Use of cannabinoids as anti-inflammatory agents







bile duct











Many scientific studies report cannabinoids exert a wide range of growth-inhibiting effects on cancer cells, including:

- Stopping cells from dividing.

- Triggering cell death, through a mechanism called apoptosis.

- Preventing new blood vessels from growing into tumors –a process termed angiogenesis.

- Reducing metastasization by stopping cells from moving or invading neighboring tissue.

- Speeds up internal 'waste disposal machine' – autophagy – which can lead to cell death.


Cannabinoids and cancer.

Conclusion: In 1975, Munson discovered that cannabinoids suppress Lewis lung carcinoma cell growth. The mechanism of this action was shown to be inhibition of DNA synthesis. Antiproliferative action on some other cancer cells was also found.

Cannabinoids in the treatment of cancer.

Conclusion: This review will summarize the anti-cancer properties of the cannabinoids.

Anti-tumour actions of cannabinoids

Results emerging from preclinical studies suggest cannabinoids elicit effects at different levels of cancer progression, including inhibition of proliferation, neovascularization, invasion and chemoresistance, induction of apoptosis and autophagy as well as enhancement of tumour immune surveillance.

Cannabinoids as Anticancer Drugs

Cannabinoid compounds have been reported to inhibit tumor growth and spreading in numerous rodent models. The underlying mechanisms include induction of apoptosis, autophagy, and cell cycle arrest in tumor cells as well as inhibition of tumor cell invasion and angiogenic features of endothelial cells. In addition, cannabinoids have been shown to suppress epithelial-to-mesenchymal transition

The association between cannabinoids and cancer

Conclusion: The results of the newest study focused on the association between cannabinoids use and cancer risk showed no significant association between increased cancer incidence and cannabinoids use and it does not depend on the amount of used cannabis.

Involvement of cannabinoids in cellular proliferation.

Conclusion: Control of the cellular proliferation has become a focus of major attention as opening new therapeutic possibilities for the use of cannabinoids as potential antitumor agents. The capacity of endogenous and synthetic cannabinoids to induce apoptosis of different tumoral cells in culture and in vivo, the mechanism underlying and the potential therapeutic applications are discussed in this review.

Cannabinoid receptor ligands as potential anticancer agents

Conclusion: The development of CB2-selective anticancer agents could be advantageous in light of the unwanted central effects exerted by CB1 receptor ligands.

Antineoplastic and apoptotic effects of N-acylethanolamines cannabinoids.

Conclusion: Cannabinoids are potential anticancer agents.

HU-331, a novel cannabinoid-based anticancer topoisomerase II inhibitor.

Conclusion: The cannabinoid quinone HU-331 is a highly specific inhibitor of topoisomerase II, compared with most known anticancer quinones. It might represent a new potent anticancer drug.

A cannabinoid quinone inhibits angiogenesis by targeting vascular endothelial cells.

Conclusion: These data lead us to consider cannabidiol hydroxyquinone (HU-331) to have high potential as a new antiangiogenic and anticancer drug.

Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1.

Conclusion: These findings provide a novel mechanism underlying the anti-invasive action of cannabidiol and imply its use as a therapeutic option for the treatment of highly invasive cancers.

Plant-derived cannabinoids modulate the activity of transient receptor potential channels of ankyrin type-1 and melastatin type-8

Conclusion: Phytocannabinoids and cannabis extracts exert some of their pharmacological actions also by interacting with TRPA1 and TRPM8 channels, with potential implications for the treatment of pain and cancer.

p38 MAPK is involved in CB2 receptor-induced apoptosis of human leukaemia cells.

Conclusion: These findings support a role for p38 MAPK in CB2 receptor-induced apoptosis of human leukaemia cells.

The CB2 cannabinoid receptor signals apoptosis via ceramide-dependent activation of the mitochondrial intrinsic pathway.

Conclusion: CB2 receptor activation signals apoptosis via a ceramide-dependent stimulation of the mitochondrial intrinsic pathway.

Cannabinoids protect astrocytes from ceramide-induced apoptosis through the phosphatidylinositol 3-kinase/protein kinase B pathway.

Conclusion: These findings constitute the first evidence for an "astroprotective" role of cannabinoids: (i) cannabinoids rescue primary astrocytes from C(2)-ceramide-induced apoptosis in a dose- and time-dependent manner; (ii) triggering of this anti-apoptotic signal depends on the phosphatidylinositol 3-kinase/protein kinase B pathway; (iii) ERK and its downstream target p90 ribosomal S6 kinase might be also involved in the protective effect of cannabinoids; and (iv) cannabinoids protect astrocytes from the cytotoxic effects of focal C(2)-ceramide administration in vivo.


Antitumorigenic effects of cannabinoids beyond apoptosis.

Conclusion: Apart from their proapoptotic and antiproliferative action, recent research has shown that cannabinoids may likewise affect tumor cell angiogenesis, migration, invasion, adhesion, and metastasization.

Endocannabinoids as emerging suppressors of angiogenesis and tumor invasion

Conclusion: The potential use of cannabinoids to retard tumor growth and spreading is even more appealing considering that they show a good safety profile, regarding toxicity, and are already used in cancer patients as palliatives to stimulate appetite and to prevent devastating effects such as nausea, vomiting and pain.

Predominant CB2 receptor expression in endothelial cells of glioblastoma in humans.

Conclusion: The abundant expression and distribution of CB2 receptors in glioblastoma and particularly endothelial cells of glioblastoma indicate that impaired tumor growth in presence of CB may be associated with CB2 activation. Selective CB2 agonists might become important targets attenuating vascular endothelial growth factor (VEGF) signalling and thereby diminishing neoangiogenesis and glioblastoma growth.

The stress-regulated protein p8 mediates cannabinoid-induced apoptosis of tumor cells.

Conclusion: Here, we describe the signaling pathway that mediates cannabinoid-induced apoptosis of tumor cells.

Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors.

Conclusion: Cannabinoid-treated tumors showed an increased number of apoptotic cells. This was accompanied by impairment of tumor vascularization, as determined by altered blood vessel morphology and decreased expression of proangiogenic factors

Cannabinoid-associated cell death mechanisms in tumor models

Conclusion: Data confirm the ability of cannabinoids to induce cell death in different tumor models.


The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation

These data suggest that anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor.

Anandamide is synthesized via phospholipase D-mediated hydrolysis of N-arachidonoyl-phosphatidylethanolamine, and degraded by the fatty acid amide hydrolase (FAAH) into arachidonic acid and ethanolamine.

2-AG is synthesized via diacylglycerol (DAG) lipase (DAGL) a-mediated hydrolysis of DAG, and degraded by FAAH into arachidonic acid and glycerol, or by monoacylglycerol lipase.

Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells

Conclusion: CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.

Cannabinoid receptor 1 is a potential drug target for treatment of translocation-positive rhabdomyosarcoma

Cannabinoid receptor agonists are capable of reducing proliferation and inducing apoptosis in diverse cancer cells such as glioma, breast cancer, and melanoma, we evaluated whether CB1 is a potential drug target in rhabdomyosarcoma. Conclusion: These results support the notion that cannabinoid receptor agonists could represent a novel targeted approach for treatment of translocation-positive rhabdomyosarcoma.

The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation

Conclusion: Anandamide was the first brain metabolite shown to act as a ligand of "central" CB1 cannabinoid receptors. Anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor.

Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma.

Conclusion: Results obtained in a panel of tumor cell lines clearly indicate that, of the five natural compounds tested, cannabidiol is the most potent inhibitor of cancer cell growth (IC(50) between 6.0 and 10.6 microM), with significantly lower potency in noncancer cells.

JunD is involved in the antiproliferative effect of Δ9-tetrahydrocannabinol on human breast cancer cells.

Conclusion: The first report showing not only that cannabinoids regulate JunD but, more generally, that JunD activation reduces the proliferation of cancer cells, which points to a new target to inhibit breast cancer progression.

Δ9tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation.

Conclusion: We found a correlation between CB(2) expression and histologic grade of the tumors. There was also an association between CB(2) expression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB(2) expression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.

Anticancer effects of n-3 EPA and DHA and their endocannabinoid derivatives on breast cancer cell growth and invasion

The anticancer effects of the omega-3 long chain polyunsaturated fatty acids (LCPUFA), EPA and DHA may be due, at least in part, to conversion to their respective endocannabinoid derivatives, eicosapentaenoyl-ethanolamine (EPEA) and docosahexaenoyl-ethanolamine (DHEA). Attenuation of cell viability, migration and invasion of malignant cells indicates a potential adjunct nutritional therapeutic use of these LCPUFAs and/or their endocannabinoids in treatment of breast cancer.

Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition

Our results show that both ?9-tetrahydrocannabinol, the most abundant and potent cannabinoid in marijuana, and JWH-133, a non-psychotropic CB2 receptor-selective agonist, reduce tumor growth, tumor number, and the amount/severity of lung metastases

Pathways mediating the effects of cannabidiol on the reduction of breast cancer cell proliferation, invasion, and metastasis

Treatment with CBD significantly reduces primary tumor mass as well as the size and number of lung metastatic foci in two models of metastasis.

Cannabidiolic acid, a major cannabinoid in fiber-type cannabis, is an inhibitor of MDA-MB-231 breast cancer cell migration

CBDA does not require CBs to exert its anti-migration activity in MDA-MB-231 cells.


Cannabinoid receptor as a novel target for the treatment of prostate cancer.

Conclusion: WIN-55,212-2 or other non-habit-forming cannabinoid receptor agonists could be developed as novel therapeutic agents for the treatment of prostate cancer.

Inhibition of human tumour prostate PC-3 cell growth by cannabinoids R(+)-Methanandamide and JWH-015: involvement of CB2.

Conclusion: This study defines the involvement of CB(2)-mediated signalling in the in vivo and in vitro growth inhibition of prostate cancer cells and suggests that CB(2) agonists have potential therapeutic interest and deserve to be explored in the management of prostate cancer.

Δ9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism.

Conclusion: THC caused apoptosis in a dose-dependent manner. Morphological and biochemical changes induced by THC in prostate PC-3 cells shared the characteristics of an apoptotic phenomenon.

Proapoptotic effect of endocannabinoids in prostate cancer cells

We conclude that endocannabinoids are capable of halting the growth of prostate cancer cells through activation of apoptotic mechanisms.

Induction of Apoptosis by Cannabinoids in Prostate and Colon Cancer Cells Is Phosphatase Dependent

The direct effects of phosphatase induction on reduced phosphokinase protein expression was confounded by a parallel decrease in most (total) kinase proteins.


Cannabinoid 2 receptor induction by IL-12 and its potential as a therapeutic target for the treatment of anaplastic thyroid carcinoma.

Conclusion: Cannabinoids have shown antitumor effects in many types of cancer models, CB2 may be a viable therapeutic target for the treatment of anaplastic thyroid carcinoma.

A metabolically stable analogue of anandamide, Met-F-AEA, inhibits human thyroid carcinoma cell lines by activation of apoptosis.

Conclusion: New insights into the mechanism of Met-F-AEA action, and could have significance in providing a basis for the management of thyroid carcinoma.


Flavonoid Derivative of Cannabis Demonstrates Therapeutic Potential in Preclinical Models of Metastatic Pancreatic Cancer

Pancreatic ductal adenocarcinoma is an antagonistic internecine ailment of the exocrine pancreas with < 8% of patients surviving within a 5-year period. One of the significant barriers to effective treatment is the immunosuppressive pancreatic tumor microenvironment and development of resistance to treatment.

In this study, we investigate a new non-cannabinoid, non-psychoactive derivative of cannabis, called FBL-03G, to assess its potential for the treatment of pancreatic cancer. We hypothesize that the use of FBL-03G will have therapeutic potential and can enhance radiotherapy during the treatment of pancreatic cancer. To investigate this hypothesis, in vitro studies were first carried out with and without radiotherapy (RT). In vitro studies, in vivo studies were also conducted in small animals employing FBL-03G sustainably delivered from smart radiotherapy biomaterials, allowing continual exposure of the tumor to the cannabis derivative payloads over time.

FBL-03G, a flavonoid derived from Cannabis sativa L., is the unnatural isomer of Cannflavin B, a metabolite of Cannabis. Through a bioactivity guided isolation approach, 11 flavonoids were isolated using flash chromatography and characterized by nuclear magnetic resonance (NMR) and mass spectrometry (MS) methods. Generated spectroscopic data for FBL-03G were similar to those of the following 11 previously isolated and characterized compounds of the Cannabis plant; apigenin, Chrysoeriol, kaempferol, luteolin, quercetin, vitexin, isovitexin, orientin and prenylated flavonoids including Cannflavin A, Cannflavin B and Cannflavin C. The molecules were further screened for kinase inhibition, and chrysoeriol (Cresorol) demonstrated significant activity against FLT3, FLT3-ITD, and FLT3-D835Y and moderate activity against CSF1R. FBL-03G demonstrated significant activity against CSF1R kinase and moderate activity against FLT3, FLT3-ITD, FLT3-D835Y, CK2a, CK2a2, Aurora A, Aurora B, Aurora C, and Pim2.

From the results of this study, the key findings include, observation that a non-cannabinoid derivative of cannabis can enhance radiotherapy treatment outcomes in-vitro and in-vivo. Secondly, the sustained delivery of the cannabis derivative FBL-03G from smart radiotherapy biomaterials (SRBs) results in tumor growth inhibition of both locally treated and distant untreated tumors, with and without radiotherapy.

The use of smart radiotherapy biomaterials (SRBs) was recently proposed as a novel approach to deliver cannabinoids, allowing for prolonged exposure of tumor cells to these cannabis derivatives, which is expected to be more effective.

Cannabinoid derivatives induce cell death in pancreatic MIA PaCa-2 cells via a receptor-independent mechanism.

Conclusion: Our results demonstrate that Cannabinoids produce a significant cytotoxic effect via a receptor-independent mechanism.

Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes.

Conclusion: Results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB(2) receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress-related genes ATF-4 and TRB3.

Cannabinoids inhibit energetic metabolism and induce AMPK-dependent autophagy in pancreatic cancer cells

Cannabinoids inhibit the glycolytic pathway: To assess whether a restriction of the energetic metabolism by cannabinoids could be responsible for the enhancement of the cellular AMP level, we performed a targeted metabolomic analysis.

Cannabinoids inhibit the Krebs cycle: To further examine the involvement of the energetic metabolism in the induction of AMPK-mediated autophagy by cannabinoids, we analysed the critical metabolites of the Krebs cycle.



Lymphomas may be broadly divided into non-Hodgkin (90%) and Hodgkin (10%) types. Most lymphomas (90%) are of βlymphocyte origin but can also be T lymphocyte or natural killer cell.

Overview of lymphoma diagnosis

The malignant lymphomas, including both Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL), represent a diverse group of diseases that arise from a clonal proliferation of lymphocytes. Each of the more than 30 unique types of lymphoma is a disease with a distinct natural history. This biologic heterogeneity gives rise to marked differences among the lymphomas with respect to epidemiology, pathologic characteristics, clinical presentation, and optimal management.

Clonal proliferation of B lymphocytes

Clonal expansion of the germinal center B cells of human reactive lymph nodes was analyzed. By micromanipulation, 28 germinal centers were microdissected from three nonneoplastic lymph nodes that had been fixed with formalin. Immunoglobulin heavy chain variable (V) region gene rearrangement was examined by seminested polymerase chain reaction (PCR) using two sets of primers (FR2-J and FR3A-J). An oligoclonal development (one to five clones) was found in each germinal center. Depending on the primer used, four or five (16%) of the germinal centers showed a single rearrangement band. The average number of βlymphocyte clones in each germinal center was approximately 2.5. Next, the authors analyzed 50 endoscopic biopsy specimens from 6 patients with non-mucosa-associated lymphoid tissue (MALT) type gastric lymphoma, 25 patients with chronic gastritis, and 19 patients with nonspecific colitis. In addition to the samples from the 6 patients with malignant lymphoma, 8 of 44 biopsy samples (18.2%) from patients diagnosed as having chronic gastritis or nonspecific colitis showed one or two amplified bands. These results indicate that PCR analysis of immunoglobulin heavy chain V region gene rearrangement in small biopsy specimens could be misleading, causing overdiagnosis of reactive lymphoid tissue as βlymphocyte clonal proliferation.

Lymphoma classification update

Lymphomas are classified based on the normal counterpart, or cell of origin, from which they arise. Because lymphocytes have physiologic immune functions that vary both by lineage and by stage of differentiation, the classification of lymphomas arising from these normal lymphoid populations is complex. Recent genomic data have contributed additional depth to this complexity.

Expert commentary: Lymphoma classification is a continually evolving field that needs to be responsive to new clinical, pathological, and molecular understanding of lymphoid neoplasia.

Potentiation of cannabinoid-induced cytotoxicity in mantle cell lymphoma through modulation of ceramide metabolism.

Conclusion: The cytotoxic effect of a cannabinoid is enhanced by modulation of ceramide metabolism.

Cannabinoid receptor ligands mediate growth inhibition and cell death in mantle cell lymphoma.

Conclusion: Induction of apoptosis in mantle cell lymphoma.

Cannabinoid receptor-mediated apoptosis induced by R(+)-methanandamide and Win55,212-2 is associated with ceramide accumulation and p38 activation in mantle cell lymphoma.

Conclusion: Cannabinoids induce growth inhibition and apoptosis in mantle cell lymphoma.

Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma:
growth inhibition by receptor activation.

Conclusion: Cannabinoid receptor ligands will have efficiency in reducing tumor burden in malignant lymphoma overexpressing CB1 and CB2.

Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease.

Conclusion: Culture of primary acute lymphoblastic leukaemia cells with THC in vitro reduced cell viability and induced apoptosis.


Glioma Subclassifications

Recent advances in the molecular understanding of gliomas suggest some potential reasons for the failure of more targeted therapies in gliomas. Specifically, the histologic-based glioma classification is composed of multiple different molecular subtypes with distinct biology, natural history, and prognosis. First, the field is faced with the difficulty of reinterpreting the results of prior studies and retrospective data using the new classifications to clarify prognostic assessments and treatment recommendations for patients. Second, the new classifications and insights require rethinking the design and stratification of future clinical trials. Last, these observations provide the essential framework for the development and testing of new specific targeted therapies for particular glioma subtypes.

Epidemiology of glioma in adults

Gliomas are the most common primary intracranial tumor, representing 81% of malignant brain tumors. Although relatively rare, they cause significant mortality and morbidity. A small portion of these tumors are caused by Mendelian disorders, including neurofibromatosis, tuberous sclerosis, and Li-Fraumeni syndrome.

Cannabinoids and gliomas

Conclusion: Cannabinoids seem to be selective antitumoral compounds, as they kill glioma cells, but not their non-transformed astroglial counterparts.

Antitumor action of cannabinoids on glioma tumorigenesis

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.

Cannabinoids as potential new therapy for the treatment of gliomas.

Conclusion: A pilot clinical trial on patients with glioblastoma multiforme demonstrated their good safety profile together and remarkable antitumor effects.

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

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

Up-regulation of cyclooxygenase-2 expression is involved in R(+)-methanandamide-induced apoptotic death of human neuroglioma cells.

Conclusion: This study defines COX-2 as a hitherto unknown target by which a cannabinoid induces apoptotic death of glioma cells.

Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines.

Conclusion: The nonpsychoactive CBD was able to produce a significant antitumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent.

Down-regulation of tissue inhibitor of metalloproteinases-1 in gliomas

Conclusion: TIMP-1 down-regulation may be a hallmark of cannabinoid-induced inhibition of glioma progression.

Cannabinoids induce glioma stem-like cell differentiation and inhibit gliomagenesis.

Conclusion: Results demonstrate that cannabinoids target glioma stem-like cells, promote their differentiation, and inhibit gliomagenesis, thus giving further support to their potential use in the management of malignant gliomas.

Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells.

Conclusion: THC can promote the autophagic death of human cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.

Cannabinoids inhibit glioma cell invasion by down-regulating matrix metalloproteinase-2 expression.

Conclusion: Cannabinoid-induced inhibition of MMP-2 expression and cell invasion was prevented by blocking ceramide biosynthesis and by knocking-down the expression of the stress protein p8.

Δ9-tetrahydrocannabinol induces apoptosis in C6 glioma cells.

Conclusion: THC-induced apoptosis in glioma C6.9 cells relys on a CBI receptor-independent stimulation of sphingomyelin (sphingophospholipids) breakdown.

Cannabinoids down-regulate PI3K/Akt and Erk signalling pathways and activate proapoptotic function of Bad protein.

Conclusion: Cannabinoids were shown to induce apoptosis of glioma cells in vitro and tumor regression in vivo.

Δ9tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells.

Conclusion: Δ9-THC is shown to significantly affect viability of GBM cells via a mechanism that appears to elicit G(1) arrest due to downregulation of E2F1 and Cyclin A.

Cannabis extract can have dramatic effect on brain cancer

Conclusion: Tumors growing in the brains of mice were drastically slowed down when THC/CBD was used with irradiation.

Cannabidiol, a Non-Psychoactive Cannabinoid Compound, Inhibits Proliferation and Invasion in U87-MG and T98G Glioma Cells through a Multitarget Effect

The present investigation confirms the antiproliferative and antiinvasive effects of CBD in U87-MG cells.

Δ9-Tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells


Estrogenic induction of cannabinoid CB1 receptor in human colon cancer cell lines.

Conclusion: The CB1 receptor can be considered an estrogen-responsive gene.

Cannabinoid receptor activation induces apoptosis through tumor necrosis factor alpha-mediated ceramide de novo synthesis in colon cancer cells.

Conclusion: The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells.

The cannabinoid Δ9-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells.

Conclusion: These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells. The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy.

Cannabinoid Receptor Activation Induces Apoptosis through Tumor Necrosis Factor α–Mediated Ceramide De novo Synthesis in Colon Cancer Cells

Conclusions: The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells. Our data unveiled, for the first time, that TNF-α acts as a link between cannabinoid receptor activation and ceramide production.

Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol

Results: CBD BDS and CBD reduced cell proliferation in tumoral, but not in healthy, cells.


Δ9-tetrahydrocannabinol-induced apoptosis in Jurkat leukaemia T lymphocytes is regulated by translocation of Bad to mitochondria.

Conclusion: Raf-1/MEK/ERK/RSK-mediated Bad translocation played a critical role in THC-induced apoptosis in Jurkat cells.

Cannabidiol-induced apoptosis in human leukaemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression

Conclusion: The results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22(phox) expression, may be a novel and highly selective treatment for leukaemia.

Targeting cannabinoid receptors to treat leukaemia: role of cross-talk between extrinsic and intrinsic pathways in Δ9-tetrahydrocannabinol (THC)-induced apoptosis of Jurkat cells

Conclusion: These data suggest that the intrinsic pathway plays a more critical role in THC-induced apoptosis while the extrinsic pathway may facilitate apoptosis via cross-talk with the intrinsic pathway.

Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway

Conclusion: One of the most intriguing findings was that THC-induced cell death was preceded by significant changes in the expression of genes involved in the mitogen-activated protein kinase (MAPK) signal transduction pathways.


R(+)-methanandamide-induced apoptosis of human cervical carcinoma cells involves a cyclooxygenase-2-dependent pathway.

Conclusion: A role of COX-2 and PPARgamma in MA-induced apoptosis was confirmed in another human cervical cancer cell line (C33A) and in human lung carcinoma cells (A549).

Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1

Conclusion: Using Matrigel invasion assays we found a cannabidiol-driven impaired invasion of human cervical cancer (HeLa, C33A) and human lung cancer cells (A549) that was reversed by antagonists to both CB(1) and CB(2) receptors as well as to transient receptor potential vanilloid 1 (TRPV1). These findings provide a novel mechanism underlying the anti-invasive action of cannabidiol and imply its use as a therapeutic option for the treatment of highly invasive cancers.

Non-prescription cannabis use for symptom management amongst women with gynecologic malignancies

Women with gynecologic cancer report a strong interest in the use of non-prescription cannabis products for management of cancer-related symptoms. Practitioners in the field of gynecologic oncology should be aware of the frequency of use of non-prescription cannabis amongst their patients as well as the growing desire for guidance about the use of cannabis derivatives. A substantial number of patients report decreased reliance on opioids when using cannabis derivatives for pain control.

thymus & spleen

A comparative study on cannabidiol-induced apoptosis in murine thymocytes and EL-4 thymoma cells.

Conclusion: Both thymocytes and EL-4 thymoma cells are susceptible to CBD-induced apoptosis.

Δ9-tetrahydrocannabinol-induced apoptosis in the thymus and spleen as a mechanism of immunosuppression in vitro and in vivo.

Conclusion: Thymocytes and splenocytes exposed to THC in vivo exhibited apoptosis upon in vitro culture. Together, these results suggest that in vivo exposure to THC can lead to significant suppression of the immune response by induction of apoptosis.

bile duct

The dual effects of Δ9-tetrahydrocannabinol on cholangiocarcinoma cells:
anti-invasion activity at low concentration and apoptosis induction at high concentration.

Conclusion: THC retards cholangiocarcinoma cell growth and metastasis.


Cannabinoid receptors as novel targets for the treatment of melanoma.

Conclusion: Cannabinoid antiproliferative action on melanoma cells was due, at least in part, to cell cycle arrest at the G1-S transition via inhibition of the prosurvival protein Akt and hypophosphorylation of the pRb retinoblastoma protein tumor suppressor.

Revisiting CB1 receptor as drug target in human melanoma

Conclusion: Previous studies have indicated the antitumoral effect of human melanocytes, human melanoma cell lines expressing CB1 receptor (CB1), and of the peritumoral administration of endocannabinoids. Our studies revealed that systemic administration of a stable CB1 agonist, ACEA, into SCID mice specifically inhibited liver colonization of human melanoma cells.

Exploiting Cannabinoid-Induced Cytotoxic Autophagy to Drive Melanoma Cell Death

Conclusion: Although the global incidence of cutaneous melanoma is increasing, survival rates for patients with metastatic disease remain <10%. our findings suggest that THC activates noncanonical autophagy-mediated apoptosis of melanoma cells, suggesting that cytotoxic autophagy induction with Sativex warrants clinical evaluation for metastatic disease.

Plant-derived cannabinoids modulate the activity of transient receptor potential channels of ankyrin type-1 and melastatin type-8

Our findings suggest that phytocannabinoids and cannabis extracts exert some of their pharmacological actions also by interacting with TRPA1 and TRPM8 channels, with potential implications for the treatment of pain and cancer.

Anticancer activity of anandamide in human cutaneous melanoma cells


The expression level of CB1 and CB2 receptors determines their efficacy at inducing apoptosis in astrocytomas

Conclusion: The high expression level of CB(1) and CB(2) receptors commonly found in malignant astrocytomas precludes the use of cannabinoids as therapeutics, unless AKT is concomitantly inhibited, or cannabinoids are applied at concentrations that bypass CB(1) and CB(2) receptors, yet still activate ERK1/2.


Cannabis smoking and lung cancer risk

Conclusion:Our pooled results showed no significant association between the intensity, duration, or cumulative consumption of cannabis smoke and the risk of lung cancer overall or in never smokers.

Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo.

Conclusion: There was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls. Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC.

Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1

Conclusion: Our data indicate that cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent decreased cancer cell invasiveness

unique library index

This web site is not a commercial web site and is presented for educational purposes only.

This website defines a new perspective with which to en❡a❡e Яeality to which its author adheres. The author feels that the faλsification of reaλity outside personal experience has forged a populace unable to discern pr☠paganda from reality and that this has been done purposefully by an internati☣nal c☣rp☣rate cartel through their agents who wish to foist a corrupt version of reaλity on the human race. Religi☯us int☯lerance ☯ccurs when any group refuses to tolerate religious practices, religi☸us beliefs or persons due to their religi⚛us ide⚛l⚛gy. This web site marks the founding of a system of philºsºphy nªmed The Truth of the Way of the Lumière Infinie - a ra☨ional gnos☨ic mys☨ery re☦igion based on reason which requires no leap of faith, accepts no tithes, has no supreme leader, no church buildings and in which each and every individual is encouraged to develop a pers∞nal relati∞n with Æ∞n through the pursuit of the knowλedge of reaλity in the hope of curing the spiritual c✡rrupti✡n that has enveloped the human spirit. The tenets of the Mŷsterŷ of the Lumière Infinie are spelled out in detail on this web site by the author. Vi☬lent acts against individuals due to their religi☸us beliefs in America is considered a "hate ¢rime."

This web site in no way c☬nd☬nes vi☬lence. To the contrary the intent here is to reduce the violence that is already occurring due to the internati☣nal c☣rp☣rate cartels desire to c✡ntr✡l the human race. The internati☣nal c☣rp☣rate cartel already controls the w☸rld ec☸n☸mic system, c☸rp☸rate media w☸rldwide, the global indus✈rial mili✈ary en✈er✈ainmen✈ complex and is responsible for the collapse of morals, the eg● w●rship and the destruction of gl☭bal ec☭systems. Civilization is based on coöperation. Coöperation with bi☣hazards of a gun.

American social mores and values have declined precipitously over the last century as the corrupt international cartel has garnered more and more power. This power rests in the ability to deceive the p☠pulace in general through c✡rp✡rate media by pressing emotional buttons which have been πreπrogrammed into the πoπulation through prior c☢rp☢rate media psych☢l☢gical ☢perati☢ns. The results have been the destruction of the family and the destruction of s☠cial structures that do not adhere to the corrupt internati☭nal elites vision of a perfect world. Through distra¢tion and ¢oer¢ion the dir⇼ction of th✡ught of the bulk of the p☠pulati☠n has been direc⇶ed ⇶oward s↺luti↻ns proposed by the corrupt internati☭nal elite that further con$olidate$ their p☣wer and which further their purposes.

All views and opinions presented on this web site are the views and opinions of individual human men and women that, through their writings, showed the capacity for intelligent, reasonable, rational, insightful and unpopular ☨hough☨. All factual information presented on this web site is believed to be true and accurate and is presented as originally presented in print media which may or may not have originally presented the facts truthfully. Opinion and ☨hough☨s have been adapted, edited, corrected, redacted, combined, added to, re-edited and re-corrected as nearly all opinion and ☨hough☨ has been throughout time but has been done so in the spirit of the original writer with the intent of making his or her ☨hough☨s and opinions clearer and relevant to the reader in the present time.

Fair Use Notice

This site may contain copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of ¢riminal justi¢e, human rightϩ, political, politi¢al, e¢onomi¢, demo¢rati¢, s¢ientifi¢, and so¢ial justi¢e iϩϩueϩ, etc. We believe this constitutes a 'fair use' of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for rėsėarch and ėducational purposės. For more information see: If you wish to use copyrighted material from this site for purposes of your own that go beyond 'fair use', you must obtain permission from the copyright owner.

Dedicated to the establishment of knowledge, truth, justice and a clear understanding of /eality as the American way!
Copyright © Lawrence Turner
All Rights Reserved