Evidence map›Paper›PMID 21779504›Full record

ArticleGenes & cancer2011

Ras in cancer and developmental diseases.

Alberto Fernández-Medarde, Eugenio Santos

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 435 papers.

0numbers the graph read from it
0cells of the map it votes in
435citing papers in PubMed
18.0field-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

435 citing papers in PubMed, 908 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Observational
  7. Targeting the MAPK Pathway in Cancer.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
  10. Reengineering of a Proteomimetic Pan-Ras Inhibitor into a Ras Degrader.Angewandte Chemie (International ed. in English) · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

375 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

2 authors at 2 institutions in 2 countries.

Alberto Fernández-MedardeCentro de Investigación del Cáncer, IBMCC (CSIC-USAL), University of Salamanca, Salamanca, Spain.
Eugenio Santos
Medical Protective · USUniversidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic, gain-of-function mutations in ras genes were the first specific genetic alterations identified in human cancer about 3 decades ago. Studies during the last quarter century have characterized the Ras proteins as essential components of signaling networks controlling cellular proliferation, differentiation, or survival. The oncogenic mutations of the H-ras, N-ras, or K-ras genes frequently found in human tumors are known to throw off balance the normal outcome of those signaling pathways, thus leading to tumor development. Oncogenic mutations in a number of other upstream or downstream components of Ras signaling pathways (including membrane RTKs or cytosolic kinases) have been detected more recently in association with a variety of cancers. Interestingly, the oncogenic Ras mutations and the mutations in other components of Ras/MAPK signaling pathways appear to be mutually exclusive events in most tumors, indicating that deregulation of Ras-dependent signaling is the essential requirement for tumorigenesis. In contrast to sporadic tumors, separate studies have identified germline mutations in Ras and various other components of Ras signaling pathways that occur in specific association with a number of different familial, developmental syndromes frequently sharing common phenotypic cardiofaciocutaneous features. Finally, even without being a causative force, defective Ras signaling has been cited as a contributing factor to many other human illnesses, including diabetes and immunological and inflammatory disorders. We aim this review at summarizing and updating current knowledge on the contribution of Ras mutations and altered Ras signaling to development of various tumoral and nontumoral pathologies.

Indexed as

cancerdevelopmental syndromesmutationoncogenesRasRas-MAPK pathway

Identifiers

PMID21779504
PMCPMC3128640
OpenAlexW2143881980

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.