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@ARTICLE{Preuss:276233,
author = {S. F. Preuss$^*$ and D. Grieshober$^*$ and H. Augustin$^*$},
title = {{S}ystemic {R}eprogramming of {E}ndothelial {C}ell
{S}ignaling in {M}etastasis and {C}achexia.},
journal = {Physiology},
volume = {38},
number = {4},
issn = {1548-9213},
address = {Stanford, Calif.},
publisher = {HighWire Press},
reportid = {DKFZ-2023-01042},
pages = {189–202},
year = {2023},
note = {#EA:A190#LA:A190#},
abstract = {Proliferating cancer cells secrete a multitude of factors
impacting metabolism, interorgan communication, and tumor
progression. The distribution of tumor-derived factors to
distant organs occurs via the circulation, which provides an
extensive reactive surface lined by endothelial cells.
Primary tumor-derived proteins impact cancer progression by
modulating endothelial cell activation at the
(pre-)metastatic niche, which affects tumor cell
dissemination as well as the outgrowth of seeded metastatic
cells into overt tumors. In addition, new insight indicates
that endothelial cell signaling contributes to metabolic
symptoms of cancer, including cancer-associated cachexia,
opening a new field of vascular metabolism research. This
review addresses how tumor-derived factors systemically
affect endothelial cell signaling and activation and impact
distant organs as well as tumor progression.},
subtyp = {Review Article},
keywords = {Humans / Endothelial Cells / Cachexia / Signal Transduction
/ Neoplasm Proteins / angiocrine signaling (Other) /
cachexia (Other) / metastasis (Other) / systemic signaling
(Other) / vascular endothelium (Other) / Neoplasm Proteins
(NLM Chemicals)},
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:37222464},
doi = {10.1152/physiol.00001.2023},
url = {https://inrepo02.dkfz.de/record/276233},
}