Evidence map›Paper›PMID 10378694›Full record

ReviewOncogene1999

The role of c-myc in cellular growth control.

E V Schmidt

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
8.7field-weighted citation impact, top 1% 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

141 citing papers in PubMed, 381 citations in OpenAlex.

  1. Trial
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  7. Development of Acridone Derivatives: TargetingAntioxidants (Basel, Switzerland) · 2023
    Article
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  10. Review
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  12. BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023
    Review
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  14. Article
  15. Article
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  19. Review
  20. Review

81 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

E V SchmidtMGH Cancer Center, Massachusetts General Hospital, Charlestown 02129, USA.
Massachusetts General Hospital · US

Funding

FUNCTIONS OF CYCLIN D1 IN BREAST CANCERR01CA069069 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SCHMIDT, EMMETT VANCE · 1997 to 2007
$2.5M
GENES REGULATED BY C-MYCR01CA063117 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SCHMIDT, EMMETT VANCE · 1994 to 2004
$1.9M
NCI NIH HHS R01-CA63117NCI NIH HHS R01-CA69069
6 · The paper itself

Abstract

Cell division is coupled to cell growth. Since some c-myc target genes are regulators of cell growth while others function in cell division pathways, c-myc is apparently poised at the interface of these processes. Cell culture systems have shown specific myc-associated growth phenotypes. Increased cell growth precedes DNA synthesis after myc activation in cells expressing myc-estrogen receptor fuson constructs and cells lacking c-myc exhibit a marked loss of protein synthesis. A number of candidate c-myc target genes regulate processes required for cell growth including rRNA transcription and processing, ribosomal protein transcription and translation, and translation initiation. These interactions all have the potential to account for the growth phenotypes in c-myc mutant cells. The ability of translation initiation factors, including eIF4E, to transform cells makes them particularly interesting targets of c-myc. Further evaluation of these target genes will provide important insights into growth control and c-myc's functions in cellular proliferation.

Indexed as

AnimalsCell DivisionGene Expression RegulationHumansProto-Oncogene Proteins c-mycProto-Oncogene Proteins c-myc

Identifiers

PMID10378694
OpenAlexW2016855149

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.