Evidence map›Paper›PMID 19010892›Full record

ArticleCancer research2008

NOTCH is part of the transcriptional network regulating cell growth and survival in mouse plasmacytomas.

Dong-Mi Shin, Daniel J Shaffer, Hongsheng Wang, Derry C Roopenian, Herbert C Morse

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Dong-Mi ShinLaboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, NIH, Rockville, Maryland 20852, USA.
Daniel J Shaffer
Hongsheng Wang
Derry C Roopenian
Herbert C Morse
National Institute of Allergy and Infectious Diseases · USJackson Laboratory · US

Funding

Lymphomas And Retroviral PathogenesisZIAAI000858 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2009 to 2018
$5.3M
Molecular Mechanisms in Innate immunityZIAAI001057 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2009 to 2018
$4.7M
CLASS I MOLECULES AND AUTOIMMUNITYR01DK056597 · NIDDK · JACKSON LABORATORY · PI ROOPENIAN, DERRY CHARLES · 1999 to 2006
$2.4M
Molecular Regulation of B-Cell Differentiation and FunctionZ01AI001024 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI MORSE, HERBERT · 2007 to 2008
$2.2M
LYMPHOMAS AND RETROVIRAL PATHOGENESISZ01AI000858 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI MORSE, HERBERT C · 2000 to 2008
$2.2M
NON H-2 HISTOCOMPATIBILITY GENES AND ANTIGENSR01AI028802 · NIAID · JACKSON LABORATORY · PI ROOPENIAN, DERRY CHARLES · 1990 to 2007
$2.1M
Molecular Mechanisms in Innate immunityZ01AI001057 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MORSE, HERBERT · 2008 to 2008
$568k
Intramural NIH HHS Z01 AI000858Intramural NIH HHS Z01 AI001024Intramural NIH HHS Z01 AI001057Intramural NIH HHS Z99 AI999999Intramural NIH HHS ZIA AI001057NIAID NIH HHS R01 AI028802NIAID NIH HHS R01AI28802NIDDK NIH HHS DK56597NIDDK NIH HHS R01 DK056597
6 · The paper itself

Abstract

Aside from Myc-activating translocations characteristic of plasmacytomas (PCT), little is known about genetic factors and signaling pathways responsible for the development of spontaneous B-cell lineage lymphomas of mice. Here, we characterized the transcriptional profiles of PCT, centroblastic diffuse large B-cell lymphomas (CBL), and high-grade splenic marginal zone B-cell lymphoma (MZL++) using high-throughput quantitative reverse transcription-PCR. Expression profiles of CBL and MZL++ were strikingly similar and quite unlike that of PCT. Among the genes expressed at significantly higher levels by PCT were a number involved in NOTCH signaling, a finding supported by gene set enrichment analyses of microarray data. To investigate the importance of this pathway, NOTCH signaling was blocked in PCT cell lines by treatment with a gamma-secretase inhibitor (GSI) or transduction of a dominant-negative mutant of MAML1. These treatments resulted in reduced expression of NOTCH transcriptional targets in association with impaired proliferation and increased apoptosis. GSI treatment of transformed plasma cells in a primary PCT also induced apoptosis. These results integrate NOTCH activation with oncogenic signaling pathways downstream of translocated Myc in the pathogenesis of mouse PCT, two signaling pathways also implicated in development of human multiple myeloma and T-cell lymphoblastic lymphoma.

Indexed as

Gene Expression ProfilingAmyloid Precursor Protein SecretasesAnimalsCell ProliferationCell SurvivalLymphoma, B-CellMiceMice, Inbred BALB COligonucleotide Array Sequence AnalysisPlasma CellsPlasmacytomaPolymerase Chain ReactionReceptors, NotchSignal TransductionAmyloid Precursor Protein SecretasesReceptors, Notch

Identifiers

PMID19010892
PMCPMC2800374
OpenAlexW2080457149

What OpenQuestion holds

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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.