Evidence map›Paper›PMID 11791181›Full record

ArticleOncogene2002

Consequences of altered TGF-beta expression and responsiveness in breast cancer: evidence for autocrine and paracrine effects.

Stephen W Tobin, Karen Douville, Ulrike Benbow, Constance E Brinckerhoff, Vincent A Memoli, Bradley A Arrick

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 64 citations in OpenAlex.

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  16. Induction of Smad1 by MT1-MMP contributes to tumor growth.International journal of cancer · 2007
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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

6 authors at 1 institution in 1 country.

Stephen W TobinDepartment of Biochemistry, Dartmouth Medical School, Hanover, New Hampshire, NH 03755, USA.
Karen Douville
Ulrike Benbow
Constance E Brinckerhoff
Vincent A Memoli
Bradley A Arrick
Dartmouth College · US

Funding

Cancer Biology and Molecular TherapeuticsT32CA009658 · NCI · DARTMOUTH COLLEGE · PI EASTMAN, ALAN R · 1991 to 2011
$3.8M
TGF-BETA AND BREAST CANCERR01CA060928 · NCI · DARTMOUTH COLLEGE · PI ARRICK, BRADLEY A · 1993 to 1995
–
NCI NIH HHS CA09658NCI NIH HHS CA60928
6 · The paper itself

Abstract

To characterize the impact of increased production of TGF-beta in a xenograft model of human breast cancer, TGF-beta-responsive MDA-231 cells were genetically modified by stable transfection so as to increase their production of active TGF-beta1. Compared with control cells, cells that produced increased amounts of TGF-beta proliferated in vitro more slowly. In vivo, however, tumors derived from these cells exhibited increased proliferation and grew at an accelerated pace. To evaluate the role of autocrine TGF-beta signaling, cells were also transfected with a dominant-negative truncated type II TGF-beta receptor (TbetaRII). Disruption of autocrine TGF-beta signaling in the TGF-beta-overexpressing cells reduced their in vivo growth rate. Co-inoculation of Matrigel with the TGF-beta-overexpressing cells expressing the truncated TbetaRII compensated for their diminished in vivo growth capacity, compared with the TGF-beta-overexpressing cells with an intact autocrine loop. Tissue invasion by the tumor was a distinctive feature of the TGF-beta-overexpressing cells, whether or not the autocrine loop was intact. Furthermore, tumors derived from TGF-beta-overexpressing cells, irrespective of the status of the autocrine TGF-beta-signaling pathway, had a higher incidence of lung metastasis. Consistent with the suggestion that TGF-beta's enhancement of invasion and metastasis is paracrine-based, we observed no significant differences among the cell clones in an in vitro invasion assay. Thus, in this experimental model system in vitro assays of cell proliferation and invasion do not accurately reflect in vivo observations, perhaps due to autocrine and paracrine effects of TGF-beta that influence the important in vivo-based phenomena of tumor growth, invasion, and metastasis.

Indexed as

Autocrine CommunicationGene Expression Regulation, NeoplasticParacrine CommunicationAnimalsBreast NeoplasmsCarcinoma, Ductal, BreastCell DivisionCollagenCulture Media, ConditionedDrug CombinationsFemaleGenes, DominantHemorrhageHumansLamininLung NeoplasmsCollagenCulture Media, ConditionedDrug CombinationsLamininmatrigelNeoplasm ProteinsProtein Serine-Threonine KinasesProteoglycansReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIRecombinant Fusion ProteinsTransforming Growth Factor beta

Identifiers

PMID11791181
OpenAlexW2317179801

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.