ArticleLeukemia research2012
Potentiation of Nilotinib-mediated cell death in the context of the bone marrow microenvironment requires a promiscuous JAK inhibitor in CML.
Article in Leukemia research, 2012. 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.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Future Directions in Chronic Phase CML Treatment.Current hematologic malignancy reports · 2021Review
- Review
- Mesenchymal soluble factors confer imatinib drug resistance in chronic myelogenous leukemia cells.Archives of medical science : AMS · 2021Article
- Contribution of the bone marrow stromal cells in mediating drug resistance in hematopoietic tumors.Current opinion in pharmacology · 2020Review
- Stem cell persistence in CML is mediated by extrinsically activated JAK1-STAT3 signaling.Leukemia · 2019Article
- A phase I clinical trial of ruxolitinib in combination with nilotinib in chronic myeloid leukemia patients with molecular evidence of disease.Leukemia research · 2018Article
- BCR-ABL1-positive microvesicles malignantly transform human bone marrow mesenchymal stem cells in vitro.Acta pharmacologica Sinica · 2017Article
- Growth of tyrosine kinase inhibitor-resistant Philadelphia-positive acute lymphoblastic leukemia: Role of bone marrow stromal cells.Oncology letters · 2017Article
- Article
- Cancer prevention and therapy through the modulation of the tumor microenvironment.Seminars in cancer biology · 2015Review
- Emerging therapeutic paradigms to target the dysregulated Janus kinase/signal transducer and activator of transcription pathway in hematological malignancies.Leukemia & lymphoma · 2014Review
- Article
- Article
- What challenges remain in chronic myeloid leukemia research?Haematologica · 2013Article
- Article
- Review
- Pushing the limits of targeted therapy in chronic myeloid leukaemia.Nature reviews. Cancer · 2012Review
- Role of STAT3 in Transformation and Drug Resistance in CML.Frontiers in oncology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In this study, we show that conditioned media (CM) generated from bone marrow (BM)-derived mesenchymal stromal cells lead to BCR-ABL independent STAT3 activation. Activation of STAT3 is important not only for survival of CML cells but also for its protection against Nilotinib (NI), within the BM microenvironment. Reducing the expression of both JAK2 and TYK2 or utilizing a pan-JAK inhibitor blocked CM-mediated STAT3 activation and sensitized CML cells to NI-mediated cell death. Finally, we demonstrate that in patient-derived primitive leukemic cells, co-cultured with BM stromal cells, inhibition of BCR-ABL and JAK activity was a successful strategy to potentiate their elimination.
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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.