Evidence map›Paper›PMID 15738393›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

MET and MYC cooperate in mammary tumorigenesis.

Alana L Welm, Suwon Kim, Bryan E Welm, J Michael Bishop

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 89 citations in OpenAlex.

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  13. Inactivation of MYC reverses tumorigenesis.Journal of internal medicine · 2014
    Review
  14. MYC activation is a hallmark of cancer initiation and maintenance.Cold Spring Harbor perspectives in medicine · 2014
    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

4 authors at 2 institutions in 1 country.

Alana L WelmG. W. Hooper Research Foundation and Department of Microbiology and Immunology, University of California, San Francisco, CA 94143, USA. awelm@itsa.ucsf.edu
Suwon Kim
Bryan E Welm
J Michael Bishop
University of California, San Francisco · USSan Francisco Foundation · US

Funding

NCI NIH HHS U01 CA84343
6 · The paper itself

Abstract

In human breast cancer, overexpression of the protooncogene MET is strongly associated with poor prognosis and high risk of metastasis. It stands out as a reliable prognostic indicator of survival and defines a set of tumors exclusive of those that express HER2 or hormone receptors. Studies have shown that overexpression of mutant forms of MET cause cancer in mice. However, MET mutations have not been found in human breast cancer, and the consequences of overexpression of normal MET are unknown. To investigate the role of MET and other putative oncogenes in breast cancer, we developed an experimental system that involves retroviral delivery of genes into primary mammary epithelial cells, followed by transplantation of the transduced cells into mammary fat pads. Using this approach, we found that overexpression of wild-type MET leads to the development of nonprogressive neoplasms. The lesions progressed to mammary adenocarcinoma when a second protooncogene, MYC, was overexpressed, indicating that MET and MYC cooperate in mammary tumorigenesis. Both the nonprogressive neoplasms and adenocarcinomas display characteristics consistent with transformation and expansion of mammary progenitor cells. The approach described here should provide a useful model with which to efficiently test effects of various genes on tumor development in the breast.

Indexed as

Genes, mycAdenocarcinomaAnimalsCells, CulturedEpithelial CellsFemaleGene ExpressionGenetic VectorsHumansKeratinsMammary Glands, AnimalMammary Neoplasms, ExperimentalMiceMice, TransgenicMutationProto-Oncogene Proteins c-metKeratinsProto-Oncogene Proteins c-met

Identifiers

PMID15738393
PMCPMC552784
OpenAlexW2063889984

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.