ReviewSmall GTPases2015
G17V RHOA: Genetic evidence of GTP-unbound RHOA playing a role in tumorigenesis in T cells.
Review in Small GTPases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Liquid biopsy in T-cell lymphoma: biomarker detection techniques and clinical application.Molecular cancer · 2024Review
- Advances in the pathogenesis and therapeutic strategies of angioimmunoblastic T-cell lymphoma.Clinical and experimental medicine · 2023Review
- Major roles of the circadian clock in cancer.Cancer biology & medicine · 2023Review
- Point Mutation Specific Antibodies in B-Cell and T-Cell Lymphomas and Leukemias: Targeting IDH2, KRAS, BRAF and Other Biomarkers RHOA, IRF8, MYD88, ID3, NRAS, SF3B1 and EZH2.Diagnostics (Basel, Switzerland) · 2021Review
- Current Progress in Investigating Mature T- and NK-Cell Lymphoma Gene Aberrations by Next-Generation Sequencing (NGS).Cancer management and research · 2021Review
- A comprehensive analysis of RHOA mutation positive and negative angioimmunoblastic T-cell lymphomas by targeted deep sequencing, expression profiling and single cell digital image analysis.International journal of molecular medicine · 2020Article
- Application of NanoString technologies in angioimmunoblastic T cell lymphoma.Genes & genomics · 2020Article
- Review
- Genetic alterations affecting GTPases and T-cell receptor signaling in peripheral T-cell lymphomas.Small GTPases · 2019Review
- CLOCK and BMAL1 stabilize and activate RHOA to promote F-actin formation in cancer cells.Experimental & molecular medicine · 2018Article
- Rho GTPases: Anti- or pro-neoplastic targets?Oncogene · 2017Review
- Rho GTPases: Regulation and roles in cancer cell biology.Small GTPases · 2016Review
- The RhoA-ROCK pathway in the regulation of T and B cell responses.F1000Research · 2016Review
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 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RHOA is a member of RHO family small GTPases. Over the past 2 decades, numerous biochemical and cell biological studies on RHOA have demonstrated signalings such as activation of RHO-associated coiled-coil forming kinases through guanine nucleotide exchange and GTP hydrolysis, cellular responses such as actin fiber formation and myocin activation, biological consequences such as cell motility and cytokineses, etc. There have also been a plenty of active discussion on the roles of RHOA in tumorigenesis, primarily based on gain- and loss-of-function experiments. However, cell-type-specific functions of RHOA have only recently been delineated by conditional gene targeting strategies. Furthermore, very little information had been available on human cancer genetics until we and others recently reported frequent somatic RHOA mutations in a distinct subtype of T-cell-type malignant lymphoma called angioimmunoblastic T-cell lymphoma (AITL), and other T-cell lymphoma with AITL-like features. The RHOA mutations were very specific to these types of lymphoma among hematologic malignancies, and a single hotspot, glycine at the 17th position, was affected by the replacement with valine (G17V). Remarkably, G17V RHOA did not bind GTP, and moreover, it inhibited the GTP binding to wild-type RHOA. How G17V RHOA contributes to T-cell lymphomagenesis needs to be clarified.
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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.