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@ARTICLE{Schmitt:143882,
author = {K. Schmitt and B. Molfenter and N. Koerich Laureano$^*$ and
B. Tawk$^*$ and M. Bieg$^*$ and X. Pastor Hostench$^*$ and
D. Weichenhan$^*$ and N. D. Ullrich and V. Shang and D.
Richter$^*$ and F. Stögbauer and L. Schroeder$^*$ and B. de
Bem Prunes and F. Visioli and P. Varvaki Rados and A. Jou
and M. Plath and P. A. Federspil and J. Thierauf and J.
Döscher and S. E. Weissinger and T. K. Hoffmann and S.
Wagner and C. Wittekindt and N. Ishaque$^*$ and R. Eils$^*$
and J. P. Klussmann and D. Holzinger$^*$ and C. Plass$^*$
and A. Abdollahi$^*$ and K. Freier and W. Weichert$^*$ and
K. Zaoui and J. Hess$^*$},
title = {{S}omatic mutations and promotor methylation of the
ryanodine receptor 2 is a common event in the pathogenesis
of head and neck cancer.},
journal = {International journal of cancer},
volume = {145},
number = {12},
issn = {1097-0215},
address = {Bognor Regis},
publisher = {Wiley-Liss},
reportid = {DKFZ-2019-01444},
pages = {3299-3310},
year = {2019},
abstract = {Genomic sequencing projects unraveled the mutational
landscape of head and neck squamous cell carcinoma (HNSCC)
and provided a comprehensive catalogue of somatic mutations.
However, the limited number of significant cancer-related
genes obtained so far only partially explains the biological
complexity of HNSCC and hampers the development of novel
diagnostic biomarkers and therapeutic targets. We pursued a
multi-scale omics approach based on whole-exome sequencing,
global DNA methylation and gene expression profiling data
derived from tumor samples of the HIPO-HNC cohort (n=87),
and confirmed new findings with datasets from The Cancer
Genome Atlas (TCGA). Promoter methylation was confirmed by
MassARRAY analysis and protein expression was assessed by
immunohistochemistry and immunofluorescence staining. We
discovered a set of cancer-related genes with frequent
somatic mutations and high frequency of promoter
methylation. This included the ryanodine receptor 2 (RYR2),
which showed variable promoter methylation and expression in
both tumor samples and cell lines. Immunohistochemical
staining of tissue sections unraveled a gradual loss of RYR2
expression from normal mucosa via dysplastic lesion to
invasive cancer, and indicated that reduced RYR2 expression
in adjacent tissue and precancerous lesions might serve as
risk factor for unfavorable prognosis and upcoming malignant
conversion. In summary, our data indicate that impaired RYR2
function by either somatic mutation or epigenetic silencing
is a common event in HNSCC pathogenesis. Detection of RYR2
expression and/or promoter methylation might enable risk
assessment for malignant conversion of dysplastic lesions.
This article is protected by copyright. All rights
reserved.},
cin = {A102 / E210 / L101 / B080 / B370 / B340 / F022 / F020 /
L701 / E221},
ddc = {610},
cid = {I:(DE-He78)A102-20160331 / I:(DE-He78)E210-20160331 /
I:(DE-He78)L101-20160331 / I:(DE-He78)B080-20160331 /
I:(DE-He78)B370-20160331 / I:(DE-He78)B340-20160331 /
I:(DE-He78)F022-20160331 / I:(DE-He78)F020-20160331 /
I:(DE-He78)L701-20160331 / I:(DE-He78)E221-20160331},
pnm = {315 - Imaging and radiooncology (POF3-315)},
pid = {G:(DE-HGF)POF3-315},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31135957},
doi = {10.1002/ijc.32481},
url = {https://inrepo02.dkfz.de/record/143882},
}