ArticleOncotarget2011
Mutant Cbl proteins as oncogenic drivers in myeloproliferative disorders.
Article in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 48 citations in OpenAlex.
- FBXO22 targets ubiquitination and degradation of c-Cbl in leukemia.Scientific reports · 2026Article
- TGF-β in hematologic malignancies: molecular functions and clinical applications.Frontiers in immunology · 2026Review
- Mastocytosis in a Case of Noonan Syndrome Caused by a De Novo PathogenicYonago acta medica · 2023Article
- Antitumor activity of miR-188-3p in gastric cancer is achieved by targeting CBL expression and inactivating the AKT/mTOR signaling.World journal of gastrointestinal oncology · 2023Article
- Genetic Disorders with Predisposition to Paediatric Haematopoietic Malignancies-A Review.Cancers · 2022Review
- Integrative Analysis for Identification of Therapeutic Targets and Prognostic Signatures in Non-Small Cell Lung Cancer.Bioinformatics and biology insights · 2022Article
- Ubiquitin Ligases CBL and CBL-B Maintain the Homeostasis and Immune Quiescence of Dendritic Cells.Frontiers in immunology · 2021Article
- The combination of FLT3 and SYK kinase inhibitors is toxic to leukaemia cells with CBL mutations.Journal of cellular and molecular medicine · 2020Article
- Ubiquitin E3 Ligase c-Cbl Is a Host Negative Regulator of Nef Protein of HIV-1.Frontiers in microbiology · 2020Article
- Computational Approaches to Prioritize Cancer Driver Missense Mutations.International journal of molecular sciences · 2018Review
- Loss of the Nuclear Pool of Ubiquitin Ligase CHIP/STUB1 in Breast Cancer Unleashes the MZF1-Cathepsin Pro-oncogenic Program.Cancer research · 2018Article
- Acquired expression ofBlood · 2017Article
- Casitas B-cell lymphoma (Cbl) proteins protect mammary epithelial cells from proteotoxicity of active c-Src accumulation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- VAV1-Cre mediated hematopoietic deletion of CBL and CBL-B leads to JMML-like aggressive early-neonatal myeloproliferative disease.Oncotarget · 2016Article
- Balancing Protein Stability and Activity in Cancer: A New Approach for Identifying Driver Mutations Affecting CBL Ubiquitin Ligase Activation.Cancer research · 2016Article
- Patterns of Transposable Element Expression and Insertion in Cancer.Frontiers in molecular biosciences · 2016Article
- Network-Based Integration of Disparate Omic Data To Identify "Silent Players" in Cancer.PLoS computational biology · 2015Article
- Mutations of c-Cbl in myeloid malignancies.Oncotarget · 2015Review
- Complementary genetic screens identify the E3 ubiquitin ligase CBLC, as a modifier of PARP inhibitor sensitivity.Oncotarget · 2015Article
- Regulation of TGF-β Signal Transduction.Scientifica · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Casitas B-lineage lymphoma (Cbl) family proteins are evolutionarily-conserved attenuators of protein tyrosine kinase (PTK) signaling. Biochemical analyses over the past two decades have firmly established that the negative regulatory functions of Cbl proteins are mediated through their ability to facilitate ubiquitination and thus promote degradation of PTKs. As aberrant activation of PTKs is frequently associated with oncogenesis, it has long been postulated that loss of normal Cbl functions may lead to unregulated activation of PTKs and cellular transformation. In the last few years, mutations in the CBL gene have been identified in a subset of human patients with myeloid malignancies. Here we discuss insights gained from the analyses of Cbl mutants both in human patients and in animal models and propose potential mechanisms of oncogenesis through this pathway.
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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.