Evidence map›Paper›PMID 25088202›Full record

ArticleOncogene2015

WEE1 murine deficiency induces hyper-activation of APC/C and results in genomic instability and carcinogenesis.

A Vassilopoulos, Y Tominaga, H-Seok Kim, T Lahusen, B Li, H Yu, D Gius, C-X Deng

Open access · bronzeAbstract read
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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Targeting WEE1 Kinase for Breast Cancer Therapeutics: An Update.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The DNA damage repair-related geneTranslational lung cancer research · 2021
    Article
  14. Wee1 Kinase: A Potential Target to Overcome Tumor Resistance to Therapy.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Review
  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

8 authors at 5 institutions in 1 country.

A Vassilopoulos1] Genetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA [2] Department of Radiation Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Y TominagaGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
H-Seok Kim1] Genetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA [2] Department of Life Science, Ewha Womans University, Seoul, South Korea.
T LahusenGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
B LiDepartment of Pharmacology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
H YuDepartment of Pharmacology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
D GiusDepartment of Radiation Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
C-X DengGenetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · USHoward Hughes Medical Institute · USNorthwestern University · USThe University of Texas Southwestern Medical Center · US

Funding

TISSUE CoreP50CA098131 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PARK, BEN HO, PIETENPOL, JENNIFER A · 2003 to 2024
$48.7M
Chemoprevention and therapeutic treatment of BRCA1 associated mammary tumorsZIADK056009 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DENG, CHUXIA · 2009 to 2014
$4.0M
Roles of BRCA1 transcription target genes in tumorigenesis and agingZIADK056011 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DENG, CHUXIA · 2009 to 2014
$3.9M
Loss of mtSIRT3, Decreased MnSOD Activity, and IR Induced Genomic InstabilityR01CA152601 · NCI · VANDERBILT UNIVERSITY · PI BONINI, MARCELO G. · 2010 to 2019
$3.5M
ROS and HIFa as molecular targets for chemoprevention in Sirt3 -/- breast cancersR01CA168292 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GIUS, DAVID · 2012 to 2016
$1.9M
SIRT3 is a Mitochondrial Tumor Suppressor in ER/PR Positive Mammary TumorsR01CA152799 · NCI · VANDERBILT UNIVERSITY · PI GIUS, DAVID · 2011 to 2015
$1.6M
Howard Hughes Medical InstituteIntramural NIH HHSNCI NIH HHS 1R01CA152601-01NCI NIH HHS BC093803NCI NIH HHS P50 CA098131NCI NIH HHS P50CA98131NCI NIH HHS R01 CA152601NCI NIH HHS R01 CA152799NCI NIH HHS R01 CA168292
6 · The paper itself

Abstract

The tyrosine kinase WEE1 controls the timing of entry into mitosis in eukaryotes and its genetic deletion leads to pre-implantation lethality in mice. Here, we show that besides the premature mitotic entry phenotype, Wee1 mutant murine cells fail to complete mitosis properly and exhibit several additional defects that contribute to the deregulation of mitosis, allowing mutant cells to progress through mitosis at the expense of genomic integrity. WEE1 interacts with the anaphase promoting complex, functioning as a negative regulator, and the deletion of Wee1 results in hyper-activation of this complex. Mammary specific knockout mice overcome the DNA damage response pathway triggered by the mis-coordination of the cell cycle in mammary epithelial cells and heterozygote mice spontaneously develop mammary tumors. Thus, WEE1 functions as a haploinsufficient tumor suppressor that coordinates distinct cell division events to allow correct segregation of genetic information into daughter cells and maintain genome integrity.

Indexed as

Anaphase-Promoting Complex-CyclosomeAnimalsCell Cycle ProteinsCell Transformation, NeoplasticEpithelial CellsFemaleGene DeletionGenomic InstabilityMammary Glands, AnimalMiceMice, KnockoutMitosisNuclear ProteinsProtein-Tyrosine KinasesTamoxifenAnaphase-Promoting Complex-CyclosomeCell Cycle ProteinsNuclear ProteinsProtein-Tyrosine KinasesTamoxifenWee1 protein, mouse

Identifiers

PMID25088202
PMCPMC5547996
OpenAlexW2080893860

What OpenQuestion holds

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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.