Evidence map›Paper›PMID 17637742›Full record

ArticleOncogene2008

Characterization of mammary tumors from Brg1 heterozygous mice.

S J Bultman, J I Herschkowitz, V Godfrey, T C Gebuhr, M Yaniv, C M Perou, T Magnuson

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Chromatin remodellers as therapeutic targets.Nature reviews. Drug discovery · 2024
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. BRG1 Is Dispensable for Sertoli Cell Development and Functions in Mice.International journal of molecular sciences · 2020
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. How to Choose a Mouse Model of Breast Cancer, a Genomic Perspective.Journal of mammary gland biology and neoplasia · 2019
    Review

44 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

7 authors at 2 institutions in 2 countries.

S J BultmanDepartment of Genetics, University of North Carolina, Chapel Hill, NC 27599-7264, USA. Scott_Bultman@med.unc.edu
J I Herschkowitz
V Godfrey
T C Gebuhr
M Yaniv
C M Perou
T Magnuson
University of North Carolina at Chapel Hill · USInstitut Pasteur · FR

Funding

GENETIC REGULATION OF MURINE PLACENTAL DEVELOPMENTR01HD036655 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAGNUSON, TERRY R · 1999 to 2018
$5.2M
NICHD NIH HHS R01 HD036655
6 · The paper itself

Abstract

Mammalian SWI/SNF-related complexes have been implicated in cancer based on some of the subunits physically interacting with retinoblastoma (RB) and other proteins involved in carcinogenesis. Additionally, several subunits are mutated or not expressed in tumor-derived cell lines. Strong evidence for a role in tumorigenesis in vivo, however, has been limited to SNF5 mutations that result primarily in malignant rhabdoid tumors (MRTs) in humans and MRTs as well as other sarcomas in mice. We previously generated a null mutation of the Brg1 catalytic subunit in the mouse and reported that homozygotes die during embryogenesis. Here, we demonstrate that Brg1 heterozygotes are susceptible to mammary tumors that are fundamentally different than Snf5 tumors. First, mammary tumors are carcinomas not sarcomas. Second, Brg1+/- tumors arise because of haploinsufficiency rather than loss of heterozygosity. Third, Brg1+/- tumors exhibit genomic instability but not polyploidy based on array comparative genomic hybridization results. We monitored Brg1+/-, Brm-/- double-mutant mice but did not observe any tumors resembling those from Snf5 mutants, indicating that the Brg1+/- and Snf5+/- tumor phenotypes do not differ simply because Brg1 has a closely related paralog whereas Snf5 does not. These findings demonstrate that BRG1 and SNF5 are not functionally equivalent but protect against cancer in different ways. We also demonstrate that Brg1+/- mammary tumors have relatively heterogeneous gene expression profiles with similarities and differences compared to other mouse models of breast cancer. The Brg1+/- expression profiles are not particularly similar to mammary tumors from Wap-T121 transgenic line where RB is perturbed. We were also unable to detect a genetic interaction between the Brg1+/- and Rb+/- tumor phenotypes. These latter findings do not support a BRG1-RB interaction in vivo.

Indexed as

HeterozygoteAdenocarcinomaAnimalsCluster AnalysisDisease Models, AnimalDNA HelicasesFemaleGene Expression ProfilingGenomic InstabilityLoss of HeterozygosityMaleMammary Neoplasms, ExperimentalMiceMutation, MissenseNuclear ProteinsOligonucleotide Array Sequence AnalysisDNA HelicasesNuclear ProteinsRetinoblastoma ProteinSMARCA4 protein, humanTranscription Factors

Identifiers

PMID17637742
OpenAlexW2062981427

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.