Evidence map›Paper›PMID 10516025›Full record

ArticleJournal of virology1999

Sequence and insertion sites of murine melanoma-associated retrovirus.

M Li, X Huang, Z Zhu, E Gorelik

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Making a virtue of necessity: the pleiotropic role of human endogenous retroviruses in cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  13. Article
  14. Endogenous retroviruses and the development of cancer.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Review
  15. Article
  16. Article
  17. Article
  18. The program of androgen-responsive genes in neoplastic prostate epithelium.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

M LiUniversity of Pittsburgh Cancer Institute, Department of Pathology, Pittsburgh, Pennsylvania 15213, USA. mengfeng@pitt.edu
X Huang
Z Zhu
E Gorelik
UPMC Hillman Cancer Center · US

Funding

H 2, ALPHA GALACTOSYL EPITOPES AND TUMOR METASTASESR01CA059903 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GORELIK, ELIESER · 1994 to 2001
$474k
NCI NIH HHS CA59903
6 · The paper itself

Abstract

We previously showed that B16 melanoma cells produce ecotropic melanoma-associated retrovirus (MelARV) which encodes a melanoma-associated antigen recognized by MM2-9B6 monoclonal antibody. The biological significance of MelARV in melanoma formation remains unknown. We found that infection of normal melanocytes with MelARV resulted in malignant transformation. It is likely that MelARV emerged from the defective Emv-2 provirus, a single copy of ecotropic provirus existing in the genome of C57BL/6 mice. In the present study, we cloned and sequenced the full-length MelARV genome and its insertion sites and we completed sequencing of the Emv-2 provirus. Our data show that MelARV has a typical full-length retroviral genome with high homology (98.54%) to Emv-2, indicating a close relationship between both viruses. MelARV probably emerged as a result of recombination between Emv-2 and an endogenous nonecotropic provirus. Some observed differences in the gag and pol regions of MelARV might account for the restoration of productivity and infectivity of a novel retrovirus that somatically emerged during melanoma formation. MelARV does not contain any oncogene and therefore might induce transformation by insertional mutagenesis. We sequenced two insertion sites of MelARV. The first insertion site represents the 3' coding region of the c-maf proto-oncogene at 67.0 centimorgans (cM) on chromosome 8. The c-maf proto-oncogene encodes a basic leucine zipper protein homologous to c-fos and c-jun. Insertion of MelARV in BL6 melanoma cells resulted in the up-regulation of c-maf. It is noteworthy that the Emv-2 provirus is also inserted into a noncoding region at 61.0 cM on the same chromosome 8. The second insertion site is the 3' noncoding region of the DNA polymerase gamma (PolG) gene on chromosome 7. The expression of PolG was not affected by the MelARV insertion. Further investigation of the biological significance of MelARV in melanoma formation is being undertaken.

Indexed as

Genome, ViralVirus IntegrationAnimalsBase SequenceBlotting, NorthernCloning, MolecularDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA Polymerase gammaGammaretrovirusMelanoma, ExperimentalMiceMice, Inbred C57BLMolecular Sequence DataMutagenesis, InsertionalPlasmidsDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA Polymerase gammaMaf protein, mouseProto-Oncogene ProteinsProto-Oncogene Proteins c-mafRNA, Viral

Identifiers

PMID10516025
PMCPMC112951
OpenAlexW2143733226

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.