Evidence map›Paper›PMID 12525640›Full record

ArticleJournal of virology2003

Genome-based identification of cancer genes by proviral tagging in mouse retrovirus-induced T-cell lymphomas.

Rachel Kim, Alla Trubetskoy, Takeshi Suzuki, Nancy A Jenkins, Neal G Copeland, Jack Lenz

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 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
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  7. SOX3 can promote the malignant behavior of glioblastoma cells.Cellular oncology (Dordrecht, Netherlands) · 2019
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  15. Sex-determining region Y-box3 (SOX3) functions as an oncogene in promoting epithelial ovarian cancer by targeting Src kinase.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

6 authors at 2 institutions in 1 country.

Rachel KimDepartment of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Alla Trubetskoy
Takeshi Suzuki
Nancy A Jenkins
Neal G Copeland
Jack Lenz
Albert Einstein College of Medicine · USNational Cancer Institute · US

Funding

LEUKEMOGENESIS BY MURINE RETROVIRUSESR01CA044822 · NCI · YESHIVA UNIVERSITY · PI LENZ, JACK R. · 1987 to 2006
$2.4M
VIRAL ONCOLOGY AND TUMOR BIOLOGYT32CA009060 · NCI · YESHIVA UNIVERSITY · PI LENZ, JACK R. · 1985 to 2001
$569k
NCI NIH HHS CA09060NCI NIH HHS CA44822NCI NIH HHS R01 CA044822NCI NIH HHS T32 CA009060
6 · The paper itself

Abstract

The identification of tumor-inducing genes is a driving force for elucidating the molecular mechanisms underlying cancer. Many retroviruses induce tumors by insertion of viral DNA adjacent to cellular oncogenes, resulting in altered expression and/or structure of the encoded proteins. The availability of the mouse genome sequence now allows analysis of retroviral common integration sites in murine tumors to be used as a genetic screen for identification of large numbers of candidate cancer genes. By positioning the sequences of inverse PCR-amplified, virus-host junction fragments within the mouse genome, 19 target genes were identified in T-cell lymphomas induced by the retrovirus SL3-3. The candidate cancer genes included transcription factors (Fos, Gfi1, Lef1, Myb, Myc, Runx3, and Sox3), all three D cyclins, Ras signaling pathway components (Rras2/TC21 and Rasgrp1), and Cmkbr7/CCR7. The most frequent target was Rras2. Insertions as far as 57 kb away from the transcribed portion were associated with substantially increased transcription of Rras2, and no coding sequence mutations, including those typically involved in Ras activation, were detected. These studies demonstrate the power of genome-based analysis of retroviral insertion sites for cancer gene discovery, identify several new genes worth examining for a role in human cancer, and implicate the pathways in which those genes act in lymphomagenesis. They also provide strong genetic evidence that overexpression of unmutated Rras2 contributes to tumorigenesis, thus suggesting that it may also do so if it is inappropriately expressed in human tumors.

Indexed as

GenomeOncogenesAnimalsDNA, ViralHumansLymphoma, T-CellMiceMutationPolymerase Chain ReactionProvirusesRetroviridaeTerminal Repeat SequencesTranscriptional ActivationDNA, Viral

Identifiers

PMID12525640
PMCPMC140962
OpenAlexW2129905381

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.