Evidence map›Paper›PMID 21807965›Full record

ArticleMolecular cancer research : MCR2011

Progressive genomic instability in the FVB/Kras(LA2) mouse model of lung cancer.

Minh D To, David A Quigley, Jian-Hua Mao, Reyno Del Rosario, Jeff Hsu, Graeme Hodgson, Tyler Jacks, Allan Balmain

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Non-cell-autonomous mechanisms of tumor initiation and relapse by chromosomal instability.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  4. Article
  5. Article
  6. Epithelial cell migration as a potential therapeutic target in early lung cancer.European respiratory review : an official journal of the European Respiratory Society · 2017
    Review
  7. Mutational landscape of EGFR-, MYC-, and Kras-driven genetically engineered mouse models of lung adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. The genetics and biology of KRAS in lung cancer.Chinese journal of cancer · 2013
    Review
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 2 institutions in 1 country.

Minh D ToHelen Diller Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94158, USA.
David A Quigley
Jian-Hua Mao
Reyno Del Rosario
Jeff Hsu
Graeme Hodgson
Tyler Jacks
Allan Balmain
Massachusetts Institute of Technology · USUniversity of California, San Francisco · US

Funding

Identification of epithelial tumor susceptiility genesU01CA084244 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 1999 to 2013
$13.3M
The role of the Kras4A isoform in epithelial carcinogenesisR01CA111834 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 2006 to 2016
$2.6M
NCI NIH HHS CA111834-01NCI NIH HHS CA84244NCI NIH HHS R01 CA111834NCI NIH HHS U01 CA084244
6 · The paper itself

Abstract

Alterations in DNA copy number contribute to the development and progression of cancers and are common in epithelial tumors. We have used array Comparative Genomic Hybridization (aCGH) to visualize DNA copy number alterations across the genomes of lung tumors in the Kras(LA2) model of lung cancer. Copy number gain involving the Kras locus, as focal amplification or whole chromosome gain, is the most common alteration in these tumors and with a prevalence that increased significantly with increasing tumor size. Furthermore, Kras amplification was the only major genomic event among the smallest lung tumors, suggesting that this alteration occurs early during the development of mutant Kras-driven lung cancers. Recurring gains and deletions of other chromosomes occur progressively more frequently among larger tumors. These results are in contrast to a previous aCGH analysis of lung tumors from Kras(LA2) mice on a mixed genetic background, in which relatively few DNA copy number alterations were observed regardless of tumor size. Our model features the Kras(LA2) allele on the inbred FVB/N mouse strain, and in this genetic background, there is a highly statistically significant increase in level of genomic instability with increasing tumor size. These data suggest that recurring DNA copy alterations are important for tumor progression in the Kras(LA2) model of lung cancer and that the requirement for these alterations may be dependent on the genetic background of the mouse strain.

Indexed as

Genes, rasGenomic InstabilityAnimalsCell Line, TumorChromosome AberrationsDisease Models, AnimalDisease ProgressionDNA Copy Number VariationsDNA, NeoplasmGene DosageGene Expression Regulation, NeoplasticLung NeoplasmsMiceMice, Inbred C57BLProto-Oncogene Proteins p21(ras)DNA, NeoplasmHras protein, mouseProto-Oncogene Proteins p21(ras)

Identifiers

PMID21807965
PMCPMC3196775
OpenAlexW2102583574

What OpenQuestion holds

Textmetadata
LicenceTDM
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.