ArticleCell reports2019
p53 Loss in Breast Cancer Leads to Myc Activation, Increased Cell Plasticity, and Expression of a Mitotic Signature with Prognostic Value.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 97 citations in OpenAlex.
- Dynamics, function, and regulation of mammary stem cells in development and disease.Experimental & molecular medicine · 2026Review
- Effect of Amino Acid Derivatives and Polyphenol Supplementation on Ovine Muscle Growth In Vitro and In Vivo.Muscles (Basel, Switzerland) · 2026Article
- Spatial ecology of breast cancer reveals co-evolution of proliferative and dormant niches.Genome medicine · 2026Article
- Wnt signaling-mediated activation of cancer cell stemness in thoracic SMARCA4-deficient undifferentiated tumor cells.Cell death discovery · 2026Article
- Article
- Genes-first and phenotypes-first paths to treatment resistance in hematological malignancies.Cell death & disease · 2025Review
- Cross-attention graph neural networks for inferring gene regulatory networks with skewed degree distribution.BMC bioinformatics · 2025Article
- PDCD11 Stabilizes C-MYC Oncoprotein by Hindering C-MYC-SKP2 Negative Feedback Loop to Facilitate Progression of p53-Mutant Breast and Colon Malignancies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrating Network Pharmacology andCombinatorial chemistry & high throughput screening · 2025Article
- Atypical cell cycle regulation promotes mammary stem cell expansion during mammary development and tumourigenesis.Breast cancer research : BCR · 2024Article
- U2AF2-SNORA68 promotes triple-negative breast cancer stemness through the translocation of RPL23 from nucleoplasm to nucleolus and c-Myc expression.Breast cancer research : BCR · 2024Article
- Article
- Degradation of MYC by the mutant p53 reactivator drug, COTI-2 in breast cancer cells.Investigational new drugs · 2023Article
- When Just One Phosphate Is One Too Many: The Multifaceted Interplay between Myc and Kinases.International journal of molecular sciences · 2023Review
- Annexin A1 is a polarity cue that directs mitotic spindle orientation during mammalian epithelial morphogenesis.Nature communications · 2023Article
- Harnessing the value of TCTP in breast cancer treatment resistance: an opportunity for personalized therapy.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- The insulin and IGF signaling pathway sustains breast cancer stem cells by IRS2/PI3K-mediated regulation of MYC.Cell reports · 2022Article
- Aberrant activation of p53/p66Shc-mInsc axis increases asymmetric divisions and attenuates proliferation of aged mammary stem cells.Cell death and differentiation · 2022Article
- Review
- Current strategies and progress for targeting the "undruggable" transcription factors.Acta pharmacologica Sinica · 2022Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of p53 function is invariably associated with cancer. Its role in tumor growth was recently linked to its effects on cancer stem cells (CSCs), although the underlying molecular mechanisms remain unknown. Here, we show that c-myc is a transcriptional target of p53 in mammary stem cells (MaSCs) and is activated in breast tumors as a consequence of p53 loss. Constitutive Myc expression in normal mammary cells leads to increased frequency of MaSC symmetric divisions, extended MaSC replicative-potential, and MaSC-reprogramming of progenitors, whereas Myc activation in breast cancer is necessary and sufficient to maintain the expanding pool of CSCs. Concomitant p53 loss and Myc activation trigger the expression of 189 mitotic genes, which identify patients at high risk of mortality and relapse, independently of other risk factors. Altogether, deregulation of the p53:Myc axis in mammary tumors increases CSC content and plasticity and is a critical determinant of tumor growth and clinical aggressiveness.
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