Towards an understanding of the role of p53 in adrenocortical carcinogenesis
Open accessAbstract
Adrenocortical carcinoma (ACC) is recognized to be a component tumor of the Li Fraumeni Syndrome (LFS), a familial cancer predisposition resulting from germline mutations in the p53 tumor-suppressor. p53 activity is tightly regulated by multiple post-translational mechanisms, disruption of which may lead to tumorigenesis. ACC is present in disproportionately high rates among p53-mutation carriers, suggesting tissue-specific manifestations of p53 deficiency. Additionally, p53-associated ACC demonstrates a strong predominance in infants and children. Several of the p53 alleles associated with pediatric ACC, however, retain significant wild-type activity and demonstrate incomplete penetrance, a finding distinct from other LFS-component tumors. In this review, we discuss the relationship between p53 and adrenocortical carcinogenesis, with specific focus on disease-specific alleles, tumorigenesis in the context of adrenal development and potential therapeutic approaches to p53-associated ACC.
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A bimodal distribution of ACC incidence was observed in a review of case series and in SEER data.
“A bimodal distribution was definitely observed in a concise review of case series reported and in the SEER data (13, 14).”
From Adrenocortical carcinoma (2014) · cites this paper as [14]
Most TP53 mutations affect the DNA binding and tetramerization domains.
“Most TP53 mutations affect the DNA binding and tetramerization domains (14).”
From Adrenocortical carcinoma (2014) · cites this paper as [14]
The p.R337H mutation is a low-penetrance tetramerization domain mutation in Southern Brazil.
“One particular hot spot mutation has been described to date, which is the low-penetrance tetramerization domain p.R337H mutation in Southern Brazil (14, 37–39).”
From Adrenocortical carcinoma (2014) · cites this paper as [14]
High-grade ACCs are enriched for mutations of TP53 and/or CTNNB1, and these mutations tend to be mutually exclusive.
“High-grade ACCs are enriched for mutations of TP53 (14, 140–142) and/or CTNNB1 (143–149), and these mutations tend to be mutually exclusive (reviewed in Ref. 150).”
From Adrenocortical carcinoma (2014) · cites this paper as [14]
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- Authors
- Wasserman, J. D., Zambetti, G. P., & Malkin, D.
- Affiliations
- University of Toronto (CA)
- St. Jude Children's Research Hospital (US)
- Corresponding author
- Wasserman, Jonathan D.
- Venue
- Molecular and Cellular Endocrinology
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 351
- Issue
- 1
- Pages
- 101-110
- ISSN
- 0303-7207 (ISSN-L)
- PMC
- PMC3288384
- OpenAlex
- W2063635264
- Cited by
- 84
- References
- 132
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 8 · 2021: 8 · 2020: 10 · 2019: 5 · 2018: 5 · 2017: 5 · 2016: 6 · 2015: 13 · 2014: 4 · 2013: 4 · 2012: 4
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes of Health Research (MOP-97834)
- National Cancer Institute (R01CA063230, CA21765, P30CA021765)
- National Institute of General Medical Sciences (R01GM083159, GM-083159)
- Topics
- Health Sciences › Medicine › Surgery › Adrenal and Paraganglionic Tumors
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- p53, adrenocortical carcinoma, Li-Fraumeni syndrome, p53 tumor suppressor, germline mutations, pediatric adrenocortical carcinoma, incomplete penetrance, adrenal development, carcinogenesis, p53-targeted therapy
- MeSH terms
- Adolescent, Adrenal Cortex Neoplasms, Alleles, Animals, Cell Transformation, Neoplastic, Child, Child, Preschool, Humans, Infant, Organ Specificity, Tumor Suppressor Protein p53, Li-Fraumeni Syndrome, Adrenocortical Carcinoma, Penetrance
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