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@ARTICLE{Janning:179072,
author = {M. Janning$^*$ and J. Süptitz and C. Albers-Leischner and
P. Delpy$^*$ and A. Tufman and J.-L. Velthaus-Rusik and M.
Reck and A. Jung$^*$ and D. Kauffmann-Guerrero and I.
Bonzheim and S. Brändlein and H.-D. Hummel and M. Wiesweg
and H.-U. Schildhaus and J. A. Stratmann and M. Sebastian
and J. Alt and J. Buth and I. Esposito and J. Berger and L.
Tögel and F. C. Saalfeld and M. Wermke and S.
Merkelbach-Bruse and A. M. Hillmer and F. Klauschen and C.
Bokemeyer and R. Buettner and J. Wolf and S. Loges$^*$},
title = {{T}reatment outcome of atypical {EGFR} mutations in the
{G}erman {N}ational {N}etwork {G}enomic {M}edicine {L}ung
{C}ancer (n{NGM}).},
journal = {Annals of oncology},
volume = {33},
number = {6},
issn = {0923-7534},
address = {Amsterdam [u.a.},
publisher = {Elsevier},
reportid = {DKFZ-2022-00448},
pages = {602-615},
year = {2022},
note = {#EA:A420#LA:A420# / 2022 Jun;33(6):602-615},
abstract = {Atypical EGFR mutations occur in $10-30\%$ of NSCLC
patients with EGFR mutations and their sensitivity to
classical EGFR-tyrosine kinase inhibitors (TKI) is highly
heterogeneous. Patients harboring one group of uncommon,
recurrent EGFR mutations (G719X, S768I, L861Q) respond to
EGFR-TKI. Exon 20 insertions are mostly insensitive to
EGFR-TKI but display sensitivity to exon 20 inhibitors.
Clinical outcome data of patients with very rare point and
compound mutations upon systemic treatments are still sparse
to date.In this retrospective, multi-center study of the
national Network Genomic Medicine (nNGM) in Germany, 856
NSCLC cases with atypical EGFR mutations including
co-occuring mutations were reported from 12 centers.
Clinical follow-up data after treatment with different
EGFR-TKI, chemotherapy and immune checkpoint inhibitors were
available from 260 patients. Response to treatment was
analyzed in three major groups: (1) uncommon mutations
(G719X, S7681, L861Q and combinations), (2) exon 20
insertions and (3) very rare EGFR mutations (very rare
single point mutations, compound mutations, exon 18
deletions, exon 19 insertions).Our study comprises the
largest thus far reported real-world cohort of very rare
EGFR single point and compound mutations treated with
different systemic treatments. We validated higher efficacy
of EGFR-TKI in comparison to chemotherapy in group 1
(uncommon), while most exon 20 insertions (group 2) were not
EGFR-TKI responsive. In addition, we found TKI sensitivity
of very rare point mutations (group 3) and of complex EGFR
mutations containing exon 19 deletions or L858R mutations
independent of the combination partner. Notably, treatment
responses in group 3 (very rare) were highly heterogeneous.
Co-occurring TP53 mutations exerted a non-significant trend
for a detrimental effect on outcome in EGFR-TKI treated
patients in groups 2 and 3 but not in group 1.Based on our
findings we propose a novel nNGM classification of uncommon
EGFR mutations.},
keywords = {EGFR (Other) / Non-small cell lung cancer (Other) /
uncommon EGFR mutations (Other)},
cin = {A420 / E260 / MU01},
ddc = {610},
cid = {I:(DE-He78)A420-20160331 / I:(DE-He78)E260-20160331 /
I:(DE-He78)MU01-20160331},
pnm = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
pid = {G:(DE-HGF)POF4-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35263633},
doi = {10.1016/j.annonc.2022.02.225},
url = {https://inrepo02.dkfz.de/record/179072},
}