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Gene expression profiling of acute graft-vs-host disease after hematopoietic stem cell transplantation

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VERNER Jan KABÁTHOVÁ Jitka TOMANCOVÁ Alexandra PAVLOVÁ Šárka TICHÝ Boris MRÁZ Marek BRYCHTOVÁ Yvona KREJČÍ Marta ZDRÁHAL Zbyněk TRBUŠEK Martin VOLEJNÍKOVÁ Jana SEDLÁČEK Petr DOUBEK Michael MAYER Jiří POSPÍŠILOVÁ Šárka

Rok publikování 2012
Druh Článek v odborném periodiku
Časopis / Zdroj Experimental Hematology
Fakulta / Pracoviště MU

Středoevropský technologický institut

Citace
www http://www.ncbi.nlm.nih.gov/pubmed/22771791
Doi http://dx.doi.org/10.1016/j.exphem.2012.06.011
Obor Onkologie a hematologie
Klíčová slova MONONUCLEAR-CELLS; ACUTE GVHD; BLOOD; MICROARRAYS; BIOMARKERS; THERAPY
Popis Acute graft-vs-host disease (aGVHD) is a frequent, life-threatening complication after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Despite that, there are no reliable molecular markers reflecting the onset or clinical course of aGVHD. We performed a pilot study on gene expression profiling in peripheral blood mononuclear cells taken from 15 patients with hematological malignancies who underwent allo-HSCT and developed aGVHD. Based on survival rates after aGVHD, patients were divided into two groups-favorable (all patients alive; median follow-up 40 months) vs unfavorable group (all patients died; median survival 2 months). Two-hundred and eighty genes differentially expressed between these two groups were identified; among them, genes responsible for cytokine signaling, inflammatory response, and regulation of cell cycle were over-represented; interleukin-8, GOS2, ANXA3, and NR4A2 were upregulated in the unfavorable group, CDKN1C was downregulated in the same group. Interestingly, the same genes were also described as overexpressed in connection with autoimmune diseases. This indicates an involvement of similar immune regulatory pathways also in aGVHD. Our data support use of gene expression profiling at aGVHD onset for a prediction of its outcomes. (C) 2012 ISEH - Society for Hematology and Stem Cells.
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