Evidence map›Paper›PMID 32054717›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2020

The Endocannabinoid System Alleviates Pain in a Murine Model of Cancer-Induced Bone Pain.

A L Thompson, S A Grenald, H A Ciccone, N BassiriRad, M J Niphakis, B F Cravatt, T M Largent-Milnes, T W Vanderah

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.1field-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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  10. Should oncologists trust cannabinoids?Frontiers in pharmacology · 2023
    Review
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  17. Article
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

8 authors at 4 institutions in 1 country.

A L ThompsonDepartment of Medical Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona (A.L.T., S.A.G., H.A.C., N.B., T.M.L.-M., T.W.V); Division of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland (S.A.G.); and The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California (M.J.N., B.F.C.).
S A GrenaldDepartment of Medical Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona (A.L.T., S.A.G., H.A.C., N.B., T.M.L.-M., T.W.V); Division of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland (S.A.G.); and The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California (M.J.N., B.F.C.).
H A CicconeDepartment of Medical Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona (A.L.T., S.A.G., H.A.C., N.B., T.M.L.-M., T.W.V); Division of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland (S.A.G.); and The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California (M.J.N., B.F.C.).
N BassiriRadDepartment of Medical Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona (A.L.T., S.A.G., H.A.C., N.B., T.M.L.-M., T.W.V); Division of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland (S.A.G.); and The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California (M.J.N., B.F.C.).
M J NiphakisDepartment of Medical Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona (A.L.T., S.A.G., H.A.C., N.B., T.M.L.-M., T.W.V); Division of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland (S.A.G.); and The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California (M.J.N., B.F.C.).
B F CravattDepartment of Medical Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona (A.L.T., S.A.G., H.A.C., N.B., T.M.L.-M., T.W.V); Division of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland (S.A.G.); and The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California (M.J.N., B.F.C.).
T M Largent-MilnesDepartment of Medical Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona (A.L.T., S.A.G., H.A.C., N.B., T.M.L.-M., T.W.V); Division of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland (S.A.G.); and The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California (M.J.N., B.F.C.).
T W VanderahDepartment of Medical Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona (A.L.T., S.A.G., H.A.C., N.B., T.M.L.-M., T.W.V); Division of Pain Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland (S.A.G.); and The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California (M.J.N., B.F.C.) vanderah@email.arizona.edu.
Johns Hopkins Medicine · USJohns Hopkins University · USScripps Research Institute · USUniversity of Arizona · US

Funding

CHEMOPROTEOMIC METHODS FOR SERINE HYDROLASE INHIBITOR DEVELOPMENTR01DA033760 · NIDA · SCRIPPS RESEARCH INSTITUTE, THE · PI CRAVATT, BENJAMIN F, SCAMPAVIA, LOUIS DANIEL · 2012 to 2021
$5.1M
Cannabinoid CB2 Agonists for Treatment of Breast Cancer-Induced Bone PainR01CA142115 · NCI · UNIVERSITY OF ARIZONA · PI VANDERAH, TODD W · 2010 to 2021
$3.3M
New Modalities for the Treatment of Pain and Drug Abuse-Biochemical CoreP01DA041307 · NIDA · UNIVERSITY OF ARIZONA · PI PORRECA, FRANK · 2017 to 2021
$3.0M
Integrated Acoustic Transfer System for HTS Library ManagementS10OD025279 · OD · SCRIPPS FLORIDA · PI SCAMPAVIA, LOUIS DANIEL · 2018 to 2018
$624k
HTS Drug  Discovery DispensersS10OD026857 · OD · SCRIPPS FLORIDA · PI SCAMPAVIA, LOUIS DANIEL · 2019 to 2019
$452k
NCI NIH HHS R01 CA142115NIDA NIH HHS P01 DA041307NIDA NIH HHS R01 DA033760NIH HHS S10 OD025279NIH HHS S10 OD026857
6 · The paper itself

Abstract

Metastatic breast cancer is prevalent worldwide, and one of the most common sites of metastasis is long bones. Of patients with disease, the major symptom is pain, yet current medications fail to adequately result in analgesic efficacy and present major undesirable adverse effects. In our study, we investigate the potential of a novel monoacylglycerol lipase (MAGL) inhibitor, MJN110, in a murine model of cancer-induced bone pain. Literature has previously demonstrated that MAGL inhibitors function to increase the endogenous concentrations of 2-arachydonylglycerol, which then activates CB1 and CB2 receptors to inhibit inflammation and pain. We demonstrate that administration of MJN110 significantly and dose dependently alleviates spontaneous pain behavior during acute administration compared with vehicle control. In addition, MJN110 maintains its efficacy in a chronic-dosing paradigm over the course of 7 days without signs of receptor sensitization. In vitro analysis of MJN110 demonstrated a dose-dependent and significant decrease in cell viability and proliferation of 66.1 breast adenocarcinoma cells to a greater extent than KML29, an alternate MAGL inhibitor, or the CB2 agonist JWH015. Chronic administration of the compound did not appear to affect tumor burden, as evidenced by radiograph or histologic analysis. Together, these data support the application for MJN110 as a novel therapeutic for cancer-induced bone pain. SIGNIFICANCE STATEMENT: Current standard of care for metastatic breast cancer pain is opioid-based therapies with adjunctive chemotherapy, which have highly addictive and other deleterious side effects. The need for effective, non-opioid-based therapies is essential, and harnessing the endogenous cannabinoid system is proving to be a new target to treat various types of pain conditions. We present a novel drug targeting the endogenous cannabinoid system that is effective at reducing pain in a mouse model of metastatic breast cancer to bone.

Indexed as

AnimalsBone NeoplasmsCancer PainCarbamatesCell Line, TumorDisease Models, AnimalDose-Response Relationship, DrugEndocannabinoidsFemaleMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CMonoacylglycerol LipasesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2SuccinimidesCarbamatesEndocannabinoidsMJN110Monoacylglycerol LipasesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2Succinimides

Identifiers

PMID32054717
PMCPMC7160863
OpenAlexW3005607082

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.