Evidence map›Paper›PMID 24076008›Full record

ReviewNeuroscience letters2013

Cancer-induced bone pain: Mechanisms and models.

A N Lozano-Ondoua, A M Symons-Liguori, T W Vanderah

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuroscience letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 2 pooled it
6.7field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 2 syntheses or guidelines pooled it, 148 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Role of TRP Channels in Cancer-Induced Bone Pain.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Article
  16. Neuropathic Pain in Cancer: What Are the Current Guidelines?Current treatment options in oncology · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Article

21 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

A N Lozano-OndouaDepartment of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ, USA.
A M Symons-Liguori
T W Vanderah
University of Arizona · US

Funding

Cannabinoid CB2 Agonists for Treatment of Breast Cancer-Induced Bone PainR01CA142115 · NCI · UNIVERSITY OF ARIZONA · PI VANDERAH, TODD W · 2010 to 2021
$3.3M
NCI NIH HHS R01 CA142115
6 · The paper itself

Abstract

Cancerous cells can originate in a number of different tissues such as prostate, breast and lung, but often go undetected and are non-painful. Many types of cancers have a propensity to metastasize to the bone microenvironment first. Tumor burden within the bone causes excruciating breakthrough pain with properties of ongoing pain that is inadequately managed with current analgesics. Part of this failure is due to the poor understanding of the etiology of cancer pain. Animal models of cancer-induced bone pain (CIBP) have revealed that the neurochemistry of cancer has features distinctive from other chronic pain states. For example, preclinical models of metastatic cancer often result in the positive modulation of neurotrophins, such as NGF and BDNF, that can lead to nociceptive sensitization. Preclinical cancer models also demonstrate nociceptive neuronal expression of acid-sensing receptors, such as ASIC1 and TRPV1, which respond to cancer-induced acidity within the bone. CIBP is correlated with a significant increase in pro-inflammatory mediators acting peripherally and centrally, contributing to neuronal hypersensitive states. Finally, cancer cells generate high levels of oxidative molecules that are thought to increase extracellular glutamate concentrations, thus activating primary afferent neurons. Knowledge of the unique neuro-molecular profile of cancer pain will ultimately lead to the development of novel and superior therapeutics for CIBP.

Indexed as

Acid Sensing Ion ChannelsAnimalsBone NeoplasmsCytokinesDisease Models, AnimalHumansMiceNerve Growth FactorsOxidative StressPainRatsAcid Sensing Ion ChannelsCytokinesNerve Growth FactorsASICCytokinesGlutamateNGFOxidative StressSyngenic tumor model

Identifiers

PMID24076008
PMCPMC4542064
OpenAlexW2036637024

What OpenQuestion holds

Textmetadata
LicenceTDM
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.