Evidence map›Paper›PMID 12915553›Full record

ArticleJournal of virology2003

Silent point mutation in an avian retrovirus RNA processing element promotes c-myb-associated short-latency lymphomas.

Tatjana S Polony, Sandra J Bowers, Paul E Neiman, Karen L Beemon

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Integration of ALV intoOncotarget · 2017
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. RNA processing control in avian retroviruses.Frontiers in bioscience : a journal and virtual library · 2008
    Review
  10. Telomerase reverse transcriptase expression elevated by avian leukosis virus integration in B cell lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  11. Article
  12. Review
  13. Article
  14. 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 2 institutions in 1 country.

Tatjana S PolonyDepartment of Biology, Johns Hopkins University, Baltimore, Maryland 21218, USA.
Sandra J Bowers
Paul E Neiman
Karen L Beemon
Fred Hutch Cancer Center · USJohns Hopkins University · US

Funding

CELLULAR AND MOLECULAR BIOLOGYT32GM007231 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VAN DOREN, MARK B · 1985 to 2020
$18.4M
RETROVIRAL REGULATORY SEQUENCES WITHIN CODING SEQUENCESR01CA048746 · NCI · JOHNS HOPKINS UNIVERSITY · PI BEEMON, KAREN L. · 1989 to 2014
$4.6M
MOLECULAR MECHANISMS IN NEOPLASIAR01CA020068 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI NEIMAN, PAUL ERIC · 1985 to 2008
$2.6M
Oncogenes and oncogenic microRNAs in chicken tumorsR01CA124596 · NCI · JOHNS HOPKINS UNIVERSITY · PI BEEMON, KAREN L. · 2008 to 2012
$1.7M
NCI NIH HHS R01 CA020068NCI NIH HHS R01 CA048746NCI NIH HHS R01 CA124596NCI NIH HHS R01CA20068NCI NIH HHS R01CA48746NIGMS NIH HHS T32 GM007231NIGMS NIH HHS T32GM07231
6 · The paper itself

Abstract

The avian leukosis virus DeltaLR-9 causes a high frequency of B-cell lymphomas within weeks after injection into 10-day-old chicken embryos. These lymphomas result from proviral integrations into the oncogene c-myb. In contrast, LR-9, which lacks the 42-nucleotide gag gene deletion of DeltaLR-9, does not cause a high frequency of c-myb-associated short-latency lymphomas. Although viral replication rates and spliced env mRNA levels were found to be similar for both viruses, DeltaLR-9 exhibited an increase in readthrough transcription compared to LR-9. The DeltaLR-9 deletion is located in the region of the gag gene corresponding to the matrix (MA) protein as well as in the negative regulator of splicing (NRS) element. To test whether disruption of the NRS or of the MA protein was responsible for inducing short-latency lymphomas, we generated viruses with NRS point mutations that maintained the wild-type Gag amino acid sequence. One of the mutant viruses induced an even higher incidence than DeltaLR-9 of short-latency lymphomas with viral integrations into c-myb. Thus, we propose that disruption of the NRS sequence promotes readthrough transcription and splicing to the downstream myb gene, causing overexpression of a slightly truncated Myb protein, which induces short-latency tumors.

Indexed as

Genes, mybAnimalsAvian LeukosisAvian Leukosis VirusBase SequenceChick EmbryoDNA, ViralGenes, envLymphoma, B-CellOncogene Proteins v-mybPoint MutationRNA, MessengerRNA Processing, Post-TranscriptionalRNA SplicingRNA, ViralSequence DeletionDNA, ViralOncogene Proteins v-mybRNA, MessengerRNA, ViralViral Matrix Proteins

Identifiers

PMID12915553
PMCPMC187396
OpenAlexW2151847115

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.