Evidence map›Paper›PMID 39587356›Full record

ArticleEuropean journal of human genetics : EJHG2025

Molecular diagnoses and candidate gene identification in the congenital heart disease cohorts of the 100,000 genomes project.

Verity Hartill, Mitra Kabir, Sunayna Best, Wasay Mohiuddin Shaikh Qureshi, Stephanie L Baross, Jenny Lord, Jing Yu, Erina Sasaki, Hazel Needham, Deborah Shears and 9 more

Abstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. 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

19 authors.

Verity HartillLeeds Institute of Medical Research, University of Leeds, St James University Hospital, Beckett Street, Leeds, UK. Verity.hartill@nhs.net.ORCID 0000-0003-2537-8205
Mitra KabirDivision of Evolution, Infection and Genomics, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Michael Smith Building, Oxford Road, Manchester, UK.
Sunayna BestYorkshire Regional Genetics Service, Leeds Teaching Hospitals NHS Trust, Chapel Allerton Hospital, Leeds, UK.
Wasay Mohiuddin Shaikh QureshiDivision of Evolution, Infection and Genomics, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Michael Smith Building, Oxford Road, Manchester, UK.
Stephanie L BarossDivision of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.ORCID 0000-0002-3111-9616
Jenny LordDepartment of Human Development and Health, Faculty of Medicine, University of Southampton, Southampton, UK.ORCID 0000-0002-0539-9343
Jing YuNovo Nordisk Research Centre Oxford, The Innovation Building, Roosevelt Dr, Headington, Oxford, OX3 7FZ, UK.
Erina SasakiOxford Centre for Genomic Medicine, ACE Building, Nuffield Orthopaedic Centre, Oxford University Hospital NHS Foundation Trust, Oxford, UK.ORCID 0000-0003-1448-1151
Hazel NeedhamDingley Specialist Childrens Centre, University of Reading Campus, Royal Berkshire NHS Foundation Trust, Berkshire, UK.ORCID 0009-0008-7881-0712
Deborah ShearsOxford Centre for Genomic Medicine, ACE Building, Nuffield Orthopaedic Centre, Oxford University Hospital NHS Foundation Trust, Oxford, UK.
Matthew RocheWindsor House Group Practice, Leeds, UK.
Elizabeth WallWest Midlands Regional Genetics Service, Birmingham Women's and Children's Hospital, Birmingham, UK.
Nicola CooperWest Midlands Regional Genetics Service, Birmingham Women's and Children's Hospital, Birmingham, UK.
Gavin RyanWest Midlands Regional Genetics Laboratory, Birmingham Women's Hospital, Mindelsohn Way, Birmingham, UK.
Jacqueline EasonNottingham Regional Genetics Service, City Hospital, Nottingham, UK.
Robert JohnsonAlder Hey Children's NHS Foundation Trust, Eaton Road, Liverpool, UK.
Bernard KeavneyDivision of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.ORCID 0000-0001-9573-0812
Kathryn E HentgesDivision of Evolution, Infection and Genomics, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Michael Smith Building, Oxford Road, Manchester, UK.ORCID 0000-0001-8917-3765
Colin A JohnsonLeeds Institute of Medical Research, University of Leeds, St James University Hospital, Beckett Street, Leeds, UK.ORCID 0000-0002-2979-8234

Funding

British Heart Foundation (BHF) Personal ChairBritish Heart Foundation (BHF) PG/20/14/35030British Heart Foundation (BHF) PG/22/11127DH | NIHR | Health Services Research Programme (NIHR Health Services Research Programme) Manchester Biomedical Research CentreDH | NIHR | Health Services Research Programme (NIHR Health Services Research Programme) RP-2016-07-011RCUK | Medical Research Council (MRC) MR/V037617/1Sir Jules Thorn Charitable Trust JTA/09Wellcome Trust
6 · The paper itself

Abstract

Congenital heart disease (CHD) describes a structural cardiac defect present from birth. A cohort of participants recruited to the 100,000 Genomes Project (100 kGP) with syndromic CHD (286 probands) and familial CHD (262 probands) were identified. "Tiering" following genome sequencing data analysis prioritised variants in gene panels linked to participant phenotype. To improve diagnostic rates in the CHD cohorts, we implemented an agnostic de novo Gene Discovery Pipeline (GDP). We assessed de novo variants (DNV) for unsolved CHD participants following filtering to select variants of interest in OMIM-morbid genes, as well as novel candidate genes. The 100kGP CHD cohorts had low rates of pathogenic diagnoses reported (combined CHD "solved" 5.11% (n = 28/548)). Our GDP provided diagnostic uplift of nearly one third (1.28% uplift; 5.11% vs. 6.39%), with a new or potential diagnosis for 9 additional participants with CHD. When a filtered DNV occurred within a non-morbid gene, our GDP prioritised biologically-plausible candidate CHD genes (n = 79). Candidate variants occurred in both genes linked to cardiac development (e.g. AKAP13 and BCAR1) and those currently without a known role (e.g. TFAP2C and SETDB1). Sanger sequencing of a cohort of patients with CHD did not identify a second de novo variant in the candidate dataset. However, literature review identified rare variants in HMCN1, previously reported as causative for pulmonary atresia, confirming the approach utility. As well as diagnostic uplift for unsolved participants of the 100 kGP, our GDP created a dataset of candidate CHD genes, which forms an important resource for further evaluation.

Indexed as

Genetic TestingHeart Defects, CongenitalCohort StudiesFemaleHumansMale

Identifiers

PMID39587356
PMCPMC12185689

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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.