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@ARTICLE{Hartmann:168225,
author = {O. Hartmann and M. Reissland and C. R. Maier$^*$ and T.
Fischer and C. Prieto-Garcia and A. Baluapuri and J. Schwarz
and W. Schmitz and M. Garrido-Rodriguez and N. Pahor and C.
C. Davies and F. Bassermann and A. Orian and E. Wolf and A.
Schulze$^*$ and M. A. Calzado and M. T. Rosenfeldt and M. E.
Diefenbacher},
title = {{I}mplementation of {CRISPR}/{C}as9 {G}enome {E}diting to
{G}enerate {M}urine {L}ung {C}ancer {M}odels {T}hat {D}epict
the {M}utational {L}andscape of {H}uman {D}isease.},
journal = {Frontiers in cell and developmental biology},
volume = {9},
issn = {2296-634X},
address = {Lausanne},
publisher = {Frontiers Media},
reportid = {DKFZ-2021-00756},
pages = {641618},
year = {2021},
abstract = {Lung cancer is the most common cancer worldwide and the
leading cause of cancer-related deaths in both men and
women. Despite the development of novel therapeutic
interventions, the 5-year survival rate for non-small cell
lung cancer (NSCLC) patients remains low, demonstrating the
necessity for novel treatments. One strategy to improve
translational research is the development of surrogate
models reflecting somatic mutations identified in lung
cancer patients as these impact treatment responses. With
the advent of CRISPR-mediated genome editing, gene deletion
as well as site-directed integration of point mutations
enabled us to model human malignancies in more detail than
ever before. Here, we report that by using
CRISPR/Cas9-mediated targeting of Trp53 and KRas, we
recapitulated the classic murine NSCLC model Trp53 fl/fl
:lsl-KRas G12D/wt . Developing tumors were indistinguishable
from Trp53 fl/fl :lsl-KRas G12D/ wt -derived tumors with
regard to morphology, marker expression, and transcriptional
profiles. We demonstrate the applicability of CRISPR for
tumor modeling in vivo and ameliorating the need to use
conventional genetically engineered mouse models.
Furthermore, tumor onset was not only achieved in
constitutive Cas9 expression but also in wild-type animals
via infection of lung epithelial cells with two discrete
AAVs encoding different parts of the CRISPR machinery. While
conventional mouse models require extensive husbandry to
integrate new genetic features allowing for gene targeting,
basic molecular methods suffice to inflict the desired
genetic alterations in vivo. Utilizing the CRISPR toolbox,
in vivo cancer research and modeling is rapidly evolving and
enables researchers to swiftly develop new, clinically
relevant surrogate models for translational research.},
keywords = {CRISPR-Cas9 (Other) / JUN (Other) / KRAS (Other) / MYC
(Other) / TP53 (Other) / lung cancer (Other) / mouse model
(Other) / non-small cell lung cancer (Other)},
cin = {A410},
ddc = {570},
cid = {I:(DE-He78)A410-20160331},
pnm = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
pid = {G:(DE-HGF)POF4-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:33738287},
pmc = {pmc:PMC7961101},
doi = {10.3389/fcell.2021.641618},
url = {https://inrepo02.dkfz.de/record/168225},
}