Evidence map›Paper›PMID 39245467›Full record

ArticleCancer science2024

Chromosome aberrations cause tumorigenesis through chromosomal rearrangements in a hepatocarcinogenesis rat model.

Kenji Nakamura, Yuji Ishii, Shinji Takasu, Moeka Namiki, Meili Soma, Norifumi Takimoto, Kohei Matsushita, Makoto Shibutani, Kumiko Ogawa

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Kenji NakamuraDivision of Pathology, National Institute of Health Sciences, Kawasaki, Japan.
Yuji IshiiDivision of Pathology, National Institute of Health Sciences, Kawasaki, Japan.ORCID https://orcid.org/0000-0002-3245-3464
Shinji TakasuDivision of Pathology, National Institute of Health Sciences, Kawasaki, Japan.
Moeka NamikiDivision of Pathology, National Institute of Health Sciences, Kawasaki, Japan.
Meili SomaDivision of Pathology, National Institute of Health Sciences, Kawasaki, Japan.
Norifumi TakimotoDivision of Pathology, National Institute of Health Sciences, Kawasaki, Japan.
Kohei MatsushitaDivision of Pathology, National Institute of Health Sciences, Kawasaki, Japan.
Makoto ShibutaniLaboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology, Tokyo, Japan.ORCID https://orcid.org/0000-0003-3417-9697
Kumiko OgawaDivision of Pathology, National Institute of Health Sciences, Kawasaki, Japan.ORCID https://orcid.org/0000-0002-4454-3838

Funding

Grant-in-Aid from the Ministry of Health, Labour, and Welfare of Japan 22KD2001
6 · The paper itself

Abstract

Chromosome aberrations (CAs), a genotoxic potential of carcinogens, are believed to contribute to tumorigenesis by chromosomal rearrangements through micronucleus formation. However, there is no direct evidence that proves the involvement of CAs in tumorigenesis in vivo. In the current study, we sought to clarify the involvement of CAs in chemical carcinogenesis using a rat model with a pure CA-inducer hepatocarcinogen, acetamide. Whole-genome analysis indicated that hepatic tumors induced by acetamide treatment for 26-30 weeks showed a broad range of copy number alterations in various chromosomes. In contrast, hepatic tumors induced by a typical mutagen (diethylnitrosamine) followed by a nonmutagen (phenobarbital) did not show such mutational patterns. Additionally, structural alterations such as translocations were observed more frequently in the acetamide-induced tumors. Moreover, most of the acetamide-induced tumors expressed c-Myc and/or MDM2 protein due to the copy number gain of each oncogene. These results suggest the occurrence of chromosomal rearrangements and subsequent oncogene amplification in the acetamide-induced tumors. Taken together, the results indicate that CAs are directly involved in tumorigenesis through chromosomal rearrangements in an acetamide-induced hepatocarcinogenesis rat model.

Indexed as

CarcinogenesisChromosome AberrationsDiethylnitrosamineAcetamidesAnimalsCarcinogensDisease Models, AnimalDNA Copy Number VariationsLiver NeoplasmsLiver Neoplasms, ExperimentalMalePhenobarbitalRatsRats, Inbred F344acetamideAcetamidesCarcinogensDiethylnitrosaminePhenobarbitalcarcinogenesischromosomal rearrangementchromosome aberrationcopy number alterationmicronucleus

Identifiers

PMID39245467
PMCPMC11531951

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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.