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@ARTICLE{Ali:186245,
author = {E. Ali and A. Trailin and F. Ambrozkiewicz and V. Liška
and K. Hemminki$^*$},
title = {{A}ctivated {H}epatic {S}tellate {C}ells in
{H}epatocellular {C}arcinoma: {T}heir {R}ole as a
{P}otential {T}arget for {F}uture {T}herapies.},
journal = {International journal of molecular sciences},
volume = {23},
number = {23},
issn = {1422-0067},
address = {Basel},
publisher = {Molecular Diversity Preservation International},
reportid = {DKFZ-2022-03039},
pages = {15292},
year = {2022},
note = {#LA:C020#},
abstract = {Hepatocellular carcinoma (HCC) is a global healthcare
challenge, which affects more than 815,000 new cases every
year. Activated hepatic stellate cells (aHSCs) remain the
principal cells that drive HCC onset and growth. aHSCs
suppress the anti-tumor immune response through interaction
with different immune cells. They also increase the
deposition of the extracellular matrix proteins, challenging
the reversion of fibrosis and increasing HCC growth and
metastasis. Therapy for HCC was reported to activate HSCs,
which could explain the low efficacy of current treatments.
Conversely, recent studies aimed at the deactivation of HSCs
show that they have been able to inhibit HCC growth. In this
review article, we discuss the role of aHSCs in HCC
pathophysiology and therapy. Finally, we provide suggestions
for the experimental implementation of HSCs in HCC
therapies.},
subtyp = {Review Article},
keywords = {fibrosis regression (Other) / hepatic stellate cells
(Other) / hepatocellular carcinoma (Other) / therapeutic
studies (Other)},
cin = {C020},
ddc = {540},
cid = {I:(DE-He78)C020-20160331},
pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
pid = {G:(DE-HGF)POF4-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:36499616},
doi = {10.3390/ijms232315292},
url = {https://inrepo02.dkfz.de/record/186245},
}