Evidence map›Paper›PMID 38255960›Full record

ArticleInternational journal of molecular sciences2024

Human Fallopian Tube-Derived Organoids with TP53 and RAD51D Mutations Recapitulate an Early Stage High-Grade Serous Ovarian Cancer Phenotype In Vitro.

Yilin Dai, Jing Xu, Xiaofeng Gong, Jinsong Wei, Yi Gao, Ranran Chai, Chong Lu, Bing Zhao, Yu Kang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
9.1field-weighted citation impact, top 2% 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

16 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  6. TP53 mutations and MDM2 polymorphisms in breast and ovarian cancers: amelioration by drugs and natural compounds.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
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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 at 2 institutions in 1 country.

Yilin DaiObstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.
Jing XuObstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.
Xiaofeng GongState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai 200438, China.
Jinsong WeiState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai 200438, China.
Yi GaoObstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.
Ranran ChaiObstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.
Chong LuObstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.ORCID 0000-0001-7189-6500
Bing ZhaoState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai 200438, China.
Yu KangObstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, China.
Obstetrics and Gynecology Hospital of Fudan University · CNFudan University · CN

Funding

Shanghai Municipal Health and Family Planning Commission 2020YJZX0202Shanghai ShenKang Hospital Development Center SHDC12020108
6 · The paper itself

Abstract

RAD51D mutations have been implicated in the transformation of normal fallopian tube epithelial (FTE) cells into high-grade serous ovarian cancer (HGSOC), one of the most prevalent and aggressive gynecologic malignancies. Currently, no suitable model exists to elucidate the role of RAD51D in disease initiation and progression. Here, we established organoids from primary human FTE and introduced TP53 as well as RAD51D knockdown to enable the exploration of their mutational impact on FTE lesion generation. We observed that TP53 deletion rescued the adverse effects of RAD51D deletion on the proliferation, stemness, senescence, and apoptosis of FTE organoids. RAD51D deletion impaired the homologous recombination (HR) function and induced G2/M phase arrest, whereas concurrent TP53 deletion mitigated G0/G1 phase arrest and boosted DNA replication when combined with RAD51D mutation. The co-deletion of TP53 and RAD51D downregulated cilia assembly, development, and motility, but upregulated multiple HGSOC-associated pathways, including the IL-17 signaling pathway. IL-17A treatment significantly improved cell viability. TP53 and RAD51D co-deleted organoids exhibited heightened sensitivity to platinum, poly-ADP ribose polymerase inhibitors (PARPi), and cell cycle-related medication. In summary, our research highlighted the use of FTE organoids with RAD51D mutations as an invaluable in vitro platform for the early detection of carcinogenesis, mechanistic exploration, and drug screening.

Indexed as

Cystadenocarcinoma, SerousOvarian NeoplasmsCarcinoma, Ovarian EpithelialDNA-Binding ProteinsFallopian TubesFemaleHumansMutationTumor Suppressor Protein p53DNA-Binding ProteinsRAD51D protein, humanTP53 protein, humanTumor Suppressor Protein p53fallopian tubeshigh-grade serous ovarian cancer (HGSOC)organoidsRAD51D

Identifiers

PMID38255960
PMCPMC10815309
OpenAlexW4390752492

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.