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@ARTICLE{Angeles:275755,
author = {A. Angeles$^*$ and F. Janke$^*$ and A.-K. Daum$^*$ and M.
Reck and M. A. Schneider and M. Thomas and P. Christopoulos
and H. Sültmann$^*$},
title = {{I}ntegrated circulating tumour {DNA} and cytokine analysis
for therapy monitoring of {ALK}-rearranged lung
adenocarcinoma.},
journal = {British journal of cancer},
volume = {129},
number = {1},
issn = {0007-0920},
address = {Edinburgh},
publisher = {Nature Publ. Group},
reportid = {DKFZ-2023-00854},
pages = {112-121},
year = {2023},
note = {#EA:B063#LA:B063# / 2023 Jul;129(1):112-121},
abstract = {Detection of circulating tumour DNA (ctDNA) in biological
fluids is a minimally invasive alternative to tissue biopsy
for therapy monitoring. Cytokines are released in the tumour
microenvironment to influence inflammation and tumorigenic
mechanisms. Here, we investigated the potential biomarker
utility of circulating cytokines vis-à-vis ctDNA in
ALK-rearranged+ lung adenocarcinoma (ALK + NSCLC) and
explored the optimal combination of molecular parameters
that could indicate disease progression.Longitudinal serum
samples (n = 296) were collected from ALK + NSCLC patients
(n = 38) under tyrosine kinase inhibitor (TKI) therapy and
assayed to quantify eight cytokines: IFN-γ, IL-1β, IL-6,
IL-8, IL-10, IL-12p70, MCP1 and TNF-α. Generalised linear
mixed-effect modelling was performed to test the performance
of different combinations of cytokines and previously
determined ctDNA parameters in identifying progressive
disease.Serum IL-6, IL-8 and IL-10 were elevated at
progressive disease, with IL-8 having the most significant
impact as a biomarker. Integrating changes in IL-8 with
ctDNA parameters maximised the performance of the
classifiers in identifying disease progression, but this did
not significantly outperform the model based on ctDNA
alone.Serum cytokine levels are potential disease
progression markers in ALK + NSCLC. Further validation in a
larger and prospective cohort is necessary to determine
whether the addition of cytokine evaluation could improve
current tumour monitoring modalities in the clinical
setting.},
cin = {B063 / HD01},
ddc = {610},
cid = {I:(DE-He78)B063-20160331 / I:(DE-He78)HD01-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37120670},
doi = {10.1038/s41416-023-02284-0},
url = {https://inrepo02.dkfz.de/record/275755},
}