Transcriptional Addiction in Cancer
By James E. Bradner, Denes Hnisz, Richard A. Young. Cell, 2017
1,026 citations recorded by the source corpus.
Summary Cancer arises from genetic alterations that invariably lead to dysregulated transcriptional programs. These dysregulated programs can cause cancer cells to become highly dependent on certain regulators of gene expression. Here we discuss how transcriptional control is disrupted by genetic alterations in cancer cells, why transcriptional dependencies can develop as a consequence of dysregulated programs, and how these dependencies provide opportunities for novel therapeutic interventions in cancer.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/bdd0c494862161587dc25e789088faa0c755f5ca
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In Molecular Biology
- Richard A. Young
- Tong Ihn Lee
- B. Abraham
- N. Hannett
- Charles H. Li
- M. Wiznerowicz
- Patrycja Czerwińska
- John N. Weinstein
Citations in the corpus
- Transcription factors activate genes through the phase separation capacity of their activation domains (2018, background): “Many malignancies bear fusion-protein translocations involving portions of TFs (Bradner et al., 2017; Kim et al., 2017; Latysheva et al., 2016).”
- Machine Learning Identifies Stemness Features Associated with Oncogenic Dedifferentiation (2018, background): “Transcriptional and epigenetic dysregulation of cancer cells frequently leads to oncogenic de-differentiation and acquisition of stemness features by altering core signaling pathways that regulate the phenotypes of normal stem cells (Bradner et al., 2017; Young, 2011).”