ReviewCancer research2010
Cbl and human myeloid neoplasms: the Cbl oncogene comes of age.
Review in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed, 128 citations in OpenAlex.
- Trial
- Juvenile myelomonocytic leukemia due to a germline CBL Y371C mutation: 35-year follow-up of a large family.Human genetics · 2015Trial
- Genetic landscape of stage II melanoma identifies CBL as a new driver gene and prognostic biomarker.British journal of cancer · 2026Article
- Somatic deficiency of the human E3 ubiquitin ligase CBL in leukocytes impairs B cell but not T cell development and function.Nature immunology · 2026Article
- Transcriptomic analysis identifies candidate molecular mechanisms underlying SCF+G-CSF-reduced neuropathology in aged APP/PS1 mice.Frontiers in aging neuroscience · 2026Article
- Locking CBL TKBD in its native conformation presents a novel therapeutic opportunity in mutant CBL-dependent leukemia.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- LNK/SH2B3 Loss Exacerbates the Development of Myeloproliferative Neoplasms in CBL-deficient Mice.Stem cell reviews and reports · 2025Article
- Autoinflammation in patients with leukocytic CBL loss of heterozygosity is caused by constitutive ERK-mediated monocyte activation.The Journal of clinical investigation · 2024Article
- Immunological and hematological findings as major features in a patient with a new germline pathogenic CBL variant.American journal of medical genetics. Part A · 2024Article
- Deciphering the Selectivity of CBL-B Inhibitors Using All-Atom Molecular Dynamics and Machine Learning.ACS medicinal chemistry letters · 2024Article
- Structure and activation of the RING E3 ubiquitin ligase TRIM72 on the membrane.Nature structural & molecular biology · 2023Article
- TAGET: a toolkit for analyzing full-length transcripts from long-read sequencing.Nature communications · 2023Article
- EGFR endocytosis: more than meets the eye.Oncotarget · 2023Article
- Comprehensive Analysis of Acquired Genetic Variants and Their Prognostic Impact in Systemic Mastocytosis.Cancers · 2022Review
- Acetylation, Phosphorylation, Ubiquitination (Oh My!): Following Post-Translational Modifications on the Ubiquitin Road.Biomolecules · 2022Review
- Clinical significance of RAS pathway alterations in pediatric acute myeloid leukemia.Haematologica · 2022Article
- Review
- The CADM1 tumor suppressor gene is a major candidate gene in MDS with deletion of the long arm of chromosome 11.Blood advances · 2022Article
- Molecular and phenotypic diversity of CBL-mutated juvenile myelomonocytic leukemia.Haematologica · 2022Article
- Somatic variation as an incidental finding in the pediatric next-generation sequencing era.Cold Spring Harbor molecular case studies · 2021Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cbl was originally discovered in 1989 as the cellular homolog of the v-Cbl oncogene, the transforming gene of the Cas NS-1 murine retrovirus that causes myeloid leukemia and lymphomas in mice. Cbl is a member of a family of RING finger ubiquitin ligases that negatively regulate signaling by tyrosine kinases and that function as adaptor proteins to regulate signaling positively. Until the past 2 years, there was little evidence that Cbl proteins were involved in human malignancies. Recent publications have shown homozygous mutations in Cbl in human myeloid neoplasms. Although in vitro and animal transformation models suggested that mutant forms of Cbl acted as an oncogene, the cellular role suggested that the protein could serve as a tumor suppressor gene. The recent data begin to reconcile this paradox as the loss of ubiquitin ligase function (the tumor suppressor function) is coupled to the maintenance of the positive signaling function (the oncogene function). These data also provide insight into potential therapeutic approaches to myeloid disorders harboring Cbl mutations.
Indexed as
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.