Evidence map›Paper›PMID 33934524›Full record

ArticleCancer medicine2021

Comprehensive mutational analysis of background mucosa in patients with Lugol-voiding lesions.

Naoki Akizue, Kenichiro Okimoto, Makoto Arai, Yosuke Hirotsu, Kenji Amemiya, Hirotaka Oura, Tatsuya Kaneko, Mamoru Tokunaga, Kentaro Ishikawa, Yuki Ohta and 12 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 56% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

22 authors at 4 institutions in 1 country.

Naoki AkizueDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kenichiro OkimotoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-5809-1254
Makoto AraiDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Yosuke HirotsuGenome Analysis Center, Yamanashi Prefectural Central Hospital, Yamanashi, Japan.ORCID 0000-0002-8002-834X
Kenji AmemiyaGenome Analysis Center, Yamanashi Prefectural Central Hospital, Yamanashi, Japan.
Hirotaka OuraDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tatsuya KanekoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Mamoru TokunagaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kentaro IshikawaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Yuki OhtaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Takashi TaidaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Keiko SaitoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Daisuke MaruokaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tomoaki MatsumuraDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tomoo NakagawaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Motoi NishimuraDivision of Clinical Genetics and Proteomics, Department of Laboratory Medicine, Chiba University Hospital, Chiba, Japan.
Tetsuhiro ChibaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0001-7179-0765
Kazuyuki MatsushitaDivision of Clinical Genetics and Proteomics, Department of Laboratory Medicine, Chiba University Hospital, Chiba, Japan.ORCID 0000-0001-6742-0761
Hitoshi MochizukiGenome Analysis Center, Yamanashi Prefectural Central Hospital, Yamanashi, Japan.
Osamu YokosukaDepartment of Gastroenterology, Japan Community Health care Organization Funabashi Central Hospital, Chiba, Japan.
Masao OmataGenome Analysis Center, Yamanashi Prefectural Central Hospital, Yamanashi, Japan.
Naoya KatoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chiba University · JPYamanashi Prefectural Central Hospital · JPChiba University Hospital · JPJapan Community Healthcare Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic mutations including the background mucosa in patients with Lugol-voiding lesions (LVLs) are still not well known. The aim of this study was to evaluate the somatic mutations of the background mucosa in patients with LVLs (Squamous cell carcinoma (SCC), intraepithelial neoplasia (IN), and hyperplasia). Twenty-five patients with LVLs (9 with SCC, 6 with IN, and 10 with hyperplasia) were included. A targeted sequence was performed for LVLs and background mucosa using an esophageal cancer panel. Each mutation was checked whether it was oncogenic or not concerning OncoKB. In LVLs, TP53 was the most dominant mutation (80%). Furthermore, 72% of TP53 mutations was putative drivers. In background mucosa, NOTCH1 was the most dominant mutation (88%) and TP53 was the second most dominant mutation (48%). Furthermore, 73% of TP53 mutations and 8% of NOTCH1 mutations were putative drivers. Putative driver mutations of TP53 had significantly higher allele frequency (AF) in SCC than in IN and hyperplasia. Conversely, putative driver mutations of NOTCH1 did not have a significant accumulation of AF in the progression of carcinogenesis. Furthermore, in SCC, AF of TP53 mutations was significantly higher in LVLs than in background mucosa, but not in IN and hyperplasia. Regarding NOTCH1, a significant difference was not observed between LVLs and background mucosa in each group. The background mucosa in patients with LVLs already had putative driver mutations such as TP53 and NOTCH1. Of these two genes, TP53 mutation could be the main target gene of carcinogenesis in esophageal SCC. Clinical Trials registry: UMIN000034247.

Indexed as

Esophageal MucosaGenes, p53MutationAgedAlcohol DrinkingAllelesCarcinogenesisCarcinoma in SituCase-Control StudiesDisease ProgressionDNA Mutational AnalysisEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleGene FrequencyHumansIodidesLugol's solutionNOTCH1 protein, humanReceptor, Notch1background mucosaesophageal squamous cell carcinomaLugol-voiding lesionsNOTCHITP53

Identifiers

PMID33934524
PMCPMC8178505
OpenAlexW3159832417

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.