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@ARTICLE{Thierauf:125397,
author = {J. Thierauf and J. A. Veit and J. Hess$^*$},
title = {{E}pithelial-to-{M}esenchymal {T}ransition in the
{P}athogenesis and {T}herapy of {H}ead and {N}eck {C}ancer.},
journal = {Cancers},
volume = {9},
number = {7},
issn = {2072-6694},
address = {Basel},
publisher = {MDPI},
reportid = {DKFZ-2017-01527},
pages = {76},
year = {2017},
abstract = {Head and neck cancer (HNC) is one of the most prevalent
human malignancies worldwide, with a high morbidity and
mortality. Implementation of interdisciplinary treatment
modalities has improved the quality of life, but only minor
changes in overall survival have been achieved over the past
decades. Main causes for treatment failure are an aggressive
and invasive tumor growth in combination with a high degree
of intrinsic or acquired treatment resistance. A subset of
tumor cells gain these properties during malignant
progression by reactivating a complex program of
epithelia-to-mesenchymal transition (EMT), which is integral
in embryonic development, wound healing, and stem cell
behavior. EMT is mediated by a core set of key transcription
factors, which are under the control of a large range of
developmental signals and extracellular cues. Unraveling
molecular principles that drive EMT provides new concepts to
better understand tumor cell plasticity and response to
established as well as new treatment modalities, and has the
potential to identify new drug targets for a more effective,
less toxic, and individualized therapy of HNC patients.
Here, we review the most recent findings on the clinical
relevance of a mesenchymal-like phenotype for HNC patients,
including more rare cases of mucosal melanoma and adenoid
cystic carcinoma.},
subtyp = {Review Article},
cin = {G405},
ddc = {610},
cid = {I:(DE-He78)G405-20160331},
pnm = {317 - Translational cancer research (POF3-317)},
pid = {G:(DE-HGF)POF3-317},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28671620},
pmc = {pmc:PMC5532612},
doi = {10.3390/cancers9070076},
url = {https://inrepo02.dkfz.de/record/125397},
}