Evidence map›Paper›PMID 20139704›Full record

ArticleCancer biology & therapy2010

Bone-specific growth inhibition of prostate cancer metastasis by atrasentan.

Justin M Drake, Joshua R Danke, Michael D Henry

Abstract read
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Article in Cancer biology & therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Review
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  15. Future perspectives of prostate cancer therapy.Translational andrology and urology · 2012
    Article
  16. Regulation of postnatal trabecular bone formation by the osteoblast endothelin A receptor.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2011
    Article
  17. Review
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  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Justin M DrakeDepartment of Molecular Physiology and Biophysics, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA, USA.
Joshua R Danke
Michael D Henry

Funding

Predoctoral Training in the Pharmacological SciencesT32GM067795 · NIGMS · UNIVERSITY OF IOWA · PI STRACK, STEFAN · 2004 to 2021
$3.4M
NIGMS NIH HHS T32 GM067795
6 · The paper itself

Abstract

Advanced prostate cancer frequently metastasizes to bone and remains an incurable disease. One recent experimental therapy involves endothelin receptor A (ETA) antagonists (e.g., atrasentan). Clinical results to date have been mixed, with atrasentan not meeting its primary endpoints in a Phase III trial. It remains an open question whether some patients might benefit from this therapy, while others may not. Preclinical data supports the concept that the endothelin signaling axis may be particularly important for tumor growth in bone, but the extent to which it is involved in metastatic colonization of other organ sites in prostate cancer remains unclear. Here we evaluate the efficacy of atrasentan in a mouse model of prostate cancer metastatic colonization. Using bioluminescence imaging, we show that atrasentan does inhibit tumor growth in, but not the initial colonization of, bony sites in intracardially-injected 22Rv1 prostate cancer cells. However, atrasentan shows little efficacy in soft tissues such as adrenal gland or liver. Our studies show that whether atrasentan exhibits significant overall antitumor efficacy and survival benefit depends on the presence of bone metastasis evident in that animal. Though in contrast to previous findings efficacy is apparent in a prostate tumor model that elicits mixed osteoblastic/osteolytic lesions. These data confirm the notion that atrasentan may exhibit selective activity against prostate cancer bone metastasis, mirroring clinical findings, and suggest that the role of endothelin signaling in bone metastasis may be more complex than previously appreciated. The model described here may provide a valuable tool for unraveling this complexity.

Indexed as

AdenocarcinomaAnimalsAntineoplastic AgentsAtrasentanBone NeoplasmsCell Growth ProcessesCell Line, TumorHumansMaleMiceProstatic NeoplasmsPyrrolidinesRandom AllocationXenograft Model Antitumor AssaysAntineoplastic AgentsAtrasentanPyrrolidines

Identifiers

PMID20139704

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.