports · 2012Review
- The interferons and their receptors--distribution and regulation.Immunology and cell biology · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Constitutive activity of Bcr-abl fusion protein kinase causes chronic myeloid leukemia (CML). Inhibitors of Bcr-abl such as imatinib mesylate have replaced the cytokine IFNα as the primary treatment for the management of patients with this malignancy. We found that pretreatment of CML cells with imatinib mesylate augments the antigrowth effects of IFNα. Furthermore, introduction of Bcr-abl into non-CML cells inhibits the cellular responses to IFNα. This inhibition is mediated via a mechanism that involves activation of protein kinase D2. The latter promotes an accelerated phosphorylation-dependent degradation of the interferon-α/β receptor 1 chain of the type I interferon receptor, leading to attenuation of IFNα signaling. We discuss the relationship between Bcr-abl activity and IFNα signaling as a molecular basis of the combination of inhibitors of Bcr-abl and IFNα for CML treatment.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.