ReviewThe Journal of clinical investigation2007
Applying the discovery of the Philadelphia chromosome.
Review in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 118 citations in OpenAlex.
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- Divergence in a eukaryotic transcription factor's co-TF dependence involves multiple intrinsically disordered regions.Nature communications · 2025Article
- Divergence in a Eukaryotic Transcription Factor's co-TF Dependence Involves Multiple Intrinsically Disordered Regions.bioRxiv : the preprint server for biology · 2025Article
- A novel imatinib analogue inhibitor of chronic myeloid leukaemia: design, synthesis and characterization-explanation of its folded conformation.Royal Society open science · 2025Article
- Exploring the Potential Role of Phytopharmaceuticals in Alleviating Toxicities of Chemotherapeutic Agents.Current protein & peptide science · 2024Review
- Therapeutic Approaches to Increase the Survival Rate of Cancer Patients in the Younger and Older Population.Current aging science · 2024Review
- BCR-ABL triggers a glucose-dependent survival program during leukemogenesis through the suppression of TXNIP.Cell death & disease · 2023Article
- Saudi Arabian CML patient with a novel four-way translocation at t(9;22;5;2)(q34;q11.2;p13;q44).Molecular genetics & genomic medicine · 2022Article
- HNRNPH1 Is a Novel Regulator Of Cellular Proliferation and Disease Progression in Chronic Myeloid Leukemia.Frontiers in oncology · 2021Article
- Cancer Research in the "Chemical Biology" Section of the JournalMolecules (Basel, Switzerland) · 2020Article
- FLT3-IRAK dual targeting: an exciting new therapeutic option guided by adaptive activation of immune response pathways.Annals of translational medicine · 2020Article
- Article
- The Anti-Cancer Multikinase Inhibitor Sorafenib Impairs Cardiac Contractility by Reducing Phospholamban Phosphorylation and Sarcoplasmic Calcium Transients.Scientific reports · 2018Article
- Using Regularization to Infer Cell Line Specificity in Logical Network Models of Signaling Pathways.Frontiers in physiology · 2018Article
- MYC-xing it up with PIK3CA mutation and resistance to PI3K inhibitors: summit of two giants in breast cancers.American journal of cancer research · 2015Review
- Cardiovascular toxicity of multi-tyrosine kinase inhibitors in advanced solid tumors: a population-based observational study.PloS one · 2015Observational
- Deregulation of cell signaling in cancer.FEBS letters · 2014Review
- Proteome Changes Induced by Imatinib and Novel Imatinib Derivatives in K562 Human Chronic Myeloid Leukemia Cells.Proteomes · 2014Article
- Growth arrest specific 2 is up-regulated in chronic myeloid leukemia cells and required for their growth.PloS one · 2014Article
- The search for ESR1 mutations in breast cancer.Nature genetics · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The identification of the Philadelphia chromosome in cells from individuals with chronic myelogenous leukemia (CML) led to the recognition that the BCR-ABL tyrosine kinase causes CML. This in turn led to the development of imatinib mesylate, a clinically successful inhibitor of the BCR-ABL kinase. Incorporating the use of markers of BCR-ABL kinase inhibition into clinical trials led to the realization that imatinib-resistant kinase domain mutations are the major cause of relapse during imatinib therapy and the subsequent development of new inhibitors to treat CML patients. The development of imatinib validates an emerging paradigm in cancer, in which a tumor is defined by genetic abnormalities and effective therapies are developed that target events critical to the growth and survival of a specific tumor.
Indexed as
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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.