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@ARTICLE{Martin:275976,
author = {S. Martin and D. Viertl and A. Janz and S. Habringer$^*$
and U. Keller$^*$ and M. Schottelius},
title = {{I}nfluence of corticosteroid treatment on {CXCR}4
expression in {DLBCL}.},
journal = {EJNMMI Research},
volume = {13},
number = {1},
issn = {2191-219X},
address = {Heidelberg},
publisher = {Springer},
reportid = {DKFZ-2023-00956},
pages = {40},
year = {2023},
note = {Short Communication},
abstract = {CXCR4-targeted radioligand therapy (RLT) with
[177Lu]Lu/[90Y]Y-PentixaTher has recently evolved as a
promising therapeutic option for patients with advanced
hematological cancers. Given their advanced disease stage,
most patients scheduled for PentixaTher RLT require
concomitant or bridging chemotherapy to prevent intermittent
tumor progression. These (mostly combination) therapies may
cause significant downregulation of tumoral CXCR4
expression, challenging the applicability of PentixaTher
RLT. This study therefore aimed at investigating the
influence of corticosteroids, a central component of these
chemotherapies, on CXCR4 regulation in diffuse large B cell
lymphoma (DLBCL).Different DLBCL cell lines (Daudi, OCI-LY1,
SUDHL-4, -5-, -6 and -8) as well as the human T-cell
lymphoma cell line Jurkat were incubated with Dexamethasone
(Dex; 0.5 and 5 µM, respectively) and Prednisolone (Pred;
5 and 50 µM, respectively) for different time points
(2 h, 24 h). Treatment-induced modulation of cellular
CXCR4 surface expression was assessed via flow cytometry
(FC) and compared to untreated cells. A radioligand binding
assay with [125I]CPCR4.3 was performed in parallel using the
same cells. To quantify potential corticosteroid treatment
effects on tumoral CXCR4 expression in vivo, OCI-LY1 bearing
NSG mice were injected 50 µg Dex/mouse i.p. (daily for
6 days). Then, a biodistribution study (1 h p.i.) using
[68Ga]PentixaTher was performed, and tracer biodistribution
in treated (n = 5) vs untreated mice (n = 5) was compared.In
the in vitro experiments, a strongly cell line-dependent
upregulation of CXCR4 was observed for both Dex and Pred
treatment, with negligible differences between the high and
low dose. While in Jurkat, Daudi and SUDHL-8 cells, CXCR4
expression remained unchanged, a 1.5- to 3.5-fold increase
in CXCR4 cell surface expression was observed for SUDHL-5 <
SUDHL-4 /-6 < OCI-LY1 via FC compared to untreated cells.
This increase in CXCR4 expression was also reflected in
correspondingly enhanced [125I]CPCR4.3 accumulation in
treated cells, with a linear correlation between FC and
radioligand binding data. In vivo, Dex treatment led to a
general increase of [68Ga]PentixaTher uptake in all organs
compared to untreated animals, as a result of a higher
tracer concentration in blood. However, we observed an
overproportionally enhanced [68Ga]PentixaTher uptake in the
OCI-LY1 tumors in treated (21.0 ± $5.5\%iD/g)$ vs untreated
(9.2 ± $2.8\%iD/g)$ mice, resulting in higher
tumor-to-background ratios in the treatment group.Overall,
corticosteroid treatment (Dex/Pred) consistently induced an
upregulation of CXCR4 expression DBLCL cells in vitro,
albeit in a very cell line-dependent manner. For the cell
line with the most pronounced Dex-induced CXCR4
upregulation, OCI-LY1, the in vitro findings were
corroborated by an in vivo biodistribution study. This
confirms that at least the corticosteroid component of
stabilizing chemotherapy regimens in DLBCL patients prior to
[177Lu]Lu-PentixaTher RLT does not lead to downregulation of
the molecular target CXCR4 and may even have a beneficiary
effect. However, further studies are needed to investigate
if and to what extent the other commonly used
chemotherapeutic agents affect CXCR4 expression on DLBCL to
ensure the choice of an appropriate treatment regimen prior
to [177Lu]Lu/[90Y]Y-PentixaTher RLT.},
keywords = {CXCR4 (Other) / Chemokine receptor regulation (Other) /
Corticosteroids (Other) / Cortisol (Other) / PentixaTher
(Other) / Radioligand therapy (Other)},
cin = {BE01},
ddc = {610},
cid = {I:(DE-He78)BE01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37162652},
doi = {10.1186/s13550-023-00993-4},
url = {https://inrepo02.dkfz.de/record/275976},
}