Evidence map›Paper›PMID 15455033›Full record

ArticlePLoS biology2004

Developmental context determines latency of MYC-induced tumorigenesis.

Shelly Beer, Anders Zetterberg, Rebecca A Ihrie, Ryan A McTaggart, Qiwei Yang, Nicole Bradon, Constadina Arvanitis, Laura D Attardi, Sandy Feng, Boris Ruebner and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
4.1field-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

89 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. NaCancer research communications · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Mouse Models of Oncoimmunology in Hepatocellular Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Review
  16. Article
  17. Article
  18. Targeting cancer stem cell pathways for cancer therapy.Signal transduction and targeted therapy · 2020
    Review
  19. Article
  20. Article

29 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

12 authors at 4 institutions in 2 countries.

Shelly BeerDivision of Oncology, Department of Medicine, Stanford University, Stanford, California, USA.
Anders Zetterberg
Rebecca A Ihrie
Ryan A McTaggart
Qiwei Yang
Nicole Bradon
Constadina Arvanitis
Laura D Attardi
Sandy Feng
Boris Ruebner
Robert D Cardiff
Dean W Felsher
Stanford University · USUniversity of California, Davis · USUniversity of California, San Francisco · USKarolinska Institutet · SE

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
X RAY INACTIVATION OF HUMAN COLORECTAL CANCER CELLSR01CA085610 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI DEWEY, WILLIAM C · 2001 to 2003
$481k
C-MYC INDUCED TUMORIGENESIS AND GENOMIC INSTABILITYK08CA075967 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI FELSHER, DEAN W · 1998 to 2002
$333k
NCI NIH HHS 5T32 CA09302-27NCI NIH HHS K08-CA75967-01NCI NIH HHS R01 CA085610NCI NIH HHS R01-CA85610NCI NIH HHS T32 CA009302
6 · The paper itself

Abstract

One of the enigmas in tumor biology is that different types of cancers are prevalent in different age groups. One possible explanation is that the ability of a specific oncogene to cause tumorigenesis in a particular cell type depends on epigenetic parameters such as the developmental context. To address this hypothesis, we have used the tetracycline regulatory system to generate transgenic mice in which the expression of a c-MYC human transgene can be conditionally regulated in murine hepatocytes. MYC's ability to induce tumorigenesis was dependent upon developmental context. In embryonic and neonatal mice, MYC overexpression in the liver induced marked cell proliferation and immediate onset of neoplasia. In contrast, in adult mice MYC overexpression induced cell growth and DNA replication without mitotic cell division, and mice succumbed to neoplasia only after a prolonged latency. In adult hepatocytes, MYC activation failed to induce cell division, which was at least in part mediated through the activation of p53. Surprisingly, apoptosis is not a barrier to MYC inducing tumorigenesis. The ability of oncogenes to induce tumorigenesis may be generally restrained by developmentally specific mechanisms. Adult somatic cells have evolved mechanisms to prevent individual oncogenes from initiating cellular growth, DNA replication, and mitotic cellular division alone, thereby preventing any single genetic event from inducing tumorigenesis.

Indexed as

Gene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticAllelesAnimalsApoptosisBlotting, NorthernBlotting, WesternCell DivisionCell NucleusCell ProliferationCell SeparationDNA ReplicationFlow CytometryHepatocytesHeterozygoteKi-67 AntigenKi-67 AntigenProto-Oncogene Proteins c-mycTumor Suppressor Protein p53

Identifiers

PMID15455033
PMCPMC519000
OpenAlexW2155234942

What OpenQuestion holds

Textmetadata
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.