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MYC on the Path to Cancer
Open accessAbstract
The MYC oncogene contributes to the genesis of many human cancers. Recent insights into its expression and function have led to therapeutic opportunities. MYC's activation by bromodomain proteins could be inhibited by drug-like molecules, resulting in tumor inhibition in vivo. Tumor growth can also be curbed by pharmacologically uncoupling bioenergetic pathways involving glucose or glutamine metabolism from Myc-induced cellular biomass accumulation. Other approaches to halt Myc on the path to cancer involve targeting Myc-Max dimerization or Myc-induced microRNA expression. Here the richness of our understanding of MYC is reviewed, highlighting new biological insights and opportunities for cancer therapies.
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“The Myc oncogene, including its three subtypes C-Myc, N-Myc, and L-Myc, is believed to act as a transcriptional “amplifier” that can trigger a variety of oncogenic transcriptional programs in different types of cancer.410,411”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [410]
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“Overexpression or hyperactivation of Myc is one of the most common occurrences in cancer, making it a key factor in oncogenesis.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [410]
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Self-citation
Metadata
- Authors
- Dang, C. V.
- Affiliations
- Abramson Cancer Center (US)
- Corresponding author
- Dang, Chi V.
- ORCID
- Dang, Chi V.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 149
- Issue
- 1
- Pages
- 22-35
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3345192
- OpenAlex
- W2021536610
- Cited by
- 3,390
- References
- 232
- Citations by year
- 2026: 218 · 2025: 267 · 2024: 300 · 2023: 299 · 2022: 280 · 2021: 332 · 2020: 283 · 2019: 250 · 2018: 209 · 2017: 215 · 2016: 215 · 2015: 166 · 2014: 179 · 2013: 144 · 2012: 33
- FWCI
- 17.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA057341, R01CA051497, P30CA016520)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- MYC oncogene, tumor initiation, bromodomain proteins, MYC inhibitors, tumor growth inhibition, bioenergetics, glucose metabolism, glutamine metabolism, biomass accumulation, microRNA expression, cancer therapy
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Humans, Neoplasms, Gene Expression Regulation, Neoplastic, Genes, myc, Proto-Oncogene Proteins c-myc, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
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