Targeting Synthetic Lethal Interactions between Myc and the eIF4F Complex Impedes Tumorigenesis
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Summary
Inhibition of eIF4F is synthetic lethal with elevated Myc in pre-malignant preB/B cells resulting in reduced numbers of cycling preB/B cells and delayed tumor onset and eIF4F suppression affected a subset of normal regenerating cells but this was well tolerated and rapidly and completely reversible.
- Type
- article
- Published
- 2012-03-01
- Cited by
- 90
- References
- 46
- Access
- Open access
- OpenAlex
- https://openalex.org/W1966826063
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:26947104
Keywords
Carcinogenesis, PI3K/AKT/mTOR pathway, Biology, Cancer research, RNA interference
References
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- Evasion of the p53 tumour surveillance network by tumour-derived MYC mutants
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- MYC as a regulator of ribosome biogenesis and protein synthesis
- Oncogene cooperation in tumor maintenance and tumor recurrence in mouse mammary tumors induced by Myc and mutant Kras
Cited by
- Hippuristanol - A potent steroid inhibitor of eukaryotic initiation factor 4A
- The spliceosome is a therapeutic vulnerability in MYC-driven cancer
- Pleiotropic antitumor effects of the pan‐HDAC inhibitor ITF2357 against c‐Myc‐overexpressing human B‐cell non‐Hodgkin lymphomas
- Tumor progression and metastasis: role of translational deregulation.
- Linking tumor mutations to drug responses via a quantitative chemical-genetic interaction map
- TARGETING THE eIF4F TRANSLATION INITIATION COMPLEX: A CRITICAL NEXUS FOR CANCER DEVELOPMENT
- Targeting the translation machinery in cancer
- Taming of the beast: Shaping Myc-dependent amplification
- Throwing a monkey wrench in the motor: targeting DExH/D box proteins with small molecule inhibitors.
- CDK9-mediated transcription elongation is required for MYC addiction in hepatocellular carcinoma
- Identification of a novel E-box binding PI polyamide inhibiting MYC-driven cell-proliferation
- Modifying chemotherapy response by targeted inhibition of eukaryotic initiation factor 4A
- Hyperactivation of mTORC1 and mTORC2 by multiple oncogenic events causes addiction to eIF4E-dependent mRNA translation in T-cell leukemia
- Flavaglines target primitive leukemia cells and enhance anti-leukemia drug activity
- Cell Intrinsic and Extrinsic Activators of the Unfolded Protein Response in Cancer: Mechanisms and Targets for Therapy
- Stable RNA interference rules for silencing
- Synthetic lethal screens as a means to understand and treat MYC-driven cancers
- Suppression of eukaryotic initiation factor 4E prevents chemotherapy-induced alopecia
- Myc and mTOR converge on a common node in protein synthesis control that confers synthetic lethality in Myc-driven cancers
- A novel Bcr-Abl–mTOR–eIF4A axis regulates IRES-mediated translation of LEF-1
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