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@ARTICLE{Schwab:300144,
author = {H. Schwab and M. Kerkhoff$^*$ and P. Plaumann$^*$ and S.
Collaud and U. Dirksen$^*$ and D. Theegarten and T. Herold
and S. Kalbourtzis and S. Bölükbas and B. Hegedüs and L.
Hegedüs},
title = {{C}haracterization of a novel sarcoma cell line with an
{EWSR}1::{POU}2{AF}3 fusion.},
journal = {Pathology $\&$ oncology research},
volume = {31},
issn = {1219-4956},
address = {Heidelberg},
publisher = {Springer},
reportid = {DKFZ-2025-00635},
pages = {1611986},
year = {2025},
abstract = {Sarcomas with an EWSR1::POU2AF3(COLCA2) fusion are a very
recently described entity of preferentially sinonasal origin
and with undifferentiated round/spindle cell morphology. We
established a novel cell line (PF1095) carrying a
EWSR1::POU2AF3 fusion from the malignant pleural effusion of
a 25-year-old sarcoma patient. The patient was first
diagnosed with poorly differentiated neuroendocrine
carcinoma based on tumor cell morphology and positivity to
markers such as EMA, synaptophysin, and CD56. Later, the
EWSR1 translocation was identified in the tumor cells with
unknown partners and the patient received chemotherapy
according to the Ewing 2008 protocol in combination with
surgery and proton beam radiotherapy. At the time of cell
line establishment, the disease progressed to pleural
sarcomatosis with pleural effusion. In the cell line, we
identified POU2AF3 as a fusion partner of EWSR1 and a TP53
frameshift deletion. Next, we determined the sensitivity of
PF1095 cells to the currently approved chemotherapies in
comparison to two conventional Ewing sarcoma lines (EW-7 and
MHH-ES1) with the two most frequent EWSR::FLI1 fusions.
Finally, we tested potential new combination therapies. We
performed cell viability, proliferation, and cell cycle
assays. We found that the proliferation rate of PF1095 cells
was much slower than the EWSR1::FLI1 fusion lines and they
also had a lower sensitivity to both irinotecan and
doxorubicin treatment. Expression level of SLFN11, a
predictor of sensitivity to DNA damaging agents, was also
lower in PF1095 cells. Combination treatment with the PARP
inhibitors olaparib and irinotecan or doxorubicin
synergistically reduced cell viability and induced cell
death and cell cycle arrest. This unique cell model provides
an opportunity to test therapeutic approaches preclinically
for this novel and aggressive sarcoma entity.},
keywords = {Humans / Oncogene Proteins, Fusion: genetics / RNA-Binding
Protein EWS: genetics / Adult / Sarcoma: genetics / Sarcoma:
pathology / Cell Line, Tumor / Cell Proliferation / Male /
EWSR1 (Other) / POU2AF3 (Other) / chemotherapy (Other) /
patient derived cell line (Other) / sarcoma (Other) /
Oncogene Proteins, Fusion (NLM Chemicals) / RNA-Binding
Protein EWS (NLM Chemicals) / EWSR1 protein, human (NLM
Chemicals)},
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:40134582},
pmc = {pmc:PMC11932835},
doi = {10.3389/pore.2025.1611986},
url = {https://inrepo02.dkfz.de/record/300144},
}