Evidence map›Paper›PMID 39172268›Full record

ArticleJournal of clinical immunology2024

De Novo Deep Intron ELANE Mutation Resulting in Severe Congenital Neutropenia.

Zhou Shu, Mengyue Deng, Tongxin Han, Huawei Mao

Abstract readCase Reports
PubMed Publisher
In one paragraph

Article in Journal of clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Cyclic neutropenia: a case report and literature review.American journal of translational research · 2025
    Article
  6. 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

4 authors.

Zhou ShuDepartment of Immunology, Ministry of Education Key Laboratory of Major Diseases in Children, Beijing Children's Hospital, National Center for Children's Health, Capital Medical University, No. 56 Nanlishi Road, Beijing, 100045, China.
Mengyue DengDepartment of Immunology, Ministry of Education Key Laboratory of Major Diseases in Children, Beijing Children's Hospital, National Center for Children's Health, Capital Medical University, No. 56 Nanlishi Road, Beijing, 100045, China.
Tongxin HanDepartment of Immunology, Ministry of Education Key Laboratory of Major Diseases in Children, Beijing Children's Hospital, National Center for Children's Health, Capital Medical University, No. 56 Nanlishi Road, Beijing, 100045, China.
Huawei MaoDepartment of Immunology, Ministry of Education Key Laboratory of Major Diseases in Children, Beijing Children's Hospital, National Center for Children's Health, Capital Medical University, No. 56 Nanlishi Road, Beijing, 100045, China. maohwei@qq.com.

Funding

Key Program of Beijing Natural Science Foundation KZ202210025030National Key Research and Development Program of China 2021YFC2702005National Science Foundation of China 81900136
6 · The paper itself

Abstract

Severe congenital neutropenia (SCN) comprises a diverse range of rare hematological disorders characterized by recurrent, often life-threatening infections that manifest within the first months of life. Mutations in the ELANE gene are the most prevalent cause of SCN. While over 230 mutations in ELANE have been documented, including substitutions, frameshifts, nonsense mutations, and splice site alterations, the occurrence of deep intronic mutations has not been previously reported. Herein, we present the case of a young girl who exhibited recurrent fever, respiratory infections, skin abscesses, and gingivitis shortly after birth. Laboratory analysis revealed markedly diminished neutrophil levels alongside elevated monocyte and eosinophil counts. Bone marrow examination disclosed a halt in myelopoiesis maturation. ELANE gene full-length sequencing identified a novel de novo deep intron mutation in ELANE (c.598 + 79G > T), subsequently confirmed by Sanger sequencing. cDNA sequencing of the patient demonstrated aberrant gene splicing. Utilizing a mini-gene splicing assay for ELANE intronic variants, we identified a mutant ELANE allele (c.597 + 1_597 + 83ins) leading to the creation of a premature termination codon (p.Gly200ValfsTer40). Confocal microscopy revealed heightened expression of myeloperoxidase and neutrophil elastase in the patient, suggesting a potential role for the unfolded protein response in the pathogenesis of the deep intron ELANE mutation. In summary, our findings illustrate the first reported instance of de novo deep intron ELANE mutations associated with SCN, underscoring the importance of exploring deep intronic regions in SCN patients lacking identifiable disease-causing gene mutations.

Indexed as

Congenital Bone Marrow Failure SyndromesIntronsLeukocyte ElastaseMutationNeutropeniaAllelesFemaleGenetic Predisposition to DiseaseHumansELANE protein, humanLeukocyte ElastaseDeep intronic mutationELANE mutationSevere neutropenia

Identifiers

What OpenQuestion holds

Textmetadata
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.