Evidence map›Paper›PMID 18697930›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

Bmi1 is critical for lung tumorigenesis and bronchioalveolar stem cell expansion.

Jennifer Shepard Dovey, Sima J Zacharek, Carla F Kim, Jacqueline A Lees

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
9.1field-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

106 citing papers in PubMed, 176 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Lung Cancer Stem Cells and Their Clinical Implications.Cold Spring Harbor perspectives in medicine · 2022
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. The Role of Polycomb Group Protein BMI1 in DNA Repair and Genomic Stability.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Recent Developments in mRNA-Based Protein Supplementation Therapy to Target Lung Diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Review

46 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

4 authors at 3 institutions in 1 country.

Jennifer Shepard DoveyDavid H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Sima J Zacharek
Carla F Kim
Jacqueline A Lees
Massachusetts Institute of Technology · USBoston Children's Hospital · USHarvard University · US

Funding

USE OF RETROVIRUS PROMOTER TRAP VECTORS TO IDENTIFY ONCOGENES AND ANTI-ONCOGENESP01CA042063 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI JACKS, TYLER E. · 1986 to 2021
$30.5M
In Vivo and In Vitro Characterization of Bronchio-Alveolar Stem CellsR01HL090136 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI KIM, CARLA F. · 2007 to 2010
$1.9M
NCI NIH HHS P01 CA042063NCI NIH HHS P01 CA42063NHLBI NIH HHS R01 HL090136NHLBI NIH HHS R01HL090136
6 · The paper itself

Abstract

Understanding the pathways that control epithelial carcinogenesis is vital to the development of effective treatments. The Polycomb group family member Bmi1 is overexpressed in numerous epithelial tumors, but its role in their development has not been established. We now show a key role for Bmi1 in lung adenocarcinoma. Whereas lung development occurs normally in Bmi1-deficient mice, loss of Bmi1 decreases the number and progression of lung tumors at a very early point in an oncogenic K-ras-initiated mouse model of lung cancer. This correlates with a defect in the ability of Bmi1-deficient putative bronchiolalveolar stem cells (BASCs) to proliferate in response to the oncogenic stimulus. Notably, in the absence of oncogenic K-ras, Bmi1-deficient BASCs show impaired proliferation and self-renewal capacity in culture and after lung injury in vivo. Abrogated lung cancer development and BASC self-renewal occur partially in a p19(ARF)-dependent manner. Our data suggest that Bmi1 deficiency suppresses tumor development by limiting the expansion potential of BASCs, the apparent lung cancer cells of origin. Because Bmi1 is elevated in additional tumor types, this suggests that Bmi1 plays a key role in regulating proliferation of both stem cells and tumor cells in diverse adult epithelial tissues.

Indexed as

AnimalsBronchiCell ProliferationCells, CulturedCell Transformation, NeoplasticLung NeoplasmsMiceMice, KnockoutNuclear ProteinsPolycomb Repressive Complex 1Proto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Pulmonary AlveoliRepressor ProteinsStem CellsBmi1 protein, mouseNuclear ProteinsPolycomb Repressive Complex 1Proto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Repressor Proteins

Identifiers

PMID18697930
PMCPMC2575250
OpenAlexW2010609944

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.