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@ARTICLE{Jurmeister:147359,
author = {P. Jurmeister$^*$ and C. Vollbrecht and A. Behnke and N.
Frost and A. Arnold and D. Treue and J.-C. Rückert and J.
Neudecker and L. Schweizer$^*$ and F. Klauschen and D. Horst
and M. Hummel and M. Dietel and M. von Laffert$^*$},
title = {{N}ext generation sequencing of lung adenocarcinoma
subtypes with intestinal differentiation reveals distinct
molecular signatures associated with histomorphology and
therapeutic options.},
journal = {Lung cancer},
volume = {138},
issn = {0169-5002},
address = {Amsterdam [u.a.]},
publisher = {Elsevier},
reportid = {DKFZ-2019-02480},
pages = {43 - 51},
year = {2019},
note = {EAL201LAL201},
abstract = {We aim to provide a better understanding of the molecular
landscape of primary lung adenocarcinomas with intestinal
differentiation.Five invasive mucinous adenocarcinomas (IMA)
and seven pulmonary enteric adenocarcinomas (PEAD) were
included in this study. Furthermore, we analyzed six
pulmonary colloid adenocarcinomas (CAD), including one
primary tumor, one metastasis, and two sample pairs
consisting of the primary colloid lung tumor and a matching
metastasis and an acinar component, respectively. All
samples were characterized using immunohistochemistry
(TTF-1, CK7, CK20, CDX2, Ki-67, ALK and PD-L1) and a next
generation sequencing panel covering 404 cancer-related
genes (FoundationOne® gene panel).While Ki-67 expression
was comparably low in IMA (range: $8-15\%)$ and in primary
CAD (range: $5-8\%),$ we observed considerably higher
proliferation rates in the non-colloid tumor compartment
$(16\%)$ and metastases $(72\%)$ from CAD, as well as in the
PEAD-group $(36-71\%).$ The overall tumor mutational burden
was lowest in IMA (2.5 mutations per megabase), intermediate
in CAD (5.8 mutations per megabase) and highest in PEAD
(16.8 mutations per megabase). KRAS mutations were frequent
in all three tumor subtypes, but TP53 mutations were mostly
limited to PEAD. While chromosomal alterations were rare in
IMA, we discovered MYC amplifications in three of four CAD.
Comparing primary and metastatic CAD, we observed the
acquisition of multiple mutations and chromosomal
alterations. PEAD had a variety of chromosomal alterations,
including two cases with RICTOR amplification. PD-L1
expression $(20\%,$ $50\%$ and $80\%$ of tumor cells) was
limited to three PEAD samples, only. In conclusion, we
provide a detailed insight into the molecular alterations
across and within the different subtypes of pulmonary
adenocarcinomas with intestinal differentiation. From a
clinical perspective, we provide data on potential treatment
strategies for patients with PEAD, including immunotherapy.},
cin = {L201},
ddc = {610},
cid = {I:(DE-He78)L201-20160331},
pnm = {899 - ohne Topic (POF3-899)},
pid = {G:(DE-HGF)POF3-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31634654},
doi = {10.1016/j.lungcan.2019.10.005},
url = {https://inrepo02.dkfz.de/record/147359},
}