ArticleCancer research2010
BRAF inactivation drives aneuploidy by deregulating CRAF.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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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
36 citing papers in PubMed, 51 citations in OpenAlex.
- Discovery of Cyclic Peptides Targeting the BRAF Dimer Interface as Dual Inhibitors.ACS pharmacology & translational science · 2026Article
- Article
- Human aneuploid cells depend on the RAF/MEK/ERK pathway for overcoming increased DNA damage.Nature communications · 2024Article
- Enzyme Is the Name-Adapter Is the Game.Cells · 2024Review
- DMM Outstanding Paper Prize 2022 winners: Tamihiro Kamata, Jennifer K. Sargent and Mark A. Warner.Disease models & mechanisms · 2023Article
- Mutation-derived, genomic instability-associated lncRNAs are prognostic markers in gliomas.PeerJ · 2023Article
- Adverse Effects of Vemurafenib on Skin Integrity: Hyperkeratosis and Skin Cancer Initiation Due to Altered MEK/ERK-Signaling and MMP Activity.Frontiers in oncology · 2022Article
- Pathway-Directed Therapy in Multiple Myeloma.Cancers · 2021Review
- Genomic and transcriptomic landscape of conjunctival melanoma.PLoS genetics · 2020Article
- Growth Inhibitory Signaling of the Raf/MEK/ERK Pathway.International journal of molecular sciences · 2020Review
- Defining Signatures of Arm-Wise Copy Number Change and Their Associated Drivers in Kidney Cancers.International journal of molecular sciences · 2019Article
- AtypicalCancers · 2019Review
- Design and Synthesis of Type-IV Inhibitors of BRAF Kinase That Block Dimerization and Overcome Paradoxical MEK/ERK Activation.Journal of medicinal chemistry · 2019Article
- B-Raf deficiency impairs tumor initiation and progression in a murine breast cancer model.Oncogene · 2019Article
- Genomic analysis reveals recurrent deletion of JAK-STAT signaling inhibitors HNRNPK and SOCS1 in mycosis fungoides.Genes, chromosomes & cancer · 2018Article
- Non-V600 BRAF mutations recurrently found in lung cancer predict sensitivity to the combination of Trametinib and Dabrafenib.Oncotarget · 2017Article
- Article
- KRASBlood · 2017Article
- Molecular signaling in multiple myeloma: association of RAS/RAF mutations and MEK/ERK pathway activation.Oncogenesis · 2017Article
- A case study of an integrative genomic and experimental therapeutic approach for rare tumors: identification of vulnerabilities in a pediatric poorly differentiated carcinoma.Genome medicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Aspartate-594 is the third most common BRAF residue mutated in human cancer. Mutants of this residue are kinase inactive, and the mechanism(s) by which they contribute to cancer has remained perplexing. Using a conditional knock-in mouse model, we show that the (D594A)Braf mutant does not drive tumor development per se but is able to induce aneuploidy in murine splenocytes and mouse embryonic fibroblasts and contributes to immortalization through the propagation of aneuploid cells. (D594A)Braf lacks kinase activity but induces the related gene product Craf as well as the mitogen-activated protein/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK pathway. Here, we show that the aneuploid phenotype is dependent on Craf. Treatment with the MEK inhibitor U0126 did not attenuate the emergence of aneuploidy but prevented the growth of aneuploid cells. These results provide a previously unidentified link between Craf and chromosomal stability, with important implications for our understanding of the development of cancers with driver mutations that hyperactivate Craf.
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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.