Evidence map›Paper›PMID 15897879›Full record

ArticleOncogene2005

G1/S transcriptional networks modulated by the HOX11/TLX1 oncogene of T-cell acute lymphoblastic leukemia.

Irene Riz, Robert G Hawley

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Proteomics identifies multipotent and low oncogenic risk stem cells of the spleen.The international journal of biochemistry & cell biology · 2010
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Transcriptional activation by TLX1/HOX11 involves Gro/TLE corepressors.Biochemical and biophysical research communications · 2009
    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

2 authors at 2 institutions in 1 country.

Irene RizDepartment of Anatomy and Cell Biology, The George Washington University Medical Center, Washington, DC 20037, USA.
Robert G Hawley
George Washington University · USWashington University Medical Center · US

Funding

Molecular Chimerism Therapy for Hemophilia AR01HL065519 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI HAWLEY, ROBERT G. · 2001 to 2009
$3.0M
IMPROVED LENTIVIRAL VECTORS FOR PRIMATE ES CELLSR24RR016209 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI THOMSON, JAMES ALEXANDER · 2002 to 2006
$2.2M
Embryoid Body-derived Hematopoietic Stem Cell LinesR01HL066305 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI HAWLEY, ROBERT G. · 2001 to 2005
$1.7M
NCRR NIH HHS R24 RR016209NCRR NIH HHS R24RR16209NHLBI NIH HHS R01 HL065519NHLBI NIH HHS R01 HL066305NHLBI NIH HHS R01HL65519NHLBI NIH HHS R01HL66305
6 · The paper itself

Abstract

The HOX11/TLX1 homeobox gene is aberrantly expressed in a subset of T-cell acute lymphoblastic leukemia (T-ALL). Here, we employed oligonucleotide microarrays to compare the expression profiles of the K3P and Sil leukemic cell lines originating from patients with HOX11+ T-ALL to that of Jurkat cells, which originated from a distinct subtype of T-ALL (TAL1+). To distinguish potential HOX11 target genes from those characteristic of the stage of HOX11 leukemic arrest, we also performed gene expression analysis on Jurkat cells, genetically engineered to express exogenous HOX11. The resulting HOX11 gene expression signature, which was validated for representative signaling pathways by transient transfection of reporter constructs, was characterized by elevated expression of transcriptional programs involved in cell proliferation, including those regulated by E2F, c-Myc and cAMP response element-binding protein. We subsequently showed that ectopic HOX11 expression resulted in hyperphosphorylation of the retinoblastoma protein (Rb), which correlated with inhibition of the major Rb serine/threonine phosphatase PP1. HOX11 also inhibited PP2A serine/threonine phosphatase activity concomitant with stimulation of the AKT/PKB signaling cascade. These results suggest that transcriptional deregulation of G1/S growth-control genes, mediated in large part through blockade of PP1/PP2A phosphatase activity, plays an important role in HOX11 pathobiology.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticAnimalsCell LineG1 PhaseGene Expression ProfilingHomeodomain ProteinsHumansLeukemia-Lymphoma, Adult T-CellMiceOligonucleotide Array Sequence AnalysisPhenotypePhosphoric Monoester HydrolasesPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene ProteinsAKT1 protein, humanHomeodomain ProteinsPhosphoric Monoester HydrolasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRetinoblastoma ProteinTLX1 protein, human

Identifiers

PMID15897879
PMCPMC2408753
OpenAlexW2168982956

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.