Evidence map›Paper›PMID 25916739›Full record

ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2015

The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids.

Sean D McAllister, Liliana Soroceanu, Pierre-Yves Desprez

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 118 citations in OpenAlex.

  1. Scoping Review and Meta-Analysis Suggests thatCannabis and cannabinoid research · 2021
    Pooled it
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  4. CNR1 and CNR2 Cannabinoid Receptor Mutations in Cancer Cells.Current issues in molecular biology · 2026
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3 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.

Sean D McAllisterCalifornia Pacific Medical Center Research Institute, 475 Brannan Street, Suite 220, San Francisco, CA, 94107, USA, mcallis@cpmcri.org.
Liliana Soroceanu
Pierre-Yves Desprez
California Pacific Medical Center · US

Funding

Cannabinoids Control Breast Cancer Progression Through Id-1R01CA135281 · NCI · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI MCALLISTER, SEAN D · 2009 to 2012
$1.4M
NCI NIH HHS R01 CA135281
6 · The paper itself

Abstract

As a therapeutic agent, most people are familiar with the palliative effects of the primary psychoactive constituent of Cannabis sativa (CS), Δ(9)-tetrahydrocannabinol (THC), a molecule active at both the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptor subtypes. Through the activation primarily of CB1 receptors in the central nervous system, THC can reduce nausea, emesis and pain in cancer patients undergoing chemotherapy. During the last decade, however, several studies have now shown that CB1 and CB2 receptor agonists can act as direct antitumor agents in a variety of aggressive cancers. In addition to THC, there are many other cannabinoids found in CS, and a majority produces little to no psychoactivity due to the inability to activate cannabinoid receptors. For example, the second most abundant cannabinoid in CS is the non-psychoactive cannabidiol (CBD). Using animal models, CBD has been shown to inhibit the progression of many types of cancer including glioblastoma (GBM), breast, lung, prostate and colon cancer. This review will center on mechanisms by which CBD, and other plant-derived cannabinoids inefficient at activating cannabinoid receptors, inhibit tumor cell viability, invasion, metastasis, angiogenesis, and the stem-like potential of cancer cells. We will also discuss the ability of non-psychoactive cannabinoids to induce autophagy and apoptotic-mediated cancer cell death, and enhance the activity of first-line agents commonly used in cancer treatment.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicCannabinoidsHumansNeoplasmsPlant ExtractsReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2Antineoplastic Agents, PhytogenicCannabinoidsPlant ExtractsReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2

Identifiers

PMID25916739
PMCPMC4470774
OpenAlexW1971210779

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.