Evidence map›Paper›PMID 41535518›Full record

ArticleHuman cell2026

Generation and characterization of human iPSC lines (FAHZJUi001-A and FAHZJUi002-A) from two familial recurrent hydatidiform mole patients carrying homozygous mutation in the NLRP7 gene.

Limeng Cai, Jiayang Wan, Yating Zhao, Yuyan Xu, Luya Cai, Li Zhang, Tingyu Gong, Jin Zhang, Jianhua Qian

Abstract read
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Article in Human cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Cancers · 2026
    Review
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

9 authors.

Limeng Cai *Department of Gynecology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Jiayang Wan *Department of Gynecology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Yating ZhaoDepartment of Gynecology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Yuyan XuCenter for Stem Cell and Regenerative Medicine, Department of Basic Medical Sciences, and Bone Marrow for Transplantation Center of the First Affiliated Hospital, Zhejiang University, Hangzhou, China.
Luya CaiDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Li ZhangCenter for Stem Cell and Regenerative Medicine, Department of Basic Medical Sciences, and Bone Marrow for Transplantation Center of the First Affiliated Hospital, Zhejiang University, Hangzhou, China.
Tingyu GongShulan International Medical College, Zhejiang Shuren University, Hangzhou, China.
Jin ZhangCenter for Stem Cell and Regenerative Medicine, Department of Basic Medical Sciences, and Bone Marrow for Transplantation Center of the First Affiliated Hospital, Zhejiang University, Hangzhou, China. zhgene@zju.edu.cn.
Jianhua QianDepartment of Gynecology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China. qianjianhua@zju.edu.cn.ORCID http://orcid.org/0000-0003-1320-6860

Funding

Key Research and Development Program of Zhejiang Province 2025C02115National Natural Science Foundation of China 82371669
6 · The paper itself

Abstract

Hydatidiform mole (HM) is a pathological pregnancy characterized by excessive trophoblast proliferation and the absence of embryonic tissue development, predominantly sporadic in onset. Recurrent hydatidiform mole (RHM) affects approximately 1%-4% of HM patients, among which familial RHM (FRHM) is extremely rare and classified as a monogenic autosomal recessive disorder. NLRP7 (NLR family, pyrin domain containing 7) is the major pathogenic gene for RHM, in which affected individuals have a profound impairment in fertility and a markedly elevated risk of malignant transformation. Yet mechanistic research remains constrained by ethical limitations in human embryo studies and the absence of animal models recapitulating HM phenotypes. Here, we report the generation and characterization of iPSC lines from FRHM patients harboring homozygous NLRP7 variants c.2078G > A (p.Arg693Gln) and c.2161 C > T (p.Arg721Trp), respectively. These cellular models offer a unique platform to dissect molecular pathways driving NLRP7-mediated reproductive failure, overcoming long-standing barriers in FRHM pathogenesis research.

Indexed as

Adaptor Proteins, Signal TransducingHomozygoteHydatidiform MoleMutationUterine NeoplasmsCell LineFemaleHumansPregnancyRecurrenceAdaptor Proteins, Signal TransducingNLRP7 protein, humanFamilial recurrent hydatidiform moleHydatidiform moleInduced pluripotency stem cellNLRP7 variant

Identifiers

PMID41535518

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