ArticleLeukemia research and treatment2012
The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia.
Article in Leukemia research and treatment, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 37 citations in OpenAlex.
- Efficacy and safety of dasatinib versus imatinib in Japanese patients with newly diagnosed chronic-phase chronic myeloid leukemia (CML-CP): Subset analysis of the DASISION trial with 2-year follow-up.International journal of hematology · 2014Trial
- Non-coding RNAs: Emerging contributors to chemoresistance in chronic myeloid leukemia.Leukemia research reports · 2025Review
- Secondary fusion proteins as a mechanism of BCR::ABL1 kinase-independent resistance in chronic myeloid leukaemia.British journal of haematology · 2023Article
- Downregulation of Stearoyl-CoA Desaturase 1 (SCD-1) Promotes Resistance to Imatinib in Chronic Myeloid Leukemia.Mediterranean journal of hematology and infectious diseases · 2023Article
- COL-3-Induced Molecular and Ultrastructural Alterations in K562 Cells.Journal of personalized medicine · 2022Article
- Therapeutic potential of thymoquinone in combination therapy against cancer and cancer stem cells.World journal of clinical oncology · 2021Review
- Overexpression of P-glycoprotein and resistance to Imatinib in chronic myeloid leukemia patients.Journal of clinical laboratory analysis · 2020Article
- A genome-scale CRISPR knock-out screen in chronic myeloid leukemia identifies novel drug resistance mechanisms along with intrinsic apoptosis and MAPK signaling.Cancer medicine · 2020Article
- MicroRNA-153-3p enhances the sensitivity of chronic myeloid leukemia cells to imatinib by inhibiting B-cell lymphoma-2-mediated autophagy.Human cell · 2020Article
- Cytotoxic Effects of Some Flavonoids and Imatinib on the K562 Chronic Myeloid Leukemia Cell Line: Data Analysis Using the Combination Index MethodBalkan medical journal · 2019Article
- Towards Comprehension of the ABCB1/P-Glycoprotein Role in Chronic Myeloid Leukemia.Molecules (Basel, Switzerland) · 2018Review
- IGF-IR determines the fates of BCR/ABL leukemia.Journal of hematology & oncology · 2015Article
- Microparticles induce multifactorial resistance through oncogenic pathways independently of cancer cell type.Cancer science · 2015Article
- Multidrug resistance in chronic myeloid leukaemia: how much can we learn from MDR-CML cell lines?Bioscience reports · 2013Review
- Emerging therapeutic strategies for targeting chronic myeloid leukemia stem cells.Stem cells international · 2013Article
- Drug resistance mediated by AEG-1/MTDH/LYRIC.Advances in cancer research · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic myeloid leukemia (CML) is a clonal hematopoietic disorder characterized by the presence of the Philadelphia chromosome which resulted from the reciprocal translocation between chromosomes 9 and 22. The pathogenesis of CML involves the constitutive activation of the BCR-ABL tyrosine kinase, which governs malignant disease by activating multiple signal transduction pathways. The BCR-ABL kinase inhibitor, imatinib, is the front-line treatment for CML, but the emergence of imatinib resistance and other tyrosine kinase inhibitors (TKIs) has called attention for additional resistance mechanisms and has led to the search for alternative drug treatments. In this paper, we discuss our current understanding of mechanisms, related or unrelated to BCR-ABL, which have been shown to account for chemoresistance and treatment failure. We focus on the potential role of the influx and efflux transporters, the inhibitor of apoptosis proteins, and transcription factor-mediated signals as feasible molecular targets to overcome the development of TKIs resistance in CML.
Identifiers
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.