ArticleMolecular oncology2020
Transcriptional profiling reveals a subset of human breast tumors that retain wt TP53 but display mutant p53-associated features.
Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- Interaction of p53 with the Δ133p53α and Δ160p53α isoforms regulates p53 conformation and transcriptional activity.Cell death & disease · 2024Article
- Machine learning analysis of gene expression reveals TP53 Mutant-like AML with wild type TP53 and poor prognosis.Blood cancer journal · 2024Article
- Pharmacological reactivation of p53 in the era of precision anticancer medicine.Nature reviews. Clinical oncology · 2024Review
- p53 deficient breast cancer cells reprogram preadipocytes toward tumor-protective immunomodulatory cells.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Integrative bioinformatic analysis of p53 and pathway alterations in two different lung cancer subtypes.Biochemistry and biophysics reports · 2023Article
- Targeting tumor-stroma communication by blocking endothelin-1 receptors sensitizes high-grade serous ovarian cancer to PARP inhibition.Cell death & disease · 2023Article
- A p53 transcriptional signature in primary and metastatic cancers derived using machine learning.Frontiers in genetics · 2022Article
- Regulation of p53 and Cancer Signaling by Heat Shock Protein 40/J-Domain Protein Family Members.International journal of molecular sciences · 2021Review
- Mutant p53 in cell-cell interactions.Genes & development · 2021Review
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
TP53 gene mutations are very common in human cancer. While such mutations abrogate the tumor suppressive activities of the wild-type (wt) p53 protein, some of them also endow the mutant (mut) protein with oncogenic gain of function (GOF), facilitating cancer progression. Yet, p53 may acquire altered functionality even without being mutated; in particular, experiments with cultured cells revealed that wtp53 can be rewired to adopt mut-like features in response to growth factors or cancer-mimicking genetic manipulations. To assess whether such rewiring also occurs in human tumors, we interrogated gene expression profiles and pathway deregulation patterns in the METABRIC breast cancer (BC) dataset as a function of TP53 gene mutation status. Harnessing the power of machine learning, we optimized a gene expression classifier for ER+Her2- patients that distinguishes tumors carrying TP53 mutations from those retaining wt TP53. Interestingly, a small subset of wt TP53 tumors displayed gene expression and pathway deregulation patterns markedly similar to those of TP53-mutated tumors. Moreover, similar to TP53-mutated tumors, these 'pseudomutant' cases displayed a signature for enhanced proliferation and had worse prognosis than typical wtp53 tumors. Notably, these tumors revealed upregulation of genes which, in BC cell lines, were reported to be positively regulated by p53 GOF mutants. Thus, such tumors may benefit from mut p53-associated activities without having to accrue TP53 mutations.
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