001     142358
005     20240229105148.0
024 7 _ |2 doi
|a 10.18632/oncotarget.24997
024 7 _ |2 pmid
|a pmid:29765529
024 7 _ |2 pmc
|a pmc:PMC5940384
037 _ _ |a DKFZ-2019-00134
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Gaiser, Timo
|b 0
245 _ _ |a MYC gene amplification is a rare event in atypical fibroxanthoma and pleomorphic dermal sarcoma.
260 _ _ |a [S.l.]
|b Impact Journals LLC
|c 2018
336 7 _ |2 DRIVER
|a article
336 7 _ |2 DataCite
|a Output Types/Journal article
336 7 _ |0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
|a Journal Article
|b journal
|m journal
|s 1549528807_657
336 7 _ |2 BibTeX
|a ARTICLE
336 7 _ |2 ORCID
|a JOURNAL_ARTICLE
336 7 _ |0 0
|2 EndNote
|a Journal Article
520 _ _ |a Atypical fibroxanthoma (AFX) and pleomorphic dermal sarcoma (PDS) are rare malignancies typically occurring in elderly patients and predominantly located in skin regions exposed to UV-light. Thus, a role of UV-radiation-induced damage for AFX and PDS tumorigenesis has been postulated. MYC gene amplification has been demonstrated as a distinctive feature of radiation-induced angiosarcoma. In order to investigate whether chronic exposure to UV-light might also lead to MYC copy number changes, 51 AFX and 24 PDS samples were retrospectively analyzed for MYC amplification by fluorescence in situ hybridization using a MYC and a CEP8 gene probe. Of the 44 analyzable AFX samples, one case showed MYC amplification (defined as a MYC/CEP8 ratio ≥2.0), whereas 13 cases demonstrated low level copy number gains (defined as MYC/CEP8 ratio ≥ 1.2-< 2.0). MYC amplification was seen in an AFX sample of extraordinary tumor thickness of 17.5 mm (vs. median 3.25 mm for all samples). Of the 24 PDS cases, five specimen demonstrated MYC low level copy number gains. Immunohistochemically, neither the AFX nor the PDS cases showed MYC protein expression. In summary, these findings rule out that MYC amplification is a major genetic driver in the process of AFX or PDS tumorigenesis. However, MYC amplification may occur as a late event during AFX development and hence might only be detectable in advanced, thick lesions.
536 _ _ |0 G:(DE-HGF)POF3-317
|a 317 - Translational cancer research (POF3-317)
|c POF3-317
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
700 1 _ |a Hirsch, Daniela
|b 1
700 1 _ |a Orouji, Azadeh
|b 2
700 1 _ |a Bach, Marisa
|b 3
700 1 _ |a Kind, Peter
|b 4
700 1 _ |a Helbig, Doris
|b 5
700 1 _ |a Quaas, Alexander
|b 6
700 1 _ |0 P:(DE-He78)a229f7724466e7efadf4a1ace1ff8af3
|a Utikal, Jochen
|b 7
|u dkfz
700 1 _ |a Marx, Alexander
|b 8
700 1 _ |0 P:(DE-HGF)0
|a Gaiser, Maria Rita
|b 9
|e Last author
773 _ _ |0 PERI:(DE-600)2560162-3
|a 10.18632/oncotarget.24997
|g Vol. 9, no. 30
|n 30
|p 21182-21189
|t OncoTarget
|v 9
|x 1949-2553
|y 2018
909 C O |o oai:inrepo02.dkfz.de:142358
|p VDB
910 1 _ |0 I:(DE-588b)2036810-0
|6 P:(DE-He78)a229f7724466e7efadf4a1ace1ff8af3
|a Deutsches Krebsforschungszentrum
|b 7
|k DKFZ
910 1 _ |0 I:(DE-588b)2036810-0
|6 P:(DE-HGF)0
|a Deutsches Krebsforschungszentrum
|b 9
|k DKFZ
913 1 _ |0 G:(DE-HGF)POF3-317
|1 G:(DE-HGF)POF3-310
|2 G:(DE-HGF)POF3-300
|a DE-HGF
|l Krebsforschung
|v Translational cancer research
|x 0
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF3
|b Gesundheit
914 1 _ |y 2018
915 _ _ |0 StatID:(DE-HGF)0200
|2 StatID
|a DBCoverage
|b SCOPUS
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|2 StatID
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920 1 _ |0 I:(DE-He78)G300-20160331
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|l KKE Dermatoonkologie
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-He78)G300-20160331
980 _ _ |a UNRESTRICTED


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
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