Evidence map›Paper›PMID 36226571›Full record

ArticleJournal of cellular and molecular medicine2022

Origin and timing of de novo variants implicated in type 2 von Willebrand disease.

Ming Chen, Ming-Ching Shen, Shun-Ping Chang, Gwo-Chin Ma, Ying-Chih Huang, Ching-Yeh Lin

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 18% 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, 8 citations in OpenAlex.

  1. Non-Inversion Variants in Sporadic Hemophilia A Rarely Recur.International journal of molecular sciences · 2026
    Article
  2. Prevalence and genetics of "de novo" MEN2 syndromes.The Journal of clinical endocrinology and metabolism · 2025
    Article
  3. Clinical utility of panel-based genetic sequencing for von Willebrand disease.Research and practice in thrombosis and haemostasis · 2025
    Article
  4. Article
  5. Genotyping R1336X and Eliminating the Pseudogene Amplification in Type 3 von Willebrand Disease Patients.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025
    Article
  6. Article
  7. 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

6 authors at 2 institutions in 1 country.

Ming ChenDepartment of Genomic Medicine, Changhua Christian Hospital, Changhua, Taiwan.
Ming-Ching ShenDepartment of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan.ORCID 0000-0001-7789-2148
Shun-Ping ChangDepartment of Genomic Medicine, Changhua Christian Hospital, Changhua, Taiwan.
Gwo-Chin MaDepartment of Genomic Medicine, Changhua Christian Hospital, Changhua, Taiwan.
Ying-Chih HuangDepartment of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan.ORCID 0000-0002-9559-9428
Ching-Yeh LinDepartment of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan.
Changhua Christian Hospital · TWNational Taiwan University Hospital · TW

Funding

Changhua Christian HospitalFondation Sanofi Espoir TW20002
6 · The paper itself

Abstract

Very few studies have shown the real origin and timing of de novo variants (DNV) implicated in von Willebrand disease (VWD). We investigated four families with type 2 VWD. First, we conducted linkage analysis using single nucleotide variant genotyping to recognize the possible provenance of DNV. Second, we performed amplification refractory mutation system-quantitative polymerase chain reaction to confirm the real origin of variant (~0% mutant cells) or presence of a genetic mosaic variant (0%-50% mutant cells) in three embryonic germ layer-derived tissues and sperm cells. Then, three possible timings of DNV were categorized based on the relative likelihood of occurrence according to the number of cell divisions during embryogenesis. Two each with type 2B VWD (proband 1 p.Arg1308Cys, proband 4 p.Arg1306Trp) and type 2A VWD (proband 2 p.Leu1276Arg, proband 3 p.Ser1506Leu) were identified. Variant origins were identified for families 1, 2 and 3 and confirmed to originate from the mother, father and father, respectively. However, the father of family 4 was confirmed to have isolated germline mosaicism with 2.2% mutant sperm cells. Further investigation confirmed the paternal grandfather to be the origin of variant. Thus, we proposed that DNV originating from the two fathers most likely occurred at the single sperm cell, the one originating from the mother occurred at the zygote during the first few cellular divisions; alternatively, in family 4, the DNV most likely occurred at the early postzygotic development in the father. Our findings are essential for understanding genetic pathogenesis and providing accurate genetic counselling.

Indexed as

von Willebrand Diseasesvon Willebrand Disease, Type 2HumansMalePedigreeSemenvon Willebrand Factorvon Willebrand Factorde novo varianttype 2 von Willebrand diseasevon Willebrand disease

Identifiers

PMID36226571
PMCPMC9639050
OpenAlexW4304889329

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.