Cannabinoid receptor CB1 regulates STAT3 activity and its expression dictates the responsiveness to SR141716 treatment in human glioma patients’ cells.

Posted on May 27, 2015 by David

“Herein we show that a majority of human brain tumor samples and cell lines over-expressed cannabinoid receptor CB1 as compared to normal human astrocytes (NHA), while uniformly expressed low levels of CB2. This finding prompted us to investigate the therapeutic exploitation of CB1 inactivation by SR141716 treatment, with regard to its direct and indirect cell-mediated effects against gliomas…

These results indicate that CB1 and STAT3 participate in a new oncogenic network in the complex biology of glioma and their expression levels in patients dictate the efficacy of the CB1 antagonist SR141716 in multimodal glioma destruction.

CB1 is implicated in the regulation of cellular processes linked to survival, proliferation, invasion and angiogenesis in several physio-pathological conditions. We shed light on previously unrecognized molecular mechanism of CB1-mediated modulation of human glioma progression and provide the first and original demonstration of CB1-STAT3 axis as a new target and predictor biomarkers of the benefit from specific therapies.

Indeed CB1 antagonism capable of tumoral cell division’ control while making the glioma immunovisible and engaging the immune system to fight it may represent a hopeful alternative to other established chemotherapeutics.

Because different aspects of glioma biology have been separately targeted with very limited success, we speculate that CB1 inhibitors which enclose in the same molecule cytotoxic potential and high activity to boost competent immune surveillance mechanisms, at a degree that seems to be correlated to the levels of CB1 immunoreactivity, might have profound implications for exploring new therapeutic anti-glioma actions.”

http://www.ncbi.nlm.nih.gov/pubmed/26008966

http://www.thctotalhealthcare.com/category/gllomas/

Id-1 is a key transcriptional regulator of glioblastoma aggressiveness and a novel therapeutic target.

Posted on May 12, 2015 by David

“Glioblastoma (GBM) is the most common form of primary adult brain tumors…

It is, therefore, essential to discover master regulators that control GBM invasiveness and target them therapeutically.

We demonstrate here that the transcriptional regulator Id-1 plays a critical role in modulating the invasiveness of GBM cell lines and primary GBM cells.

Furthermore, we show that a non-toxic compound, cannabidiol, significantly down-regulates Id-1 gene expression and associated glioma cell invasiveness…

Our results suggest that Id-1 regulates multiple tumor-promoting pathways in GBM, and that drugs targeting Id-1 represent a novel and promising strategy for improving the therapy and outcome of GBM patients.

We previously showed a strong correlation between Id-1 expression and the invasive and metastatic behavior of breast cancer cells.”

“Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells… CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells… Moreover, reducing Id-1 expression with cannabinoids could also provide a therapeutic strategy for the treatment of additional aggressive cancers because Id-1 expression was found to be up-regulated during the progression of almost all types…” http://mct.aacrjournals.org/content/6/11/2921.long

“In this report, we show that Id-1 is a key regulator of brain tumor cell invasiveness and neurosphere growth, and that Id-1 expression is specifically up-regulated in tissues from patients with high-grade gliomas. Importantly, we demonstrate that targeting Id-1 expression using either genetic approaches or the non-toxic cannabinoid, cannabidiol (CBD), leads to a significant reduction in the invasion of both GBM cell lines and patient-derived primary GBM cultures. CBD also significantly inhibits GBM dispersal ex vivo, and reduces tumor growth and Id-1 expression in vivo.

Consistent with the breast cancer study, we found that the non-psychoactive cannabinoid CBD significantly down-regulated Id-1 expression in serum-derived and primary GBM cells. As expected, we observed robust inhibition of glioma cell invasiveness.

In conclusion, our results establish Id-1 as a key regulator of both invasion and stemness in GBM cells and demonstrate that the non-toxic cannabinoid compound CBD down-regulates Id-1 expression and tumor aggressiveness in culture and in vivo.

The data also shed light on some of the key pathways that control GBM cell dispersal and progression. A greater understanding of these pathways may lead to more effective therapies for cancer patients including the additional refinement of cannabinoid analogs targeting Id-1.

We expect our efforts to ultimately translate to the development of future clinical trials with nontoxic compounds that target the expression of Id-1, a master regulator of GBM aggressiveness.

With its lack of systemic toxicity and psychoactivity, CBD is an ideal candidate agent in this regard and may prove useful in combination with front-line agents for the treatment of patients with aggressive and high-grade GBM tumors.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3594064/

“McAllister Lab… Cannabidiol inhibits tumor (glioblastoma) progression in mouse models of brain cancer. Mice bearing human brain tumors derived from glioblastoma were treated with the naturally occurring cannabinoid, cannabidiol (CBD).” http://www.cpmcri-currents.org/our-people/discovery-investigators/mcallister-lab

“New Study Finds Cannabis Compound Could Have Even Greater Reach in Inhibiting Aggressive Cancer than Previously Thought. Researchers at California Pacific Medical Center Research Institute (CPMCRI, a Sutter Health affiliate) have found that a compound in cannabis previously shown to decrease metastatic breast cancer now shows promise in stopping aggressive brain cancer as well. The findings are particularly important given the safety of the cannabis compound and the fact that patients with advanced brain cancer have few options for treatment.” http://www.cpmc.org/about/press/news2012/cannabis-brain.html

http://www.thctotalhealthcare.com/category/brain-cancer/

Glioblastoma progression in mouse models of brain cancer, after treatment with CBD

Arachidonylethanolamide induces apoptosis of human glioma cells through vanilloid receptor-1.

Posted on May 7, 2015 by David

“The anti-tumor properties of cannabinoids have recently been evidenced, mainly with delta9-tetrahydrocannabinol (THC).

Here we investigated whether the most potent endogenous cannabinoid, arachidonylethanolamide (AEA), could be a candidate.

We observed that AEA induced apoptosis in long-term and recently established glioma cell lines via aberrantly expressed vanilloid receptor-1 (VR1).

In contrast with their role in THC-mediated death, both CB1 and CB2 partially protected glioma against AEA-induced apoptosis.

These data show that the selective targeting of VR1 by AEA or more stable analogues is an attractive research area for the treatment of glioma.”

http://www.ncbi.nlm.nih.gov/pubmed/15453094

http://www.thctotalhealthcare.com/category/gllomas/

It’s “BRAIN TUMOR AWARENESS MONTH”. Please, BE AWARE:

Posted on May 2, 2015 by David

“A glioma is a primary brain tumor that originates from the supportive cells of the brain, called glial cells.” http://neurosurgery.ucla.edu/body.cfm?id=159

“Long-term use of both mobile and cordless phones is associated with an increased risk for glioma, the most common type of brain tumor, the latest research on the subject concludes.” http://www.medscape.com/viewarticle/834888

“Remarkably, cannabinoids kill glioma cells selectively and can protect non-transformed glial cells from death… cannabinoids-the active components of the plant Cannabis sativa.” http://www.ncbi.nlm.nih.gov/pubmed/15275820

Green Party politician Ian Driver wants a Cannabis cafe to open in Kent

“Molecular mechanisms involved in the antitumor activity of cannabinoids… Cannabinoids, the active components of Cannabis sativa, have been shown to exert antiproliferative and proapoptotic effects on a wide spectrum of tumor cells… Of interest, cannabinoids have displayed great potency in reducing the growth of glioma tumors… Cannabinoids appear to be selective antitumoral agents as they kill glioma cells without affecting the viability of non-transformed cells. Cannabinoids have been proven to inhibit glioma tumor growth… Since cannabinoids kill tumor cells without toxicity on their non transformed counterparts, they can represent a class of new potential anticancer drugs.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835116/
“Antitumor effects of THC.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240145/

“…cannabidiol (CBD), a non-psychoactive cannabinoid, is able to kill glioma cells, both in vivo and in vitro, independently of cannabinoid receptor stimulation… CBD exerts its antitumoral effects through modulation of the LOX pathway and of the endocannabinoid system…” http://www.ncbi.nlm.nih.gov/pubmed/18028339

“Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines… Marijuana and its derivatives have been used in medicine for many centuries… cannabinoids (CBs) have been shown to possess antitumor properties… the nonpsychoactive CBD was able to produce a significant antitumor activity both in vitro and in vivo,” http://jpet.aspetjournals.org/content/308/3/838.long

“Cannabinoids appear to be selective antitumoral agents as they kill glioma cells without affecting the viability of nontransformed counterparts… good safety profile… remarkable antitumor effects… anticancer activity of cannabinoids.” http://www.ncbi.nlm.nih.gov/pubmed/18088200

“Marijuana Could Cure Cancer And Brain Tumors, Suggests Study” http://www.newseveryday.com/articles/13835/20150416/marijuana-fight-both-cancer-brain-tumour-research.htm

“Marijuana can kill cancer cells and even shrink brain tumours, amazing new findings reveal” http://www.mirror.co.uk/lifestyle/health/marijuana-can-kill-cancer-cells-5502082

“Cannabis extract shrinks brain tumours” http://www.newscientist.com/article/dn6283-cannabis-extract-shrinks-brain-tumours.html#.VUSoGlU4nTY

“Cannabis chemicals slows down brain cancer tumour: British Scientists” http://timesofindia.indiatimes.com/home/science/Cannabis-chemicals-slows-down-brain-cancer-tumour-British-Scientists/articleshow/45166303.cms

“Cannabis reduce tumour growth in cancer patients” http://timesofindia.indiatimes.com/home/science/Cannabis-reduce-tumour-growth-in-cancer-patients/articleshow/38456886.cms

“Cannabis can cure cancer and even shrink brain tumours” http://timesofindia.indiatimes.com/home/science/Cannabis-can-cure-cancer-and-even-shrink-brain-tumours/articleshow/46902373.cms

“Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis. Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death.” https://medicine.yale.edu/cancer/patient/programs/sarcoma/info/info.aspx?id=CDR683767

“Study: Thinking Can Speed Up Brain Tumour Growth”
http://au.ibtimes.com/study-thinking-can-speed-brain-tumour-growth-1443392

“Cannabis Significantly Prevents Tumour Growth in Cancer Patients” http://au.ibtimes.com/cannabis-significantly-preventstumour-growth-cancer-patients-1347319

“Cannabis Extracts ‘Drastically Reduce’ Brain Tumour Size” http://www.ibtimes.co.uk/cannabis-extracts-drastically-reduce-brain-tumour-size-1475399

“Brain Tumors And Cell Phone Use Found To Be Linked (Again)” http://www.medicaldaily.com/brain-tumors-and-cell-phone-use-found-be-linked-again-310460

“Brain Tumors Removed Through The Eye Socket In Revolutionary Operation” http://www.medicaldaily.com/brain-tumors-removed-through-eye-socket-revolutionary-operation-319650

“Cannabis Shrinks Brain Tumors Associated With Highly Aggressive Form Of Cancer” http://www.medicaldaily.com/cannabis-shrinks-brain-tumors-associated-highly-aggressive-form-cancer-310720

“Towards the use of cannabinoids as antitumour agents. Various reports have shown that cannabinoids (the active components of marijuana and their derivatives) can reduce tumour growth and progression in animal models of cancer, in addition to their well-known palliative effects on some cancer-associated symptoms. This article discusses our current understanding of cannabinoids as antitumour agents” http://www.ncbi.nlm.nih.gov/pubmed/22555283

“…antitumor effects of cannabinoids in gliomas… canabinnoids exercised selective antitumoral action in several distinct tumor models. Thereby, normal cells used as controls were not affected. The safety factor in the cannabinoids’ administration has also been demonstrated in vivo. The various cannabinoids tested in multiple tumor models showed antitumoral effects both in vitro and in vivo. These findings indicate that cannabinoids are promising compounds for the treatment of gliomas.” http://www.ncbi.nlm.nih.gov/pubmed/24142199

“The tumors regressed over the same period of time that cannabis was consumed via inhalation, raising the possibility that the cannabis played a role in the tumor regression.” http://www.ncbi.nlm.nih.gov/pubmed/21336992

“CB1 and CB2 expression levels have been detected in human tumors, including those of brain. Cannabinoids-endocannabinoids exert anti-inflammatory, anti-proliferative, anti-invasive, anti-metastatic and pro-apoptotic effects in different cancer types, both in vitro and in vivo animal models, after local or systemic administration. We present the available experimental and clinical data, to date, regarding the antitumor action of cannabinoids on the tumorigenesis of gliomas.”
http://www.ncbi.nlm.nih.gov/pubmed/25472761

“The efficacy of cannabinoids against high-grade glioma in animal models, mediated by two specific receptors, CB1 and CB2, raised promises for targeted treatment of the most frequent and malignant primary brain tumors… The high levels of CB2 expression would predestine those tumors to be vulnerable to cannabinoid treatment.” http://www.ncbi.nlm.nih.gov/pubmed/17239827

“Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis… molecular mechanisms of action of cannabinoids as antitumor agents. Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death… these compounds have been shown to induce apoptosis (programmed cell death) in glioma cells in culture and induce regression of glioma tumors in mice and rats, while they protect normal glial cells…” http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4

“As a therapeutic agent, most people are familiar with the palliative effects of the primary psychoactive constituent of Cannabis sativa (CS), Δ9-tetrahydrocannabinol (THC), a molecule active at both the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors… however, several studies have now shown that CB1 and CB2 receptor agonists can act as direct antitumor agents in a variety of aggressive cancers.” http://www.ncbi.nlm.nih.gov/pubmed/25916739

“CANNABIS can help cancer patients: Drug kills cancer cells and shrinks brain tumours, report reveals.” http://www.dailymail.co.uk/health/article-3036667/How-cannabis-help-cancer-patients-Drug-kills-cancer-cells-shrinks-brain-tumours-report-reveals.html

“Active Component In Marijuana Targets Aggressive Brain Cancer Cells… cannabinoids such as THC had anticancer effects in mice with human brain cancer cells AND PEOPLE with brain tumors.” http://www.webmd.com/cancer/brain-cancer/news/20090401/marijuana-chemical-may-fight-brain-cancer

“Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673842/

“Active Ingredient in Marijuana Inhibits Cancer Growth…the cannabinoids found in marijuana may aid in brain tumor treatment…cannabinoids inhibited genes needed for the production of vascular growth factor (VEGF) in laboratory mice with glioma brain tumors AND TWO PATIENTS with late-stage glioblastoma multiforme, a form of brain cancer.” http://www.webmd.com/cancer/news/20040815/marijuana-stall-brain-tumor-growth

“Cannabinoids Inhibit the Vascular Endothelial Growth Factor Pathway in Gliomas… Because blockade of the VEGF pathway constitutes one of the most promising antitumoral approaches currently available, the present findings provide a novel pharmacological target for cannabinoid-based therapies.” http://cancerres.aacrjournals.org/content/64/16/5617.long

“Marijuana’s Active Ingredient Targets Deadly Brain Cancer… cannabinoids could stop growth and kill cancer cells but did not harm normal cells.” http://www.webmd.com/cancer/news/20000228/marijuanas-active-ingredient-targets-deadly-brain-cancer

“Anti-tumoral action of cannabinoids: Involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation” http://www.nature.com/nm/journal/v6/n3/abs/nm0300_313.html

“Cannabinoids, the active components of Cannabis sativa L., inhibit tumor growth in laboratory animals by inducing apoptosis of tumor cells and inhibiting tumor angiogenesis. It has also been reported that cannabinoids inhibit tumor cell invasiveness… Local administration of Delta(9)-tetrahydrocannabinol (THC), the major active ingredient of cannabis, down-regulated TIMP-1 expression in mice bearing subcutaneous gliomas… THC also depressed TIMP-1 expression in cultures of various human glioma cell lines as well as in primary tumor cells obtained from a glioblastoma multiforme patient… TIMP-1 down-regulation may be a hallmark of cannabinoid-induced inhibition of glioma progression.” http://www.ncbi.nlm.nih.gov/pubmed/17675107

“Cannabinoids, the active components of Cannabis sativa L… inhibit tumor growth by inducing apoptosis of tumor cells and impairing tumor angiogenesis… these compounds inhibit tumor cell spreading… Local administration of Delta(9)-tetrahydrocannabinol (THC), the major active ingredient of cannabis, down-regulated MMP-2 expression in gliomas generated in mice… MMP-2 down-regulation constitutes a new hallmark of cannabinoid antitumoral activity.” http://www.ncbi.nlm.nih.gov/pubmed/18339876

“Cannabinoids, the active components of Cannabis sativa… Cannabinoids exert various palliative effects in cancer patients. In addition, cannabinoids inhibit the growth of different types of tumor cells, including glioma cells… Of interest, cannabinoids seem to be selective antitumoral compounds, as they kill glioma cells, but not their non-transformed astroglial counterparts.” http://www.ncbi.nlm.nih.gov/pubmed/17952650

http://www.thctotalhealthcare.com/category/brain-cancer/

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

Posted on April 29, 2015 by David

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.”

http://www.ncbi.nlm.nih.gov/pubmed/25916739

http://www.thctotalhealthcare.com/category/cancer/

Cannabidiol stimulates Aml-1a-dependent glial differentiation and inhibits glioma stem-like cells proliferation by inducing autophagy in a TRPV2-dependent manner.

Posted on April 24, 2015 by David

“Glioma stem-like cells (GSCs) correspond to a tumor cell subpopulation, involved in glioblastoma multiforme (GBM) tumor initiation and acquired chemoresistance. Currently, drug-induced differentiation is considered as a promising approach to eradicate this tumor-driving cell population.

Recently, the effect of cannabinoids (CBs) in promoting glial differentiation and inhibiting gliomagenesis has been evidenced. Herein, we demonstrated that cannabidiol (CBD) by activating Transient Receptor Potential Vanilloid-2 (TRPV2) triggers GSCs differentiation activating the autophagic process and inhibits GSCs proliferation and clonogenic capability.

Above all, CBD and carmustine (BCNU) in combination overcome the high resistance of GSCs to BCNU treatment, by inducing apoptotic cell death…

Altogether, these results support a novel mechanism by which CBD inducing TRPV2-dependent autophagic process stimulates Aml-1a-dependent GSCs differentiation, abrogating the BCNU chemoresistance in GSCs.”

http://www.ncbi.nlm.nih.gov/pubmed/25903924

http://www.thctotalhealthcare.com/category/gllomas/

The antitumor action of cannabinoids on glioma tumorigenesis.

Posted on December 5, 2014 by David

“Cannabinoids are a class of chemical compounds with a wide spectrum of pharmacological effects, mediated by two specific plasma membrane receptors (CB1 and CB2).

Recently, CB1 and CB2 expression levels have been detected in human tumors, including those of brain.

Cannabinoids-endocannabinoids exert anti-inflammatory, anti-proliferative, anti-invasive, anti-metastatic and pro-apoptotic effects in different cancer types, both in vitro and in vivo in animal models, after local or systemic administration.

We present the available experimental and clinical data, to date, regarding the antitumor action of cannabinoids on the tumorigenesis of gliomas.”

http://www.ncbi.nlm.nih.gov/pubmed/25472761

http://www.thctotalhealthcare.com/category/gllomas/

The Combination of Cannabidiol and Δ9-Tetrahydrocannabinol Enhances the Anticancer Effects of Radiation in an Orthotopic Murine Glioma Model.

Posted on November 16, 2014 by David

“High-grade glioma is one of the most aggressive cancers in adult humans and long-term survival rates are very low as standard treatments for glioma remain largely unsuccessful.

Cannabinoids have been shown to specifically inhibit glioma growth as well as neutralize oncogenic processes such as angiogenesis.

In an attempt to improve treatment outcome, we have investigated the effect of Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) both alone and in combination with radiotherapy in a number of glioma cell lines (T98G, U87MG, and GL261).

Cannabinoids were used in two forms, pure (P) and as a botanical drug substance (BDS).

Results demonstrated a duration- and dose-dependent reduction in cell viability with each cannabinoid and suggested that THC-BDS was more efficacious than THC-P, whereas, conversely, CBD-P was more efficacious than CBD-BDS.

…increase in radiosensitivity was associated with an increase in markers of autophagy and apoptosis.

These in vitro results were recapitulated in an orthotopic murine model for glioma, which showed dramatic reductions in tumor volumes when both cannabinoids were used with irradiation.

Taken together, our data highlight the possibility that these cannabinoids can prime glioma cells to respond better to ionizing radiation, and suggest a potential clinical benefit for glioma patients by using these two treatment modalities.”

http://www.ncbi.nlm.nih.gov/pubmed/25398831

http://www.thctotalhealthcare.com/category/gllomas/

Anti-Cancer Effects In Active Component Of Marijuana

Posted on July 21, 2014 by David

“Guillermo Velasco and colleagues, at Complutense University, Spain, have provided evidence that suggests that cannabinoids such as the main active component of marijuana (THC) have anticancer effects on human brain cancer cells.

In the study, THC was found to induce the death of various human brain cancer cell lines and primary cultured human brain cancer cells by a process known as autophagy. Consistent with the in vitro data, administration of THC to mice with human tumors decreased tumor growth and induced the tumor cells to undergo autophagy.

As analysis of tumors from two patients with recurrent glioblastoma multiforme (a highly aggressive brain tumor) receiving intracranial THC administration showed signs of autophagy, the authors suggest that cannabinoid administration may provide a new approach to targeting human cancers.”

http://www.medicalnewstoday.com/releases/144770.php

“Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673842/

Distinctive pattern of cannabinoid receptor type II (CB2) expression in adult and pediatric brain tumors.

Posted on March 4, 2014 by David

Unlike the abundantly expressed CB1, the CB2 receptor shows a restricted distribution in normal brain. Although brain tumors constitute the second most common malignancy in children and the prevalence of histological types of brain tumors vary significantly between the adult and pediatric populations, cannabinoid receptor expression in pediatric tumors remains unknown.

In the present study, we compared the expression of the CB2 receptor in paraffin-embedded sections from primary brain tumors of adult and pediatric patients. Most glioblastomas expressed very high levels of CB2 receptors and the expression correlated with tumor grade.

Interestingly, some benign pediatric astrocytic tumors, such as subependymal giant cell astrocytoma (SEGA), which may occasionally cause mortality owing to progressive growth, also displayed high CB2 immunoreactivity.

The high levels of CB2 expression would predestine those tumors to be vulnerable to cannabinoid treatment.

In contrast, all examined cases of embryonal tumors (medulloblastoma and S-PNET), the most frequently diagnosed malignant brain tumors in childhood, showed no or trace CB2 immunoreactivity.

Our results suggest that the CB2 receptor expression depends primarily on the histopathological origin of the brain tumor cells and differentiation state, reflecting the tumor grade.”

http://www.ncbi.nlm.nih.gov/pubmed/17239827