% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Isermann:296069,
author = {T. Isermann$^*$ and C. Sers$^*$ and C. J. Der and B.
Papke$^*$},
title = {{KRAS} inhibitors: resistance drivers and combinatorial
strategies.},
journal = {Trends in cancer},
volume = {11},
number = {2},
issn = {2405-8033},
address = {Amsterdam},
publisher = {Elsevier},
reportid = {DKFZ-2025-00017},
pages = {91-116},
year = {2025},
note = {2025 Feb;11(2):91-116},
abstract = {In 1982, the RAS genes HRAS and KRAS were discovered as the
first human cancer genes, with KRAS later identified as one
of the most frequently mutated oncogenes. Yet, it took
nearly 40 years to develop clinically effective inhibitors
for RAS-mutant cancers. The discovery in 2013 by Shokat and
colleagues of a druggable pocket in KRAS paved the way to
FDA approval of the first covalently binding KRASG12C
inhibitors, sotorasib and adagrasib, in 2021 and 2022,
respectively. However, rather than marking the end of a
successful assault on the Mount Everest of cancer research,
this landmark only revealed new challenges in RAS drug
discovery. In this review, we highlight the progress on
defining resistance mechanisms and developing combination
treatment strategies to improve patient responses to KRAS
therapies.},
subtyp = {Review Article},
keywords = {KRAS (Other) / colorectal carcinoma (Other) / drug
resistance (Other) / non-small cell lung cancer (Other) /
pancreatic ductal adenocarcinoma (Other)},
cin = {BE01},
ddc = {610},
cid = {I:(DE-He78)BE01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39732595},
doi = {10.1016/j.trecan.2024.11.009},
url = {https://inrepo02.dkfz.de/record/296069},
}