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@ARTICLE{Augustin:178400,
author = {H. Augustin$^*$ and G. Y. Koh},
title = {{A}ntiangiogenesis: {V}essel {R}egression, {V}essel
{N}ormalization, or {B}oth?},
journal = {Cancer research},
volume = {82},
number = {1},
issn = {0008-5472},
address = {Philadelphia, Pa.},
publisher = {AACR},
reportid = {DKFZ-2022-00037},
pages = {15 - 17},
year = {2022},
note = {DKFZ-ZMBH Alliance / #EA:A190#},
abstract = {The concepts of antiangiogenic tumor therapy were pioneered
on the assumption that the inhibition of tumor angiogenesis
should lead to the complete regression of the
tumor-associated vasculature and thereby hold the tumor in
an avascular dormant state. Yet, clinical trials revealed
limited efficacy of angiogenesis inhibitors when used as
monotherapy. Instead, antiangiogenic drugs proved effective
to extend overall survival when used in combination with
chemotherapy. This counterintuitive observation-inhibition
of tumor vascularization should lead to less and not more
delivery of chemotherapy to the tumor-led to the concepts of
'vessel normalization.' This refers to the notion that
antiangiogenic drugs prune the most immature tumor vessels
and spare mature vessels, thereby resulting in a more
normal-appearing vasculature that leads to better access of
chemotherapy to the tumor. The concepts of vessel
normalization were first laid out in a landmark publication
in Cancer Research in 2004. More than 600 studies on
different aspects of vessel normalization have been
published since then. Nevertheless, it is to this day less
clear than ever to what extent vessel regression (leading to
tumor starvation) and vessel normalization (facilitating
chemotherapy) contribute to the clinical efficacy of
antiangiogenic tumor therapy. This 'Landmark Commentary'
puts the concepts of tumor vessel normalization in
historical context and develops thereupon some of the most
burning questions in the field of translational angiogenesis
research that need to be answered to further advance the
application of tumor vascular stroma reprogramming
therapies.See related article by Tong and colleagues, Cancer
Res 2004;64:3731-6.},
cin = {A190},
ddc = {610},
cid = {I:(DE-He78)A190-20160331},
pnm = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
pid = {G:(DE-HGF)POF4-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:34983784},
doi = {10.1158/0008-5472.CAN-21-3515},
url = {https://inrepo02.dkfz.de/record/178400},
}