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cancer

breast

prostate

thyroid

pancreas

colon

bile duct

gastric

thymus

lung

lymphoma

glioma

cervical

leukemia

melanoma

astrocytomas

tumor


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 neighbouring 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.

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.

Endocannabinoids in the immune system and cancer.

Conclusion: The experimental evidence reviewed in this article argues in favor of the therapeutic potential of these compounds in immune disorders and cancer.

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 CB(2)-selective anticancer agents could be advantageous in light of the unwanted central effects exerted by CB(1) 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.


tumor

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


breast

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.

Δ9-tetrahydrocannabinol 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.


prostate

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.


thyroid

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.

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.


pancreas

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.


lymphoma

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 leukemia cells with THC in vitro reduced cell viability and induced apoptosis.


glioma

Cannabinoids and gliomas

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

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


colon

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.


gastric

Effect of a synthetic cannabinoid agonist on the proliferation and invasion of gastric cancer cells.

Conclusion: Cannabinoids as a new gastric cancer therapy.

Pharmacological synergism between cannabinoids and paclitaxel in gastric cancer cell lines

Conclusion: Cannabinoids as a good palliative agent for cancer patients receiving paclitaxel.


leukemia

Δ9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemia 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 leukemia 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 leukemia.

Targeting cannabinoid receptors to treat leukemia: 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.


cervical

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.


thymus

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.


melanoma

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.


astrocytomas

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.


lung

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





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