Evidence map›Paper›PMID 8821090›Full record

ReviewCancer metastasis reviews1995

Oncogenes as inducers of tumor angiogenesis.

J Rak, J Filmus, G Finkenzeller, S Grugel, D Marmé, R S Kerbel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer metastasis reviews, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 234 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. G12V and G12A KRAS mutations are associated with poor outcome in patients with metastatic colorectal cancer treated with bevacizumab.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Pericytes on the tumor vasculature: jekyll or hyde?Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2013
    Article
  16. The role of platelets in tumour growth.Klinicka onkologie : casopis Ceske a Slovenske onkologicke spolecnosti · 2012
    Review
  17. Imaging hypoxia in gliomas.The British journal of radiology · 2011
    Review
  18. Review
  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

6 authors at 3 institutions in 2 countries.

J RakDivision of Cancer Biology Research, Sunnybrook Health Science Centre, Toronto, Ontario, Canada.
J Filmus
G Finkenzeller
S Grugel
D Marmé
R S Kerbel
Institute of Molecular Biology · DEUniversity of Toronto · CASunnybrook Health Science Centre · CA

Funding

TUMOR-HOST INTERACTIONS IN HUMAN MELANOMA METASTASISR01CA041233 · NCI · TORONTO-SUNNYBROOK REGIONAL CANCER CTR · PI KERBEL, ROBERT S · 1986 to 2013
$2.4M
NCI NIH HHS CA-41233
6 · The paper itself

Abstract

Dominantly acting transforming oncogenes are generally considered to contribute to tumor development and progression by their direct effects on tumor cell proliferation and differentiation. However, the growth of solid tumors beyond 1-2 mm in diameter requires the induction and maintenance of a tumor blood vessel supply, which is attributed in large part to the production of angiogenesis promoting growth factors by tumor cells. The mechanisms which govern the expression of angiogenesis growth factors in tumor cells are largely unknown, but dominantly acting oncogenes may have a much greater impact than hitherto realized. An example of this is the induction of expression of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) by mutant H- or K-ras oncogenes, as well as v-src and v-raf, in transformed fibroblasts or epithelial cells. Besides VEGF/VPF, mutant ras genes are known to upregulate the expression of a variety of other growth factors thought to have direct or indirect stimulating effects on angiogenesis, e.g. TGF-beta and TGF-alpha. This effect may be mediated through the ras-raf-MAP kinase signal transduction pathway, resulting in activation of transcription factors such as AP1, which can then bind to relevant sites in the promoter regions of genes encoding angiogenesis growth factors. In principle, similar events could take place after activation or overexpression of many other oncogenes, especially those which can mediate their function through ras-dependent signal transduction pathways. The regulatory effect of oncogenes on mediators of angiogenesis has some potentially important therapeutic consequences. For example, it strengthens the rationale of pharmacologically targeting oncogene products, such as mutant RAS proteins, as an anti-tumor therapeutic strategy. Such drugs may attack the source of one or more angiogenic growth factors and by doing so, function, at least in part, as anti-angiogenic agents in vivo.

Indexed as

OncogenesGenes, rasGenes, srcGenes, Tumor SuppressorHumansMutationNeoplasmsNeovascularization, PathologicUp-Regulation

Identifiers

PMID8821090
OpenAlexW1976697969

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.