Evidence map›Paper›PMID 25298229›Full record

ArticleVirchows Archiv : an international journal of pathology2014

Acinar cell carcinomas of the pancreas: a molecular analysis in a series of 57 cases.

Frank Bergmann, Sebastian Aulmann, Bence Sipos, Matthias Kloor, Anja von Heydebreck, Johannes Schweipert, Andreas Harjung, Philipp Mayer, Werner Hartwig, Gerhard Moldenhauer and 9 more

Abstract read
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In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

44 citing papers in PubMed, 73 citations in OpenAlex.

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  13. Neuroendocrine neoplasms of the pancreas: diagnosis and pitfalls.Virchows Archiv : an international journal of pathology · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. [Rare pancreatic tumors].Der Pathologe · 2021
    Review
  18. Review
  19. RAF1 rearrangements are common in pancreatic acinar cell carcinomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Article
  20. Successful BRAF/MEK inhibition in a patient withCold Spring Harbor molecular case studies · 2020
    Article
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

19 authors at 5 institutions in 2 countries.

Frank BergmannInstitute of Pathology, University of Heidelberg, Im Neuenheimer Feld 224, D-69120, Heidelberg, Germany, frank.bergmann@med.uni-heidelberg.de.
Sebastian Aulmann
Bence Sipos
Matthias Kloor
Anja von Heydebreck
Johannes Schweipert
Andreas Harjung
Philipp Mayer
Werner Hartwig
Gerhard Moldenhauer
David Capper
Gerhard Dyckhoff
Kolja Freier
Esther Herpel
Anja Schleider
Peter Schirmacher
Gunhild Mechtersheimer
Günter Klöppel
Hendrik Bläker
Heidelberg University · DECharité - Universitätsmedizin Berlin · DEMerck (Germany) · DETechnical University of Munich · DEUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic acinar cell carcinomas (PACs) are rare but are distinct aggressive neoplasms that phenotypically differ from pancreatic ductal adenocarcinomas (PDACs) and pancreatic neuroendocrine neoplasms (PNENs). Despite recent work on the genetic changes of PACs, their molecular pathogenesis is still poorly understood. In this study, we focus on a comparative genomic hybridization analysis. Based on frequent chromosomal imbalances, the involvement of DCC and c-MYC in the pathogenesis of PACs is further investigated. Moreover, we examine markers harboring potential therapeutic relevance (K-RAS, BRAF, EGFR, MGMT, HSP90, L1CAM, Her2). PACs revealed a microsatellite stable, chromosomal unstable genotype, defined by recurrent chromosomal losses of 1p, 3p, 4q, 5q, 6q, 8p, 9p, 11q, 13q, 16q, and 18, as well as gains of 1q, 7, 8q, 12, 17q, and 20q. Subsets of PAC displayed reduction/loss of DCC (79 %) and c-MYC-amplification (17 %). Significant EGFR expression occurred in 42 %, HSP90 expression in 98 %, L1CAM expression in 72 %, and loss of MGMT in 26 %. Two cases carried a K-RAS mutation. Mutations of EGFR or BRAF were not detected. All cases were Her2/neu-negative. PACs display characteristic chromosomal imbalances which are distinctly different from those in pancreatic ductal adenocarcinomas and pancreatic neuroendocrine neoplasms. Our findings suggest that DCC and c-MYC alterations may play an important role in the pathogenesis of PACs. Furthermore, EGFR, MGMT, HSP90, and L1CAM may be useful as therapeutic markers and predictors of response to therapy in a subset of PACs.

Indexed as

AdolescentAdultAgedBiomarkers, TumorCarcinoma, Acinar CellChildChromosome AberrationsComparative Genomic HybridizationDNA Mutational AnalysisFemaleHumansImmunohistochemistryIn Situ Hybridization, FluorescenceMaleMiddle AgedPancreatic NeoplasmsBiomarkers, Tumor

Identifiers

PMID25298229
OpenAlexW2093232036

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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.