ArticleAmerican journal of cancer research2011
Mechanisms of aneuploidy induction by RAS and RAF oncogenes.
Article in American journal of cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- RIPOR2 promotes multinucleation of melanoma cells downstream of the RAS/ERK oncogenic pathway.iScience · 2026Article
- Single amino-acid differences define H2B variants and modify chromatin accessibility to induce EMT in breast cancer.Oncogene · 2026Article
- Hyper-active RAS/MAPK introduces cancer-specific mitotic vulnerabilities.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The RAS GTPase RIT1 compromises mitotic fidelity through spindle assembly checkpoint suppression.Current biology : CB · 2021Article
- Perspective: Potential Impact and Therapeutic Implications of Oncogenic PI3K Activation on Chromosomal Instability.Biomolecules · 2019Review
- Over-expressed, N-terminally truncated BRAF is detected in the nucleus of cells with nuclear phosphorylated MEK and ERK.Heliyon · 2018Article
- The Role of Aneuploidy in Cancer Evolution.Cold Spring Harbor perspectives in medicine · 2017Review
- Deregulated ERK1/2 MAP kinase signaling promotes aneuploidy by a Fbxw7β-Aurora A pathway.Cell cycle (Georgetown, Tex.) · 2016Article
- Oncogenic mutations produce similar phenotypes in Drosophila tissues of diverse origins.Biology open · 2014Article
- Upregulation of the Na⁺-coupled phosphate cotransporters NaPi-IIa and NaPi-IIb by B-RAF.The Journal of membrane biology · 2014Article
- Ras/Raf/MEK/ERK Pathway Activation in Childhood Acute Lymphoblastic Leukemia and Its Therapeutic Targeting.Frontiers in oncology · 2014Review
- Up-regulation of hERG K⁺ channels by B-RAF.PloS one · 2014Article
- Hematopoietic expression of oncogenic BRAF promotes aberrant growth of monocyte-lineage cells resistant to PLX4720.Molecular cancer research : MCR · 2013Article
- Aneuploidy in health, disease, and aging.The Journal of cell biology · 2013Review
- A double-edged sword: how oncogenes and tumor suppressor genes can contribute to chromosomal instability.Frontiers in oncology · 2013Article
- Distinct requirement for an intact dimer interface in wild-type, V600E and kinase-dead B-Raf signalling.The EMBO journal · 2012Article
- K-In vivo (Athens, Greece)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Most cancers progress with the accumulation of genetic mutations with time and this is frequently associated with the acquisition of genomic instability in the form of whole chromosome changes, chromosomal rearrangements, gene amplifications or smaller changes at the nucleotide level. Whole chromosome instability (W-CIN), characterised by aneuploidy, is a major form of genomic instability observed in human cancers and several lines of evidence now support the argument that W-CIN is a promoter of tumourigenesis rather than being a passenger event. The primary mechanism proposed for evolution of CIN is abnormalities in mitosis/cytokinesis. However, mutations in genes directly involved in controlling mitosis/cytokinesis are rare in human cancers and so the mechanisms underpinning the evolution of CIN in cancers are not currently clear. On the other hand, mutations in RAS or BRAF are frequently found in human cancers, many of which demonstrate CIN, suggesting a possible link between deregulated signaling through the RAS/RAF/MEK/ERK pathway and CIN. In this review, we focus on a potential relationship between deregulated RAS/RAF signaling and CIN, and discuss possible mechanisms connecting the two.
Indexed as
Identifiers
22016838PMC3196290W1597530217What 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.