2024-04-02
> Alcoholic hepatitis (AH) is the most severe form of alcoholic liver disease and occurs in patients with excessive alcohol intake It is characterized by marked hepatocellular damage, steatosis and pericellular fibrosis. Patients with severe AH have a poor short-term prognosis. Unfortunately, current therapies (i.e. corticosteroids and pentoxyphylline) are not effective in many patients and novel targeted therapies are urgently needed. The development of such therapies is hampered by a poor knowledge of the underlying molecular mechanisms. Based on studies from animal models, TNF alfa was proposed to play a pivotal role in the mechanisms of AH. Consequently, drugs interfering TNF alfa were tested in these patients. The results were disappointing due to an increased incidence of severe infections. Unluckily, there are not experimental models that mimic the main findings of AH in humans. To overcome this limitation, translational studies with human samples are required. We previously analyzed samples from patients with biopsy-proven AH. In these previous studies, we identified CXC chemokines as a potential therapeutic target for these patients. We expanded these previous observations by performing a high-throughout transcriptome analysis.
The data has been downloaded from GEO.
gcel = getGEOSuppFiles("GSE28619")
system("tar xvf GSE28619/GSE28619_RAW.tar")
gse28619raw = ReadAffy()
gse28619 = rma(gse28619raw)
type = factor(rep(1:2,c(7,15)),levels=1:2,labels=c("control","alcoholic"))
pData(gse28619) = data.frame(type)
experimentdata0 = new('MIAME', name ='Juanjo Lozano et al.',
lab ='CIBEREHD',
contact ='juanjo.lozano@ciberehd.org',
title = 'Transcriptome analysis identifies TNF
superfamily receptors as potential therapeutic
targets in alcoholic hepatitis.',
abstract = 'Alcoholic hepatitis (AH) is the most severe
form of alcoholic liver disease and occurs in patients
with excessive alcohol intake It is characterized by
marked hepatocellular damage, steatosis and pericellular
fibrosis. Patients with severe AH have a poor short-term
prognosis. Unfortunately, current therapies (i.e.
corticosteroids and pentoxyphylline) are not effective
in many patients and novel targeted therapies are urgently
needed. The development of such therapies is hampered by a
poor knowledge of the underlying molecular mechanisms.
Based on studies from animal models, TNF alfa was proposed
to play a pivotal role in the mechanisms of AH.
Consequently, drugs interfering TNF alfa were tested
in these patients. The results were disappointing due
to an increased incidence of severe infections.
Unluckily, there are not experimental models that
mimic the main findings of AH in humans. To overcome
this limitation, translational studies with human samples
are required. We previously analyzed samples from
patients with biopsy-proven AH. In these previous studies,
we identified CXC chemokines as a potential therapeutic
target for these patients. We expanded these previous
observations by performing a high-throughout transcriptome
analysis.',
url = 'http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE28619')
experimentData(gse28619) = experimentdata0
Additional identifiers per gene.
Saving the ExpressionSet
.