Evidence map›Paper›PMID 14524530›Full record

ArticleClinical & experimental metastasis2003

Inhibition of alpha(v)beta3 integrin reduces angiogenesis, bone turnover, and tumor cell proliferation in experimental prostate cancer bone metastases.

Jeffrey A Nemeth, Michael L Cher, Zhao Zhou, Chadwick Mullins, Sunita Bhagat, Mohit Trikha

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & experimental metastasis, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
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  3. Mechanically Triggered DNA Nanovehicles for Targeted Dual-Drug Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  9. Preclinical evaluation of aAmino acids · 2019
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  10. Mesenchymal Stromal Cells: Emerging Roles in Bone Metastasis.International journal of molecular sciences · 2018
    Review
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  13. Circulating tumor-associated neutrophils (cTAN) contribute to circulating tumor cell survival by suppressing peripheral leukocyte activation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  14. Article
  15. Review
  16. Article
  17. Targeting bone physiology for the treatment of metastatic prostate cancer.Clinical advances in hematology & oncology : H&O · 2013
    Review
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Jeffrey A NemethDepartment of Oncology Research, Centocor, Inc., Malvern, Pennsylvania 19355, USA.
Michael L Cher
Zhao Zhou
Chadwick Mullins
Sunita Bhagat
Mohit Trikha
Wayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The growth of metastatic prostate cancer cells in the bone involves an intimate interaction between the tumor cells and various elements of the bone microenvironment, resulting in increased rate of bone turnover and rapid tumor growth. The alpha(v)beta3 integrin has been shown to play an important role in tumor growth and angiogenesis, and is known to be critical to osteoclast formation and activity. This study was designed to examine the role of alpha(v)beta3 expressed by cells native to the bone in the growth and pathogenesis of prostate cancer bone metastases. Human prostate cancer cells which do not express alpha(v)beta3 or alpha(IIb)beta3 integrins were injected directly into human bone fragments previously implanted subcutaneously in SCID mice (SCID-human-bone model). At the same time treatment with anti-beta3 antibody fragment (m7E3 F(ab')2) i.p. at 300 microg/dose 3 x per week was initiated and continued for 2 weeks. In this system, m7E3 F(ab')2 only recognizes human bone-derived alpha(v)beta3. Antibody inhibition of alpha(v)beta3 integrin in vivo resulted in a specific reduction in the proportion of antigenically-human blood vessels within tumor-bearing bone implants (from 73.5% +/- 3.93 in controls to 17.74% +/- 5.64 in treated animals). Proliferation of the alpha(v)beta3-negative tumor cells was also reduced, although the overall vessel density was maintained by compensating mouse vasculature. Blockage of human bone-derived alpha(v)beta3 also significantly reduced the recruitment of osteoclasts in response to tumor cells, as well as degradation of calcified bone tissue. Together these observations confirm the importance of alpha(v)beta3 in bone metabolism and angiogenesis, and point to the role of these processes in controlling growth of metastatic prostate cancer cells in the bone.

Indexed as

Neovascularization, PathologicAnimalsApoptosisBone and BonesBone NeoplasmsCell DivisionFlow CytometryHumansImmunohistochemistryIntegrin alphaVbeta3MaleMiceMice, SCIDMicroscopy, FluorescenceNeoplasm MetastasisOsteoclastsIntegrin alphaVbeta3

Identifiers

PMID14524530
OpenAlexW1546251826

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.