Evidence map›Paper›PMID 19530243›Full record

ArticleGenes, chromosomes & cancer2009

Recurrent chromosomal rearrangements implicate oncogenes contributing to T-cell lymphomagenesis in Lck-MyrAkt2 transgenic mice.

Roman A Timakhov, Yinfei Tan, Mamta Rao, Zemin Liu, Deborah A Altomare, Jianming Pei, David L Wiest, Olga O Favorova, Janice E Knepper, Joseph R Testa

Abstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2009. 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
0.5field-weighted citation impact, top 34% 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, 18 citations in OpenAlex.

  1. Tcf-1 promotes genomic instability and T cell transformation in response to aberrant β-catenin activation.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  8. Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2015
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  9. Article
  10. β-Catenin induces T-cell transformation by promoting genomic instability.Proceedings of the National Academy of Sciences of the United States of America · 2014
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  11. Article
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  14. GSK690693 delays tumor onset and progression in genetically defined mouse models expressing activated Akt.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010
    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

10 authors at 3 institutions in 2 countries.

Roman A TimakhovHuman Genetics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Yinfei Tan
Mamta Rao
Zemin Liu
Deborah A Altomare
Jianming Pei
David L Wiest
Olga O Favorova
Janice E Knepper
Joseph R Testa
Fox Chase Cancer Center · USVillanova University · USPirogov Russian National Research Medical University · RU

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
Basis for Lymphomagenesis in Akt2 Transgenic MiceR01CA077429 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI TESTA, JOSEPH R. · 1998 to 2013
$4.7M
REGULATION OF APOPTOSIS IN NEUROBLASTOMAR01CA069276 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CASTLE, VALERIE P · 1997 to 2005
$1.0M
NCI NIH HHS CA06927NCI NIH HHS CA77429NCI NIH HHS P30 CA006927NCI NIH HHS R01 CA069276NCI NIH HHS R01 CA077429
6 · The paper itself

Abstract

The oncogene v-akt was isolated from a retrovirus that induced naturally occurring thymic lymphomas in AKR mice. We hypothesized that constitutive activation of Akt2 could serve as a first hit for the clonal expansion of malignant T-cells by promoting cell survival and genomic instability, leading to chromosome alterations. Furthermore, genes that cooperate with Akt2 to promote malignant transformation may reside at translocation/inversion junctions found in spontaneous thymic lymphomas from transgenic mice expressing constitutively active Akt2 specifically in T cells. Cytogenetic analysis revealed that thymic tumors from multiple founder lines exhibited either of two recurrent chromosomal rearrangements, inv(6)(A2B1) or t(14;15)(C2;D1). Fluorescence in situ hybridization, array CGH, and PCR analysis were used to delineate the inv(6) and t(14;15) breakpoints. Both rearrangements involved T-cell receptor loci. The inv(6) results in robust upregulation of the homeobox/transcription factor gene Dlx5 because of its relocation near the Tcrb enhancer. The t(14;15) places the Tcra enhancer in the vicinity of the Myc proto-oncogene, resulting in upregulated Myc expression. These findings suggest that activation of the Akt pathway can act as the initial hit to promote cell survival and genomic instability, whereas the acquisition of T-cell-specific overexpression of Dlx5 or Myc leads to lymphomagenesis.

Indexed as

Gene RearrangementOncogenesAnimalsBase SequenceChromosome AberrationsChromosome BreakageComparative Genomic HybridizationHumansIn Situ Hybridization, FluorescenceLymphocyte Specific Protein Tyrosine Kinase p56(lck)Lymphoma, T-CellMiceMice, TransgenicMolecular Sequence DataProto-Oncogene MasProto-Oncogene ProteinsAkt2 protein, mouseLymphocyte Specific Protein Tyrosine Kinase p56(lck)MAS1 protein, humanProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-akt

Identifiers

PMID19530243
PMCPMC2739734
OpenAlexW2041638651

What OpenQuestion holds

Textmetadata
LicenceTDM
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.