MDM2 Gene Amplification Is Correlated to Tumor Progression but not to the Presence of SNP309 or TP53 Mutational Status in Primary Colorectal Cancers
Abstract
Mdm2 is the main regulator of p53 and is amplified in ∼7% of all human cancers. MDM2 gene amplification as well as expression has been correlated to an increased tumorigenic potential. We have analyzed the prevalence of MDM2 gene amplifications and SNP309 in 284 colorectal tumors using a relatively new highly sensitive PCR/ligase detection reaction method in relation to TP53 mutational status and genomic instability. We found MDM2 to be amplified in 9% of the 284 colorectal cancers analyzed and a significantly higher proportion of tumors with high MDM2 gene amplification retained a wild-type p53 gene (P = 0.058). MDM2 gene amplification was significantly correlated to advanced tumor stage. Several small-molecule MDM2 antagonists have already been identified that either physically inhibit the p53-MDM2 binding or the E3 ligase function of MDM2. Our results suggest that MDM2 is a promising target for this type of cancer therapy in a substantial subgroup of colorectal cancers. (Mol Cancer Res 2008;6(2):205–11)
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MDM2 and MDMX are deregulated in many human cancers and act oncogenically mainly by inhibiting p53.
“The MDM2 and MDMX (also known as HDMX and MDM4) proteins are deregulated in many human cancers and exert their oncogenic activity predominantly by inhibiting the p53 tumour suppressor.”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [4]
Amplification of MDM genes or altered expression of MDM proteins is a feature of many tumours.
“Amplification of MDM genes or altered expression of MDM proteins is a feature of many tumours3–10 (Table 1).”
From MDM2, MDMX and p53 in oncogenesis and cancer therapy (2013) · cites this paper as [4]
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References 40 · Cited by 54
- Authors
- Forslund, A., Zeng, Z., Qin, L.-X., Rosenberg, S., Ndubuisi, M., Pincas, H., Gerald, W., Notterman, D. A., Barany, F., & Paty, P. B.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Cornell University (US)
- 4Department of Microbiology, Weill Medical College of Cornell University, New York, New York;
- Princeton University (US)
- Venue
- Molecular Cancer Research
- Published
- 2008-02-01
- Volume
- 6
- Issue
- 2
- Pages
- 205-211
- ISSN
- 1541-7786 (ISSN-L)
- 1557-3125
- OpenAlex
- W2025439169
- Cited by
- 54
- References
- 40
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 5 · 2016: 6 · 2015: 4 · 2014: 7 · 2013: 2
- FWCI
- 1.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P01CA065930, P01 CA65930)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Keywords
- MDM2 amplification, colorectal cancer, p53, SNP309, TP53 mutation, tumor progression, tumor stage, genomic instability, MDM2 inhibitors, E3 ubiquitin ligase, therapeutic target
- MeSH terms
- Adult, Aged, Aged, 80 and over, DNA Mutational Analysis, Female, Gene Amplification, Genotype, Humans, Male, Middle Aged, Mutation, Reference Standards, Colorectal Neoplasms, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, In Situ Hybridization, Fluorescence, Disease Progression, Polymorphism, Single Nucleotide, Proto-Oncogene Proteins c-mdm2
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