ArticleProceedings of the National Academy of Sciences of the United States of America2010
Inactivation of p53 in breast cancers correlates with stem cell transcriptional signatures.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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.
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Who cites it
99 citing papers in PubMed, 154 citations in OpenAlex.
- Prognostic interaction between expression of p53 and estrogen receptor in patients with node-negative breast cancer: results from IBCSG Trials VIII and IX.Breast cancer research : BCR · 2012Trial
- HNF4α controls growth, identity, and KRAS inhibitor response in invasive mucinous adenocarcinoma of the lung.The Journal of clinical investigation · 2026Article
- p53 regulates the expression of histone modifiers to restrict stemness and maintain differentiated luminal identity in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Overexpression of ornithine decarboxylase 1 mediates the immune-deserted microenvironment and poor prognosis in diffuse large B-cell lymphoma.Journal of the National Cancer Center · 2025Article
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- Activating p53 abolishes self-renewal of quiescent leukaemic stem cells in residual CML disease.Nature communications · 2024Article
- Lung adenocarcinomas with isolated TP53 mutation: A comprehensive clinical, cytopathologic and molecular characterization.Cancer medicine · 2024Article
- Article
- A genetic mosaic mouse model illuminates the pre-malignant progression of basal-like breast cancer.Disease models & mechanisms · 2023Article
- Evolutionary determinants of curability in cancer.Nature ecology & evolution · 2023Review
- Convergent TP53 loss and evolvability in cancer.BMC ecology and evolution · 2023Review
- Loss of p53 enhances the tumor-initiating potential and drug resistance of clonogenic multiple myeloma cells.Blood advances · 2023Article
- Current view of liver cancer cell-of-origin and proposed mechanisms precluding its proper determination.Cancer cell international · 2023Review
- Low-intensity pulsed ultrasound-generated singlet oxygen induces telomere damage leading to glioma stem cell awakening from quiescence.iScience · 2022Article
- Whence CRIPTO: The Reemergence of an Oncofetal Factor in 'Wounds' That Fail to Heal.International journal of molecular sciences · 2021Review
- p53 and Tumor Suppression: It Takes a Network.Trends in cell biology · 2021Review
- Bridging Tumorigenesis and Therapy Resistance With a Non-Darwinian and Non-Lamarckian Mechanism of Adaptive Evolution.Frontiers in oncology · 2021Article
- The p53-53BP1-Related Survival of A549 and H1299 Human Lung Cancer Cells after Multifractionated Radiotherapy Demonstrated Different Response to Additional Acute X-ray Exposure.International journal of molecular sciences · 2020Article
- Cell surface GRP78 promotes stemness in normal and neoplastic cells.Scientific reports · 2020Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Breast cancer comprises a heterogeneous set of diseases distinguishable from one another by pathologic presentation and molecular signatures. However, each breast cancer subtype is also heterogeneous. Some of the heterogeneity may be attributable to genetic instability, but recent data emphasize that developmental plasticity may also contribute. The p53 tumor suppressor could constitute a nodal control point underlying both sources of heterogeneity because it is frequently inactivated during malignant progression and has recently been shown to function as a potent barrier preventing fully differentiated cells from reverting to pluripotent stem cells after expression of appropriate oncogenes. Using archival microarray datasets, we tested the hypothesis that a p53 mutation could allow cells within a tumor to acquire a stem cell-like state by looking for coordinate expression of stem cell identity genes. We show that breast and lung cancers with p53 mutations do exhibit stem cell-like transcriptional patterns. Such tumors were also depleted for differentiation genes regulated by the polycomb repressor complex 2. These data are consistent with a model in which loss of p53 function enables acquisition of stem cell properties, which are positively selected during tumor progression.
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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.