Evidence map›Paper›PMID 21779503›Full record

ArticleGenes & cancer2011

KRAS Mouse Models: Modeling Cancer Harboring KRAS Mutations.

Rónán C O'Hagan, Joerg Heyer

Open access · bronzeAbstract read
In one paragraph

Article in Genes & cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. [Pathology of liver tumours in animal models].Pathologie (Heidelberg, Germany) · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Models of pancreatic ductal adenocarcinoma.Cancer metastasis reviews · 2021
    Review
  8. Article
  9. Article
  10. Cell Type-specific Adaptive Signaling Responses to KRASClinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  11. Review
  12. Current methods in translational cancer research.Cancer metastasis reviews · 2021
    Review
  13. Review
  14. Review
  15. Review
  16. Article
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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

2 authors.

Rónán C O'HaganAVEO Pharmaceuticals, Cambridge, MA, USA.
Joerg Heyer

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KRAS is a potent oncogene and is mutated in about 30% of all human cancers. However, the biological context of KRAS-dependent oncogenesis is poorly understood. Genetically engineered mouse models of cancer provide invaluable tools to study the oncogenic process, and insights from KRAS-driven models have significantly increased our understanding of the genetic, cellular, and tissue contexts in which KRAS is competent for oncogenesis. Moreover, variation among tumors arising in mouse models can provide insight into the mechanisms underlying response or resistance to therapy in KRAS-dependent cancers. Hence, it is essential that models of KRAS-driven cancers accurately reflect the genetics of human tumors and recapitulate the complex tumor-stromal intercommunication that is manifest in human cancers. Here, we highlight the progress made in modeling KRAS-dependent cancers and the impact that these models have had on our understanding of cancer biology. In particular, the development of models that recapitulate the complex biology of human cancers enables translational insights into mechanisms of therapeutic intervention in KRAS-dependent cancers.

Indexed as

interpatient tumor variationmouse models harboring KRAS mutationtumor contexttumor genetics

Identifiers

PMID21779503
PMCPMC3128636
OpenAlexW1999732485

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.