Evidence map›Paper›PMID 15902260›Full record

ArticleNature2005

The Ter mutation in the dead end gene causes germ cell loss and testicular germ cell tumours.

Kirsten K Youngren, Douglas Coveney, Xiaoning Peng, Chitralekha Bhattacharya, Laura S Schmidt, Michael L Nickerson, Bruce T Lamb, Jian Min Deng, Richard R Behringer, Blanche Capel and 3 more

Open access · greenAbstract read
In one paragraph

Article in Nature, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed, 2 pooled it
7.2field-weighted citation impact, top 2% 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

178 citing papers in PubMed, 2 syntheses or guidelines pooled it, 371 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  12. Gonocytes in Transition: Establishing the Male Germline Identity.Advances in experimental medicine and biology · 2026
    Review
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118 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

13 authors at 5 institutions in 1 country.

Kirsten K YoungrenDepartment of Genetics and.
Douglas Coveney
Xiaoning Peng
Chitralekha Bhattacharya
Laura S Schmidt
Michael L Nickerson
Bruce T Lamb
Jian Min Deng
Richard R Behringer
Blanche Capel
Edward M Rubin
Joseph H Nadeau
Angabin Matin
The University of Texas MD Anderson Cancer Center · USCase Western Reserve University · USDuke University · USLawrence Berkeley National Laboratory · USScience Applications International Corporation (United States) · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
GENETIC CONTROL OF SUSCEPTIBILITY TO TESTICULAR CANCERR01CA075056 · NCI · PACIFIC NORTHWEST RESEARCH INSTITUTE · PI NADEAU, JOSEPH H. · 1998 to 2014
$5.7M
ORGAN SPECIFIC MECHANISMS OF VASCULAR DEVELOPMENTR01HL063054 · NHLBI · DUKE UNIVERSITY · PI CAPEL, BLANCHE · 1999 to 2007
$1.5M
Testicular Cancer Susceptibility Genes on Mouse Chr 19.R01CA093754 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MATIN, ANGABIN · 2003 to 2009
$1.4M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA075056NCI NIH HHS R01 CA093754NHLBI NIH HHS R01 HL063054
6 · The paper itself

Abstract

In mice, the Ter mutation causes primordial germ cell (PGC) loss in all genetic backgrounds. Ter is also a potent modifier of spontaneous testicular germ cell tumour (TGCT) susceptibility in the 129 family of inbred strains, and markedly increases TGCT incidence in 129-Ter/Ter males. In 129-Ter/Ter mice, some of the remaining PGCs transform into undifferentiated pluripotent embryonal carcinoma cells, and after birth differentiate into various cells and tissues that compose TGCTs. Here, we report the positional cloning of Ter, revealing a point mutation that introduces a termination codon in the mouse orthologue (Dnd1) of the zebrafish dead end (dnd) gene. PGC deficiency is corrected both with bacterial artificial chromosomes that contain Dnd1 and with a Dnd1-encoding transgene. Dnd1 is expressed in fetal gonads during the critical period when TGCTs originate. DND1 has an RNA recognition motif and is most similar to the apobec complementation factor, a component of the cytidine to uridine RNA-editing complex. These results suggest that Ter may adversely affect essential aspects of RNA biology during PGC development. DND1 is the first protein known to have an RNA recognition motif directly implicated as a heritable cause of spontaneous tumorigenesis. TGCT development in the 129-Ter mouse strain models paediatric TGCT in humans. This work will have important implications for our understanding of the genetic control of TGCT pathogenesis and PGC biology.

Indexed as

AllelesAnimalsBase SequenceBody WeightChromosome MappingChromosomes, MammalianDisease Models, AnimalGene Expression ProfilingGenetic Complementation TestGerm CellsIn Situ HybridizationMaleMiceMutationNeoplasm ProteinsNeoplasms, Germ Cell and EmbryonalDnd1 protein, mouseNeoplasm ProteinsRNA, Messenger

Identifiers

PMID15902260
PMCPMC1421521
OpenAlexW1997928390

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.