Evidence map›Paper›PMID 19038005›Full record

ArticleCancer science2009

Transforming growth factor-beta signaling at the tumor-bone interface promotes mammary tumor growth and osteoclast activation.

Mitsuru Futakuchi, Kalyan C Nannuru, Michelle L Varney, Anguraj Sadanandam, Kimihisa Nakao, Kiyofumi Asai, Tomoyuki Shirai, Shin-ya Sato, Rakesh K Singh

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
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  7. Article
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  14. Article
  15. PRDX4 and Its Roles in Various Cancers.Technology in cancer research & treatment · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. What Is Breast in the Bone?International journal of molecular sciences · 2016
    Review
  20. Novel therapeutic targets in myeloma bone disease.British journal of pharmacology · 2014
    Review
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

9 authors at 4 institutions in 3 countries.

Mitsuru FutakuchiDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5845, USA.
Kalyan C Nannuru
Michelle L Varney
Anguraj Sadanandam
Kimihisa Nakao
Kiyofumi Asai
Tomoyuki Shirai
Shin-ya Sato
Rakesh K Singh
University of Nebraska Medical Center · USInstitute of Neurobiology and Molecular Medicine · ITNagoya City University · JPSociety of Environmental Toxicology and Chemistry · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Steven H Caplan · 1985 to 2026
$55.0M
NCI NIH HHS CA71781NCI NIH HHS P30 CA036727NCI NIH HHS P30CA036727
6 · The paper itself

Abstract

Understanding the cellular and molecular changes in the bone microenvironment is important for developing novel therapeutics to control breast cancer bone metastasis. Although the underlying mechanism(s) of bone metastasis has been the focus of intense investigation, relatively little is known about complex molecular interactions between malignant cells and bone stroma. Using a murine syngeneic model that mimics osteolytic changes associated with human breast cancer, we examined the role of tumor-bone interaction in tumor-induced osteolysis and malignant growth in the bone microenvironment. We identified transforming growth factor-beta receptor 1 (TGF-betaRI) as a commonly upregulated gene at the tumor-bone (TB) interface. Moreover, TGF-betaRI expression and activation, analyzed by nuclear localization of phospho-Smad2, was higher in tumor cells and osteoclasts at the TB interface as compared to the tumor-alone area. Furthermore, attenuation of TGF-beta activity by neutralizing antibody to TGF-beta or TGF-betaRI kinase inhibitor reduced mammary tumor-induced osteolysis, TGF-betaRI expression and its activation. In addition, we demonstrate a potential role of TGF-beta as an important modifier of receptor activator of NF-kappaB ligand (RANKL)-dependent osteoclast activation and osteolysis. Together, these studies demonstrate that inhibition of TGF-betaRI signaling at the TB interface will be a therapeutic target in the treatment of breast cancer-induced osteolysis.

Indexed as

AnimalsBone NeoplasmsCell DifferentiationCell Line, TumorFemaleMammary Neoplasms, ExperimentalMiceMice, Inbred BALB COsteoclastsOsteolysisProtein Serine-Threonine KinasesRANK LigandReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISignal TransductionTransforming Growth Factor betaProtein Serine-Threonine KinasesRANK LigandReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ITransforming Growth Factor beta

Identifiers

PMID19038005
PMCPMC11159074
OpenAlexW2059860426

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.