Evidence map›Paper›PMID 26943575›Full record

ArticleOncotarget2016

Oncogene and therapeutic target analyses in atypical fibroxanthomas and pleomorphic dermal sarcomas.

Doris Helbig, Michaela Angelika Ihle, Katharina Pütz, Iliana Tantcheva-Poor, Cornelia Mauch, Reinhard Büttner, Alexander Quaas

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
7.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.

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  18. Optimized PD-L1 scoring of gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Doris HelbigDepartment of Dermatology, University Hospital Cologne, Cologne, Germany.
Michaela Angelika IhleInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
Katharina PützInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
Iliana Tantcheva-PoorDepartment of Dermatology, University Hospital Cologne, Cologne, Germany.
Cornelia MauchDepartment of Dermatology, University Hospital Cologne, Cologne, Germany.
Reinhard BüttnerInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
Alexander QuaasInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
University Hospital Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUntil now, almost nothing is known about the tumorigenesis of atypical fibroxanthoma (AFX) and pleomorphic dermal sarcoma (PDS). Our hypothesis is that AFX is the non-infiltrating precursor lesion of PDS. MATERIALS AND

methodsWe performed the world-wide most comprehensive immunohistochemical and mutational analysis in well-defined AFX (n=5) and PDS (n=5).

resultsIn NGS-based mutation analyses of selected regions by a 17 hotspot gene panel of 102 amplicons we could detect TP53 mutations in all PDS as well as in the only analyzed AFX and PDS of the same patient. Besides, we detected mutations in the CDKN2A, HRAS, KNSTRN and PIK3CA genes.Performing immunohistochemistry for CTNNB1, KIT, CDK4, c-MYC, CTLA-4, CCND1, EGFR, EPCAM, ERBB2, IMP3, INI-1, MKI67, MDM2, MET, p40, TP53, PD-L1 and SOX2 overexpression of TP53, CCND1 and CDK4 was seen in AFX as well as in PDS. IMP3 was upregulated in 2 AFX (weak staining) and 4 PDS (strong staining).FISH analyses for the genes FGFR1, FGFR2 and FGFR3 revealed negative results in all tumors.

conclusionsUV-induced TP53 mutations as well as CCND1/CDK4 changes seem to play essential roles in tumorigenesis of PDS. Furthermore, we found some more interesting mutated genes in other oncogene pathways (activating mutations of HRAS and PIK3CA). All AFX and PDS investigated immunohistochemically presented with similar oncogene expression profiles (TP53, CCND1, CDK4 overexpression) and the single case with an AFX and PDS showed complete identical TP53 and PIK3CA mutation profiles in both tumors. This reinforces our hypothesis that AFX is the non-infiltrating precursor lesion of PDS.

Indexed as

AgedAged, 80 and overBiomarkers, TumorDNA Mutational AnalysisFemaleHigh-Throughput Nucleotide SequencingHumansImmunohistochemistryIn Situ Hybridization, FluorescenceMaleMutationOncogenesSarcomaSkin NeoplasmsXanthomatosisBiomarkers, Tumoratypical fibroxanthomaCCND1CDK4pleomorphic dermal sarcomaTP53

Identifiers

PMID26943575
PMCPMC5008321
OpenAlexW2325428530

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.