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@ARTICLE{Hamid:283200,
author = {R. Hamid and M. Alaziz and A. S. Mahal and A. W. Ashton and
N. Halama$^*$ and D. Jaeger$^*$ and X. Jiao and R. G.
Pestell},
title = {{T}he {R}ole and {T}herapeutic {T}argeting of {CCR}5 in
{B}reast {C}ancer.},
journal = {Cells},
volume = {12},
number = {18},
issn = {2073-4409},
address = {Basel},
publisher = {MDPI},
reportid = {DKFZ-2023-01965},
pages = {2237},
year = {2023},
abstract = {The G-protein-coupled receptor C-C chemokine receptor 5
(CCR5) functions as a co-receptor for the entry of HIV into
immune cells. CCR5 binds promiscuously to a diverse array of
ligands initiating cell signaling that includes guided
migration. Although well known to be expressed on immune
cells, recent studies have shown the induction of CCR5 on
the surface of breast cancer epithelial cells. The function
of CCR5 on breast cancer epithelial cells includes the
induction of aberrant cell survival signaling and tropism
towards chemo attractants. As CCR5 is not expressed on
normal epithelium, the receptor provides a potential useful
target for therapy. Inhibitors of CCR5 (CCR5i), either small
molecules (maraviroc, vicriviroc) or humanized monoclonal
antibodies (leronlimab) have shown anti-tumor and
anti-metastatic properties in preclinical studies. In early
clinical studies, reviewed herein, CCR5i have shown
promising results and evidence for effects on both the tumor
and the anti-tumor immune response. Current clinical studies
have therefore included combination therapy approaches with
checkpoint inhibitors.},
subtyp = {Review Article},
keywords = {CCR5 (Other) / breast cancer (Other) / triple-negative
breast cancer (Other)},
cin = {D240 / D120},
ddc = {570},
cid = {I:(DE-He78)D240-20160331 / I:(DE-He78)D120-20160331},
pnm = {314 - Immunologie und Krebs (POF4-314)},
pid = {G:(DE-HGF)POF4-314},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37759462},
doi = {10.3390/cells12182237},
url = {https://inrepo02.dkfz.de/record/283200},
}