Evidence map›Paper›PMID 16943588›Full record

ArticleEndocrine2006

Expression and functional analysis of menin in a multiple endocrine neoplasia type 1 (MEN1) patient with somatic loss of heterozygosity in chromosome 11q13 and unidentified germline mutation of the MEN1 gene.

Junko Naito, Hiroshi Kaji, Hideaki Sowa, Riko Kitazawa, Sohei Kitazawa, Toshihiko Tsukada, Geoffrey N Hendy, Toshitsugu Sugimoto, Kazuo Chihara

Abstract readCase Reports
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In one paragraph

Article in Endocrine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

2 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Menin and bone metabolism.Journal of bone and mineral metabolism · 2012
    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

9 authors at 3 institutions in 2 countries.

Junko NaitoDivision of Endocrinology/Metabolism, Neurology and Hematology/Oncology, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Japan.
Hiroshi Kaji
Hideaki Sowa
Riko Kitazawa
Sohei Kitazawa
Toshihiko Tsukada
Geoffrey N Hendy
Toshitsugu Sugimoto
Kazuo Chihara
Kobe University · JPMcGill University · CAShimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In some patients with multiple endocrine neoplasia type 1 (MEN1) it is not possible to identify a germline mutation in the MEN1 gene. We sought to document the loss of expression and function of the MEN1 gene product, menin, in the tumors of such a patient. The proband is an elderly female patient with primary hyperparathyroidism, pancreatic islet tumor, and breast cancer. Her son has primary hyperparathyroidism. No germline MEN1 mutation was identified in the proband or her son. However, loss of heterozygosity at the MEN1 locus and complete lack of menin expression were demonstrated in the proband's tumor tissue. The proband's cultured parathyroid cells lacked the normal reduction in proliferation and parathyroid hormone secretion in response to transforming growth factor- beta. This assessment provided insight into the molecular pathogenesis of the patient and provides evidence for a critical requirement for menin in the antiproliferative action of transforming growth factor-beta.

Indexed as

Chromosomes, Human, Pair 11Loss of HeterozygosityAgedFemaleGerm-Line MutationHumansHypercalcemiaHyperthyroidismLiver NeoplasmsMicrosatellite RepeatsMultiple Endocrine Neoplasia Type 1Parathyroid HormoneParathyroid NeoplasmsPolymorphism, GeneticProto-Oncogene ProteinsTransforming Growth Factor betaMEN1 protein, humanParathyroid HormoneProto-Oncogene ProteinsTransforming Growth Factor beta

Identifiers

PMID16943588
OpenAlexW1992743440

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.