Myb proteins inhibit fibroblast transformation by v-Rel.

Shu-Ling Fu, Brigitte Ganter, Joseph S Lipsick

Open access · goldAbstract read

In one paragraph

Article in Molecular cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it

0cells of the map it votes in

2citing papers in PubMed

0.3field-weighted citation impact, top 41% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

c-Myb regulates matrix metalloproteinases 1/9, and cathepsin D: implications for matrix-dependent breast cancer cell invasion and metastasis.Molecular cancer · 2012
Article
Potential tumor suppressor role for the c-Myb oncogene in luminal breast cancer.PloS one · 2010
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

3 authors at 1 institution in 1 country.

Shu-Ling FuDepartments of Pathology and Genetics, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305-5324, USA. slfu@ym.edu.tw

Brigitte Ganter

Joseph S Lipsick

Stanford University · US

Funding

MECHANISM OF TRANSFORMATION BY THE V-MYB ONCOGENESR01CA043592 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI LIPSICK, JOSEPH STEVEN · 1987 to 2005

$1.5M

NCI NIH HHS R01 CA043592NCI NIH HHS R01 CA43592

6 · The paper itself

Abstract

Genes that cause cancer have been divided into two general classes--oncogenes that act in a dominant fashion to transform normal cells into a malignant state, and tumor suppressor genes that act in a dominant fashion to prevent such transformation. In this report, we demonstrate that both the v-myb retroviral oncogene, which causes leukemic transformation of hematopoietic cells, and the c-myb proto-oncogene can also function as inhibitors of fibroblast transformation by the v-rel oncogene. These results imply that the myb genes can function either as oncogenes or as tumor suppressors in different cellular contexts.

Indexed as

Cell Transformation, NeoplasticActinsAnimalsCell ExtractsCell NucleusChickensFibroblastsMiceOncogene Proteins v-mybOncogene Proteins v-relProto-Oncogene Proteins c-mybProvirusesQuailReceptors, EstrogenActinsCell ExtractsOncogene Proteins v-mybOncogene Proteins v-relProto-Oncogene Proteins c-mybReceptors, Estrogen

Identifiers

PMID17081304

DOI10.1186/1476-4598-5-54

PMCPMC1635057

OpenAlexW2149977805

What OpenQuestion holds

Textmetadata

LicenceCC BY

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.