Evidence map›Paper›PMID 28500274›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Combined HMG-COA reductase and prenylation inhibition in treatment of CCM.

Sayoko Nishimura, Ketu Mishra-Gorur, JinSeok Park, Yulia V Surovtseva, Said M Sebti, Andre Levchenko, Angeliki Louvi, Murat Gunel

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  8. Brain and/or Spinal Cord Tumors Accompanied with Other Diseases or Syndromes.Advances in experimental medicine and biology · 2023
    Article
  9. Article
  10. Bringing CCM into a dish: cell culture models for cerebral cavernous malformations.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2021
    Article
  11. Article
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  14. Cerebrovascular disorders associated with genetic lesions.Cellular and molecular life sciences : CMLS · 2019
    Review
  15. Article
  16. Article
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Sayoko NishimuraDepartment of Neurosurgery, Yale School of Medicine, New Haven, CT 06520.
Ketu Mishra-GorurDepartment of Neurosurgery, Yale School of Medicine, New Haven, CT 06520.
JinSeok ParkDepartment of Biomedical Engineering, Yale University, New Haven, CT 06520.
Yulia V SurovtsevaYale Center for Molecular Discovery, Yale University, West Haven, CT 06516.
Said M SebtiDepartment of Drug Discovery, Chemical Biology and Molecular Medicine Program, Moffitt Cancer Center, Tampa, FL 33612.
Andre LevchenkoDepartment of Biomedical Engineering, Yale University, New Haven, CT 06520.
Angeliki LouviDepartment of Neurosurgery, Yale School of Medicine, New Haven, CT 06520; angeliki.louvi@yale.edu murat.gunel@yale.edu.
Murat GunelDepartment of Neurosurgery, Yale School of Medicine, New Haven, CT 06520; angeliki.louvi@yale.edu murat.gunel@yale.edu.
Yale University · USMoffitt Cancer Center · US

Funding

Systems analysis of phenotypic switch in control of cancer invasionU54CA209992 · NCI · YALE UNIVERSITY · PI LEVCHENKO, ANDRE · 2016 to 2021
$10.1M
Functional Genomics of the Cavernous Malformation GeneR01NS046521 · NINDS · YALE UNIVERSITY · PI GUNEL, MURAT · 2004 to 2013
$4.2M
NCI NIH HHS U54 CA209992NINDS NIH HHS R01 NS046521
6 · The paper itself

Abstract

Cerebral cavernous malformations (CCMs) are common vascular anomalies that develop in the central nervous system and, more rarely, the retina. The lesions can cause headache, seizures, focal neurological deficits, and hemorrhagic stroke. Symptomatic lesions are treated according to their presentation; however, targeted pharmacological therapies that improve the outcome of CCM disease are currently lacking. We performed a high-throughput screen to identify Food and Drug Administration-approved drugs or other bioactive compounds that could effectively suppress hyperproliferation of mouse brain primary astrocytes deficient for CCM3. We demonstrate that fluvastatin, an inhibitor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase and the

Indexed as

AnimalsAstrocytesDiphosphonatesDrosophilaDrug Evaluation, PreclinicalDrug Therapy, CombinationEndothelial CellsFatty Acids, MonounsaturatedFemaleFluvastatinHemangioma, Cavernous, Central Nervous SystemHigh-Throughput Screening AssaysHydroxymethylglutaryl-CoA Reductase InhibitorsImidazolesIndolesMaleDiphosphonatesFatty Acids, MonounsaturatedFluvastatinHydroxymethylglutaryl-CoA Reductase InhibitorsImidazolesIndolesZoledronic Acidcerebral cavernous malformationsfluvastatinhigh-throughput screenmevalonate pathwayzoledronic acid

Identifiers

PMID28500274
PMCPMC5448170
OpenAlexW2612135927

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.