Evidence map›Paper›PMID 14991527›Full record

ArticleJournal of human genetics2004

Rapid isolation of viral integration site reveals frequent integration of HTLV-1 into expressed loci.

Tatsuhiko Ozawa, Takahiro Itoyama, Naoki Sadamori, Yasuaki Yamada, Tomoko Hata, Masao Tomonaga, Masaharu Isobe

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

12 citing papers in PubMed, 30 citations in OpenAlex.

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  11. Correction of chromosomal mutation and random integration in embryonic stem cells with helper-dependent adenoviral vectors.Proceedings of the National Academy of Sciences of the United States of America · 2005
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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

7 authors at 3 institutions in 1 country.

Tatsuhiko OzawaLaboratory of Molecular and Cellular Biology, Department of Materials and Biosystem Engineering, Faculty of Engineering, Toyama University, 3190 Gofuku, Toyama 930-8555, Japan.
Takahiro ItoyamaLaboratory of Molecular and Cellular Biology, Department of Materials and Biosystem Engineering, Faculty of Engineering, Toyama University, 3190 Gofuku, Toyama 930-8555, Japan.
Naoki SadamoriDepartment of Nursing, Siebold University of Nagasaki, Nagasaki 851-2195, Japan.
Yasuaki YamadaDivision of Laboratory Medicine, Department of Translational Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan.
Tomoko HataDepartment of Hematology, Molecular Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
Masao TomonagaDepartment of Hematology, Molecular Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
Masaharu IsobeLaboratory of Molecular and Cellular Biology, Department of Materials and Biosystem Engineering, Faculty of Engineering, Toyama University, 3190 Gofuku, Toyama 930-8555, Japan. isobe@eng.toyama-u.ac.jp.
Nagasaki University · JPUniversity of Toyama · JPUniversity of Nagasaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although there is tight association of the human T-cell leukemia virus type-1 (HTLV-1) with adult T-cell leukemia/lymphoma (ATLL), it has remained unresolved whether the HTLV-1 integration into the host genome has any role in the development of this disease. We isolated a total of 58 HTLV-1 integration sites using newly developed, adaptor-ligated PCR from 33 ATLL patients and five ATLL cell lines. We compared our data as well as the previously reported ones with the complete human genomic sequence for the location of its placement, structure, and expression of genes nearby the integration site. The chromosomal target for integration was selected at random, but the integration favorably occurred within the transcription units; more than 59.5% of total integration was observed within the transcriptional unit. All inserted genes by HTLV-1 integration were expressed in normal T cells. Upregulation of genes due to viral integration was found in two out of nine ATLL cases; about 4.4- and 102-fold elevated ankyrin-1 ( ANK-1) and gephyrin ( GPHN) gene expressions were observed, respectively. These data suggest that the preferential integration of HTLV-1 into an expressed locus occasionally causes deregulation of corresponding gene, which may lead to leukemogenesis of a fraction of ATLL.

Indexed as

Virus IntegrationAnkyrinsCarrier ProteinsCell Line, TumorChromosome MappingDatabases as TopicGene Expression Regulation, NeoplasticGenome, HumanHTLV-I InfectionsHumansHuman T-lymphotropic virus 1Leukemia-Lymphoma, Adult T-CellMembrane ProteinsPolymerase Chain ReactionProvirusesReverse Transcriptase Polymerase Chain ReactionANK1 protein, humanAnkyrinsCarrier ProteinsgephyrinMembrane ProteinsRNA, Messenger

Identifiers

PMID14991527
OpenAlexW2051404329

What OpenQuestion holds

Textmetadata
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.