Evidence map›Paper›PMID 19688092›Full record

ArticlePloS one2009

Hes1 potentiates T cell lymphomagenesis by up-regulating a subset of notch target genes.

Darryll D Dudley, Hong-Cheng Wang, Xiao-Hong Sun

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  18. Critical roles of NOTCH1 in acute T-cell lymphoblastic leukemia.International journal of hematology · 2011
    Review
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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

3 authors at 1 institution in 1 country.

Darryll D DudleyImmunobiology and Cancer Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Hong-Cheng Wang
Xiao-Hong Sun
Oklahoma Medical Research Foundation · US

Funding

Molecular Basis of Immunity - Kirschtein-NRSAT32AI007633 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CUNNINGHAM, MADELEINE W. · 2001 to 2022
$4.0M
Notch-induced protein degradation in lymphopoiesisR01AI056129 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI SUN, XIAO-HONG · 2003 to 2013
$3.8M
MOLECULAR MECHANISMS OF T CELL LEUKEMOGENESIS BY TALR01CA077553 · NCI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI SUN, XIAO-HONG · 1999 to 2009
$2.5M
NCI NIH HHS CA77553NCI NIH HHS R01 CA077553NIAID NIH HHS AI56129NIAID NIH HHS F32-AI07633NIAID NIH HHS R01 AI056129NIAID NIH HHS T32 AI007633
6 · The paper itself

Abstract

backgroundHairy/Enhancer of Split (Hes) proteins are targets of the Notch signaling pathway and make up a class of basic helix-loop-helix (bHLH) proteins that function to repress transcription. Data from Hes1 deficient mice suggested that Hes1, like Notch1, is necessary for the progression of early T cell progenitors. Constitutive activation of Notch is known to cause T cell leukemia or lymphoma but whether Hes1 has any oncogenic activity is not known. METHODOLOGY/PRINCIPAL

findingsWe generated mice carrying a Hes1 transgene under control of the proximal promote of the lck gene. Hes1 expression led to a reduction in numbers of total thymocytes, concomitant with the increased percentage and number of immature CD8+ (ISP) T cells and sustained CD25 expression in CD4+CD8+ double positive (DP) thymocytes. Hes1 transgenic mice develop thymic lymphomas at about 20 weeks of age with a low penetrance. However, expression of Hes1 significantly shortens the latency of T cell lymphoma developed in Id1 transgenic mice, where the function of bHLH E proteins is inhibited. Interestingly, Hes1 increased expression of a subset of Notch target genes in pre-malignant ISP and DP thymocytes, which include Notch1, Notch3 and c-myc, thus suggesting a possible mechanism for lymphomagenesis. CONCLUSIONS/SIGNIFICANCE: We have demonstrated for the first time that Hes1 potentiates T cell lymphomagenesis, by up-regulating a subset of Notch target genes and by causing an accumulation of ISP thymocytes particularly vulnerable to oncogenic transformation.

Indexed as

Up-RegulationAnimalsBase SequenceBasic Helix-Loop-Helix ProteinsDNA PrimersFlow CytometryHomeodomain ProteinsLymphoma, T-CellMiceMice, TransgenicPolymerase Chain ReactionReceptors, NotchTranscription Factor HES-1Basic Helix-Loop-Helix ProteinsDNA PrimersHes1 protein, mouseHomeodomain ProteinsReceptors, NotchTranscription Factor HES-1

Identifiers

PMID19688092
PMCPMC2722736
OpenAlexW2092852989

What OpenQuestion holds

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LicenceCC BY
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.