ArticleOncotarget2017
Whole-exome sequencing reveals genetic variants in ERC1 and KCNG4 associated with complete hydatidiform mole in Chinese Han women.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular Basis of Hydatidiform Moles-A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Defects in meiosis I contribute to the genesis of androgenetic hydatidiform moles.The Journal of clinical investigation · 2024Article
- Genetic screening of Chinese patients with hydatidiform mole by whole-exome sequencing and comprehensive analysis.Journal of assisted reproduction and genetics · 2022Article
Corrections and comments
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Authors and funding
34 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complete hydatidiform mole (CHM) is a rare pregnancy-related disease with invasive potential. The genetics underlying the sporadic form of CHM have not been addressed previously, but maternal genetic variants may be involved in biparental CHM. We performed whole-exome sequencing of 51 patients with CHM and 47 healthy women to identify genetic variants associated with CHM. In addition, candidate variants were analyzed using single base extension and Matrix Assisted Laser Desorption/Ionization-Time of Flight Mass Spectrometry in 199 CHM patients and 400 healthy controls. We validated candidate variants using Sanger sequencing in 250 cases and 652 controls, including 205 new controls. Two single nucleotide polymorphisms, c.G48C(p.Q16H) in
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