Evidence map›Paper›PMID 12967477›Full record

ArticleCancer science2003

Svi3: A provirus common integration site in c-myc in SL/Kh pre-B lymphomas.

Guang Jin, Tatsuaki Tsuruyama, Yoshihiro Yamada, Hiroshi Hiai

Open access · bronzeAbstract read
In one paragraph

Article in Cancer science, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 41% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
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

4 authors at 1 institution in 1 country.

Guang JinDepartment of Pathology and Biology of Diseases, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Tatsuaki Tsuruyama
Yoshihiro Yamada
Hiroshi Hiai
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spontaneous pre-B lymphomas in SL/Kh mice occur by somatic acquisition of a provirus genome of endogenous murine leukemia virus (MuLV). Inverse PCR amplification and sequence analyses of a provirus and its host flanking fragment revealed a proviral insertion into c-myc in 3 out of 60 SL/Kh pre-B lymphomas, named Svi3 lymphomas (SL/Kh virus integration site-3). Southern blot analysis revealed that two lymphomas had clonal integration in c-myc exon 1 and the other, in the promoter region. In 2 out of 3 Svi3 lymphomas, a fusion transcript of provirus 3' long terminal repeat and c-myc and a normal full-length c-myc transcript were obtained, but in one Svi3 lymphoma, only the normal transcript was obtained. All three Svi3 lymphomas had increased c-myc expression, producing normal 67-kDa c-Myc protein. Svi3 lymphomas had more mature phenotypes in the steps of early B-cell differentiation than Svi1 lymphomas, in which c-myc expression was indirectly up-regulated by provirus integration into Stat5a.

Indexed as

Milk ProteinsVirus Integration3' Untranslated RegionsAnimalsBlotting, NorthernBlotting, SouthernDNA-Binding ProteinsDNA, NeoplasmDNA PrimersExonsGenes, mycIntronsLeukemia Virus, MurineLymphoma, B-CellMiceMice, Inbred Strains3' Untranslated RegionsDNA-Binding ProteinsDNA, NeoplasmDNA PrimersMilk ProteinsStat5a protein, mouseSTAT5 Transcription FactorTrans-Activators

Identifiers

PMID12967477
PMCPMC11160231
OpenAlexW2147997973

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.