Abstract |
Therapeutics that disrupt the p53-MDM2 interaction show promise for cancer treatment but surprisingly have different biological outcomes. A study by Enge et al. in this issue of Cancer Cell shows that the ability of MDM2 to target hnRNP K for degradation contributes to the decision to induce apoptosis rather than cell-cycle arrest.
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Authors | Christine M Eischen, Guillermina Lozano |
Journal | Cancer cell
(Cancer Cell)
Vol. 15
Issue 3
Pg. 161-2
(Mar 03 2009)
ISSN: 1878-3686 [Electronic] United States |
PMID | 19249672
(Publication Type: Journal Article, Review, Comment)
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Chemical References |
- Antineoplastic Agents
- Tumor Suppressor Protein p53
- Proto-Oncogene Proteins c-mdm2
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Topics |
- Animals
- Antineoplastic Agents
(pharmacology)
- Apoptosis
(physiology)
- Cell Cycle
(drug effects)
- Gene Expression Regulation
- Humans
- Neoplasms
(drug therapy, metabolism)
- Proto-Oncogene Proteins c-mdm2
(metabolism)
- Tumor Suppressor Protein p53
(metabolism)
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