Evidence map›Paper›PMID 39946193›Full record

ArticleJCI insight2025

Genotype-phenotype correlation in multiple endocrine neoplasia type 1.

Charlita C Worthy, Rana Tora, Chandra N Uttarkar, James M Welch, Lynn Bliss, Craig Cochran, Anisha Ninan, Sheila Kumar, Stephen Wank, Sungyoung Auh and 5 more

Abstract read
In one paragraph

Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. 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

15 authors.

Charlita C WorthyMetabolic Diseases Branch.
Rana ToraMetabolic Diseases Branch.
Chandra N UttarkarMetabolic Diseases Branch.
James M WelchMetabolic Diseases Branch.
Lynn BlissMetabolic Diseases Branch.
Craig CochranMetabolic Diseases Branch.
Anisha NinanMetabolic Diseases Branch.
Sheila KumarDigestive Diseases Branch, and.
Stephen WankDigestive Diseases Branch, and.
Sungyoung AuhBiostatistics Program, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA.
Lee S WeinsteinMetabolic Diseases Branch.
William F SimondsMetabolic Diseases Branch.
Sunita K AgarwalMetabolic Diseases Branch.
Jenny E BlauMetabolic Diseases Branch.
Smita JhaMetabolic Diseases Branch.

Funding

Hyperparathyroidism-- Etiology, Diagnosis And TreatmentZIADK043006 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JHA, SMITA · 2011 to 2025
$8.9M
Institute for Clinical and Translational ResearchKL2TR000425 · NCATS · JOHNS HOPKINS UNIVERSITY · PI FORD, DANIEL ERNEST · 2012 to 2012
$0k
Intramural NIH HHS ZIA DK043006NCATS NIH HHS KL2 TR000425
6 · The paper itself

Abstract

BACKGROUNDAmong patients with multiple endocrine neoplasia type 1 (MEN1), 80% develop duodenopancreatic neuroendocrine tumors (dpNETs), of whom 15%-25% die of metastasis. There is a need to identify biomarkers to predict aggressive disease. MEN1 genotype affords an attractive possibility as a biomarker, as it remains constant during life. Currently, patients are clinically diagnosed with MEN1 by the presence of ≥2 primary endocrine tumors (pituitary, parathyroid, and pancreas) or ≥1 primary endocrine tumor with a positive family history. From 10% to 30% of patients diagnosed clinically with MEN1 have no pathogenic germline MEN1 variants.METHODSThis was a retrospective study of 162 index patients or probands with genotype-positive and 47 with genotype-negative MEN1 enrolled from 1977 to 2022.RESULTSCompared with patients with genotype-negative disease, patients with genotype-positive disease were younger at diagnosis and had an increased frequency of recurrent parathyroid tumors, dpNETs, and angiofibromas or collagenomas. We propose a weighted scoring system to diagnose genotype-positive MEN1 based on clinical characteristics. No evidence of MEN1 mosaicism was seen in 30 tumors from 17 patients with genotype-negative MEN1. Patients with germline MEN1 variants in exons 2 and 3 had a reduced risk of distant metastases.CONCLUSIONThe clinical course of genotype-negative MEN1 is distinct from genotype-positive disease, raising uncertainty about the benefits of lifetime surveillance in patients with genotype-negative disease. MEN1 mosaicism is rare.TRIAL REGISTRATION ClinicalTrials.gov NCT04969926FUNDINGIntramural Research Program of National Institute of Diabetes and Digestive and Kidney Diseases, NIH (ZIA DK043006-46).

Indexed as

Multiple Endocrine Neoplasia Type 1Proto-Oncogene ProteinsAdolescentAdultAgedFemaleGenetic Association StudiesGenotypeGerm-Line MutationHumansMaleMiddle AgedNeuroendocrine TumorsPhenotypeRetrospective StudiesYoung AdultMEN1 protein, humanProto-Oncogene ProteinsCalciumDiagnostic imagingEndocrinologyGeneticsMolecular diagnosisOncology

Identifiers

PMID39946193
PMCPMC11949022

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.