Evidence map›Paper›PMID 32098350›Full record

ArticleCancers2020

Genomic Characterization of Non-Invasive Differentiated-Type Gastric Cancer in the Japanese Population.

Koki Nakamura, Yuji Urabe, Kenichi Kagemoto, Ryo Yuge, Ryohei Hayashi, Atsushi Ono, C Nelson Hayes, Shiro Oka, Masanori Ito, Takashi Nishisaka and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. World journal of gastrointestinal oncology · 2025
    Review
  2. Review
  3. Journal of clinical medicine · 2023
    Article
  4. Polymorphism in autophagy-related genes LRP1 and CAPZA1 may promote gastric mucosal atrophy.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023
    Article
  5. Article
  6. Article
  7. 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

15 authors at 3 institutions in 1 country.

Koki NakamuraDepartment of Gastroenterology and Metabolism, Institute of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.ORCID 0000-0002-3036-234X
Yuji UrabeDepartment of Gastroenterology and Metabolism, Institute of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Kenichi KagemotoDepartment of Gastroenterology and Metabolism, Institute of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Ryo YugeDepartment of Endoscopy, Hiroshima University Hospital, Hiroshima 734-8551, Japan.
Ryohei HayashiDepartment of Endoscopy, Hiroshima University Hospital, Hiroshima 734-8551, Japan.
Atsushi OnoDepartment of Gastroenterology and Metabolism, Institute of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
C Nelson HayesDepartment of Gastroenterology and Metabolism, Institute of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Shiro OkaDepartment of Gastroenterology and Metabolism, Institute of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Masanori ItoDepartment of Gastroenterology and Metabolism, Institute of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Takashi NishisakaDepartment of Pathology and Laboratory Medicine, Hiroshima Prefectural Hospital, Hiroshima 734-8551, Japan.
Kazuaki TanabeDepartment of Health Care for Adults, Graduate School of Biochemical & Health Sciences, Hiroshima 734-8551, Japan.
Koji ArihiroDepartment of Anatomical Pathology, Hiroshima University Hospital, Hiroshima, Hiroshima 734-8551, Japan.
Hideki OhdanDepartment of Gastroenterological and Transplant Surgery, Graduate School of Biochemical & Health Sciences, Hiroshima 734-8551, Japan.
Shinji TanakaDepartment of Endoscopy, Hiroshima University Hospital, Hiroshima 734-8551, Japan.
Kazuaki ChayamaDepartment of Gastroenterology and Metabolism, Institute of Biomedical and Health Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Hiroshima University · JPHiroshima University Hospital · JPHiroshima Prefectural Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsRecent genomic characterization of gastric cancer (GC) by sequencing has revealed a large number of cancer-related genes. Research to characterize the genomic landscape of cancer has focused on established invasive cancer to develop biomarkers for therapeutic or diagnostic targets, and nearly all GC reports have been about advanced GC. The aim of this study is to identify recurrently mutated genes in non-invasive GC and, in particular, the driver mutations that are associated with the development of GC. METHODS AND

resultsWe performed whole-exome sequencing of 19 fresh frozen specimens of differentiated-type non-invasive GC and targeted sequencing for 168 genes of 30 formalin-fixed paraffin-embedded archival specimens of differentiated-type non-invasive GC. We found that TP53 and LRP1 are significantly associated with non-invasive GC. It has been reported that LPR1 is associated with CagA autophagy in gastric mucosa. Therefore, we downloaded RNA sequence data for gastric cancer from the The Cancer Genome Atlas (TCGA) Genomic Data Commons Data Portal and examined the differences in LRP1 gene expression levels. The expression level was significantly lower in cases without LRP1 mutation than in cases with LRP1 mutation. Based on these results, fluorescent immunostaining for CagA was performed for 49 of the above samples to evaluate CagA accumulation within the cancerous tissue. Accumulation of CagA was significantly greater when an LRP1 mutation was present than without a mutation.

conclusionThese data suggest that LRP1 mutation is an important change promoting the transformation of gastric mucosa to GC early in the carcinogenesis of cancer.

Indexed as

CagAdriver mutationgastric cancerHelicobacter pyloriLRP1

Identifiers

PMID32098350
PMCPMC7072322
OpenAlexW3008266283

What OpenQuestion holds

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LicenceCC BY
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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.