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Updated: May 26, 2026

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes
Published on: May 23, 2025
Finding cancer's weakest link
Nicole M Sodir1, Gerard I Evan
1Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, CA 94143, USA.
Abstract:
The biological programs of vertebrates exhibit a remarkable degree of functional degeneracy, adaptive compensation and robustness, to preserve homeostasis and generate reproducible phenotypic outputs irrespective of variations in signal strength, noise and quality. Cancers are difficult to treat not only because they are so mechanistically diverse but also because they adapt or evolve in response to any pharmacological elective pressure we impose upon them. Hence, an ideal cancer drug target would exert a function both necessary for cancer cell survival and functionally non-redundant, rendering it impossible for tumor cells to compensate for, or evolve independence from, the inhibitory effect of any drug aimed at that target. In this review, we discuss the unique, non-degenerate and highly pleiotropic role played by Myc in coordinating, engaging and maintaining the diverse intracellular and extracellular programs required for cell proliferation in vivo. These properties make Myc a compelling candidate cancer drug target, at least in principle: an assertion recently reinforced by new in vivo genetic data.
Insights
Myc is a crucial protein for cell proliferation that cancer cells cannot compensate for when targeted. This makes Myc an ideal target for novel cancer drug development, offering a promising therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Systems Biology
Background:
- Vertebrate biological systems possess inherent robustness and adaptability to maintain homeostasis.
- Cancer cells are mechanistically diverse and can evolve resistance to therapies.
- Identifying non-redundant targets is crucial for effective cancer drug development.
Purpose of the Study:
- To review the role of Myc in coordinating cellular programs essential for proliferation.
- To evaluate Myc as a potential cancer drug target due to its unique properties.
Main Methods:
- Literature review of Myc's function in cell proliferation.
- Analysis of Myc's role in cancer cell survival and adaptation.
- Discussion of in vivo genetic data supporting Myc as a drug target.
Main Results:
- Myc plays a unique, non-degenerate, and pleiotropic role in coordinating proliferation programs.
- Myc's function is essential for cancer cell survival in vivo.
- Myc's critical role makes it difficult for cancer cells to compensate for its inhibition.
Conclusions:
- Myc's essential and non-redundant functions present it as a compelling cancer drug target.
- Targeting Myc could overcome cancer cell adaptive resistance mechanisms.
- Recent in vivo data reinforce Myc's potential as a therapeutic target in oncology.
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