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@ARTICLE{Gewalt:301327,
author = {T. Gewalt and A. M. Dmitrieva and F. Elsner and X. Zhao and
D. D. Sieber and I. G. Kocak and Q. Yang and C. V. Orschel
and N. M. Eckert and B. Goebel and M. Nill and F. Peter and
A. Hartmann and F. Beleggia and M. Odenthal and H. C.
Reinhardt$^*$ and R. T. Ullrich and F. Graw and L. Meder},
title = {{TAT}-{CRE} inhalation enables tumor induction
corresponding to adenoviral {C}re-recombinase in a lung
cancer mouse model.},
journal = {Communications biology},
volume = {8},
number = {1},
issn = {2399-3642},
address = {London},
publisher = {Springer Nature},
reportid = {DKFZ-2025-00999},
pages = {741},
year = {2025},
abstract = {Cre-recombinase inducible model systems are extensively
used in cancer research to manipulate gene expression in
specific tissues and induce autochthonous tumor growth.
These systems often involve the cross-breeding of
genetically engineered organisms containing loxP-flanked
alleles with those expressing Cre-recombinase. This
approach, while effective, has the challenge of requiring
high numbers of animals due to breeding requirements. Other
frequently used tumor induction methods in cancer research
involve the direct application of viral Cre-recombinase
vectors. This approach presents the challenge of the
accessibility of facilities that meet the necessary safety
level. In this context, we perform a comprehensive
comparison between TAT-CRE (biosafety level S1) and
adenoviral Cre-recombinase induced (biosafety level S2) lung
adenocarcinomas driven by KrasG12D expression and Trp53
depletion. We use in vivo lung tumor monitoring via computed
tomography, single-cell RNA sequencing, immunohistochemistry
and flow cytometry to elucidate similarities and differences
between TAT-CRE and adenoviral Cre-recombinase induced lung
adenocarcinomas. TAT-CRE induced lung tumors present
differences in micro-vessels and macrophages but with
corresponding tumor onset and growth characteristics
compared to adenoviral-Cre recombinase induced lung tumors.
Taken together, TAT-CRE is a valuable genetic engineering
safety level S1 alternative for cancer induction and may be
implemented in other cancer models than lung cancer.},
keywords = {Animals / Integrases: genetics / Integrases: metabolism /
Integrases: administration $\&$ dosage / Lung Neoplasms:
genetics / Lung Neoplasms: pathology / Lung Neoplasms:
metabolism / Mice / Adenoviridae: genetics / Disease Models,
Animal / Adenocarcinoma of Lung: genetics / Adenocarcinoma
of Lung: pathology / Administration, Inhalation / Mice,
Inbred C57BL / Tumor Suppressor Protein p53: genetics / Cre
recombinase (NLM Chemicals) / Integrases (NLM Chemicals) /
Tumor Suppressor Protein p53 (NLM Chemicals)},
cin = {ED01},
ddc = {570},
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:40360735},
doi = {10.1038/s42003-025-08146-0},
url = {https://inrepo02.dkfz.de/record/301327},
}