ArticleAmerican journal of cancer research2017
Targeting NRAS
Article in American journal of cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 5 citations in OpenAlex.
- Feline Alimentary Lymphomas: Established Concepts and an Underexplored Molecular Landscape.Current issues in molecular biology · 2026Review
- Review
- Conformational plasticity of RAS Q61 family of neoepitopes results in distinct features for targeted recognition.Nature communications · 2023Article
- NRAS expression is associated with prognosis and tumor immune microenvironment in lung adenocarcinoma.Journal of cancer research and clinical oncology · 2022Article
- KRAS gene polymorphisms are associated with the risk of glioma: a two-center case-control study.Translational pediatrics · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells require vascular supply for their growth, and they express proangiogenic growth factors that promote the formation of vascular networks. Many oncogenic mutations that may potentially lead to tumor angiogenesis have been identified. Somatic mutations in the small GTPase NRAS are the most common activating lesions found in human cancer and are generally associated with poor response to standard therapies. However, the mechanisms by which NRAS mutations affect tumor angiogenesis are largely unknown. Therefore, we investigated the role of NRAS
Indexed as
Identifiers
28469956PMC5411791W2975275600What 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.