Does AL amyloidosis have a unique genomic profile? Gene
expression profiling meta-analysis and literature overview

J 2016

Does AL amyloidosis have a unique genomic profile? Gene expression profiling meta-analysis and literature overview

KRYUKOV, Fedor; Elena Vladimirovna KRYUKOVA; Lucie BROŽOVÁ; Zuzana KUFOVA; Jana FILIPOVA et al.

Základní údaje

Originální název

Does AL amyloidosis have a unique genomic profile? Gene expression profiling meta-analysis and literature overview

Autoři

KRYUKOV, Fedor; Elena Vladimirovna KRYUKOVA; Lucie BROŽOVÁ; Zuzana KUFOVA; Jana FILIPOVA; Katerina GROWKOVA; Tereza SEVCIKOVA; Jiří JARKOVSKÝ a Roman HÁJEK

Vydání

Gene, Amsterdam, Elsevier Science, 2016, 0378-1119

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

Genetika a molekulární biologie

Stát vydavatele

Nizozemské království

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 2.415

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14110/16:00093200

Organizační jednotka

Lékařská fakulta

Klíčová slova anglicky

AL amyloidosis; Monoclonal gammapaties; Gene expression profile; Ribosome; Meta-analysis

Štítky

EL OK

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 26. 1. 2017 14:09, Soňa Böhmová

Anotace

V originále

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. (C) 2016 Elsevier B.V. All rights reserved.

Citovat

KRYUKOV, Fedor; Elena Vladimirovna KRYUKOVA; Lucie BROŽOVÁ; Zuzana KUFOVA; Jana FILIPOVA; Katerina GROWKOVA; Tereza SEVCIKOVA; Jiří JARKOVSKÝ a Roman HÁJEK. Does AL amyloidosis have a unique genomic profile? Gene expression profiling meta-analysis and literature overview. Gene. Amsterdam: Elsevier Science, 2016, roč. 591, č. 2, s. 490-498. ISSN 0378-1119. Dostupné z: https://doi.org/10.1016/j.gene.2016.06.017.

@article{1369821,
   author = {Kryukov, Fedor and Kryukova, Elena Vladimirovna and Brožová, Lucie and Kufova, Zuzana and Filipova, Jana and Growkova, Katerina and Sevcikova, Tereza and Jarkovský, Jiří and Hájek, Roman},
   article_location = {Amsterdam},
   article_number = {2},
   doi = {https://doi.org/10.1016/j.gene.2016.06.017},
   keywords = {AL amyloidosis; Monoclonal gammapaties; Gene expression profile; Ribosome; Meta-analysis},
   language = {eng},
   issn = {0378-1119},
   journal = {Gene},
   title = {Does AL amyloidosis have a unique genomic profile? Gene expression profiling meta-analysis and literature overview},
   volume = {591},
   year = {2016}
}

TY  - JOUR
ID  - 1369821
AU  - Kryukov, Fedor - Kryukova, Elena Vladimirovna - Brožová, Lucie - Kufova, Zuzana - Filipova, Jana - Growkova, Katerina - Sevcikova, Tereza - Jarkovský, Jiří - Hájek, Roman
PY  - 2016
TI  - Does AL amyloidosis have a unique genomic profile? Gene expression profiling meta-analysis and literature overview
JF  - Gene
VL  - 591
IS  - 2
SP  - 490-498
EP  - 490-498
PB  - Elsevier Science
SN  - 03781119
KW  - AL amyloidosis
KW  - Monoclonal gammapaties
KW  - Gene expression profile
KW  - Ribosome
KW  - Meta-analysis
N2  - 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. (C) 2016 Elsevier B.V. All rights reserved.
ER  -

KRYUKOV, Fedor; Elena Vladimirovna KRYUKOVA; Lucie BROŽOVÁ; Zuzana KUFOVA; Jana FILIPOVA; Katerina GROWKOVA; Tereza SEVCIKOVA; Jiří JARKOVSKÝ a Roman HÁJEK. Does AL amyloidosis have a unique genomic profile? Gene expression profiling meta-analysis and literature overview. \textit{Gene}. Amsterdam: Elsevier Science, 2016, roč.~591, č.~2, s.~490-498. ISSN~0378-1119. Dostupné z: https://doi.org/10.1016/j.gene.2016.06.017.

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