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  The structural impact of cancer-associated missense mutations in oncogenes and tumor suppressors

Stehr, H., Jang, S. H., Duarte, J. M., Wierling, C., Lehrach, H., Lappe, M., et al. (2011). The structural impact of cancer-associated missense mutations in oncogenes and tumor suppressors. Molecular Cancer, 10, 54. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21575214 http://www.molecular-cancer.com/content/pdf/1476-4598-10-54.pdf.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-7902-2 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-7903-F
Genre: Journal Article

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 Creators:
Stehr, H.1, Author              
Jang, S. H., Author
Duarte, J. M.1, Author              
Wierling, C.2, Author              
Lehrach, H.3, Author              
Lappe, M.1, Author              
Lange, B. M., Author
Affiliations:
1Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433554              
2Systems Biology (Christoph Wierling), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479656              
3Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433550              

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Free keywords: Databases, Genetic; Humans; Models, Genetic; Models, Molecular; Molecular Sequence Annotation; Molecular Structure; Mutation, Missense/*genetics; Neoplasms/*genetics/*pathology; Oncogene Proteins/*chemistry/*genetics; Polymorphism, Single Nucleotide/genetics; Protein Stability; Tumor Suppressor Proteins/*chemistry/*genetics
 Abstract: BACKGROUND: Current large-scale cancer sequencing projects have identified large numbers of somatic mutations covering an increasing number of different cancer tissues and patients. However, the characterization of these mutations at the structural and functional level remains a challenge. RESULTS: We present results from an analysis of the structural impact of frequent missense cancer mutations using an automated method. We find that inactivation of tumor suppressors in cancer correlates frequently with destabilizing mutations preferably in the core of the protein, while enhanced activity of oncogenes is often linked to specific mutations at functional sites. Furthermore, our results show that this alteration of oncogenic activity is often associated with mutations at ATP or GTP binding sites. CONCLUSIONS: With our findings we can confirm and statistically validate the hypotheses for the gain-of-function and loss-of-function mechanisms of oncogenes and tumor suppressors, respectively. We show that the distinct mutational patterns can potentially be used to pre-classify newly identified cancer-associated genes with yet unknown function.

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 Dates: 2011
 Publication Status: Published in print
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Title: Molecular Cancer
Source Genre: Journal
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Pages: - Volume / Issue: 10 Sequence Number: - Start / End Page: 54 Identifier: ISSN: 1476-4598 (Electronic) 1476-4598 (Linking)