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@ARTICLE{Ceranski:274241,
author = {A. K. Ceranski$^*$ and M. J. Carreño-Gonzalez$^*$ and A.
Ehlers$^*$ and M. Colombo$^*$ and F. Cidre-Aranaz$^*$ and T.
Grünewald$^*$},
title = {{H}ypoxia and {HIF}s in {E}wing sarcoma: new perspectives
on a multi-facetted relationship.},
journal = {Molecular cancer},
volume = {22},
number = {1},
issn = {1476-4598},
address = {London},
publisher = {Biomed Central},
reportid = {DKFZ-2023-00527},
pages = {49},
year = {2023},
note = {#EA:B410#LA:B410#},
abstract = {Hypoxia develops during the growth of solid tumors and
influences tumoral activity in multiple ways. Low oxygen
tension is also present in the bone microenvironment where
Ewing sarcoma (EwS) - a highly aggressive pediatric cancer -
mainly arises. Hypoxia inducible factor 1 subunit alpha
(HIF-1-a) is the principal molecular mediator of the hypoxic
response in cancer whereas EWSR1::FLI1 constitutes the
oncogenic driver of EwS. Interaction of the two proteins has
been shown in EwS. Although a growing body of studies
investigated hypoxia and HIFs in EwS, their precise role for
EwS pathophysiology is not clarified to date. This review
summarizes and structures recent findings demonstrating that
hypoxia and HIFs play a role in EwS at multiple levels. We
propose to view hypoxia and HIFs as independent protagonists
in the story of EwS and give a perspective on their
potential clinical relevance as prognostic markers and
therapeutic targets in EwS treatment.},
subtyp = {Review Article},
keywords = {ARNT (Other) / Ewing sarcoma (Other) / HIF-1-a (Other) /
HIF-1-b (Other) / hypoxia (Other)},
cin = {B410 / HD01},
ddc = {570},
cid = {I:(DE-He78)B410-20160331 / I:(DE-He78)HD01-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:36915100},
doi = {10.1186/s12943-023-01750-w},
url = {https://inrepo02.dkfz.de/record/274241},
}