Evidence map›Paper›PMID 24276244›Full record

ArticleOncogene2015

Selective roles of E2Fs for ErbB2- and Myc-mediated mammary tumorigenesis.

L Wu, A de Bruin, H Wang, T Simmons, W Cleghorn, L E Goldenberg, E Sites, A Sandy, A Trimboli, S A Fernandez and 3 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The broken cycle: E2F dysfunction in cancer.Nature reviews. Cancer · 2019
    Review
  10. Expressions and prognostic values of theCancer management and research · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. E2F3 transcription factor: A promising biomarker in lung cancer.Cancer biomarkers : section A of Disease markers · 2017
    Article
  17. Review
  18. Article
  19. Article
  20. Article
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

13 authors at 3 institutions in 1 country.

L Wu1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
A de Bruin1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
H Wang1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
T Simmons1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
W Cleghorn1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
L E Goldenberg1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
E Sites1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
A Sandy1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
A Trimboli1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
S A FernandezCenter for Biostatistics, Ohio State University, Columbus, OH, USA.
C EngGenomic Medicine Institute, Cleveland Clinic, Cleveland, OH, USA.
C ShapiroDivision of Hematology & Oncology, College of Medicine, Ohio State University, Columbus, OH, USA.
G Leone1] Department of Molecular Genetics, College of Biological Sciences, Ohio State University, Columbus, OH, USA [2] Human Cancer Genetics Program, Comprehensive Cancer Center, Ohio State University, Columbus, OH, USA [3] Department of Molecular Virology Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus, OH, USA.
The Ohio State University · USCancer Genetics (United States) · USCleveland Clinic · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Suppression of Mammary Tumorigenesis by Stromal p53P01CA097189 · NCI · OHIO STATE UNIVERSITY · PI FERNANDEZ, SOLEDAD A · 2004 to 2016
$16.1M
Tumor Suppressor Roles of E2F7 & E2F8 in Hepatocellular Carcinoma (HCC)R01CA121275 · NCI · OHIO STATE UNIVERSITY · PI LEONE, GUSTAVO WALTER · 2008 to 2018
$3.1M
E2F3 and embryonic developmentR01HD047470 · NICHD · OHIO STATE UNIVERSITY · PI LEONE, GUSTAVO WALTER · 2004 to 2008
$1.6M
E2F3 GENE LOCUS IN THE CONTROL OF CELL PROLIFERATIONR01CA085619 · NCI · OHIO STATE UNIVERSITY · PI LEONE, GUSTAVO WALTER · 2001 to 2005
$1.4M
E2F AND THE CONTROL OF APOPTOSISR01CA082259 · NCI · OHIO STATE UNIVERSITY · PI LEONE, GUSTAVO WALTER · 1999 to 2003
$840k
NCI NIH HHS P01 CA097189NCI NIH HHS P01CA097189NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA082259NCI NIH HHS R01 CA085619NCI NIH HHS R01 CA121275NCI NIH HHS R01CA121275NCI NIH HHS R01CA82259NCI NIH HHS R01CA85619NICHD NIH HHS R01 HD047470NICHD NIH HHS R01HD047470
6 · The paper itself

Abstract

Previous studies have demonstrated that cyclin D1, an upstream regulator of the Rb/E2F pathway, is an essential component of the ErbB2/Ras (but not the Wnt/Myc) oncogenic pathway in the mammary epithelium. However, the role of specific E2fs for ErbB2/Ras-mediated mammary tumorigenesis remains unknown. Here, we show that in the majority of mouse and human primary mammary carcinomas with ErbB2/HER2 overexpression, E2f3a is up-regulated, raising the possibility that E2F3a is a critical effector of the ErbB2 oncogenic signaling pathway in the mammary gland. We examined the consequence of ablating individual E2fs in mice on ErbB2-triggered mammary tumorigenesis in comparison to a comparable Myc-driven mammary tumor model. We found that loss of E2f1 or E2f3 led to a significant delay in tumor onset in both oncogenic models, whereas loss of E2f2 accelerated mammary tumorigenesis driven by Myc-overexpression. Furthermore, southern blot analysis of final tumors derived from conditionally deleted E2f3(-/loxP) mammary glands revealed that there is a selection against E2f3(-/-) cells from developing mammary carcinomas, and that such selection pressure is higher in the presence of ErbB2 activation than in the presence of Myc activation. Taken together, our data suggest oncogenic activities of E2F1 and E2F3 in ErbB2- or Myc-triggered mammary tumorigenesis, and a tumor suppressor role of E2F2 in Myc-mediated mammary tumorigenesis.

Indexed as

AllelesAnimalsBreast NeoplasmsCarcinogenesisCell ProliferationE2F1 Transcription FactorE2F2 Transcription FactorE2F3 Transcription FactorErb-b2 Receptor Tyrosine KinasesFemaleGene DeletionHumansMammary Neoplasms, AnimalMammary Neoplasms, ExperimentalMicePhosphorylationE2f1 protein, mouseE2F1 Transcription FactorE2f2 protein, mouseE2F2 Transcription FactorE2f3 protein, mouseE2F3 Transcription FactorErbb2 protein, mouseErb-b2 Receptor Tyrosine KinasesProto-Oncogene Proteins c-myc

Identifiers

PMID24276244
PMCPMC4032808
OpenAlexW2167918456

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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.