Evidence map›Paper›PMID 24393766›Full record

ReviewOncotarget2014

NF2/merlin in hereditary neurofibromatosis 2 versus cancer: biologic mechanisms and clinical associations.

Rebecca Dunbar Schroeder, Laura S Angelo, Razelle Kurzrock

Open access · hybridAbstract readReview
In one paragraph

Review in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Role ofCancers · 2024
    Review
  5. Review
  6. Article
  7. Translational cancer research · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Cerebrospinal Fluid Hyaluronan and Neurofibromatosis Type 2.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2018
    Article
  17. Review
  18. Article
  19. Article
  20. A Unified Methodological Framework for Vestibular Schwannoma Research.Journal of visualized experiments : JoVE · 2017
    Article
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

3 authors at 1 institution in 1 country.

Rebecca Dunbar SchroederDepartment of Investigational Cancer Therapeutics (Phase I Program), The University of Texas MD Anderson Cancer Center, Houston, TX.
Laura S Angelo
Razelle Kurzrock
The University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inactivating germline mutations in the tumor suppressor gene NF2 cause the hereditary syndrome neurofibromatosis 2, which is characterized by the development of neoplasms of the nervous system, most notably bilateral vestibular schwannoma. Somatic NF2 mutations have also been reported in a variety of cancers, but interestingly these mutations do not cause the same tumors that are common in hereditary neurofibromatosis 2, even though the same gene is involved and there is overlap in the site of mutations. This review highlights cancers in which somatic NF2 mutations have been found, the cell signaling pathways involving NF2/merlin, current clinical trials treating neurofibromatosis 2 patients, and preclinical findings that promise to lead to new targeted therapies for both cancers harboring NF2 mutations and neurofibromatosis 2 patients.

Indexed as

Genes, Neurofibromatosis 2AnimalsGerm-Line MutationHumansNervous System NeoplasmsNeurofibromatosis 2Signal Transduction

Identifiers

PMID24393766
PMCPMC3960189
OpenAlexW2138938916

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.