The DOI matches its Crossref record; 116 of the 116 references it cites were found in a registry or an index.
Targeting Mdm2 and Mdmx in Cancer Therapy: Better Living through Medicinal Chemistry?
Open accessAbstract
Genomic and proteomic profiling of human tumor samples and tumor-derived cell lines are essential for the realization of personalized therapy in oncology. Identification of the changes required for tumor initiation or maintenance will likely provide new targets for small-molecule and biological therapeutics. For example, inactivation of the p53 tumor suppressor pathway occurs in most human cancers. Although this can be due to frank p53 gene mutation, almost half of all cancers retain the wild-type p53 allele, indicating that the pathway is disabled by other means. Alternate mechanisms include deletion or epigenetic inactivation of the p53-positive regulator arf, methylation of the p53 promoter, or elevated expression of the p53 regulators Mdm2 and Mdmx. This review discusses current models of p53 regulation by Mdm2 and Mdmx and presents the rationale for design of future Mdmx-specific therapeutics based on our knowledge of its structure and biological functions.
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“Although the Mdmx–p53 interaction is sufficiently different to limit the efficacy of Mdm2 antagonists [104], structural data will inform medicinal chemistry efforts to develop Mdmx-specific drugs.”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [104]
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Ferroptosis as a p53-mediated activity during tumour suppression
Jiang, L., Kon, N., Li, T., Wang, S.-J., Su, T., Hibshoosh, H., Baer, R., & Gu, W. (2015) · Nature · doi:10.1038/nature14344 · Cited by 3,398
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MDM2, MDMX and p53 in oncogenesis and cancer therapy
Wade, M., Li, Y.-C., & Wahl, G. M. (2013) · Nature Reviews Cancer · doi:10.1038/nrc3430 · Cited by 1,279
Self-citationAwakening guardian angels: drugging the p53 pathway
Brown, C. J., Lain, S., Verma, C. S., Fersht, A. R., & Lane, D. P. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2763 · Cited by 881
The p53 orchestra: Mdm2 and Mdmx set the tone
Wade, M., Wang, Y. V., & Wahl, G. M. (2010) · Trends in Cell Biology · doi:10.1016/j.tcb.2010.01.009 · Cited by 450
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Metadata
- Authors
- Wade, M., & Wahl, G. M.
- Affiliations
- Salk Institute for Biological Studies (US)
- Venue
- Molecular Cancer Research
- Published
- 2009-01-01
- Volume
- 7
- Issue
- 1
- Pages
- 1-11
- ISSN
- 1541-7786 (ISSN-L)
- 1557-3125
- PMC
- PMC2629357
- OpenAlex
- W2161785833
- Cited by
- 170
- References
- 116
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 5 · 2022: 6 · 2021: 5 · 2020: 10 · 2019: 2 · 2018: 2 · 2017: 7 · 2016: 9 · 2015: 15 · 2014: 14 · 2013: 21 · 2012: 18
- FWCI
- 2.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA061449, R01‑CA61449)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- MDM2, MDMX, p53 regulation, cancer therapy, small molecule drugs, p53 inactivation, ARF, epigenetic silencing, precision oncology, structure-based drug design
- MeSH terms
- Animals, Humans, Mice, Transgenic, Mutation, Neoplasms, Nuclear Proteins, Proto-Oncogene Proteins, Transcription, Genetic, Transcriptional Activation, Gene Expression Regulation, Neoplastic, Genes, p53, Tumor Suppressor Protein p53, Cell Cycle Proteins, Dimerization, Mice, Proto-Oncogene Proteins c-mdm2
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