ArticleCell cycle (Georgetown, Tex.)2014
Reinforcing targeted therapeutics with phenotypic stability factors.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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
13 citing papers in PubMed, 23 citations in OpenAlex.
- P4HA2: A link between tumor-intrinsic hypoxia, partial EMT and collective migration.Advances in cancer biology - metastasis · 2022Article
- Transcriptional and post-transcriptional control of epithelial-mesenchymal plasticity: why so many regulators?Cellular and molecular life sciences : CMLS · 2022Review
- Breast Cancer Resistance to Cyclin-Dependent Kinases 4/6 Inhibitors: Intricacy of the Molecular Mechanisms.Frontiers in oncology · 2021Review
- Molecular mechanisms of resistance to CDK4/6 inhibitors in breast cancer: A review.International journal of cancer · 2019Review
- Phenotypic Plasticity and Cell Fate Decisions in Cancer: Insights from Dynamical Systems Theory.Cancers · 2017Review
- Deciphering Epithelial-Mesenchymal Transition Regulatory Networks in Cancer through Computational Approaches.Frontiers in oncology · 2017Review
- Distinguishing mechanisms underlying EMT tristability.Cancer convergence · 2017Article
- 3,6-dihydroxyflavone suppresses the epithelial-mesenchymal transition in breast cancer cells by inhibiting the Notch signaling pathway.Scientific reports · 2016Article
- Stability of the hybrid epithelial/mesenchymal phenotype.Oncotarget · 2016Article
- Notch-Jagged signalling can give rise to clusters of cells exhibiting a hybrid epithelial/mesenchymal phenotype.Journal of the Royal Society, Interface · 2016Article
- Expression of Ovol2 is related to epithelial characteristics and shows a favorable clinical outcome in hepatocellular carcinoma.OncoTargets and therapy · 2016Article
- Article
- Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis.Frontiers in oncology · 2015Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulated cell cycle progression can often be traced to intrinsic defects in specific regulatory proteins in cancer cells. Knowledge of these primary defects has led to targeted approaches that exploit the defects and spare normal cells. However, the success of such targeted approaches is still hit-or-miss. Genetic and epigenetic variability inherent in most tumors often results in phenotypic heterogeneity that, in turn, results in de novo or acquired resistance to therapeutic agents. The ability of cells to compensate and adapt to the inhibition of a specific cell cycle mediator is not remarkable. What is novel and of great potential importance is that the ability of cells to exhibit such adaptability varies markedly. "Phenotypic stability factors" that restrict the ability of cells to undergo epithelial-mesenchymal transitions (EMT) may dictate the success or failure of targeted therapies by interfering with compensatory changes such as deregulation of CDK2 activity. Identification of existing and new agents that induce and maintain phenotypic stability factors will inform and enable synergistic approaches to the eradication of even the most aggressive tumors.
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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.