Evidence map›Paper›PMID 26311541›Full record

ArticleJournal of human genetics2015

Setleis syndrome due to inheritance of the 1p36.22p36.21 duplication: evidence for lack of penetrance.

Beom Hee Lee, Christos Kasparis, Brenden Chen, Hui Mei, Lisa Edelmann, Celia Moss, David D Weaver, Robert J Desnick

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In one paragraph

Article in Journal of human genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

3 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

8 authors at 4 institutions in 3 countries.

Beom Hee LeeDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Christos KasparisDepartment of Dermatology, Birmingham Children's Hospital, National Health Service Foundation Trust, Birmingham, UK.
Brenden ChenDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Hui MeiDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Lisa EdelmannDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Celia MossDepartment of Dermatology, Birmingham Children's Hospital, National Health Service Foundation Trust, Birmingham, UK.
David D WeaverDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Robert J DesnickDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Icahn School of Medicine at Mount Sinai · USBirmingham Children's Hospital · GBIndiana University School of MedicineUlsan College · KR

Funding

T32 training grant in medical genetics.T32GM082773 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Laszlo Tamas Kozicz, Eva Morava-Kozicz · 2008 to 2026
$4.9M
6 · The paper itself

Abstract

Setleis syndrome, focal facial dermal dysplasia type III (FFDD3, MIM #227260), is characterized by scar-like bitemporal lesions and other ocular and facial dysmorphic features. The syndrome results from recessive mutations in the TWIST2 gene, encoding a basic helix-loop-helix transcription factor or de novo genomic duplication or triplication, which include 1.3 Mb at 1p36.22p36.21, or other yet undefined lesions, emphasizing the syndrome's genetic heterogeneity. Recently, three patients were reported with 1p36.22p36.21 duplications/triplication that had the characteristic FFDD3 features and developmental delay or intellectual disabilities. Here, we describe a male with this microduplication, and the typical FFDD3 phenotype, but normal intelligence. Notably, his duplication was inherited from his father who did not have any FFDD3 manifestations, indicating lack of penetrance of the 1p36.22p36.21 microduplication. These findings emphasize phenotypic heterogeneity of the 1p36.22p36.21 copy number variant and the importance of screening the parents of patients with the 1p36.22p36.21 copy number variant to determine whether the duplication/triplication is de novo or inherited, for informed reproductive and genetic counseling.

Indexed as

Chromosome DuplicationChromosomes, Human, Pair 1Ectodermal DysplasiaFemaleFocal Dermal HypoplasiaFocal Facial Dermal DysplasiasHumansMalePedigreePenetrancePhenotypeRepressor ProteinsSkin DiseasesTwist-Related Protein 1Young AdultRepressor ProteinsTWIST2 protein, humanTwist-Related Protein 1

Identifiers

PMID26311541
OpenAlexW2262124295

What OpenQuestion holds

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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.