Evidence map›Paper›PMID 7612899›Full record

ReviewBreast cancer research and treatment1995

Aberrant function of the Ras signal transduction pathway in human breast cancer.

G J Clark, C J Der

Abstract readReview
PubMed Publisher
In one paragraph

Review in Breast cancer research and treatment, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 13% 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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 214 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
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  6. Article
  7. Arene Ru(II) Complexes Acted as PotentialMolecules (Basel, Switzerland) · 2022
    Article
  8. Article
  9. Cancers · 2022
    Article
  10. Review
  11. Review
  12. Article
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  18. Article
  19. Article
  20. Functional SNP in stem of mir-146a affects Her2 status and breast cancer survival.Cancer biomarkers : section A of Disease markers · 2016
    Article

4 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 1 institution in 1 country.

G J ClarkDepartment of Pharmacology, University of North Carolina at Chapel Hill 27599, USA.
C J Der
University of North Carolina at Chapel Hill · US

Funding

BIOLOGICAL ACTIVITY OF RAS ONCOGENESR01CA042978 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1986 to 2017
$5.9M
KREV-1 AND SUPPRESSION OF RAS ONCOGENE TRANSFORMATIONR01CA052072 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J · 1990 to 1994
–
FUNCTION OF RAS ONCOGENE PROTEIN RELATED RAB PROTEINSR01CA055008 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J · 1991 to 1995
–
NCI NIH HHS CA42978NCI NIH HHS CA52072NCI NIH HHS CA55008
6 · The paper itself

Abstract

Although ras mutations are infrequent (approximately 5%) in breast cancers, there is considerable evidence that suggests that the pathways which Ras services may still be deregulated in breast cancer cells. The recent identification of many of the components of the Ras signal transduction pathway has defined a network of proto-oncogene proteins controlling diverse signaling events that regulate cell growth and differentiation. Consequently, mutations that perturb the function of any one component of this signal pathway may trigger the same oncogenic events as mutation of ras itself. Moreover, several Ras-related proteins have recently been demonstrated to possess the ability to trigger malignant transformation via signaling pathways shared with Ras proteins. Thus, it is possible that the aberrant function of Ras-related proteins may contribute to breast cancer development. Consequently, it is important not to dismiss the Ras pathway in the development of breast cancer merely because of the infrequent detection of mutations in ras itself, but rather to consider the influence of aberrations upstream or downstream of Ras and of certain Ras-related proteins in the development of breast cancer. Finally, the critical importance of components upstream and downstream of Ras provides additional targets for rational drug design approaches to block the aberrant function of Ras signaling in human tumors.

Indexed as

Genes, rasMutationSignal TransductionApoptosisBreast NeoplasmsHumansProto-Oncogene MasProto-Oncogene Proteins p21(ras)HRAS protein, humanMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins p21(ras)

Identifiers

PMID7612899
OpenAlexW2088428799

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.