cbd oil cures cancer

December 15, 2021 By admin Off

In 2021, scientists reported the final results of a phase 1 study to treat people with recurrent glioblastoma (a type of brain tumour that has come back). The study looked at Sativex in combination with the chemotherapy drug temozolomide.

A drug called dexanabinol which is a man made form of a chemical similar to that found in cannabis has been trialled in a phase 1 trial. This is an early trial that tries to work out whether or not the drug works in humans, what the correct dose is and what the side effects might be. The results are not available yet. You can read about the trial on our clinical trials database.

You could talk with your cancer specialist about the possibility of joining a clinical trial. Trials can give access to new drugs in a safe and monitored environment.

We need more research to know if cannabis or the chemicals in it can treat cancer.

There are different types of oil made from parts of the cannabis plant. Some are sold legally in health food stores as a food supplement. Other types of oil are illegal.

Sativex and cancer pain.

Cannabis oil comes from the flowers, leaves and stalks of the cannabis plant. Cannabis oil often contains high levels of the psychoactive ingredient THC. Cannabis oil is illegal in the UK.

There are trials looking at whether Sativex can help with cancer pain that has not responded to other painkillers.

Different types of cannabis have differing amounts of these and other chemicals in them. This means they can have different effects on the body.

There has been a lot of interest into whether cannabinoids might be useful as a cancer treatment. The scientific research done so far has been laboratory research, with mixed results, so we do not know if cannabinoids can treat cancer in people.

However, this phase 1 study only involved 27 patients, which was too small to learn about any potential benefits of Sativex. The study wanted to find out if Sativex and temozolomide was safe to take by patients.

Scientists also discovered that cannabinoids can:

Results have shown that different cannabinoids can:

Clinical trials need to be done in large numbers where some patients have the drug and some don’t. Then you can compare how well the treatment works.

CBD oil comes from the flowers of the cannabis plant and does not contain the psychoactive substance THC. It can be sold in the UK as a food supplement but not as a medicine. There is no evidence to support its use as a medicine.

Researchers found that adding Sativex caused side effects, which included, vomiting, dizziness, fatigue, nausea and headache but patients found the side effects manageable.

Other research.

Cannabis is a class B drug and illegal in the UK.

Cannabis is a plant. It is known by many names including marijuana, weed, hemp, grass, pot, dope, ganja and hash.

Prescription drugs such as Nabilone can cause side effects. This can include:

Cannabis products can be smoked, vaporized, ingested (eating or drinking), absorbed through the skin (in a patch) or as a cream or spray.

THC is a psychoactive substance that can create a ‘high’ feeling. It can affect how your brain works, changing your mood and how you feel.

Hemp oil comes from the seeds of a type of cannabis plant that doesn’t contain the main psychoactive ingredient THC. Hemp seed oil is used for various purposes including as a protein supplement for food, a wood varnish and an ingredient in soaps.

The plant produces a resin that contains a number of substances or chemicals. These are called cannabinoids. Cannabinoids can have medicinal effects on the body. The main cannabinoids are:

Word of caution.

Cannabis that contains high levels of THC can cause panic attacks, hallucinations and paranoia.

This means a cannabis based product used to relieve symptoms.

Some cannabis based products are available on prescription as medicinal cannabis. The following medicines are sometimes prescribed to help relieve symptoms.

Cannabis has been used medicinally and recreationally for hundreds of years.

Researchers now plan to run a larger phase 2 trial, to find out if this treatment is effective and who might benefit from it.

CBD is a cannabinoid that may relieve pain, lower inflammation and decrease anxiety without the psychoactive ‘high’ effect of THC.

Many of the studies done so far have been small and in the laboratory. There have been a few studies involving people with cancer.

A Cochrane review in 2015 looked at all the research available looking into cannabis based medicine as a treatment for nausea and sickness in people having chemotherapy for cancer. It reported that many of the studies were too small or not well run to be able to say how well these medicines work. They say that they may be useful if all other medicines are not working.

There is some evidence that CBD oil could be effective against some rare childhood epilepsies. But again, more data is needed before we can draw any firm conclusions. Studies also show that CBD oil could be beneficial for managing anxiety and insomnia in some people, and early research also suggests a possible use of CBD for the treatment of certain types of pain.

There is no evidence that CBD oil can be used to treat cancer in people. CBD does show promise for the management of some cancer related symptoms, including pain and anxiety, however, more research into appropriate amounts of CBD and its effects on humans is necessary.

This is why research and regulated clinical trials are so important. They enable us to make informed decisions on what treatments are likely to work best based on solid evidence.

One study of cannabis users found they had a lower risk of bladder cancer, but their risk of developing prostate cancer increased.

Some cannabinoids inhibit the growth of tumour cells in test tubes and mice, but others encourage growth. Human studies are still small and hard to come by.

But I’ve heard about someone who was cured when they used CBD oil!

We don’t know yet whether cannabis, or any of the chemicals in cannabis, are useful to treat cancer. But it’s an important topic to discuss. And because we believe in the power of research, we dug into the science to answer some of the top questions you might have on cannabis and its effect on cancer.

Relatively. The doses sold in UK health stores are generally too low to cause any serious harm. Side effects of CBD include nausea, fatigue and diarrhoea. Most importantly, it can affect certain medications and you should always check with your GP before trying CBD oil. Because CBD oil is freely available to purchase in stores, it is not as tightly regulated as medicines.

This is difficult to answer, as research into cannabis and the chemicals in cannabis is still in its infancy. Most of the research so far has involved work in cells and mice. THC and CBD are two of the main cannabinoids found in the cannabis plant.

Walking along your local high street, you’ve probably noticed shops selling CBD oil, along with all sorts of health claims – including the possibility that it could even be used to combat cancer. But could this be true? Could cannabis really cure cancer? We asked our experts to delve into the research.

The problem with these stories is that it’s difficult to know whether you have all of the facts. It’s impossible to make any kind of judgement without knowing about the type of cancer, other treatment and the person’s medical history.

In 2021, a new clinical trial was launched in the UK to test whether a cannabis-based mouth spray could treat brain tumours and help patients live longer.

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Can CBD oil be used to treat cancer?

Massi et al. explored how CBD modulates 5-lipoxygenase (5-LOX), COX-2, and the endocannabinoid system in GBMs [68,73,76]. They found that 5-LOX, but not COX-2, was decreased by CBD in vivo. CBD treatment also resulted in increased expression of fatty acid amide hydrolase (FAAH), which reduces the level of AEA, suggesting that CBD may inhibit the production of inflammatory mediators by indirectly attenuating the endocannabinoid system in GBMs.

Our understanding of CBD’s effects on leukemia and lymphoma has expanded in recent years (Table S5). EL-4 and Jurkat cell lines are the commonly used models for lymphoma and leukemia, respectively. CBD induced a dose- and time-dependent killing effect on these leukemia and lymphoma cell lines, whereas peripheral blood monomolecular cells were more resistant to CBD [105,106,107,108,109].

There are also a few case studies that described the use of CBD in patients with high-grade gliomas [80,81]. Two patients were treated with procarbazine, lomustine, and vincristine along with CBD (one patient at 100–200 mg/day orally and the other at 300–450 mg/day orally) for about two years [80]. Both patients did not have any disease progression for two years after treatment. Adverse effects of the treatment included rash, moderate nausea, vomiting, and fatigue, without any lymphopenia, thrombocytopenia, hepatic toxicity, or neurotoxicity. In a case series describing nine patients with grade IV GBM, mean survival with the combination of surgery, radio- and chemo-therapy, and CBD (200–400 mg/day) was prolonged to 22.3 months, and two patients had no signs of disease progression for three or more years [81].

2. The Interplays between Reactive Oxygen Species (ROS), ER Stress, Inflammation, and Cancers.

Tissue microenvironment often plays an important role in supporting tumor establishment, expansion, and metastasis. The tumor microenvironment is primarily comprised of infiltrated leukocytes, including tumor-associated macrophages (TAMs), dendritic cells, and myeloid-derived suppressor cells (MDSC) [51]. The crosstalk between the infiltrated cells and tumor cells could suppress the immune response and create a pro-survival environment for tumor cells.

CBD, alone or with other agents, has been shown to successfully induce cell death, inhibit cell migration and invasion in vitro, decrease tumor size, vascularization, growth, and weight, and increase survival and induce tumor regression in vivo [58,59,62,65,68,70,71,74]. Regarding CBD’s anti-proliferative action on GBM, data show that apoptosis occurs independent of CB 1 , CB 2 , and TRPV1, but is dependent on TRPV2 [58,65,66,67,69,72]. Specifically, Ivanov et al. found that CBD, γ-irradiation, and ATM inhibitor KU60019 upregulate TNF/ TNFR1 and TRAIL/ TRAIL-R2 signaling along with DR5 within the extrinsic apoptotic pathway [61,64]. CBD also activates the JNK-AP1 and NF-κB pathways to induce cell death. Less emphasis has been placed on the role of autophagy or cell cycle arrest in CBD-mediated effects on glial cells [57,58,64,72,74].

Glioma is the most common primary brain malignancy. The grade IV glioma, also called glioblastoma multiforme (GBM) or glioblastoma, is one of the most aggressive types of cancer. The prognosis of GBM is very poor with only 4–5% survival within five years. Current treatment modalities include surgery, followed by radiotherapy and chemotherapy with Temozolomide (TMZ) or Carmustine (BCNU). Unfortunately, most GBM tumors are resistant to these treatments.

An alternative targeted therapy for CRC cancer, TNF-related apoptosis-inducing ligand (TRAIL), has also displayed resistance that can be overcome with the addition of CBD (4 µM) in HCT116, HT29, and DLD-1 cells [103]. CBD and TRAIL increased apoptosis through the activation of ER stress-related genes, including PERK, CHOP, and DR5. In vivo, TRAIL with CBD showed a significant decrease in tumor growth and an increased number of apoptotic cells. Altogether, these FOLFOX and TRAIL therapy studies suggest that CBD may be considered as a therapeutic option for CRC or, perhaps, as an adjunctive treatment to work synergistically with conventional chemotherapies. Currently, there are no clinical trials related to CBD in CRC, however, these findings related to the synergistic effects of CBD with chemotherapies are very promising and make a good case for a clinical trial in the future.

UPR is a well-studied cellular process ( Figure 3 A). It is primarily regulated by the 78-kDa glucose-regulated protein (GRP78), which is also known as the binding immunoglobulin protein (BiP) [49]. Under non-stress conditions, GRP78 binds and inhibits three transmembrane proteins: inositol-requiring enzymes 1α (IRE1α), pancreatic endoplasmic reticulum kinase (PERK), as well as the activating transcription factor 6 (ATF6) [48,49]. Whereas under ER stress conditions, GRP78 binds the unfolded proteins, dissociates from PERK, IRE1α, and ATF6, and results in the activation of three distinct, but interconnecting, pathways. Downstream of the PERK and ATF6 cascades, CHOP activity is increased.

Taha et al. studied patients with stage IV non-small cell lung cancer, clear cell renal cell carcinoma, and advanced melanoma treated with nivolumab immunotherapy (anti-PD-1 agents) and patients who had additionally used cannabis, including CBD and Δ 9 -THC [117]. They showed a decreased response rate to treatment in groups using cannabis with nivolumab, whereas patients not using cannabis were 3.17 times more likely to respond to treatment with nivolumab. However, cannabis use resulted in no significant difference in overall survival and progression-free survival. This group suggested that there may be a possible negative interaction between cannabis and immunotherapy.

Taken together, CBD has been consistently shown to be efficacious in many breast cancer cells and mouse models when it comes to its anti-proliferative and pro-apoptotic effects, while the mechanisms of these effects may vary. At this point, there is an urgent need for clinical trials looking at the anti-tumor effect of CBD for breast cancers, as this seems to be the next logical step in the progression of developing CBD as a treatment alternative for breast cancers.

3.4. Colorectal Cancer.

McKallip et al. [106] found that in both EL-4 and Jurkat cells, CBD’s anti-proliferative effects were mediated through CB 2 , but independent of CB 1 and TRPV1 [106]. However in a separate study Olivas-Aguirre et al. showed CBD’s effects to be independent of the endocannabinoid receptors and plasma membrane Ca 2+ channels in Jurkat cells [110]. These conflicting results need to be resolved by future studies. Despite this, the majority of research on leukemia/lymphomas confirmed apoptosis as the mechanism by which CBD-mediated cell death occurs, either alone or in combination with other treatment modalities, including γ-irradiation, Δ 9 -THC, vincristine, and cytarbine [105,106,107,110]. One study also demonstrated that CBD decreased tumor burden and induced apoptosis in vivo [106]. Kalenderoglou et al. found that CBD can induce cell cycle arrest in Jurkat cells, with increased cells in G1 phase [108]. CBD treatment also resulted in changes to cell morphology, including decreased size of cells, extensive vacuolation, swollen mitochondria, disassembled ER and Golgi, and plasma membrane blebbing [108,110].

ROS refer to various oxygen-containing species that are energetically unstable and highly reactive with a variety of biomolecules, including amino acids, lipids and nucleic acids. Commonly seen ROS include superoxide (O 2 − ), peroxide (O 2 −2 ), hydrogen peroxide (H 2 O 2 ), and hydroxyl free radical (OH − ) [41,42,43,44]. The most common sources of ROS are the electron transport chain in the mitochondria and the NADPH oxidase (NOX) family of transmembrane enzymes ( Figure 2 ). Certain enzymes and organelles, such as peroxisomes and ER, can also produce ROS. ROS can directly oxidize nucleic acids, proteins, and lipids thus altering or disrupting their functions [45].

Endoplasmic reticulum (ER) homeostasis, stress, and the unfolded protein response (UPR). ( A ) ER homeostasis is mediated by 78-kDa glucose-regulated protein (GRP78). Under stress conditions, GRP78 dissociates from pancreatic endoplasmic reticulum kinase (PERK), inositol-requiring enzymes 1α (IRE1α), as well as the activating transcription factor 6 (ATF6), leading to activation of their downstream signaling cascades in order to restore ER homeostasis. ( B ) When ER homeostasis fails to be restored, excessive UPR could lead to apoptosis, primarily via upregulation of C/EBP homologous protein (CHOP). PM: cytoplasmic membrane; eIF2α: eukaryotic initiation factor 2α; ATF4: activating transcription factor 4; GADD34: DNA damage inducible protein 34; XPB1: X-box-binding protein (XBP1s: spliced form); ERO1α: endoplasmic reticulum oxidoreductase 1α; PDI: protein disulfide isomerase; DR5: death receptor 5; TRAIL: TNF related apoptosis-inducing ligand; IP3R: inositol 1,4,5-triphosphate receptor; BAP31: B cell receptor-associated protein 31; Bid: BH3 Interacting Domain Death Agonist; TRAF2: tumor necrosis factor receptor-associated factor 2; RIDD: regulated IRE1-dependent decay; ASK1: apoptosis signal-regulating kinase 1; JNK: JUN N-terminal kinase; E2F7: E2F transcription factor 7; E2F1: E2F transcription factor 1.

Kalenderoglou et al. explored CBD’s effects on the mTOR pathway in Jurkat cells [108]. They found that CBD reduced the phosphorylation of AKT and ribosomal protein S6. They also tested CBD’s effects with different nutrient and oxygen conditions and found that CBD’s anti-proliferative effects alone or together with doxorubicin were greater with 1% serum than 5% serum. Olivas-Aguirre et al. found that when Jurkat cells were treated with lower concentrations of CBD, proliferation still occurred (at 1 µM CBD) and autophagy was increased at 10 µM CBD [110]. However, at higher concentrations (30 µM), the intrinsic apoptotic pathway was activated, resulting in cytochrome c release and Ca 2+ overload within the mitochondria. In Burkitt lymphoma cell lines, Jiyoye and Mutu I, AF1q stimulated cell proliferation and reduced ICAM-1 expression, through which cells became resistant to chemotherapies [104]. After exposure to CBD for 24 h, the chemo-resistant effect was dramatically attenuated.

Evasion of the attack by the immune system is essential during the development of cancers. This is accomplished through dynamic interactions between different cytokines and their receptors in the tumor microenvironment. Tumors actively secrete different cytokines that attract a variety of infiltrating cells, such as TAMs, dendritic cells, MSDCs, and immunosuppressive regulatory T cells, which in turn help tumors to evade the attack by the immune system ( Figure 4 A). Cytokines released from myeloid cells can also induce genomic instability in tumor cells by directly damaging DNA or epigenetically altering the expression of genes ( Figure 4 B).

2.1. ROS and Cancers.

Tissue inhibitor of MMPs (TIMPs) were evaluated and are related to the anti-invasive effect of CBD and were found to be induced by CBD in a time- and concentration-dependent manner [93]. CBD-mediated upregulation of TIMP-1 was attributed to the activation of CB 1 , CB 2 , and TRPV1. CBD also activated p38 MAPK and p42/44 MAPK, two downstream targets of TRPV1. To connect CB 1 , CB 2 , and TRPV1 to the activation of MAPK and TIMP-1, Ramer et al. investigated the expression and function of intercellular adhesion molecule-1 (ICAM-1), a transmembrane glycoprotein involved in tumor metastasis [91] ( Figure 5 A). Time- and concentration-dependent increase of ICAM-1 was observed in CBD-treated A549, H358, H460, and cells from a patient with brain metastatic NSCLC. An increase in the expression of TIMP-1 mRNA was also observed, but it occurred after an increase of ICAM-1 mRNA. The expression of ICAM-1 was dependent on the activation of p42/44 MAPK and p38 MAPK. In the in vivo A549 model displaying CBD’s anti-invasive properties, both ICAM-1 and TIMP-1 were also upregulated. Inactivation of ICAM-1 using a neutralizing antibody and siRNA led to a decrease in TIMP-1 activation as well as a reduction in CBD’s anti-invasive properties. These data suggest that the MAPKs activate ICAM-1, which then stimulates the function of TIMP-1 that, in turn, suppresses tumor invasion.

Similar to the CRCs, Sreevalsan et al. found that dual-specificity phosphatases and protein tyrosine phosphatases were also induced by CBD in LNCaP cells [98]. Inhibition of the phosphatases with the phosphatase inhibitor, SOV, decreased PARP cleavage. Additionally, CBD enhanced the phosphorylation of p38 MAPK. Most recently, Kosgodage et al. found that in PC3, CBD treatment (1 µM and 5 µM) reduced the release of EMV [89,114]. CBD was also shown to reduce mitochondrial-associated proteins, prohibitin, and STAT3, which may account for the decrease of EMV.

Melanoma cancer cell lines (B16 and A375) express the endocannabinoid receptors, CB 1 , and CB 2 [120]. Previous studies have also shown that activation of these receptors with Δ 9 -THC decreased melanoma growth, proliferation, angiogenesis, and metastasis in vivo [120]. While Δ 9 -THC looks promising as a treatment modality of melanoma, there has been little research on the effects of CBD on melanoma. A recent study by Simmerman et al. tested CBD in a murine melanoma model (B16F10) [121]. They set up three groups of mice: control (ethanol- and PBS-treated), cisplatin-treated (5 mg/kg intraperitoneal once per week), and CBD-treated (5 mg/kg intraperitoneal twice a week). Survival time was significantly increased, and tumor size was significantly decreased in CBD-treated mice compared to control mice, but to a lesser effect when compared to that of cisplatin-treated mice. Quality of life was subjectively described, and CBD-treated mice were found to have a better quality of life, improved movement, and less hostile interaction/fighting compared to both controls and cisplatin-treated mice. This study did not include a group of CBD and cisplatin combination treatment. More research is required to understand the effects of CBD on human melanoma cells.

Taken together, these studies suggest that through CB 1 , CB 2 , and TRPV1 receptors, CBD activates p38 MAPK and p42/44 MAPK, which first induce ICAM-1 and then TIMP-1. The upregulation of ICAM-1 and TIMP-1 then attenuates the invasion of lung cancers ( Figure 5 A).

ER is an important organelle that plays a critical role in post-translational modification and folding of proteins, calcium homeostasis, and other biological processes [48,49]. Accumulation of unfolded and/or misfolded proteins triggers the unfolded protein response (UPR), which helps to re-balance the ER homeostasis. UPR temporarily halts protein synthesis and attempts to correct and re-fold proteins. In the case that the unfolded and/or misfolded proteins cannot be corrected in time, they will then be targeted for protein degradation.

Kosgodage et al. showed that breast cancer cells treated with CBD had increased sensitization to cisplatin. CBD significantly decreased the release of exosomes and microvesicles (EMV) (at 100–200 nm), which typically aid the spread of tumors and cause chemo-resistance [89]. However, in these same MDA-MB-231 cells, there was an increase in the release of the larger EMVs (201–500 nm). These cells displayed a concentration-dependent increase in ROS, proton leakage, mitochondrial respiration, and ATP levels. The authors attributed these effects to either a higher sensitivity or a sign of pseudo-apoptotic responses occurring, where the apoptotic factors such as ROS are still at a lower level resulting in the conversion of apoptosomes into EMVs. CBD inhibited paclitaxel-induced neurotoxicity through a 5-HT1A receptor system without conditioned reward or cognitive impairment [85]. It also decreased the viability of both 4T1 and MDA-MB-231 cells. Thus, CBD may be a viable adjunctive treatment for breast cancers as it can sensitize cells, allowing for potentially lower doses of such toxic chemicals to be prescribed.