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@ARTICLE{May:148910,
author = {V. May and S. Berchtold$^*$ and A. Berger and S. Venturelli
and M. Burkard and C. Leischner and N. P. Malek and U. M.
Lauer$^*$},
title = {{C}hemovirotherapy for pancreatic cancer: {G}emcitabine
plus oncolytic measles vaccine virus.},
journal = {Oncology letters},
volume = {18},
number = {5},
issn = {1792-1082},
address = {Athens},
publisher = {Spandidos Publ.},
reportid = {DKFZ-2020-00068},
pages = {5534-5542},
year = {2019},
note = {LA:L801},
abstract = {Oncolytic virotherapy with vaccine viruses employs
replicative vectors, which quite selectively infect tumor
cells leading to massive virus replication followed by
subsequent profound tumor cell death (oncolysis). Measles
vaccine virus (MeV) has already shown great oncolytic
activity against different types of cancers, including
pancreatic cancer. Gemcitabine is a first line
chemotherapeutic drug used for pancreatic cancer in
palliative treatment plans. Furthermore, this drug can be
used to induce senescence, a permanent cell cycle arrest, in
tumor cells. In our preclinical work, three
well-characterized immortalized human pancreatic cancer cell
lines were used to investigate the combinatorial effect of
MeV-based virotherapy together with the chemotherapeutic
compound gemcitabine. Viability assays revealed that the
combination of only small amounts of MeV together with
subtherapeutic concentrations of gemcitabine resulted in a
tumor cell mass reduction of $>50\%.$ To further investigate
the replication of the oncolytic MeV vectors under these
distinct combinatorial conditions, viral growth curves were
generated. As a result, viral replication was found to be
only slightly diminished in the presence of gemcitabine. As
gemcitabine induces senescence, the effect of MeV on that
phenomenon was explored using a senescence-associated
β-galactosidase assay. Notably, gemcitabine-induced tumor
cell senescence was not impaired by MeV. Accordingly, the
chemovirotherapeutic combination of gemcitabine plus
oncolytic MeV constitutes a novel therapeutic option for
advanced pancreatic carcinoma that is characterized by the
mutual improvement of the effectiveness of each therapeutic
component.},
cin = {L801},
ddc = {610},
cid = {I:(DE-He78)L801-20160331},
pnm = {899 - ohne Topic (POF3-899)},
pid = {G:(DE-HGF)POF3-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31612061},
pmc = {pmc:PMC6781561},
doi = {10.3892/ol.2019.10901},
url = {https://inrepo02.dkfz.de/record/148910},
}