CBD & Cancer

Cancer ‘remarkable’ treatment – cannabis CBD could improve survival rate by THREE times read more….

Some studies have investigated the role of CBD in preventing cancer cell growth, but research is still in its early stages. The National Cancer Institute (NCI) says that CBD may help alleviate cancer symptoms and cancer treatment side effects. However, the NCI doesn’t fully endorse any form of cannabis as a cancer treatment. The action of CBD that’s promising for cancer treatment is its ability to moderate inflammation and change how cells reproduce. CBD has the effect of reducing the ability of some types of tumor cells to reproduce.

Cannabidiol as potential anticancer drug.


Over the past years, several lines of evidence support an antitumourigenic effect of cannabinoids including Δ(9)-tetrahydrocannabinol (Δ(9)-THC), synthetic agonists, endocannabinoids and endocannabinoid transport or degradation inhibitors. Indeed, cannabinoids possess anti-proliferative and pro-apoptotic effects and they are known to interfere with tumour neovascularization, cancer cell migration, adhesion, invasion and metastasization. However, the clinical use of Δ(9)-THC and additional cannabinoid agonists is often limited by their unwanted psychoactive side effects, and for this reason interest in non-psychoactive cannabinoid compounds with structural affinity for Δ(9)-THC, such as cannabidiol (CBD), has substantially increased in recent years. The present review will focus on the efficacy of CBD in the modulation of different steps of tumourigenesis in several types of cancer and highlights the importance of exploring CBD/CBD analogues as alternative therapeutic agents.

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


Although cannabinoids exhibit a broad variety of anticarcinogenic effects, their potential use in cancer therapy is limited by their psychoactive effects. Here we evaluated the impact of cannabidiol, a plant-derived non-psychoactive cannabinoid, on cancer cell invasion. 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). The decrease of invasion by cannabidiol appeared concomitantly with upregulation of tissue inhibitor of matrix metalloproteinases-1 (TIMP-1). Knockdown of cannabidiol-induced TIMP-1 expression by siRNA led to a reversal of the cannabidiol-elicited decrease in tumor cell invasiveness, implying a causal link between the TIMP-1-upregulating and anti-invasive action of cannabidiol. P38 and p42/44 mitogen-activated protein kinases were identified as upstream targets conferring TIMP-1 induction and subsequent decreased invasiveness. Additionally, in vivo studies in thymic-aplastic nude mice revealed a significant inhibition of A549 lung metastasis in cannabidiol-treated animals as compared to vehicle-treated controls. Altogether, 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.

CBD may help to alleviate some of the symptoms of cancer and side effects from treatment such as nausea, poor sleep, anxiety, depression and pain.

The following information relates to the role of other cannabinoids and cancer not just CBD – remember CBD or Cannabidiol is one of many cannabinoids found in cannabis.


In addition to the well-known palliative effects of cannabinoids on some cancer-associated symptoms, a large body of evidence shows that these molecules can decrease tumour growth in animal models of cancer. They do so by modulating key cell signalling pathways involved in the control of cancer cell proliferation and survival. In addition, cannabinoids inhibit angiogenesis and decrease metastasis in various tumour types in laboratory animals. In this review, we discuss the current understanding of cannabinoids as antitumour agents, focusing on recent discoveries about their molecular mechanisms of action, including resistance mechanisms and opportunities for their use in combination therapy. Those observations have already contributed to the foundation for the development of the first clinical studies that will analyze the safety and potential clinical benefit of cannabinoids as anticancer agents.


Preparations of Cannabis sativa L. (marijuana) have been used for many centuries both medicinally and recreationally. However, the chemical structures of their unique active components—the cannabinoids—were not elucidated until the 1960s. Three decades later, the first solid clues to cannabinoid molecular action were established, which led to an impressive expansion of basic cannabinoid research and a renaissance in the study of the therapeutic effects of cannabinoids in various fields, including oncology. Today, it is widely accepted that, of the approximately 108 cannabinoids produced by C. sativa, Δ9-tetrahydrocannabinol (thc) is the most relevant because of its high potency and abundance in plant preparations.

Tetrahydrocannabinol exerts a wide variety of biologic effects by mimicking endogenous substances—the endocannabinoids anandamide and 2-arachidonoylglycerol—that engage specific cell-surface cannabinoid receptors. So far, two major cannabinoid-specific receptors—cb1 and cb2—have been cloned from mammalian tissues and characterized. In addition, other receptors such as the transient receptor potential cation channel subfamily V, member 1, and the orphan G protein–coupled receptor 55 have been proposed to act as endocannabinoid receptors. Most of the effects produced by cannabinoids in the nervous system and in non-neural tissues rely on cb1 receptor activation. In contrast, the cb2 receptor was initially described to be present in the immune system, but was more recently shown to also be expressed in cells from other origins. Notably, expression of the cb1 and cb2 receptors has been found in many types of cancer cells, but not necessarily correlating with the expression of those receptors in the tissue of origin continue reading https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791144/


It is widely believed that strategies aimed at reducing mortality from cancer should consist of targeted therapies capable of providing the most efficacious and selective treatment for each individual tumour and patient. Thus, the major focus of anticancer drug development has progressively moved from nonspecific chemotherapies to molecularly-targeted inhibitors. However, despite the huge amount of preclinical literature on how these rationally designed compounds work, their use in clinical practice is still limited.

How do cannabinoid-based medicines fit into this ongoing scenario? Consider glioma, the type of cancer in which the most detailed cannabinoid research has been conducted to date. As discussed here, engagement of a molecular target (the cb receptors) by a family of selective drugs (thc and other cannabinoid agonists) inhibits tumour growth in animal models through a well-established mechanism of action that also seems to operate in human patients. Moreover, cannabinoids potentiate the antitumour efficacy of temozolomide and alk inhibitors in mice harbouring gliomas. Those findings provide preclinical proof-of-concept that “cannabinoid sensitizers” could improve the clinical efficacy of classical cytotoxic drugs in glioblastoma and perhaps other highly malignant tumours such as pancreatic cancer, melanoma, and hepatocellular carcinoma. However, further research is required to define the precise molecular cross-talk between cannabinoids and chemotherapeutic drugs and to optimize the pharmacology of preclinical cannabinoid-based combination therapies.

With respect to patient stratification, the particular individuals that are potentially responsive to cannabinoid administration should be unequivocally determined. To that end, high-throughput approaches should be implemented to find cannabinoid therapy–associated biomarkers in tumour biopsies or, ideally, in easily acquired fluids containing circulating cancer cells or enhanced levels of resistance factors that might have been released by cancer cells. Such biomarkers would conceivably relate to cannabinoid pharmacodynamics—namely, expression and activity of cannabinoid receptors and their downstream cell-death-inducing effectors. The approach would be analogous to the biochemical evaluation of estrogen and ErbB2 receptors, which respectively predict benefit from endocrine therapies and trastuzumab in breast cancer. Predictive markers to define the sensitivity of a particular tumour to cannabinoid-based therapies could also include the status of growth factors, such as mdk in gliomas, and their receptors and signalling partners.

To summarize, cannabinoids induce tumour cell death and inhibit tumour angiogenesis and invasion in animal models of cancer, and there are indications that they act similarly in patients with glioblastoma. Given that cannabinoids show an acceptable safety profile, clinical trials testing them as single drugs or, ideally, in combination therapies in glioblastoma and other types of cancer are both warranted and urgently needed.

The content on these pages are in no way intended to offer any related health benefits to our products but merely to share opinions and any research findings.

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