ArticleOncogenesis2018
Vav1 mutations identified in human cancers give rise to different oncogenic phenotypes.
Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 16 citations in OpenAlex.
- Sam68 is a druggable vulnerability point in cancer stem cells.Cancer metastasis reviews · 2024Review
- A Systematic Compilation of Human SH3 Domains: A Versatile Superfamily in Cellular Signaling.Cells · 2023Review
- Review
- Vav1 Promotes B-Cell Lymphoma Development.Cells · 2022Article
- Naturally Occurring Genetic Alterations in Proximal TCR Signaling and Implications for Cancer Immunotherapy.Frontiers in immunology · 2021Review
- QuaDMutNetEx: a method for detecting cancer driver genes with low mutation frequency.BMC bioinformatics · 2020Article
- Targeting Rac and Cdc42 GEFs in Metastatic Cancer.Frontiers in cell and developmental biology · 2020Review
- Rac-GEF/Rac Signaling and Metastatic Dissemination in Lung Cancer.Frontiers in cell and developmental biology · 2020Article
- RAC1 Takes the Lead in Solid Tumors.Cells · 2019Review
- Specific copy number changes as potential predictive markers for adjuvant chemotherapy in non-small cell lung cancer.Translational lung cancer research · 2018Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vav1 is physiologically active as a GDP/GTP nucleotide exchange factor (GEF) in the hematopoietic system. Overexpression of Vav1 in multiple tumor types is known to enhance oncogenicity, yet whether or not Vav1 is a bona fide oncogene is still a matter of debate. Although mutations in Vav1 were recently identified in human cancers of various origins, the functional activities of these mutants are not known. We tested the transforming potential of three mutations identified in human lung adenocarcinoma: E59K, D517E, and L801P. Results from several assays indicative of transforming activities such as rate of proliferation, growth in agar, and generation of tumors in NOD/SCID mice clearly indicated that E59K and D517E are highly transforming but L801P at the SH3 domain is not. The acquired oncogenic activity of these mutants can be attributed to their enhanced activity as GEFs for Rho/Rac GTPases. Deciphering of the mechanisms leading to overactivity of the tested mutants revealed that the E59K mutation facilitates cleavage of a truncated protein that is uncontrollably active as a GEF, while D517E generates a highly stable overexpressed protein that is also more active as a GEF than wild-type Vav1. These findings support the classification of Vav1 as a bona fide oncogene in human cancer.
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.