ArticleNature communications2022
p53 wild-type colorectal cancer cells that express a fetal gene signature are associated with metastasis and poor prognosis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Stemness in Colon Cancer.Methods in molecular biology (Clifton, N.J.) · 2027Article
- A Generalizable Multimodal Model for Treatment-Stratified Risk and Survival Assessment under Real-World Constraints: A Multi-Center Study of Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identifying phenotype-genotype-function coupling in 3D organoid imaging using Shape, Appearance and Motion Phenotype Observation Tool (SPOT).Nature communications · 2026Article
- Article
- APC coordinates GSK3 phosphorylation of SETD8 to suppress colorectal cancer.Cell reports · 2026Article
- A Plastic EMP1+ to LGR5+ Cell State Conversion as a Bypass to KRASG12D Pharmacologic Inhibition in Metastatic Colorectal Cancer.Cancer discovery · 2026Article
- Epigenetic Gatekeeping of Intestinal Stem Cell Transformation.bioRxiv : the preprint server for biology · 2026Article
- ColoStem, a core oncofetal signature that identifies poor prognosis colorectal tumors.British journal of cancer · 2026Article
- Fueling the Seed: Growth Factors and Cytokines Driving Cancer Stem Cells in Gynecological Malignancies.International journal of molecular sciences · 2025Review
- Impact of TP53, KRAS, and APC Mutations on Neoadjuvant Chemotherapy Outcomes in Locally Advanced Rectal Cancer.Cancer science · 2025Article
- Defining the mucosal ecosystem: epithelial-mesenchymal interdependence in gastrointestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- Article
- Model systems and unique biological features of high and low-grade colorectal cancer (CRC) revealed by xenografting 84 human CRC cell lines.Communications biology · 2025Article
- Review
- Establishment of a novel mouse model of colorectal cancer by orthotopic transplantation.BMC cancer · 2025Article
- Article
- USP36 promotes colorectal cancer progression through inhibition of p53 signaling pathway via stabilizing RBM28.Oncogene · 2024Article
- Cancer drug-tolerant persister cells: from biological questions to clinical opportunities.Nature reviews. Cancer · 2024Review
- Mechanisms of metastatic colorectal cancer.Nature reviews. Gastroenterology & hepatology · 2024Review
- Patient-Derived Organoids as Therapy Screening Platforms in Cancer Patients.Advanced healthcare materials · 2024Review
Corrections and comments
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Authors and funding
27 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current therapy against colorectal cancer (CRC) is based on DNA-damaging agents that remain ineffective in a proportion of patients. Whether and how non-curative DNA damage-based treatment affects tumor cell behavior and patient outcome is primarily unstudied. Using CRC patient-derived organoids (PDO)s, we show that sublethal doses of chemotherapy (CT) does not select previously resistant tumor populations but induces a quiescent state specifically to TP53 wildtype (WT) cancer cells, which is linked to the acquisition of a YAP1-dependent fetal phenotype. Cells displaying this phenotype exhibit high tumor-initiating and metastatic activity. Nuclear YAP1 and fetal traits are present in a proportion of tumors at diagnosis and predict poor prognosis in patients carrying TP53 WT CRC tumors. We provide data indicating the higher efficacy of CT together with YAP1 inhibitors for eradication of therapy resistant TP53 WT cancer cells. Together these results identify fetal conversion as a useful biomarker for patient prognosis and therapy prescription.
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