Evidence map›Paper›PMID 16088401›Full record

ArticleVirchows Archiv : an international journal of pathology2005

Expression of small intestinal and colonic phenotypes in complete intestinal metaplasia of the human stomach.

Harunari Tanaka, Tetsuya Tsukamoto, Tsutomu Mizoshita, Ken-ichi Inada, Naotaka Ogasawara, Xueyuan Cao, Sosuke Kato, Takashi Joh, Masae Tatematsu

Abstract read
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In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 18% 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, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Barrett oesophagus: lessons on its origins from the lesion itself.Nature reviews. Gastroenterology & hepatology · 2015
    Review
  6. Article
  7. Article
  8. Gastric-and-intestinal mixed-type intestinal metaplasia: aberrant expression of transcription factors and stem cell intestinalization.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2006
    Review
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

9 authors at 2 institutions in 1 country.

Harunari TanakaDivision of Oncological Pathology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Nagoya, 464-8681, Japan.
Tetsuya Tsukamoto
Tsutomu Mizoshita
Ken-ichi Inada
Naotaka Ogasawara
Xueyuan Cao
Sosuke Kato
Takashi Joh
Masae Tatematsu
Aichi Cancer Center · JPNagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incomplete intestinal metaplasia (IM) that is reported to be a risk factor for gastric carcinogenesis in man usually features sulfomucin production and thus is considered of colonic type. To cast light on the underlying mechanisms, we here examined the proportions of colonic and small intestinal phenotypes in IM by immunohistochemistry and real-time reverse transcription-polymerase chain reaction at the single isolated gland level. Carbonic anhydrase 1 (CA1) is a specific marker of colonic epithelial cells, whereas sucrase is specific to absorptive cells of the small intestine. Totals of 139 (23.5%) and 452 (76.5%) IM glands were judged to be CA1 positive and CA1 negative, respectively, in resected pyloric mucosa from cancer patients. The average score for MUC5AC in CA1-positive IMs was significantly lower than in CA1-negative counterpart tissue (P<0.0001), whereas the opposite was the case for sucrase (P<0.0001). High iron diamine-Alcian blue staining revealed CA1 expression to coincide with type I complete IM. The expression of CA1 mRNA strongly correlated with that of sucrase-isomaltase, and inversely with that of MUC5AC in isolated IM glands. In conclusion, CA1 could be colocalized with small intestinal proteins such as sucrase, but only rarely with the gastric mucin, MUC5AC. Its expression warrants further study, with the focus on stimulation and/or suppression mechanisms by gastric and intestinal transcription factors.

Indexed as

BiomarkersCarbonic Anhydrase IColonGastric MucosaHumansImmunoenzyme TechniquesIntestine, SmallMetaplasiaMucin 5ACMucinsPhenotypeReverse Transcriptase Polymerase Chain ReactionRNA, MessengerStomachSucrase-Isomaltase ComplexBiomarkersCarbonic Anhydrase IMUC5AC protein, humanMucin 5ACMucinsRNA, MessengerSucrase-Isomaltase Complex

Identifiers

PMID16088401
OpenAlexW2049948596

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.