Evidence map›Paper›PMID 10675330›Full record

ArticleThe EMBO journal2000

C-cell hyperplasia, pheochromocytoma and sympathoadrenal malformation in a mouse model of multiple endocrine neoplasia type 2B.

C L Smith-Hicks, K C Sizer, J F Powers, A S Tischler, F Costantini

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. Thyroid C-Cell Biology and Oncogenic Transformation.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2025
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  12. Drosophila Model in Cancer: An Introduction.Advances in experimental medicine and biology · 2019
    Review
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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

5 authors at 3 institutions in 1 country.

C L Smith-HicksDepartment of Genetics and Development, College of Physicians and Surgeons, Columbia University, 701 W. 168th Street, New York, NY 10032, USA.
K C Sizer
J F Powers
A S Tischler
F Costantini
Columbia University · USTufts Medical Center · USTufts University · US

Funding

THE DETERMINANTS OF MUTATIONP01CA023767 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI AXEL, RICHARD · 1985 to 2008
$8.3M
CHROMAFFIN CELL PROLIFERATION IN NEOPLASTIC PROGRESSIONR01CA048017 · NCI · TUFTS UNIVERSITY BOSTON · PI TISCHLER, ARTHUR S · 1988 to 2006
$1.5M
PHEOCHROMOCYTOMAS FROM NEUROFIBROMATOSIS KNOCKOUT MICER01NS037685 · NINDS · TUFTS MEDICAL CENTER · PI TISCHLER, ARTHUR S · 1999 to 2003
$1.1M
NCI NIH HHS CA23767NCI NIH HHS CA48017NCI NIH HHS P01 CA023767NCI NIH HHS R01 CA048017NINDS NIH HHS NS37685NINDS NIH HHS R01 NS037685
6 · The paper itself

Abstract

Dominantly inherited multiple endocrine neoplasia type 2B (MEN2B) is characterized by tumors of the thyroid C-cells and adrenal chromaffin cells, together with ganglioneuromas of the gastrointestinal tract and other developmental abnormalities. Most cases are caused by substitution of threonine for Met918 in the RET receptor tyrosine kinase, which is believed to convert the RET gene to an oncogene by altering the enzyme's substrate specificity. We report the production of a mouse model of MEN2B by introduction of the corresponding mutation into the ret gene. Mutant mice displayed C-cell hyperplasia and chromaffin cell hyperplasia progressing to pheochromocytoma. Homozygotes did not develop gastrointestinal ganglioneuromas, but displayed ganglioneuromas of the adrenal medulla, enlargement of the associated sympathetic ganglia and a male reproductive defect. Surprisingly, homozygotes did not display any developmental defects attributable to a loss-of-function mutation. Thus, while our results support the conclusion that the Met918Thr substitution is responsible for MEN2B, they suggest that the substrate specificity of the RET kinase does not interfere with its normal role in the development of the kidneys and enteric nervous system.

Indexed as

Drosophila ProteinsAdrenal Gland NeoplasmsAdrenal GlandsAnimalsBase SequenceDisease Models, AnimalDNA PrimersFemaleGanglia, SympatheticGanglioneuromaGerm-Line MutationHumansHyperplasiaInfertility, MaleMaleMiceDNA PrimersDrosophila ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesRet protein, DrosophilaRet protein, mouse

Identifiers

PMID10675330
PMCPMC305599
OpenAlexW2064068457

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.