ArticleDisease models & mechanisms2021
TP53 loss initiates chromosomal instability in fallopian tube epithelial cells.
Article in Disease models & mechanisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- A system-level metastable model of cancer evolution: integrating replication stress, cell cycle deregulation and chromosomal instability.Annals of medicine · 2026Review
- Pan-cancer Myc modulator that targets Myc-α-tubulin interaction to drive selective mitotic catastrophe.Scientific reports · 2025Article
- Coordinated protein modules define DNA damage responses to carboplatin at single-cell resolution in human ovarian carcinoma models.Cell reports. Medicine · 2025Article
- Aged and BRCA-Mutated Stromal Cells Drive Epithelial Cell Transformation.Cancer discovery · 2025Article
- Role of DNA methylation and non‑coding RNAs expression in pathogenesis, detection, prognosis, and therapy‑resistant ovarian carcinoma (Review).Molecular medicine reports · 2025Review
- Chronic Viral Mimicry Induction following p53 Loss Promotes Immune Evasion.Cancer discovery · 2025Article
- Metabolic Reprogramming Shapes the Progression and Therapeutic Landscape of Ovarian Cancer.Cancer management and research · 2025Review
- Interplay of replication stress response and immune microenvironment in high-grade serous ovarian cancer.Frontiers in cell and developmental biology · 2025Review
- Intrinsic PARG inhibitor sensitivity is mimicked byNAR cancer · 2024Article
- Aneuploidy and complex genomic rearrangements in cancer evolution.Nature cancer · 2024Review
- Rescue of p53 functions by in vitro-transcribed mRNA impedes the growth of high-grade serous ovarian cancer.Cancer communications (London, England) · 2024Article
- Mutational spectrum of breast cancer by shallow whole-genome sequencing of cfDNA and tumor gene panel analysis.PloS one · 2024Article
- Article
- Biallelic MAD2L1BP (p31comet) mutation is associated with mosaic aneuploidy and juvenile granulosa cell tumors.JCI insight · 2023Article
- The Tumor Suppressor BRCA1/2, Cancer Susceptibility and Genome Instability in Gynecological and Mammary Cancers.Asian Pacific journal of cancer prevention : APJCP · 2023Review
- Gain-of-function p53Scientific reports · 2023Article
- HRD effects on first-line adjuvant chemotherapy and PARPi maintenance therapy in Chinese ovarian cancer patients.NPJ precision oncology · 2023Article
- Molecular Management of High-Grade Serous Ovarian Carcinoma.International journal of molecular sciences · 2022Review
- The Genomic Landscape of Early-Stage Ovarian High-Grade Serous Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Pan-cancer Analysis of Homologous Recombination Repair-associated Gene Alterations and Genome-wide Loss-of-Heterozygosity Score.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
High-grade serous ovarian cancer (HGSOC) originates in the fallopian tube epithelium and is characterized by ubiquitous TP53 mutation and extensive chromosomal instability (CIN). However, direct causes of CIN, such as mutations in DNA replication and mitosis genes, are rare in HGSOC. We therefore asked whether oncogenic mutations that are common in HGSOC can indirectly drive CIN in non-transformed human fallopian tube epithelial cells. To model homologous recombination deficient HGSOC, we sequentially mutated TP53 and BRCA1 then overexpressed MYC. Loss of p53 function alone was sufficient to drive the emergence of subclonal karyotype alterations. TP53 mutation also led to global gene expression changes, influencing modules involved in cell cycle commitment, DNA replication, G2/M checkpoint control and mitotic spindle function. Both transcriptional deregulation and karyotype diversity were exacerbated by loss of BRCA1 function, with whole-genome doubling events observed in independent p53/BRCA1-deficient lineages. Thus, our observations indicate that loss of the key tumour suppressor TP53 is sufficient to deregulate multiple cell cycle control networks and thereby initiate CIN in pre-malignant fallopian tube epithelial cells. This article has an associated First Person interview with the first author of the paper.
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Registered trials
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.