Evidence map›Paper›PMID 24590585›Full record

ArticleVirchows Archiv : an international journal of pathology2014

APC alterations are frequently involved in the pathogenesis of acinar cell carcinoma of the pancreas, mainly through gene loss and promoter hypermethylation.

Daniela Furlan, Nora Sahnane, Barbara Bernasconi, Milo Frattini, Maria Grazia Tibiletti, Francesca Molinari, Alessandro Marando, Lizhi Zhang, Alessandro Vanoli, Selenia Casnedi and 7 more

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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 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

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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

33 citing papers in PubMed, 74 citations in OpenAlex.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

17 authors at 9 institutions in 4 countries.

Daniela FurlanDepartment of Surgical and Morphological Sciences, University of Insubria, Varese, Italy.
Nora Sahnane
Barbara Bernasconi
Milo Frattini
Maria Grazia Tibiletti
Francesca Molinari
Alessandro Marando
Lizhi Zhang
Alessandro Vanoli
Selenia Casnedi
Volkan Adsay
Kenji Notohara
Luca Albarello
Sofia Asioli
Fausto Sessa
Carlo Capella
Stefano La Rosa
University of Insubria · ITOspedale di Circolo e Fondazione Macchi · ITEmory University · USHôpital d'Hautepierre · FRKurashiki Central Hospital · JPMayo Clinic in Arizona · USSan Raffaele University of Rome · ITUniversity of Pavia · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic and epigenetic alterations involved in the pathogenesis of pancreatic acinar cell carcinomas (ACCs) are poorly characterized, including the frequency and role of gene-specific hypermethylation, chromosome aberrations, and copy number alterations (CNAs). A subset of ACCs is known to show alterations in the APC/β-catenin pathway which includes mutations of APC gene. However, it is not known whether, in addition to mutation, loss of APC gene function can occur through alternative genetic and epigenetic mechanisms such as gene loss or promoter methylation. We investigated the global methylation profile of 34 tumor suppressor genes, CNAs of 52 chromosomal regions, and APC gene alterations (mutation, methylation, and loss) together with APC mRNA level in 45 ACCs and related peritumoral pancreatic tissues using methylation-specific multiplex ligation probe amplification (MS-MLPA), fluorescence in situ hybridization (FISH), mutation analysis, and reverse transcription-droplet digital PCR. ACCs did not show an extensive global gene hypermethylation profile. RASSF1 and APC were the only two genes frequently methylated. APC mutations were found in only 7 % of cases, while APC loss and methylation were more frequently observed (48 and 56 % of ACCs, respectively). APC mRNA low levels were found in 58 % of cases and correlated with CNAs. In conclusion, ACCs do not show extensive global gene hypermethylation. APC alterations are frequently involved in the pathogenesis of ACCs mainly through gene loss and promoter hypermethylation, along with reduction of APC mRNA levels.

Indexed as

DNA MethylationGenes, APCPromoter Regions, GeneticCarcinoma, Acinar CellDNA Mutational AnalysisGene DosageGenes, Tumor SuppressorHumansIn Situ Hybridization, FluorescenceMultiplex Polymerase Chain ReactionPancreatic NeoplasmsReverse Transcriptase Polymerase Chain Reaction

Identifiers

PMID24590585
OpenAlexW2071270420

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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.