Evidence map›Paper›PMID 27767239›Full record

ArticleHistopathology2017

Morphology and genetics of pyloric gland adenomas in familial adenomatous polyposis.

Wenzel M Hackeng, Elizabeth A Montgomery, Francis M Giardiello, Aatur D Singhi, Marija Debeljak, James R Eshleman, Michael Vieth, G Johan Offerhaus, Laura D Wood, Lodewijk A A Brosens

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In one paragraph

Article in Histopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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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

10 authors at 5 institutions in 3 countries.

Wenzel M HackengDepartment of Pathology, University Medical Center Utrecht, Utrecht, the Netherlands.
Elizabeth A MontgomeryDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Francis M GiardielloDepartments of Medicine, Oncology Center and Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Aatur D SinghiDepartment of Pathology, University of Pittsburgh, Pittsburgh, PA, USA.
Marija DebeljakDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
James R EshlemanDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Michael ViethInstitut für Pathologie, Klinikum Bayreuth GmbH, Bayreuth, Germany.
G Johan OfferhausDepartment of Pathology, University Medical Center Utrecht, Utrecht, the Netherlands.
Laura D WoodDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Lodewijk A A BrosensDepartment of Pathology, University Medical Center Utrecht, Utrecht, the Netherlands.
Johns Hopkins Medicine · USJohns Hopkins University · USBayreuth Medical Center · DEUniversity Medical Center Utrecht · NLUniversity of Pittsburgh · US

Funding

Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
Curcumin chemoprevention in familial adenomatous polyposisR01CA134620 · NCI · JOHNS HOPKINS UNIVERSITY · PI GIARDIELLO, FRANCIS M · 2010 to 2015
$2.7M
NCI NIH HHS P50 CA062924NCI NIH HHS R01 CA134620
6 · The paper itself

Abstract

aimsGastric pyloric gland adenomas (PGAs) are rare epithelial polyps that are found more commonly in autoimmune atrophic gastritis and familial adenomatous polyposis (FAP). Little is known about the morphology and genetics of PGAs in FAP. PGAs in FAP are studied morphologically and genetically. Findings in FAP-associated PGAs are compared to sporadic PGAs and related lesions such as oxyntic gland adenoma (OGA) to increase our understanding of these rare polyps. METHODS AND

resultsSeven PGAs and 18 fundic gland polyps (FGPs) from FAP patients were collected. KRAS and GNAS mutations were determined in six PGAs and 18 FGPs. Immunohistochemistry was applied on five PGAs to provide further confirmation of the histological subtypes and genetic alterations. Morphology of all PGAs was studied and compared to literature on sporadic PGAs and related lesions. All successfully sequenced PGAs (six of six) carried GNAS mutations and half of the successfully sequenced PGAs carried a KRAS mutation (three of six). Nuclear β-catenin was seen only in one PGA with focal high-grade dysplasia. Morphologically, PGAs in FAP showed overlapping features with OGA.

conclusionFamilial adenomatous polyposis-associated PGAs have a similar genetic background as sporadic PGAs, i.e. KRAS and GNAS mutation. Based on morphological findings in FAP associated PGAs, it is hypothesized that PGAs and OGAs are closely related lesions.

Indexed as

AdenomaAdenomatous Polyposis ColiAdultAgedChromograninsDNA Mutational AnalysisFemaleGastric MucosaGTP-Binding Protein alpha Subunits, GsHumansImmunohistochemistryMaleMiddle AgedMutationProto-Oncogene Proteins p21(ras)Reverse Transcriptase Polymerase Chain ReactionChromograninsGNAS protein, humanGTP-Binding Protein alpha Subunits, GsKRAS protein, humanProto-Oncogene Proteins p21(ras)familial adenomatous polyposisfundic gland polypgastric adenomaoxyntic gland adenomapyloric gland adenoma

Identifiers

PMID27767239
PMCPMC5300963
OpenAlexW2533575211

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.