Evidence map›Paper›PMID 9927682›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Ectopic expression of E47 or E12 promotes the death of E2A-deficient lymphomas.

I Engel, C Murre

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 107 citations in OpenAlex.

  1. T Cell Development: From T-Lineage Specification to Intrathymic Maturation.Advances in experimental medicine and biology · 2025
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  10. E proteins in lymphocyte development and lymphoid diseases.Current topics in developmental biology · 2014
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  19. Transcriptional regulator Id2 controls survival of hepatic NKT cells.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
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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

2 authors at 1 institution in 1 country.

I EngelDepartment of Biology, University of California at San Diego, La Jolla, CA 92093-0366, USA.
C Murre
University of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mice with null mutations in the E2A gene are highly susceptible to the spontaneous development of thymic lymphomas. To understand better how E2A deficiency may contribute to lymphomagenesis, we have observed the consequences of enforced expression of the E2A gene products E12 and E47 in cell lines derived from lymphomas that arose spontaneously in E2A-deficient mice. E2A-expressing cells are steadily eliminated from lymphoma cultures into which E47 or E12 was introduced. The mechanism underlying the loss of E2A-expressing cells does not involve an arrest in cell-cycle progression. Rather, the E2A proteins activate a programmed cell death pathway in these lymphomas. This E2A-mediated cell death appears to be preceded by a loss of mitochondrial transmembrane potential. These data provide direct evidence that E2A gene products can act as tumor suppressors.

Indexed as

Adenovirus E2 ProteinsAnimalsCell CycleCell DeathDNA-Binding ProteinsHelix-Loop-Helix MotifsHumansIntracellular MembranesLymphomaLymphoma, T-CellMembrane PotentialsMiceMice, KnockoutMitochondriaRecombinant ProteinsTCF Transcription FactorsAdenovirus E2 ProteinsDNA-Binding ProteinsRecombinant ProteinsTCF7L1 protein, humanTcf7l1 protein, mouseTCF Transcription FactorsTranscription Factor 7-Like 1 ProteinTranscription Factors

Identifiers

PMID9927682
PMCPMC15339
OpenAlexW2077799380

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.