Evidence map›Paper›PMID 25026295›Full record

ReviewOncotarget2014

The NF1 gene revisited - from bench to bedside.

Yoon-Sim Yap, John R McPherson, Choon-Kiat Ong, Steven G Rozen, Bin-Tean Teh, Ann S G Lee, David F Callen

Open access · diamondAbstract 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 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 4% 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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.

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50 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 2 countries.

Yoon-Sim YapDivision of Medical Oncology, National Cancer Centre Singapore, Singapore; Faculty of Health Sciences, School of Medicine, University of Adelaide, Australia.
John R McPhersonCentre for Computational Biology, Cancer and Stem Cell Biology Program, Duke- National University of Singapore Graduate Medical School, Singapore, Singapore.
Choon-Kiat OngLaboratory of Cancer Epigenome, Division of Medical Sciences, National Cancer Centre Singapore, Singapore; Division of Cancer and Stem Cell Biology, Duke-National University of Singapore Graduate Medical School, Singapore.
Steven G RozenCentre for Computational Biology, Cancer and Stem Cell Biology Program, Duke- National University of Singapore Graduate Medical School, Singapore, Singapore.
Bin-Tean TehLaboratory of Cancer Epigenome, Division of Medical Sciences, National Cancer Centre Singapore, Singapore; Division of Cancer and Stem Cell Biology, Duke-National University of Singapore Graduate Medical School, Singapore; Cancer Science Institute of Singapore, NUS, Singapore.
Ann S G LeeLaboratory of Molecular Oncology, Division of Medical Sciences, National Cancer Centre, Singapore, Singapore; Office of Clinical & Academic Faculty Affairs, Duke-NUS Graduate Medical School, Singapore; Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
David F CallenCancer Therapeutics Laboratory, Centre for Personalised Cancer Medicine, University of Adelaide, Australia.
National University of Singapore · SGNational Cancer Centre Singapore · SGUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurofibromatosis type 1 (NF1) is a relatively common tumour predisposition syndrome related to germline aberrations of NF1, a tumour suppressor gene. The gene product neurofibromin is a negative regulator of the Ras cellular proliferation pathway, and also exerts tumour suppression via other mechanisms. Recent next-generation sequencing projects have revealed somatic NF1 aberrations in various sporadic tumours. NF1 plays a critical role in a wide range of tumours. NF1 alterations appear to be associated with resistance to therapy and adverse outcomes in several tumour types. Identification of a patient's germline or somatic NF1 aberrations can be challenging, as NF1 is one of the largest human genes, with a myriad of possible mutations. Epigenetic factors may also also contribute to inadequate levels of neurofibromin in cancer cells. Clinical trials of NF1-based therapeutic approaches are currently limited. Preclinical studies on neurofibromin-deficient malignancies have mainly been on malignant peripheral nerve sheath tumour cell lines or xenografts derived from NF1 patients. However, the emerging recognition of the role of NF1 in sporadic cancers may lead to the development of NF1-based treatments for other tumour types. Improved understanding of the implications of NF1 aberrations is critical for the development of novel therapeutic strategies.

Indexed as

Genes, Neurofibromatosis 1AnimalsHumansNeoplasmsNeurofibromin 1Neurofibromin 1

Identifiers

PMID25026295
PMCPMC4171599
OpenAlexW1522859997

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.