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@ARTICLE{Lckerath:274566,
author = {K. Lückerath$^*$ and M. Trajkovic-Arsic$^*$ and C. E.
Mona},
title = {{F}ibroblast {A}ctivation {P}rotein {I}nhibitor
{T}heranostics: {P}reclinical {C}ombination {T}reatment.},
journal = {PET clinics},
volume = {18},
number = {3},
issn = {1556-8598},
address = {Orlando, Fla. [u.a.]},
publisher = {Elsevier},
reportid = {DKFZ-2023-00643},
pages = {409-418},
year = {2023},
note = {2023 Jul;18(3):409-418},
abstract = {Fibroblast activation protein (FAP)-radioligand therapy
might be effective in some patients without being curative.
FAP-radioligands deliver ionizing radiation directly to FAP+
cancer-associated fibroblasts and, in some cancers, to FAP+
tumor cells; in addition, they indirectly irradiate FAP-
cells in tumor tissue via cross-fire and bystander effects.
Here, we discuss the potential to improve FAP-radioligand
therapy through interfering with DNA damage repair,
immunotherapy, and co-targeting cancer-associated
fibroblasts. As the molecular and cellular effects of
FAP-radioligands on the tumor and its microenvironment have
not been investigated yet, we call for future research to
close this gap in knowledge, which prevents the development
of more effective FAP-radioligand therapies.},
subtyp = {Review Article},
keywords = {Combination therapy (Other) / Fibroblast activation protein
(Other) / Radioligand (Other) / Theranostics (Other) / Tumor
microenvironment (Other)},
cin = {ED01},
ddc = {610},
cid = {I:(DE-He78)ED01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:36990945},
doi = {10.1016/j.cpet.2023.02.006},
url = {https://inrepo02.dkfz.de/record/274566},
}