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@ARTICLE{Noronha:180826,
author = {A. Noronha and N. Belugali Nataraj and J. Sang Lee and B.
Zhitomirsky and Y. Oren and S. Oster and M. Lindzen and S.
Mukherjee and R. Will$^*$ and S. Ghosh and A. Simoni-Nieves
and A. Verma and R. Chatterjee and S. Borgoni$^*$ and W.
Robinson and S. Sinha and A. Brandis and D. L. Kerr and W.
Wu and A. Sekar and S. Giri and Y. Chung and D. Drago-Garcia
and B. P. Danysh and M. Lauriola and M. Fiorentino and A.
Ardizzoni and M. Oren and C. M. Blakely and J. Ezike and S.
Wiemann$^*$ and L. Parida and T. G. Bivona and R. I. Aqeilan
and J. S. Brugge and A. Regev and G. Getz and E. Ruppin and
Y. Yarden},
title = {{AXL} and error-prone {DNA} replication confer drug
resistance and offer strategies to treat {EGFR}-mutant lung
cancer.},
journal = {Cancer discovery},
volume = {12},
number = {11},
issn = {2159-8274},
address = {Philadelphia, Pa.},
reportid = {DKFZ-2022-01582},
pages = {2666-2683},
year = {2022},
note = {2022 Nov 2;12(11):2666-2683 / Genomics and Proteomics Core
Facility, German Cancer Research Center (DKFZ),
ImNeuenheimer Feld 580, 69120, Heidelberg, GermanyDivision
of Molecular Genome Analysis, German Cancer Research Center
(DKFZ), ImNeuenheimer Feld 580, 69120, Heidelberg, Germany},
abstract = {Anti-cancer therapies have been limited by emergence of
mutations and other adaptations. In bacteria, antibiotics
activate the SOS response, which mobilizes error-prone
factors that allow for continuous replication at the cost of
mutagenesis. We investigated whether treatment of lung
cancer with EGFR inhibitors (EGFRi) similarly engages
hypermutators. In cycling drug-tolerant persister (DTP)
cells and in EGFRi-treated patients presenting residual
disease we observed upregulation of GAS6, while ablation of
GAS6's receptor, AXL, eradicated resistance. Reciprocally,
AXL overexpression enhanced DTP survival and accelerated the
emergence of T790M, an EGFR mutation typical to resistant
cells. Mechanistically, AXL induces low-fidelity DNA
polymerases and activates their organizer, RAD18, by
promoting neddylation. Metabolomics uncovered another
hypermutator, AXL-driven activation of MYC and increased
purine synthesis that is unbalanced by pyrimidines. Aligning
anti-AXL combination treatments with the transition from
DTPs to resistant cells cured patient-derived xenografts.
Hence, similar to bacteria, tumors tolerate therapy by
engaging pharmacologically targetable endogenous mutators.},
cin = {B050 / W111},
ddc = {610},
cid = {I:(DE-He78)B050-20160331 / I:(DE-He78)W111-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35895872},
doi = {10.1158/2159-8290.CD-22-0111},
url = {https://inrepo02.dkfz.de/record/180826},
}