Evidence map›Paper›PMID 22140379›Full record

ArticleMolecular syndromology2010

Refinement of the Region for Split Hand/Foot Malformation 5 on 2q31.1.

A Theisen, J A Rosenfeld, K Shane, K L McBride, J F Atkin, C Gaba, J Hoo, T W Kurczynski, R E Schnur, L B Coffey and 26 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular syndromology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. The molecular genetics of human appendicular skeleton.Molecular genetics and genomics : MGG · 2022
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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

36 authors at 18 institutions in 3 countries.

A TheisenSignature Genomic Laboratories, Spokane, Wash.
J A Rosenfeld
K Shane
K L McBride
J F Atkin
C Gaba
J Hoo
T W Kurczynski
R E Schnur
L B Coffey
E H Zackai
L Schimmenti
N Friedman
M Zabukovec
S Ball
R Pagon
A Lucas
C K Brasington
J E Spence
S Sparks
V Banks
W Smith
T Friedberg
P R Wyatt
M Aust
R Tervo
A Crowley
D Skidmore
A N Lamb
B Ravnan
T Sahoo
R Schultz
B S Torchia
M Sgro
D Chitayat
L G Shaffer
Signature Research (United States) · USCarolinas Medical Center · USThe Ohio State University · USCleveland Clinic · USRowan University · USUniversity of Toledo · USUniversity of Toronto · CAVirginia Mason Memorial · USYork Central Hospital · CAAkron Children's Hospital · USCalifornia Maritime Academy · USChildren's Hospital of Philadelphia · USGillette Children's Specialty Healthcare · USIzaak Walton Killam Health Centre · CAMaine Medical Center · USMount Sinai Hospital · CASignature Analytics (United States) · USUniversity of Minnesota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Deletions that encompass 2q31.1 have been proposed as a microdeletion syndrome with common clinical features, including intellectual disability/developmental delay, microcephaly, cleft palate, growth delay, and hand/foot anomalies. In addition, several genes within this region have been proposed as candidates for split hand-foot malformation 5 (SHFM5). Methods: To delineate the genotype-phenotype correlation between deletions of this region, we identified 14 individuals with deletions at 2q31.1 detected by microarray analysis for physical and developmental disabilities. Results: All subjects for whom detailed clinical records were available had neurological deficits of varying degree. Seven subjects with deletions encompassing the HOXD cluster had hand/foot anomalies of varying severity, including syndactyly, brachydactyly, and ectrodactyly. Of 7 subjects with deletions proximal to the HOXD cluster, 5 of which encompassed DLX1/DLX2, none had clinically significant hand/foot anomalies. In contrast to previous reports, the individuals in our study did not display a characteristic gestalt of dysmorphic facial features. Conclusion: The absence of hand/foot anomalies in any of the individuals with deletions of DLX1/DLX2 but not the HOXD cluster supports the hypothesis that haploinsufficiency of the HOXD cluster, rather than DLX1/DLX2, accounts for the skeletal abnormalities in subjects with 2q31.1 microdeletions.

Identifiers

PMID22140379
PMCPMC3214950
OpenAlexW1963885049

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Registered trials

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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.