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Does AL amyloidosis have a unique genomic profile? Gene expression profiling meta-analysis and literature overview
F. Kryukov, E. Kryukova, L. Brozova, Z. Kufova, J. Filipova, K. Growkova, T. Sevcikova, J. Jarkovsky, R. Hajek,
Jazyk angličtina Země Nizozemsko
Typ dokumentu dopisy, metaanalýza, přehledy
Grantová podpora
NV15-29667A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Odkazy
PubMed
27288311
DOI
10.1016/j.gene.2016.06.017
Knihovny.cz E-zdroje
- MeSH
- amyloidóza genetika MeSH
- geny pro lehké řetězce imunoglobulinů * MeSH
- lidé MeSH
- paraproteinemie genetika MeSH
- stanovení celkové genové exprese MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- dopisy MeSH
- metaanalýza MeSH
- přehledy MeSH
Immunoglobulin light chain amyloidosis (ALA) is a plasma cell dyscrasia characterized by deposition of amyloid fibrils in various organs and tissues. The current paper is devoted to clarify if ALA has a unique gene expression profile and to its pathogenetic argumentation. The meta-analysis of ALA patients vs. healthy donors, monoclonal gammopathy of undetermined significance, smoldering and multiple myeloma patients' cohorts have revealed molecular signature of ALA consists of 256 genes representing mostly ribosomal proteins and immunoglobulin regions. This signature appears pathogenetically supported and elucidates for the first time the role of ribosome dysfunction in ALA. In summary of our findings with literature overview, we hypothesize that ALA development is associated not only with changes in genes, coding amyloidogenic protein itself, but with post-transcriptional disbalance as well. Based on our data analysis in ALA, ribosome machinery is impaired and the affected link mainly involves translational initiation, elongation and co-translational protein folding.
Department of Haematooncology Faculty of Medicine University of Ostrava Czech Republic
Department of Haematooncology University Hospital Ostrava Czech Republic
Institute of Biostatistics and Analyses Faculty of Medicine Masaryk University Brno Czech Republic
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- $a Kryukov, Fedor $u Department of Haematooncology, Faculty of Medicine, University of Ostrava, Czech Republic; Department of Haematooncology, University Hospital Ostrava, Czech Republic. Electronic address: f.kryukov@gmail.com.
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- $a Immunoglobulin light chain amyloidosis (ALA) is a plasma cell dyscrasia characterized by deposition of amyloid fibrils in various organs and tissues. The current paper is devoted to clarify if ALA has a unique gene expression profile and to its pathogenetic argumentation. The meta-analysis of ALA patients vs. healthy donors, monoclonal gammopathy of undetermined significance, smoldering and multiple myeloma patients' cohorts have revealed molecular signature of ALA consists of 256 genes representing mostly ribosomal proteins and immunoglobulin regions. This signature appears pathogenetically supported and elucidates for the first time the role of ribosome dysfunction in ALA. In summary of our findings with literature overview, we hypothesize that ALA development is associated not only with changes in genes, coding amyloidogenic protein itself, but with post-transcriptional disbalance as well. Based on our data analysis in ALA, ribosome machinery is impaired and the affected link mainly involves translational initiation, elongation and co-translational protein folding.
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