ArticlePloS one2009
ERK2, but not ERK1, mediates acquired and "de novo" resistance to imatinib mesylate: implication for CML therapy.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 47 citations in OpenAlex.
- A customized mass array panel forJournal of mass spectrometry and advances in the clinical lab · 2023Article
- BRD4 degradation blocks expression of MYC and multiple forms of stem cell resistance in PhAmerican journal of hematology · 2022Article
- Verbascoside potentiates the effect of tyrosine kinase inhibitors on the induction of apoptosis and oxidative stress via the Abl-mediated MAPK signalling pathway in chronic myeloid leukaemia.Experimental and therapeutic medicine · 2022Article
- Chronic Myeloid Leukemia: Modern therapies, current challenges and future directions.Blood reviews · 2021Review
- Inhibition of Skp2 Sensitizes Chronic Myeloid Leukemia Cells to Imatinib.Cancer management and research · 2020Article
- A Novel Naphthoquinone-Coumarin Hybrid That Inhibits BCR-ABL1-STAT5 Oncogenic Pathway and Reduces Survival in Imatinib-Resistant Chronic Myelogenous Leukemia Cells.Frontiers in pharmacology · 2018Article
- Article
- KPT-330 inhibition of chromosome region maintenance 1 is cytotoxic and sensitizes chronic myeloid leukemia to Imatinib.Cell death discovery · 2018Article
- Novel Molecular Challenges in Targeting Anaplastic Lymphoma Kinase in ALK-Expressing Human Cancers.Cancers · 2017Review
- Contributions of MET activation to BCR-ABL1 tyrosine kinase inhibitor resistance in chronic myeloid leukemia cells.Oncotarget · 2017Article
- CM363, a novel naphthoquinone derivative which acts as multikinase modulator and overcomes imatinib resistance in chronic myelogenous leukemia.Oncotarget · 2017Article
- MicroRNAs mediated regulation of MAPK signaling pathways in chronic myeloid leukemia.Oncotarget · 2016Review
- p38MAPK and Chemotherapy: We Always Need to Hear Both Sides of the Story.Frontiers in cell and developmental biology · 2016Review
- Redundancy in the World of MAP Kinases: All for One.Frontiers in cell and developmental biology · 2016Review
- Article
- Grb10 is involved in BCR-ABL-positive leukemia in mice.Leukemia · 2015Article
- MAPK15 mediates BCR-ABL1-induced autophagy and regulates oncogene-dependent cell proliferation and tumor formation.Autophagy · 2015Article
- A therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid leukemia.Science translational medicine · 2014Article
- Small G proteins Rac1 and Ras regulate serine/threonine protein phosphatase 5 (PP5)·extracellular signal-regulated kinase (ERK) complexes involved in the feedback regulation of Raf1.The Journal of biological chemistry · 2014Article
- Snail promotes epithelial mesenchymal transition in breast cancer cells in part via activation of nuclear ERK2.PloS one · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to Imatinib Mesylate (IM) is a major problem in Chronic Myelogenous Leukaemia management. Most of the studies about resistance have focused on point mutations on BCR/ABL. However, other types of resistance that do not imply mutations in BCR/ABL have been also described. In the present report we aim to study the role of several MAPK in IM resistance not associate to BCR/ABL mutations. Therefore we used an experimental system of resistant cell lines generated by co-culturing with IM (K562, Lama 84) as well as primary material from resistant and responder patient without BCR/ABL mutations. Here we demonstrate that Erk5 and p38MAPK signaling pathways are not implicated in the acquired resistance phenotype. However, Erk2, but not Erk1, is critical for the acquired resistance to IM. In fact, Bcr/Abl activates preferentially Erk2 in transient transfection in a dose dependent fashion through the c-Abl part of the chimeric protein. Finally, we present evidences demonstrating how constitutive activation of Erk2 is a de novo mechanism of resistance to IM. In summary our data support the use of therapeutic approaches based on Erk2 inhibition, which could be added to the therapeutic armamentarium to fight CML, especially when IM resistance develops secondary to Erk2 activation.
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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.