Evidence map›Paper›PMID 26273102›Full record

ReviewEndocrine-related cancer2015

15 YEARS OF PARAGANGLIOMA: Clinical manifestations of paraganglioma syndromes types 1-5.

Diana E Benn, Bruce G Robinson, Roderick J Clifton-Bligh

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Endocrine-related cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 2 pooled it
21.8field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 2 syntheses or guidelines pooled it, 194 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. A Recurrent Tympanicum Paraganglioma With a SDHD Pathogenic Variant: First Reported Case.World journal of otorhinolaryngology - head and neck surgery · 2026
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  19. Jugular Foramen Paragangliomas.Advances and technical standards in neurosurgery · 2024
    Article
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33 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

3 authors at 2 institutions in 1 country.

Diana E BennCancer GeneticsKolling Institute, Royal North Shore Hospital, University of Sydney, St Leonards, New South Wales 2065, Australia.
Bruce G RobinsonCancer GeneticsKolling Institute, Royal North Shore Hospital, University of Sydney, St Leonards, New South Wales 2065, Australia.
Roderick J Clifton-BlighCancer GeneticsKolling Institute, Royal North Shore Hospital, University of Sydney, St Leonards, New South Wales 2065, Australia jclifton@med.usyd.edu.au.
University of Sydney · AURoyal North Shore Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The paraganglioma (PGL) syndromes types 1-5 are autosomal dominant disorders characterized by familial predisposition to PGLs, phaeochromocytomas (PCs), renal cell cancers, gastrointestinal stromal tumours and, rarely, pituitary adenomas. Each syndrome is associated with mutation in a gene encoding a particular subunit (or assembly factor) of succinate dehydrogenase (SDHx). The clinical manifestations of these syndromes are protean: patients may present with features of catecholamine excess (including the classic triad of headache, sweating and palpitations), or with symptoms from local tumour mass, or increasingly as an incidental finding on imaging performed for some other purpose. As genetic testing for these syndromes becomes more widespread, presymptomatic diagnosis is also possible, although penetrance of disease in these syndromes is highly variable and tumour development does not clearly follow a predetermined pattern. PGL1 syndrome (SDHD) and PGL2 syndrome (SDHAF2) are notable for high frequency of multifocal tumour development and for parent-of-origin inheritance: disease is almost only ever manifest in subjects inheriting the defective allele from their father. PGL4 syndrome (SDHB) is notable for an increased risk of malignant PGL or PC. PGL3 syndrome (SDHC) and PGL5 syndrome (SDHA) are less common and appear to be associated with lower penetrance of tumour development. Although these syndromes are all associated with SDH deficiency, few genotype-phenotype relationships have yet been established, and indeed it is remarkable that such divergent phenotypes can arise from disruption of a common molecular pathway. This article reviews the clinical presentations of these syndromes, including their component tumours and underlying genetic basis.

Indexed as

Neoplastic Syndromes, HereditaryParagangliomaGenetic CounselingGenetic TestingHumansgastrointestinal stromal tumourparagangliomaphaeochromocytomarenal cancersuccinate dehydrogenase

Identifiers

PMID26273102
PMCPMC4532956
OpenAlexW1891996119

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.