The DOI matches its Crossref record; 231 of the 232 references it cites were found in a registry or an index.
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]
In the citing paper
“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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Citations
Cites
Takahashi, K., & Yamanaka, S. (2006) · Cell · doi:10.1016/j.cell.2006.07.024 · Cited by 26,673
Identification of c- MYC as a Target of the APC Pathway
He, T.-C., Sparks, A. B., Rago, C., Hermeking, H., Zawel, L., da Costa, L. T., Morin, P. J., Vogelstein, B., & Kinzler, K. W. (1998) · Science · doi:10.1126/science.281.5382.1509 · Cited by 4,566
The landscape of somatic copy-number alteration across human cancers
Beroukhim, R., Mermel, C. H., Porter, D., Wei, G., Raychaudhuri, S., Donovan, J., Barretina, J., Boehm, J. S., Dobson, J., Urashima, M., et al. (2010) · Nature · doi:10.1038/nature08822 · Cited by 4,017
BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc
Delmore, J. E., Issa, G. C., Lemieux, M. E., Rahl, P. B., Shi, J., Jacobs, H. M., Kastritis, E., Gilpatrick, T., Paranal, R. M., Qi, J., et al. (2011) · Cell · doi:10.1016/j.cell.2011.08.017 · Cited by 2,888
Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes
Land, H., Parada, L. F., & Weinberg, R. A. (1983) · Nature · doi:10.1038/304596a0 · Cited by 2,804
c-Myc-regulated microRNAs modulate E2F1 expression
O'Donnell, K. A., Wentzel, E. A., Zeller, K. I., Dang, C. V., & Mendell, J. T. (2005) · Nature · doi:10.1038/nature03677 · Cited by 2,347
Self-citationAmplification of N- myc in Untreated Human Neuroblastomas Correlates with Advanced Disease Stage
Brodeur, G. M., Seeger, R. C., Schwab, M., VARMUS, H. E., & Bishop, J. M. (1984) · Science · doi:10.1126/science.6719137 · Cited by 2,261
Cell-specific regulation of the c-myc gene by lymphocyte mitogens and platelet-derived growth factor
Kelly, K., Cochran, B., Stiles, C. D., & Leder, P. (1983) · Cell · doi:10.1016/0092-8674(83)90092-2 · Cited by 2,227
The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation
Wang, R., Dillon, C. P., Shi, L. Z., Milasta, S., Carter, R., Finkelstein, D., McCormick, L. L., Fitzgerald, P., Chi, H., Munger, J., et al. (2011) · Immunity · doi:10.1016/j.immuni.2011.09.021 · Cited by 2,140 · cited 2×
“Loss of Myc was associated with profoundly diminished expression of genes involved in metabolism and the inability for normal primary T cells to grow and proliferate (Wang et al., 2011a).”
BackgroundGao, P., Tchernyshyov, I., Chang, T.-C., Lee, Y.-S., Kita, K., Ochi, T., Zeller, K. I., De Marzo, A. M., Van Eyk, J. E., Mendell, J. T., et al. (2009) · Nature · doi:10.1038/nature07823 · Cited by 2,124
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Cited by
Sorted by citations
The PI3K Pathway in Human Disease
Fruman, D. A., Chiu, H., Hopkins, B. D., Bagrodia, S., Cantley, L. C., & Abraham, R. T. (2017) · Cell · doi:10.1016/j.cell.2017.07.029 · Cited by 2,749
Regulation and Function of the PD-L1 Checkpoint
Sun, C., Mezzadra, R., & Schumacher, T. N. (2018) · Immunity · doi:10.1016/j.immuni.2018.03.014 · Cited by 2,248
Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways
Wee, P., & Wang, Z. (2017) · Cancers · doi:10.3390/cancers9050052 · Cited by 2,027
The multifaceted roles of fatty acid synthesis in cancer
Röhrig, F., & Schulze, A. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.89 · Cited by 1,651
Transcriptional Amplification in Tumor Cells with Elevated c-Myc
Lin, C. Y., Lovén, J., Rahl, P. B., Paranal, R. M., Burge, C. B., Bradner, J. E., Lee, T. I., & Young, R. A. (2012) · Cell · doi:10.1016/j.cell.2012.08.026 · Cited by 1,543
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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