ArticleOncogene2010
Deletion of p53 in human mammary epithelial cells causes chromosomal instability and altered therapeutic response.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
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- Expanding the bat toolbox: Carollia perspicillata bat cell lines and reagents enable the characterization of viral susceptibility and innate immune responses.PLoS biology · 2025Article
- The cytidine deaminase APOBEC3A regulates nucleolar function to promote cell growth and ribosome biogenesis.PLoS biology · 2024Article
- Mixed responses to targeted therapy driven by chromosomal instability through p53 dysfunction and genome doubling.Nature communications · 2024Article
- Evolutionary history of adenomas to colorectal cancer in FAP families.Frontiers in genetics · 2024Article
- Article
- HOXA5-Mediated Stabilization of IκBα Inhibits the NF-κB Pathway and Suppresses Malignant Transformation of Breast Epithelial Cells.Cancer research · 2022Article
- Origin and Therapies of Osteosarcoma.Cancers · 2022Review
- Evaluation of twoMolecular therapy. Methods & clinical development · 2021Article
- Epithelial p53 Status Modifies Stromal-Epithelial Interactions During Basal-Like Breast Carcinogenesis.Journal of mammary gland biology and neoplasia · 2021Article
- CBFB cooperates with p53 to maintain TAp73 expression and suppress breast cancer.PLoS genetics · 2021Article
- The Nek2 centrosome-mitotic kinase contributes to the mesenchymal state, cell invasion, and migration of triple-negative breast cancer cells.Scientific reports · 2021Article
- AKT1 E17K Inhibits Cancer Cell Migration by Abrogating β-Catenin Signaling.Molecular cancer research : MCR · 2021Article
- Myricetin Apoptotic Effects on T47D Breast Cancer Cells is a P53-Independent Approach.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Oncogenic TRIM37 Links Chemoresistance and Metastatic Fate in Triple-Negative Breast Cancer.Cancer research · 2020Article
- Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome.Nature communications · 2020Article
- Clinical Implications of Chromosomal Instability (CIN) and Kinetochore Abnormalities in Breast Cancers.Molecular diagnosis & therapy · 2019Review
- Spontaneously slow-cycling subpopulations of human cells originate from activation of stress-response pathways.PLoS biology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The TP53 tumor suppressor gene is the most commonly mutated gene in human cancers. To evaluate the biological and clinical relevance of p53 loss, human somatic cell gene targeting was used to delete the TP53 gene in the non-tumorigenic epithelial cell line, MCF-10A. In all four p53-/- clones generated, cells acquired the capability for epidermal growth factor-independent growth and were defective in appropriate downstream signaling and cell cycle checkpoints in response to DNA damage. Interestingly, p53 loss induced chromosomal instability leading to features of transformation and the selection of clones with varying phenotypes. For example, p53-deficient clones were heterogeneous in their capacity for anchorage-independent growth and invasion. In addition, and of clinical importance, the cohort of p53-null clones showed sensitivity to chemotherapeutic interventions that varied depending not only on the type of chemotherapeutic agent, but also on the treatment schedule. In conclusion, deletion of the TP53 gene from MCF-10A cells eliminated p53 functions, as well as produced p53-/- clones with varying phenotypes possibly stemming from the distinct chromosomal changes observed. Such a model system will be useful to further understand the cancer-specific phenotypic changes that accompany p53 loss, as well as help to provide future treatment strategies for human malignancies that harbor aberrant p53.
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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.