Evidence map›Paper›PMID 37715023›Full record

ArticleBritish journal of cancer2023

Histological diagnosis of polyploidy discriminates an aggressive subset of hepatocellular carcinomas with poor prognosis.

Takanori Matsuura, Yoshihide Ueda, Yoshiyuki Harada, Kazuki Hayashi, Kisara Horisaka, Yoshihiko Yano, Shinichi So, Masahiro Kido, Takumi Fukumoto, Yuzo Kodama and 2 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 21 citations in OpenAlex.

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  15. Targeting chromosomal instability in patients with cancer.Nature reviews. Clinical oncology · 2024
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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

12 authors at 2 institutions in 1 country.

Takanori MatsuuraDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Yoshihide UedaDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Yoshiyuki HaradaDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Kazuki HayashiDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Kisara HorisakaDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Yoshihiko YanoDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Shinichi SoDivision of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Masahiro KidoDivision of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Takumi FukumotoDivision of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
Yuzo KodamaDivision of Gastroenterology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Eiji HaraDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.ORCID 0000-0001-7821-3960
Tomonori MatsumotoDepartment of Molecular Microbiology, Research Institute for Microbial Diseases, Osaka University, Suita, Japan. tomomatsumoto@biken.osaka-u.ac.jp.ORCID 0000-0003-4483-2178
Kobe University · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough genome duplication, or polyploidization, is believed to drive cancer evolution and affect tumor features, its significance in hepatocellular carcinoma (HCC) is unclear. We aimed to determine the characteristics of polyploid HCCs by evaluating chromosome duplication and to discover surrogate markers to discriminate polyploid HCCs.

methodsThe ploidy in human HCC was assessed by fluorescence in situ hybridization for multiple chromosomes. Clinicopathological and expression features were compared between polyploid and near-diploid HCCs. Markers indicating polyploid HCC were explored by transcriptome analysis of cultured HCC cells.

resultsPolyploidy was detected in 36% (20/56) of HCCs and discriminated an aggressive subset of HCC that typically showed high serum alpha-fetoprotein, poor differentiation, and poor prognosis compared to near-diploid HCCs. Molecular subtyping revealed that polyploid HCCs highly expressed alpha-fetoprotein but did not necessarily show progenitor features. Histological examination revealed abundant polyploid giant cancer cells (PGCCs) with a distinct appearance and frequent macrotrabecular-massive architecture in polyploid HCCs. Notably, the abundance of PGCCs and overexpression of ubiquitin-conjugating enzymes 2C indicated polyploidy in HCC and efficiently predicted poor prognosis in combination.

conclusionsHistological diagnosis of polyploidy using surrogate markers discriminates an aggressive subset of HCC, apart from known HCC subgroups, and predict poor prognosis in HCC.

Indexed as

Carcinoma, HepatocellularLiver Neoplasmsalpha-FetoproteinsHumansIn Situ Hybridization, FluorescencePolyploidyPrognosisalpha-Fetoproteins

Identifiers

PMID37715023
PMCPMC10576083
OpenAlexW4386773977

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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.