Evidence map›Paper›PMID 34514550›Full record

ArticleJournal of gastroenterology2021

APC mutations are common in adenomas but infrequent in adenocarcinomas of the non-ampullary duodenum.

Kenichi Ishizu, Taiki Hashimoto, Tomoaki Naka, Yasushi Yatabe, Motohiro Kojima, Takeshi Kuwata, Satoru Nonaka, Ichiro Oda, Minoru Esaki, Masashi Kudo and 4 more

Abstract read
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In one paragraph

Article in Journal of gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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    Review
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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

14 authors at 4 institutions in 3 countries.

Kenichi IshizuDivision of Diagnostic Pathology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Taiki HashimotoDivision of Diagnostic Pathology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Tomoaki NakaDivision of Diagnostic Pathology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Yasushi YatabeDivision of Diagnostic Pathology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Motohiro KojimaDivision of Pathology, Research Center for Innovative Oncology, National Cancer Center, Chiba, Japan.
Takeshi KuwataDivision of Pathology, Research Center for Innovative Oncology, National Cancer Center, Chiba, Japan.
Satoru NonakaEndoscopy Division, National Cancer Center Hospital, Tokyo, Japan.
Ichiro OdaEndoscopy Division, National Cancer Center Hospital, Tokyo, Japan.
Minoru EsakiDepartment of Hepatobiliary and Pancreatic Surgery, National Cancer Center Hospital, Tokyo, Japan.
Masashi KudoDepartment of Hepatobiliary and Pancreatic Surgery, National Cancer Center Hospital East, Chiba, Japan.
Naoto GotohdaDepartment of Hepatobiliary and Pancreatic Surgery, National Cancer Center Hospital East, Chiba, Japan.
Teruhiko YoshidaDivision of Genetics, National Cancer Center Research Institute, Tokyo, Japan.
Takaki YoshikawaDepartment of Gastric Surgery, National Cancer Center Hospital, Tokyo, Japan.
Shigeki SekineDivision of Diagnostic Pathology, National Cancer Center Hospital, 5-1-1, Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan. ssekine@ncc.go.jp.ORCID 0000-0003-0884-8981
National Cancer Center Hospital East · JPTokyo National Hospital · JPNational Cancer Center · USNational Cancer Centre Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies highlighted the clinicopathological heterogeneity of non-ampullary duodenal adenomas and adenocarcinomas, but the detailed process of the malignant transformation remains unclear.

methodsWe analyzed 144 adenomas and 54 adenocarcinomas of the non-ampullary duodenum for immunohistochemical phenotypes, genetic alterations, and mismatch repair (MMR) status to probe their histogenetic relationship.

resultsThe median ages of patients with adenoma and adenocarcinoma were the same (66 years). Adenomas were histologically classified as intestinal-type adenoma (n = 124), pyloric gland adenoma (PGA, n = 10), gastric-type adenoma, not otherwise specified (n = 9), and foveolar-type adenoma (n = 1). Protein-truncating APC mutations were highly frequent in adenomas (85%), with the highest prevalence in intestinal-type adenomas (89%), but rare in adenocarcinomas (9%; P = 2.1 × 10

conclusionThe discrepant APC mutation frequency between adenomas and adenocarcinomas suggests that APC-mutated adenomas, which constitute the large majority of non-ampullary duodenal adenomas, are less prone to malignant transformation. Non-ampullary duodenal adenocarcinomas frequently exhibit MMR deficiency and should be subject to MMR testing to determine appropriate clinical management, including the identification of patients with Lynch syndrome.

Indexed as

AdenocarcinomaAdenomatous Polyposis Coli ProteinAgedDuodenal NeoplasmsFemaleHumansJapanMaleMiddle AgedAdenomatous Polyposis Coli ProteinAPC protein, humanAPCDuodenal adenocarcinomaMismatch repair deficiencyNon-ampullary duodenal adenoma

Identifiers

PMID34514550
OpenAlexW3200546016

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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.