Evidence map›Paper›PMID 17062721›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2006

Treatment-related osteoporosis in men with prostate cancer.

Matthew R Smith

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 62 citations in OpenAlex.

  1. Denosumab and changes in bone turnover markers during androgen deprivation therapy for prostate cancer.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2011
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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

1 author at 1 institution in 1 country.

Matthew R SmithMassachusetts General Hospital, Boston, Massachusetts 02114, USA. smith.matthew@mgh.harvard.edu
Massachusetts General Hospital · US

Funding

Midcareer Investigator AwardK24CA121990 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI SMITH, MATTHEW RAYMOND · 2007 to 2016
$1.9M
NCI NIH HHS K24 CA121990
6 · The paper itself

Abstract

The intended therapeutic effect of gonadotropin-releasing hormone (GnRH) agonists is hypogonadism, a major cause of acquired osteoporosis in men. Consistent with this observation, GnRH agonists increase bone turnover and decrease bone mineral density, a surrogate for fracture risk. Large claims-based analyses and other retrospective studies provide compelling evidence that GnRH agonists increase risk of clinical fractures. Estrogens play a central role in homeostasis of the normal male skeleton, and estrogen deficiency rather than testosterone deficiency seems to be primarily responsible for the adverse skeletal effects of GnRH agonists. In randomized controlled trials, bisphosphonates (pamidronate and zoledronic acid) and selective estrogen receptor modulators (raloxifene and toremifene) increased bone mineral density in GnRH agonist-treated men. Two ongoing large randomized placebo-controlled studies will prospectively define fracture outcomes in men with prostate cancer and assess the efficacy of novel pharmacologic interventions (AMG162, toremifene) during GnRH agonist treatment.

Indexed as

Antineoplastic AgentsBone Density Conservation AgentsHumansMaleOsteoporosisProstatic NeoplasmsRandomized Controlled Trials as TopicAntineoplastic AgentsBone Density Conservation Agents

Identifiers

PMID17062721
PMCPMC3047394
OpenAlexW2111536069

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.