Evidence map›Paper›PMID 37396703›Full record

ArticleWorld journal of virology2023

Re-analysis of hepatitis B virus integration sites reveals potential new loci associated with oncogenesis in hepatocellular carcinoma.

Ryuta Kojima, Shingo Nakamoto, Tadayoshi Kogure, Yaojia Ma, Keita Ogawa, Terunao Iwanaga, Na Qiang, Junjie Ao, Ryo Nakagawa, Ryosuke Muroyama and 4 more

Abstract read
In one paragraph

Article in World journal of virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Review
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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

14 authors.

Ryuta KojimaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Shingo NakamotoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan. nakamotoer@faculty.chiba-u.jp.
Tadayoshi KogureDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Yaojia MaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Keita OgawaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Terunao IwanagaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Na QiangDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Junjie AoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Ryo NakagawaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Ryosuke MuroyamaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Masato NakamuraDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Tetsuhiro ChibaDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Jun KatoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Naoya KatoDepartment of Gastroenterology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC). HBV DNA can get integrated into the hepatocyte genome to promote carcinogenesis. However, the precise mechanism by which the integrated HBV genome promotes HCC has not been elucidated.

aimTo analyze the features of HBV integration in HCC using a new reference database and integration detection method.

methodsPublished data, consisting of 426 Liver tumor samples and 426 paired adjacent non-tumor samples, were re-analyzed to identify the integration sites. Genome Reference Consortium Human Build 38 (GRCh38) and Telomere-to-Telomere Consortium CHM13 (T2T-CHM13 (v2.0)) were used as the human reference genomes. In contrast, human genome 19 (hg19) was used in the original study. In addition, GRIDSS VIRUSBreakend was used to detect HBV integration sites, whereas high-throughput viral integration detection (HIVID) was applied in the original study (HIVID-hg19).

resultsA total of 5361 integration sites were detected using T2T-CHM13. In the tumor samples, integration hotspots in the cancer driver genes, such as

conclusionGRIDSS VIRUSBreakend using T2T-CHM13 is accurate and sensitive in detecting HBV integration. Re-analysis provides new insights into the regions of HBV integration and their potential roles in HCC development.

Indexed as

CarcinomaHepatitis B virusHepatocellularVirus integration

Identifiers

PMID37396703
PMCPMC10311580

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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.