Evidence map›Paper›PMID 28746835›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2017

Genetic ataxia telangiectasia porcine model phenocopies the multisystemic features of the human disease.

Rosanna Beraldi, David K Meyerholz, Alexei Savinov, Attila D Kovács, Jill M Weimer, Jordan A Dykstra, Ryan D Geraets, David A Pearce

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Porcine Models of Pancreatic Cancer.Frontiers in oncology · 2019
    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

8 authors at 2 institutions in 1 country.

Rosanna BeraldiPediatric and Rare Diseases Group Sanford Research, Sioux Falls, SD 57104, USA; Sanford School of Medicine at the University of South Dakota, Sioux Falls, SD 57105, USA.
David K MeyerholzDepartment of Pathology, University of Iowa, Iowa City, IA 52242, USA.
Alexei SavinovDiabetes Group Sanford Research, Sioux Falls, SD 57105, USA; Sanford School of Medicine at the University of South Dakota, Sioux Falls, SD 57105, USA.
Attila D KovácsPediatric and Rare Diseases Group Sanford Research, Sioux Falls, SD 57104, USA; Sanford School of Medicine at the University of South Dakota, Sioux Falls, SD 57105, USA.
Jill M WeimerPediatric and Rare Diseases Group Sanford Research, Sioux Falls, SD 57104, USA; Sanford School of Medicine at the University of South Dakota, Sioux Falls, SD 57105, USA.
Jordan A DykstraPediatric and Rare Diseases Group Sanford Research, Sioux Falls, SD 57104, USA.
Ryan D GeraetsPediatric and Rare Diseases Group Sanford Research, Sioux Falls, SD 57104, USA; Sanford School of Medicine at the University of South Dakota, Sioux Falls, SD 57105, USA.
David A PearcePediatric and Rare Diseases Group Sanford Research, Sioux Falls, SD 57104, USA; Sanford School of Medicine at the University of South Dakota, Sioux Falls, SD 57105, USA. Electronic address: David.Pearce@SanfordHealth.org.
Sanford Research · USUniversity of Iowa · US

Funding

Yeast 2 HybridP20GM103620 · NIGMS · SANFORD RESEARCH/USD · PI ROUX, KYLE J · 2013 to 2023
$24.2M
The Impact of PD-1 Inhibition on Immune-Response to ChemoradiotherapyP20GM103548 · NIGMS · SANFORD RESEARCH/USD · PI MISKIMINS, W KEITH · 2012 to 2020
$20.8M
YEAST BTNLP AND HUMAN CLN3P IN YEASTR01NS036610 · NINDS · UNIVERSITY OF ROCHESTER · PI PEARCE, DAVID A. · 1997 to 2010
$3.3M
The Autoimmune Response of Battens DiseaseR01NS044310 · NINDS · UNIVERSITY OF ROCHESTER · PI PEARCE, DAVID A. · 2003 to 2011
$2.3M
Development of a Porcine Model of Ataxia-TelangiectasiaR44NS076075 · NINDS · EXEMPLAR GENETICS, LLC · PI ROGERS, CHRISTOPHER · 2012 to 2013
$1.2M
NIGMS NIH HHS P20 GM103548NIGMS NIH HHS P20 GM103620NINDS NIH HHS R01 NS036610NINDS NIH HHS R01 NS044310NINDS NIH HHS R44 NS076075
6 · The paper itself

Abstract

Ataxia telangiectasia (AT) is a progressive multisystem autosomal recessive disorder caused by mutations in the AT-mutated (ATM) gene. Early onset AT in children is characterized by cerebellar degeneration, leading to motor impairment. Lung disease and cancer are the two most common causes of death in AT patients. Accelerated thymic involution may contribute to the cancer, and recurrent and/or chronic respiratory infections may be a contributing factor to lung disease in AT. AT patients have fertility issues, are highly sensitive to ionizing radiation and they present oculocutaneous telangiectasia. Current treatments only slightly ameliorate disease symptoms; therapy that alters or reverses the course of the disease has not yet been discovered. Previously, we have shown that ATM

Indexed as

Ataxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsDisease Models, AnimalSwineAnimalsAnimals, Genetically ModifiedFemaleHumansPurkinje CellsAtaxia Telangiectasia Mutated ProteinsImmunologyInfertilityNeurodegenerativep53Thymus

Identifiers

PMID28746835
PMCPMC5687068
OpenAlexW2738492515

What OpenQuestion holds

Textmetadata
LicenceTDM
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.