Evidence map›Paper›PMID 36892636›Full record

ArticleVirchows Archiv : an international journal of pathology2023

Molecular comparison of concurrent components of high-grade dysplasia, adenocarcinoma, and sarcomatoid carcinoma in a case of sarcomatoid carcinoma of the gallbladder.

Katsuya Hirose, Yuko Omori, Yusuke Ono, Yusuke Mizukami, Yoshiki Kaneko, Tsunehiko Maruyama, Haruo Ohtani, Toru Furukawa

Abstract read
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In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2023. 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
–field-weighted citation impact, top 95% 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, 0 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

8 authors at 3 institutions in 1 country.

Katsuya HiroseDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1, Seiryo-Machi, Aoba-Ku, Sendai, 980-8575, Japan.
Yuko OmoriDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1, Seiryo-Machi, Aoba-Ku, Sendai, 980-8575, Japan.
Yusuke OnoInstitute of Biomedical Research, Sapporo Higashi Tokusyukai Hospital, Sapporo, Japan.
Yusuke MizukamiInstitute of Biomedical Research, Sapporo Higashi Tokusyukai Hospital, Sapporo, Japan.
Yoshiki KanekoDepartment of Surgery, Mito Saiseikai General Hospital, Mito, Japan.
Tsunehiko MaruyamaDepartment of Surgery, Mito Saiseikai General Hospital, Mito, Japan.
Haruo OhtaniDepartment of Pathology, Mito Saiseikai General Hospital, Mito, Japan.
Toru FurukawaDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, 2-1, Seiryo-Machi, Aoba-Ku, Sendai, 980-8575, Japan. toru.furukawa@med.tohoku.ac.jp.ORCID http://orcid.org/0000-0002-1083-2324
Mito Saiseikai General Hospital · JPTohoku University · JPAsahikawa Medical University · JP

Funding

Japan Society for the Promotion of Science JP22H02839
6 · The paper itself

Abstract

Detailed genetic and immunohistochemical features of a sarcomatoid carcinoma of the gallbladder were reported. Studied was a resected gallbladder tumor involving the transverse colon, which was consisted of 3 histopathological neoplastic components, i.e., high-grade dysplasia, adenocarcinoma, and sarcomatoid carcinoma. The targeted amplicon sequencing showed somatic mutations in TP53 (p.S90fs) and ARID1A (c.4993 + 1G > T) in all of the 3 components. Copy numbers of CDKN2A and SMAD4 were decreased in the adenocarcinoma and the sarcomatoid component. Immunohistochemistry showed loss of expression of p53 and ARID1A in all components. p16 expression was lost in the adenocarcinoma and the sarcomatoid component, while SMAD4 expression was lost only in the latter. These results suggest that this sarcomatoid carcinoma may have developed by progression from high-grade dysplasia via adenocarcinoma with sequential accumulation of molecular aberrations involving p53, ARID1A, p16, and SMAD4. This information should serve to understand the molecular mechanism of this very intractable tumor.

Indexed as

AdenocarcinomaCarcinomaGallbladder NeoplasmsHumansTumor Suppressor Protein p53Tumor Suppressor Protein p53ARID1AGallbladderMolecular alterationsp16p53Sarcomatoid carcinomaSMAD4

Identifiers

PMID36892636
OpenAlexW4323652479

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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.