The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
MYC and Prostate Cancer
Open accessAbstract
Prostate cancer, the majority of which is adenocarcinoma, is the most common epithelial cancer affecting a majority of elderly men in Western nations. Its manifestation, however, varies from clinically asymptomatic insidious neoplasms that progress slowly and do not threaten life to one that is highly aggressive with a propensity for metastatic spread and lethality if not treated in time. A number of somatic genetic and epigenetic alterations occur in prostate cancer cells. Some of these changes, such as loss of the tumor suppressors PTEN and p53, are linked to disease progression. Others, such as ETS gene fusions, appear to be linked more with early phases of the disease, such as invasion. Alterations in chromosome 8q24 in the region of MYC have also been linked to disease aggressiveness for many years. However, a number of recent studies in human tissues have indicated that MYC appears to be activated at the earliest phases of prostate cancer (e.g., in tumor-initiating cells) in prostatic intraepithelial neoplasia, a key precursor lesion to invasive prostatic adenocarcinoma. The initiation and early progression of prostate cancer can be recapitulated in genetically engineered mouse models, permitting a richer understanding of the cause and effects of loss of tumor suppressors and activation of MYC. The combination of studies using human tissues and mouse models paints an emerging molecular picture of prostate cancer development and early progression. This picture reveals that MYC contributes to disease initiation and progression by stimulating an embryonic stem cell-like signature characterized by an enrichment of genes involved in ribosome biogenesis and by repressing differentiation. These insights pave the way to potential novel therapeutic concepts based on MYC biology.
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Cites
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Cited by
The PI3K-AKT-mTOR Pathway and Prostate Cancer: At the Crossroads of AR, MAPK, and WNT Signaling
Shorning, B. Y., Dass, M. S., Smalley, M. J., & Pearson, H. B. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21124507 · Cited by 616
Hörnberg, E., Ylitalo, E. B., Crnalic, S., Antti, H., Stattin, P., Widmark, A., Bergh, A., & Wikström, P. (2011) · PLoS ONE · doi:10.1371/journal.pone.0019059 · Cited by 498
The inflammatory microenvironment and microbiome in prostate cancer development
Sfanos, K. S., Yegnasubramanian, S., Nelson, W. G., & De Marzo, A. M. (2018) · Nature Reviews Urology · doi:10.1038/nrurol.2017.167 · Cited by 469
Self-citationCarabet, L. A., Rennie, P. S., & Cherkasov, A. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms20010120 · Cited by 172
USP22 regulates oncogenic signaling pathways to drive lethal cancer progression
Schrecengost, R. S., Dean, J. L., Goodwin, J. F., Schiewer, M. J., Urban, M. W., Stanek, T. J., Sussman, R. T., Hicks, J. L., Birbe, R. C., Draganova-Tacheva, R. A., et al. (2014) · Cancer Research · doi:10.1158/0008-5472.can-13-1954 · Cited by 126
Metadata
- Authors
- Koh, C. M., Bieberich, C. J., Dang, C. V., Nelson, W. G., Yegnasubramanian, S., & De Marzo, A. M.
- Venue
- Genes & Cancer
- Publisher
- SAGE Publications
- Published
- 2010-06-01
- Volume
- 1
- Issue
- 6
- Pages
- 617-628
- ISSN
- 1947-6019 (ISSN-L)
- 1947-6027
- OpenAlex
- W2147200519
- Cited by
- 296
- References
- 12
- FWCI
- 10.33
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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