Evidence map›Paper›PMID 37460656›Full record

ArticleEuropean journal of human genetics : EJHG2023

Nemaline myopathy: reclassification of previously reported variants according to ACMG guidelines, and report of novel genetic variants.

Alireza Haghighi, Zahra Alvandi, Yalda Nilipour, Amirreza Haghighi, Ruth Kornreich, Shahriar Nafissi, Robert J Desnick

Open access · greenAbstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2023. 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
1.3field-weighted citation impact, top 17% 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, 4 citations in OpenAlex.

  1. 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

7 authors at 5 institutions in 2 countries.

Alireza HaghighiDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA. ahaghighi@bwh.harvard.edu.ORCID 0000-0003-0683-4922
Zahra Alvandi *Department of Surgery, Harvard Medical School, Boston, MA, 02115, USA.ORCID 0000-0003-0097-4713
Yalda Nilipour *Pediatric Pathology Research Center, Research Institute for Children's Health, and Mofid Children Hospital, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Amirreza HaghighiDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Ruth KornreichDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Shahriar NafissiDepartment of Neurology, Neuromuscular Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.ORCID 0000-0003-4763-4310
Robert J DesnickDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Broad Institute · USIcahn School of Medicine at Mount Sinai · USBoston Children's Hospital · USShahid Beheshti University of Medical Sciences · IRShariati Hospital · IR

Funding

Discovery of Novel Genetic Variants Underlying Unexplained Hypertrophic Cardiomyopathy by Whole Genome Sequencing, RNA-seq and iPSC modelingK08HL150284 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI HAGHIGHI, ALIREZA · 2020 to 2024
$832k
NHLBI NIH HHS K08 HL150284
6 · The paper itself

Abstract

Nemaline myopathy (NM) is a heterogeneous genetic neuromuscular disorder characterized by rod bodies in muscle fibers resulting in multiple complications due to muscle weakness. NM patients and their families could benefit from genetic analysis for early diagnosis, carrier and prenatal testing; however, clinical classification of variants is subject to change as further information becomes available. Reclassification can significantly alter the clinical management of patients and their families. We used the newly published data and ACMG/AMP guidelines to reassess NM-associated variants previously reported by clinical laboratories (ClinVar). Our analyses on rare variants that were not canonical loss-of-function (LOF) resulted in the downgrading of ~29% (28/97) of variants from pathogenic or likely-pathogenic (P/LP) to variants of uncertain significance (VUS). In addition, we analyzed the splicing effect of variants identified in NM patients by clinical laboratories or research, using an accurate in silico prediction tool that applies a deep-learning network. We identified 55 rare variants that may impact splicing (cryptic splicing). We also analyzed six new NM families and identified eight variants in NEB and ACTA1, including three novel variants: homozygous pathogenic c.164A > G (p.Tyr55Cys), and homozygous likely pathogenic c.980T > C (p.Met327Thr) in ACTA1, and heterozygous VUS c.18694-3T > G in NEB. This study demonstrates the importance of reclassifying variants to facilitate more definitive "calls" on causality or no causality in clinical genetic testing of patients with NM. Reclassification of ~150 variants is now available for improved clinical management, risk counseling and screening of NM patients.

Indexed as

Myopathies, NemalineGenetic TestingHeterozygoteHumansMutationRNA Splicing

Identifiers

PMID37460656
PMCPMC10620380
OpenAlexW4384627449

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.