SelTarbase, a database of human mononucleotide-microsatellite mutations and their potential impact to tumorigenesis and immunology. Woerner, S., M., Yuan, Y., P., Benner, A., Korff, S., von Knebel Doeberitz, M., & Bork, P. Nucleic Acids Res, 38(Database issue):D682-9. Website abstract bibtex About 15% of human colorectal cancers and, at varying degrees, other tumor entities as well as nearly all tumors related to Lynch syndrome are hallmarked by microsatellite instability (MSI) as a result of a defective mismatch repair system. The functional impact of resulting mutations depends on their genomic localization. Alterations within coding mononucleotide repeat tracts (MNRs) can lead to protein truncation and formation of neopeptides, whereas alterations within untranslated MNRs can alter transcription level or transcript stability. These mutations may provide selective advantage or disadvantage to affected cells. They may further concern the biology of microsatellite unstable cells, e.g. by generating immunogenic peptides induced by frameshifts mutations. The Selective Targets database (http://www.seltarbase.org) is a curated database of a growing number of public MNR mutation data in microsatellite unstable human tumors. Regression calculations for various MSI-H tumor entities indicating statistically deviant mutation frequencies predict TGFBR2, BAX, ACVR2A and others that are shown or highly suspected to be involved in MSI tumorigenesis. Many useful tools for further analyzing genomic DNA, derived wild-type and mutated cDNAs and peptides are integrated. A comprehensive database of all human coding, untranslated, non-coding RNA- and intronic MNRs (MNR_ensembl) is also included. Herewith, SelTarbase presents as a plenty instrument for MSI-carcinogenesis-related research, diagnostics and therapy.
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title = {SelTarbase, a database of human mononucleotide-microsatellite mutations and their potential impact to tumorigenesis and immunology},
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pages = {D682-9},
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notes = {<m:note>Woerner, Stefan M<m:linebreak/>Yuan, Yan P<m:linebreak/>Benner, Axel<m:linebreak/>Korff, Sebastian<m:linebreak/>von Knebel Doeberitz, Magnus<m:linebreak/>Bork, Peer<m:linebreak/>Research Support, Non-U.S. Gov't<m:linebreak/>England<m:linebreak/>Nucleic acids research<m:linebreak/>gkp839<m:linebreak/>Nucleic Acids Res. 2010 Jan;38(Database issue):D682-9. Epub 2009 Oct 9.</m:note>},
abstract = {About 15% of human colorectal cancers and, at varying degrees, other tumor entities as well as nearly all tumors related to Lynch syndrome are hallmarked by microsatellite instability (MSI) as a result of a defective mismatch repair system. The functional impact of resulting mutations depends on their genomic localization. Alterations within coding mononucleotide repeat tracts (MNRs) can lead to protein truncation and formation of neopeptides, whereas alterations within untranslated MNRs can alter transcription level or transcript stability. These mutations may provide selective advantage or disadvantage to affected cells. They may further concern the biology of microsatellite unstable cells, e.g. by generating immunogenic peptides induced by frameshifts mutations. The Selective Targets database (http://www.seltarbase.org) is a curated database of a growing number of public MNR mutation data in microsatellite unstable human tumors. Regression calculations for various MSI-H tumor entities indicating statistically deviant mutation frequencies predict TGFBR2, BAX, ACVR2A and others that are shown or highly suspected to be involved in MSI tumorigenesis. Many useful tools for further analyzing genomic DNA, derived wild-type and mutated cDNAs and peptides are integrated. A comprehensive database of all human coding, untranslated, non-coding RNA- and intronic MNRs (MNR_ensembl) is also included. Herewith, SelTarbase presents as a plenty instrument for MSI-carcinogenesis-related research, diagnostics and therapy.},
bibtype = {article},
author = {Woerner, S M and Yuan, Y P and Benner, A and Korff, S and von Knebel Doeberitz, M and Bork, P},
journal = {Nucleic Acids Res},
number = {Database issue}
}
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