Cancer and Cannabis Oil

Cancer is referred to medically as a malignant neoplasm, cancer is a broad term, covering a range of various diseases (around 200 in total), all of which involve unregulated cell growth.
Cannabis oil has been shown to be effective in fighting even the most aggressive of cancers.

The main conventional therapies for treating cancer are surgery, radiotherapy and chemotherapy. A common question we get asked here at bud Buddies is: “Should I have chemotherapy?” Unfortunately, this is a question we cannot answer and the best advice we can offer is to research as much as you can and make an informed decision.
Please Note: There is preclinical evidence that combining cannabinoids with conventional therapies may be more effective than either alone, so please consider all the factors before coming to a conclusion regarding how to treat your cancer.
Here is an interview conducted with Professor Manuel Guzman by one of our founders Jeff Ditchfield.

Below is referenced from: The Medical Cannabis Guidebook by Jeff Ditchfield

Chemotherapy, The Double Edged Sword?
A team of researchers looking into why cancer cells are so resilient accidentally made a far more important discovery, the team discovered that chemotherapy actually heavily damages healthy cells and subsequently triggers them to release a protein that sustains and fuels tumour growth and makes the tumour highly resistant to future treatment. Reporting their findings in the journal Nature Medicine, the scientists state that their findings were ‘completely unexpected’. Dr Peter Nelson and his team at the Fred Hutchinson Cancer Research Center in Seattle, U.S.A. found after extensive research that chemotherapy can help cancer to survive, grow faster, and resist treatment. The team were trying to explain why cancer is so resilient in the body, yet so easy to kill in the lab, and realized that the culprit is the interaction of chemotherapy and healthy cells surrounding the targeted tumours.
When used on cancer, chemotherapy slows or stops the reproduction of rapidly dividing cells found in tumours, but the new research shows it also damages the DNA of neighbouring fibroblast cells, which normally help heal wounds. Once hit by the chemo, the fibroblast cells churn out 30 times more of a protein called WNT16B than normal. This protein encouraged prostate tumours to grow and spread into surrounding tissue, as well as to resist chemotherapy. The team examined cancer cells from prostate, breast and ovarian cancer patients who had been treated with chemotherapy and found similar results. This follows similar research which found that expensive cancer drugs make tumours ‘metasize’ and grow massively in size after taking them. As a result, the drugs killed the patients more quickly.
“If cancer specialists were to admit publicly that chemotherapy is of limited usefulness and is often dangerous, the public might demand a radical change in direction – possibly toward unorthodox and nontoxic methods, and toward cancer prevention. The use of chemotherapy is even advocated by those members of the establishment who realize how ineffective and dangerous it can be.”
Ralph W. Moss.

Adverse effects
Common side-effects include: Depression of the immune system, which can result in potentially fatal infections such as typhlitis. Although patients are advised to take infection-reducing steps, about 85% of infections are due to naturally occurring microorganisms in the patient’s own gastrointestinal tract, oral cavity and skin.

The treatment is physically exhausting for the patient, who might already be very tired from cancer-related fatigue. It may produce mild to severe anaemia and a tendency to bleed easily. Medications that kill rapidly dividing cells or blood cells are likely to reduce the number of platelets in the blood, which can result in bruises and bleeding. Gastrointestinal distress is common alongside nausea and vomiting. Chemotherapy induces nausea and vomiting. Nausea and vomiting are two of the most feared cancer treatment-related side-effects for cancer patients and their families. In 1983, Coates et al. found that patients receiving chemotherapy ranked nausea and vomiting as the first- and second-most-severe side-effects, respectively. Malnutrition and dehydration can result when the patient does not eat or drink enough, or when the patient vomits frequently, because of gastrointestinal damage. This can result in rapid weight loss, or occasionally in weight gain, if the patient eats too much in an effort to allay nausea or heartburn. Weight gain can also be caused by some steroid medications.

NOTE: As previously mentioned, some laboratory studies have indicated that combining chemotherapy with cannabinoids can be more effective against certain cancer types than either cannabinoids or chemotherapy alone.
The paper below came to some very interesting conclusions regarding cannabinoids (CBD and THC) and the oral chemotherapy drug Temozolomide:

“Cannabinoids: Potential anticancer agents”

“ ………. these compounds have been shown to inhibit the growth of tumour cells in culture and animal models by modulating key cell-signalling pathways. Cannabinoids are usually well tolerated and do not produce the generalised toxic effects of conventional chemotherapies”
Download the .pdf: Here
The paper below by Professor Manuel Guzman, Dr Guillermo Velasco and Dr Cristina Sanchez (who are conducting research into the anticancer effects of cannabinoids), looked into the mechanisms of antitumour action in this experiment.

“Towards the use of cannabinoids as anticancer agents”
“A considerable amount of the research that has been conducted so far on the mechanism of cannabinoid antitumour activity has focused on glioma cells. Initial studies showed that THC and other cannabinoids induce the apoptotic death of glioma cells through CB1- and CB2-dependent stimulation of the de novo synthesis of the pro-apoptotic sphingolipid ceramide”
Download the .pdf: Here

Cannabinoids and cancer: pros and cons of an antitumour strategy
“Indeed, cannabinoids have the advantage of being well tolerated in animal studies and they do not present the generalized toxic effects of most conventional chemotherapeutic agents. Routes of cannabinoids administration have been recently studied. THC is rapidly absorbed after inhalation and its effects become apparent within minutes. Grotenhermen showed that THC oral administration was associated with slow onset of action and with accidental over dosage. In fact, maximum THC serum concentration measured after smoke intake is 2–3-fold higher than maximum serum concentration achievable with oral or rectal THC administration. The inhalation may have pharmacokinetic advantages, but it requires use of higher potency cannabinoids and strategy aimed at eliminating carcinogenic products combustion: for this purpose, Geiringer proposed the vaporization lacking the carcinogenic compounds formed during combustion”. Download the .pdf: Here

Anticancer mechanisms of cannabinoids
“Cannabinoids impair tumour progression at various levels. Their most prevalent effect is the induction of cancer cell death by apoptosis and the inhibition of cancer cell proliferation. At least one of those actions has been demonstrated in almost all cancer cell types tested. In addition, in vivo experiments have shown that cannabinoids impair tumour angiogenesis and block invasion and metastasis.”

“CANNABINOID-BASED COMBINATION THERAPIES: The use of combinational anticancer therapies has a number of theoretical advantages over single-agent strategies, because they allow for the simultaneous targeting of tumour growth, progression, and spread at various levels. In line with that idea, recent observations suggest that the combined administration of cannabinoids with other anticancer drugs acts synergistically to reduce tumour growth. For example, the administration of THC and Temozolomide exerts strong antitumour action in glioma xenografts, an effect that is also evident in Temozolomide resistant tumours. A similar effect was observed when THC and CBD were combined with radiotherapy in animal models of glioma.
Download the .pdf: Here

Cannabidiol (CBD) as potential anticancer drug
“Collectively, the non-psychoactive plant-derived CBD exhibits pro-apoptotic and antiproliferative actions in different types of tumours and may also exert antimigratory, antiinvasive, antimetastatic and perhaps antiangiogenic properties. On the basis of these results, evidence is emerging to suggest that CBD is a potent inhibitor of both cancer growth and spread. Interestingly, the anticancer effect of this compound seems to be selective for cancer cells, at least in vitro, since it does not affect normal cell lines”
Download the .pdf: Here

Cancer Pain
“Cancer pain is often cited incorrectly as inflammatory pain; evidence from clinical studies and preclinical models strongly suggest that cancer pain can exist in a sterile tissue environment. Compelling evidence that cancer pain is not inflammatory pain is the meagre evidence supporting the role of non-steroidal antiinflammatory drugs; their role in clinical management of cancer pain is often considered controversial” Read more: Here

Pain caused by cancer can be extreme and debilitating
“Over half of all cancer patients will experience severe, uncontrollable pain during the course of their disease, and the management of pain is a primary challenge for the cancer patient and the treating oncologist”
Mechanisms of Cancer Pain is a very informative guide: Read More: Here

Cancer and cannabinoids by cancer type
In this section we have available for download academic & scientific papers regarding cannabinoids and their anticancer properties, for your ease of reference we have ordered these papers by cancer type.

Breast Cancer
One in ten women are affected by breast cancer and it is the most prominent form of cancer in women, (25% of all cancer cases).

Early indications of breast cancer can include a lump or lumps appearing, a change in the shape of the breast, a dimpling of the skin, fluid excreting from a nipple, or a red (or yellow) scaly patches of skin. In advanced stages sufferers may also experience pain, swollen lymph nodes and shortness of breath.
Confirmation of diagnosis is initially made by taking a biopsy, a range of further tests can determine if the cancer has spread beyond the breast (metastasized).
Conventional therapies involve surgery which can vary from removing tumour(s) from the breast, to complete breast removal (mastectomy).
Outcomes for breast cancer vary enormously depending on the cancer form and the extent of disease, however, generally the survival rates in the developed world are considered high, with around 80% surviving for at least 5 years from diagnosis, in developing countries survival rates are much lower.

Cannabinoids: A new hope for breast cancer therapy?
Experimental evidence accumulated during the last decade supports that cannabinoids, the active components of Cannabis Sativa and their derivatives, possess anticancer activity. Thus, these compounds exert antiproliferative, pro-apoptotic, antimigratory and antiinvasive actions in a wide spectrum of cancer cells in culture. Moreover, tumour growth, angiogenesis and metastasis are hampered by cannabinoids in xenograft-based and genetically-engineered mouse models of cancer.

This review summarizes our current knowledge on the antitumour potential of cannabinoids in breast cancer, which suggests that cannabinoid-based medicines may be useful for the treatment of most breast tumour subtypes:

Cannabinoids and hormone-sensitive breast cancer
The presence of estrogen receptors (ER) and/or progesterone receptors (PR) in breast cancer cells, as determined by immunohistochemistry-based methods, defines a subgroup of breast tumours that may respond to endocrine therapy. Specifically, these patients are treated with surgical and/or pharmacological approaches that block estrogenic signalling, which has pro-proliferative and pro-survival features. The targeted strategies include the removal of the endogenous source of estrogens (the ovaries) and/or the use of selective estrogen receptor modulators, such as the widely used tamoxifen, or inhibitors of aromatase, the main enzyme responsible for estrogen synthesis. It has been demonstrated that cannabinoids modulate pivotal tumour progression-related aspects of ER+/PR+ breast cancer cells.

Thus, anandamide inhibits basal and prolactin- and nerve growth factor (NGF)-induced proliferation of MCF-7 and EFM-19 cells in culture. This effect is mediated by the activation of CB1 receptors and is not accompanied by cancer cell death. Anandamide produces this antiproliferative action by blocking the progression through the cell cycle, specifically by preventing the transition from the G1 to the S phase, and by inhibiting adenylyl cyclase and thus activating the Raf-1/ERK/MAPK cascade, which, upon sustained activation, ultimately down-regulates prolactin and TrkA NGF receptors.

The proliferation of the ER/PR+ human breast cancer cell line
EVSA-T is also decreased in response to THC. Once again, the cell cycle is targeted: a blockade in the transition from G2 to mitosis via CB2 receptors, produced by the inhibition of CDK1, was observed. Cell cycle arrest is ensued by apoptotic cell death and the activation of the transcription factor JunD, owing to upregulation of gene expression and translocation to the nucleus, is essential for these actions.

Besides cancer cell proliferation, cannabinoids impair ER+/PR+ cancer cell migration and invasion in culture. Specifically, selective activation of CB2 receptors in MCF-7 cells that overexpress the chemokine receptor CXCR4 inhibited chemotaxis and wound healing as induced by the CXCR4 ligand CXCL1220. The CXCL12/CXCR4 signalling axis plays a pivotal role in directing breast cancer cells to distant sites and, therefore, the aforementioned finding suggests that cannabinoids may modulate hormone-sensitive breast cancer metastasis. However, the experimental support for this notion is still weak and further research with more complex models should be performed to validate it.

Cannabinoids and HER2-positive breast cancer
The breast tumours that express the tyrosine kinase receptor HER2, as determined by immunohistochemistry and fluorescence in situ hybridization (FISH) approaches, constitute another well defined breast cancer histopathological subtype. HER2 belongs to the epidermal growth factor receptor (EGFR) family, which consists of four members (ErbB1/HER1/EGFR, ErbB2/HER2, ErbB3/HER3 and ErbB4/HER4). They all have intrinsic tyrosine kinase activity and, upon ligand binding and subsequent dimerization, they activate a number of oncogenic processes, including cell proliferation and survival.

Strong preclinical evidence suggests that cannabinoids may be useful for the treatment of this particular subset of patients. THC treatment reduces not only tumour growth but also the number of tumours generated per animal (mice) and the percentage of animals with lung metastases. THC action relies on the impairment of cancer cell proliferation, via inhibition of the pro-tumorigenic kinase AKT, and on the induction of cancer cell death by apoptosis. A reduction in the number of tumour blood vessels is also observed, suggesting that tumour angiogenesis is impaired by THC.
Xenograft-based approaches strengthen the hypothesis that HER2-overexpressing tumours may be sensitive to cannabinoids.
Of interest, the antitumour effect of cannabinoids in all the HER2-positive breast cancer models used so far is mediated by the activation of CB2 receptors. Thus, the antitumour action of THC in the MMTV-neu model is mimicked by the CB2-selective agonist JWH-133. In the same line, the growth-inhibiting effect cannabinoid antitumour action may have important clinical implications since the psychotropic effects associated to these compounds are mediated by the activation of CB1 (and not CB2) receptors present in the brain. Therefore, a CB2-directed therapy may be, in principle, efficacious in curbing the growth of these tumours and would be devoid of the classical cannabis-associated psychotropic side effects.

Cannabinoids and triple-negative breast cancer
The remaining group of breast tumors according to immunopathological criteria is the triple-negative one. This definition refers to the lack of expression of ER, PR and HER2. To date, there is no standard targeted therapy for these patients, whose prognosis is very poor as a group. Efforts are being made to improve chemotherapy responses and they include, for example, the combined use of angiogenesis inhibitors such as Avastin.
Both in vitro and in vivo preclinical evidence indicates that triple-negative breast cancer may be treated with cannabinoids. A battery of synthetic cannabinoids has been tested in the human triple-negative breast cancer cell line MDA-MB-231, and all of them produced an inhibition of cell proliferation. For example, the metabolically stable analogue of anandamide Met-F-AEA reduces MDA-MB-231 proliferation without inducing cell death32 by arresting cells in the S phase of the cell cycle. This effect is accompanied by a decrease in the activity of the cyclin-dependent kinase CDK2 and the modulation of the levels of other important cell cycle regulators. CB1 receptors seem to be the primary target of Met-F-AEA action in this model. The synthetic cannabinoids WIN 55,212-2 (a CB1 and CB2 mixed agonist) and JWH-133 also produce an inhibition of MDA-MB-231 proliferation by blocking the progression trough the cell cycle, but in this case

  1. the cells are retained in the G0/G1 compartment,
  2. this effect is connected to apoptosis, and
  3. it is mediated by both CB1 and CB2 and receptors

Whether these differences are agonist-specific or due to other experimental issues has not been clarified. Interestingly, the cannabinoid proliferation-inhibiting effect is reproduced in vivo, both in a xenograft-based and in the PyMT genetically engineered model of triple-negative breast cancer.
The observations suggest that cannabinoids, via CB1 and/or CB2 receptors, confer a less invasive phenotype to triple negative breast cancer cells in culture, and allows hypothesizing that these compounds may reduce the cancer cell metastatic potential in vivo.

Phytocannabinoids other than THC have been shown as well to exert antitumour actions in breast cancer. The most studied in the triple-negative context has been cannabidiol (CBD). This compound displays low affinity for CB1 and CB2 receptors and, although its mechanism of action is not completely understood, it is emerging as an attractive potential therapeutic tool for a number of conditions.

The inhibition of breast cancer cell proliferation by CBD has been corroborated in vivo. Treatment of subcutaneous xenografts generated from MDA-MB-231 cells in immune-deficient mice resulted in a marked reduction of tumour growth. Similar results were observed in orthotropic xenografts generated from 4T1 triple-negative breast cancer murine cells in syngeneic BALB/c mice, although in this case tumours acquired resistance to CBD after 3 weeks of treatment and, from that time onwards, grew as fast as the vehicle-treated tumours at the end of the experiment.

As for other cannabinoids, CBD action on triple-negative breast cancer cells impacts not only proliferation but also metastasis-related capabilities. Thus, MDA-MB-231 and 4T1 cell invasion was hampered in culture by CBD. Most important, this compound reduced the number of lung metastases generated by intraplantar injection of MDA-MB-231 cells, by injection of 4T1 cells into the tail vein, and by spontaneous formation from 4T1 orthotopic xenografts.

Cannabinoids and triple-negative breast cancer
This definition refers to the lack of expression of ER, PR and HER2. To date, there is no standard targeted therapy for these patients, whose prognosis is very poor as a group. Efforts are being made to improve chemotherapy responses and they include, for example, the combined use of angiogenesis inhibitors such as Avastin.

Both in vitro and in vivo preclinical evidence indicates that triple-negative breast cancer may be treated with cannabinoids. A battery of synthetic cannabinoids has been tested in the human triple-negative breast cancer cell line MDA-MB-231, and all of them produced an inhibition of cell proliferation.

Interestingly, the cannabinoid proliferation-inhibiting effect is reproduced in vivo, both in a xenograft-based and in the PyMT genetically engineered model of triple-negative breast cancer. In these two models, a significant reduction in tumour growth is observed upon JWH-133 treatment, and the analysis of the tumours revealed a significant decrease in the number of cancer cells undergoing proliferation.

Phytocannabinoids other than THC have been shown as well to exert antitumour actions in breast cancer. The most studied in the triple-negative context has been cannabidiol (CBD). This compound displays low affinity for CB1 and CB2 receptors8 and, although its mechanism of action is not completely understood, it is emerging as an attractive potential therapeutic tool for a number of conditions.

The inhibition of breast cancer cell proliferation by CBD has been corroborated in vivo. Treatment of subcutaneous xenografts generated from MDA-MB-231 cells in immune-deficient mice resulted in a marked reduction of tumour growth. Similar results were observed in orthotopic xenografts generated from 4T1 triple-negative breast cancer murine cells in syngenic BALB/c mice, although in this case tumours acquired resistance to CBD after 3 weeks of treatment and, from that time onwards, grew as fast as the vehicle-treated tumours at the end of the experiment.
As for other cannabinoids, CBD action on triple-negative breast cancer cells impacts not only proliferation but also metastasis-related capabilities.
Of interest, the sensitivity of human breast cancer cells to cannabinoids in culture correlates with their aggressiveness. For example, we showed that ER- cell lines were more susceptible to cannabinoid treatment than ER+ cells.
An additional characteristic of cannabinoids, which may have important clinical implications, is their safety. Cannabinoid-based medicines have been proven very safe in thousands of patients enrolled in multiple clinical trials over the last couple of years and within them, cancer patients, whom use them for the management of pain, nausea and vomiting.

NOTE: There is preclinical evidence showing that the combination of cannabinoids with other established anticancer agents not only has positive effects but, instead, induces a synergistic action.

There is compelling evidence showing that cannabinoids have antitumour activity in preclinical models of breast cancer. These data come not only from cell culture systems but also from more complex and clinically relevant animal models. This antitumour action is produced by the blockade of several hallmarks of cancer (sustained cancer cell proliferation, metastasis and angiogenesis) rather than by the targeting of a unique process, and the compounds are not only effective but safe.

An important question is
Which cannabinoid(s) is/are the best to be tested in patients? In our opinion, the most reasonable candidate would be adding to a standard chemotherapy or immunotherapy a mixture of a cannabinoid targeting CB1 and/or CB2 receptors plus CBD. This combination would have the advantage of two cannabinoid compounds acting through different mechanisms of action that would theoretically produce (as it has been demonstrated in mice bearing gliomas) a cooperating antitumour effect. In addition, the presence of CBD in the drug cocktail would possibly attenuate non-desired effects of psychoactive cannabinoids and would provide some of the palliative effects that this compound exerts per se. Read the full text: Here

CBD, Breast Cancer Cell Proliferation, Invasion, and Metastasis
We found that systemic administration of CBD could lead to a significant reduction in primary tumour growth and metastasis in immune competent mouse models of breast cancer. The primary tumours acquired resistance to the inhibitory properties of CBD by approximately day 25”
Download the .pdf: Here

Antitumour Activity of Plant Cannabinoids – the effect of CBD on breast carcinoma
“CBD always exhibited the highest potency, Cannabidiol acid (CBD-a) was the least potent compound. Among the other plant cannabinoids, cannabigerol (CBG) was almost always the second most potent compound, followed by cannabichromene. The effect of the two Cannabis extracts (enriched in cannabidiol or THC) was next investigated, and in some circumstances, the cannabidiol-rich extract appeared slightly more potent than pure cannabidiol”
Download the .pdf: Here

 JunD is involved in the antiproliferative effect of THC on human breast cancer cells
“Data presented herein demonstrate the involvement of the AP-1 transcription factor JunD in the antiproliferative effect of THC in breast cancer cells. Nonetheless, considering the intricacy of AP-1 complex regulation, which includes regulation of phosphorylation states as well as protein–protein and protein–DNA interactions), the participation of other AP-1 family members in THC signalling may not be ruled out.
Download the .pdf: Here

Brain Cancers
Glioma is the term for a tumour in the brain or spine, malignant gliomas are very difficult to treat and the prognosis is generally poor.
Many academic studies into gliomas have shown that utilising both THC and CBD is more effective than either is alone.
This is illustrated in the below paper which reports on how CBD enhances the effects of THC on human glioblastoma cell proliferation and survival.
“CBD enhances the inhibitory effects of Δ9-THC on glioblastoma cell growth. It has been suggested that non-psychoactive cannabinoid constituents can either potentiate or inhibit the actions of THC”
The report goes on to say:
“When applied in combination at the predicted IC80 concentration, Δ 9 -THC and CBD produced a greater than additive inhibition of cell growth in SF126 and U251 cells”

The World Health Organization classifies gliomas according to their cellular features and their grade of malignancy (from I to IV).
Glioblastoma multiforme (GBM), or grade IV astrocytoma, is the most frequent class of malignant primary brain tumours and one of the most aggressive forms of cancer. As a consequence, survival after diagnosis is normally just 6 to 12 months, which is due mainly to the high invasiveness and proliferation rate of GBM.
In addition, GBM exhibits a high resistance to standard chemotherapy and radiotherapy. These malignant features may be related to the varying mutations frequently found in these tumours that impact different key pathways involved in the control of cell proliferation, survival, differentiation, and DNA repair.
Current standard therapeutic strategies for the treatment of GBM are only palliative and include surgical resection and focal radiotherapy, and/or chemotherapeutic agents such as Temozolomide.

 Cannabinoids induce cell death via stimulation of ER stress in human glioma cells
“In this study we show that cannabinoids, a new family of potential antitumoural agents, induce autophagy of cancer cells and that this process mediates the cell death–promoting activity of these compounds”
“Our findings suggest that THC — via activation of the CB1 receptor and stimulation of ceramide synthesis de novo — activates an early ER stress response that leads to increased phosphorylation of eIF2α on Ser51. Experiments performed with eIF2α S51A mutant cells have shown that phosphorylation of this residue, which is known to attenuate general protein translation while enhancing the expression of several genes related with the ER stress response, is required for the upregulation of the stress protein p8 and its ER stress–related downstream targets ATF4, CHOP, and TRB3 as well as for the induction of autophagy by cannabinoids”
Download the .pdf: Here

Cannabinoids and Gliomas
“Oo immunotherapy or gene therapy trial performed to date has been significantly successful. It is therefore essential to develop new therapeutic strategies for the management of GBM, which will most likely require a combination of therapies to obtain significant clinical results”
Download the .pdf: Here

CBD enhances the inhibitory effects of THC on glioblastoma cell proliferation and survival
“The CB1 and CB2 receptor agonist, Δ 9 -THC, can inhibit glioblastoma cell proliferation in culture and in vivo and is currently being used in a clinical trial (4). CBD, a cannabinoid constituent with negligible affinity for CB1 and CB2 receptors, can also inhibit the proliferation of glioblastoma in culture and in vivo (7,16)
Download the .pdf: Here

Is the most frequent extracranial solid tumour in childhood, accounting for approximately 8% of childhood cancers. Approximately 40% of neuroblastoma tumours are classified as high-risk. Treatment for children with high-risk NBL involves multimodality therapy, including chemotherapy, autologous stem-cell transplantation, surgery, radiation therapy, and immunotherapy. Despite these aggressive approaches, children with NBL have very poor outcomes, and the survivors experience serious side effects related to treatment toxicity.

In vitro and in vivo efficacy of non-psychoactive cannabidiol in neuroblastoma
“Tumour growth was significantly reduced in THC and CBD treated mice than in the vehicle-treated or untreated mice. Interestingly, response to treatment was observed to be better in the group treated with CBD than in the group treated with THC

To summarize, THC and CBD both suppressed the SKN-SH tumour xenograft growth rate, with CBD treatment demonstrating a better effect”
Download the .pdf: Here

Studies have shown that THC kills leukaemia cells and therefore cannabis oil can be an effective treatment for this condition.
Mykayla Comstock is a 7-year-old leukaemia patient who has consumed cannabis oil since her diagnosis.
You can read more of Mykala’s remarkable story: Here

CBD -Induced Apoptosis in Human Leukaemia Cells:
“In summary, the current study demonstrates that CBD induced apoptosis may constitute a novel approach to treat malignancies of the immune system. Here we found that the CBD-induced apoptosis was dependent on CB2 receptor signalling. CB2 is expressed almost exclusively on immune cells. Furthermore, we demonstrated, for the first time, that exposure of leukaemia cells to CBD led to increased production of ROS which was mediated through regulation of Nox4 and p22phox, suggesting a novel role of CBD in the regulation of ROS production in leukaemia cells”
Download the .pdf: Here

THC Induced Apoptosis in Leukaemia T Cells – Regulated by Translocation of Bad to Mitochondria
“it was shown that cannabinoids were cytotoxic in leukemic cells and that they inhibited neuronal progenitor cell differentiation through attenuation of the ERK pathway”
Download the .pdf: Here

Hepatocellular carcinoma (HCC) is the most frequent primary solid tumour of the liver, and it is estimated to account for 5% of all malignant neoplasia. Its aggressiveness and extensive dissemination lead to poor patient prognosis. Although there has been a great research effort made in order to come up with efficient therapeutic strategies, the incidence and mortality of HCC have increased in the United States and Europe in the past decade and therefore innovative research findings are necessary to understand the etiology of cancer and to improve the treatment and survival of patients.

Antitumoural action of cannabinoids on hepatocellular carcinoma
“We here illustrate that the cannabinoids THC and JWH-015 exert antitumour effect against the human HCC cell lines HepG2 and HUH-7 in vitro and in vivo through PPAR g. The activation of PPAR g by cannabinoids is independent of the signalling cascades previously described”
Download the .pdf: Here

Pancreatic Cancer
Pancreatic cancer is one of the most aggressive cancers, sufferers have a poor prognosis, the five-year survival rate is less than 5%. Due to the localised nature of this form of cancer sufferers have no symptoms or warning signs, so diagnosis is usually made at the latter stages of the disease when the cancer has metastasised.
“The American Cancer Society estimates that 45,220 Americans will be diagnosed with pancreatic cancer in 2013, and that 38,460 will die from the disease”
Read more from “Progress in Pancreatic Cancer”: Here

Cannabinoids Induce Apoptosis of Pancreatic Tumour Cells
“Activation of the CB2 cannabinoid receptor induces apoptosis of pancreatic tumour cells in vitro”
“Moreover, our results also show that cannabinoids exert a strong inhibitory effect on the spreading of pancreatic tumour cells not only to adjacent locations such as spleen but also to distal tissues such as liver, diaphragm, stomach, and intestine, thus suggesting that these agents may also decrease the propagation of pancreatic tumour cells”
Download the .pdf: Here

Prostate is the most common cancer in men (besides non-melanoma skin cancer) and the second most common cause of cancer death in the United States.
During its early stages this disease is usually asymptomatic and exhibits slow progression, which carries the risk of having it diagnosed at an advanced stage. Research indicates a direct correlation between the appearance of symptoms and the spreading of the cancer or metastasis. This late diagnosis may decrease the treatment options available for patients and also the chances of recovery.
Despite the fact that a higher percentage of men have localized disease at presentation, metastatic prostate cancer remains an important clinical problem, both in terms of the number of affected men and its impact on their quality of life.

Proapoptotic effect of endocannabinoids in prostate cancer
“in accordance with our findings, we conclude that endocannabinoids are capable of halting the growth of prostate cancer cells through activation of apoptotic mechanisms. Furthermore, we suggest that this effect may be through the modulation of the Erk and Akt signalling pathways by endocannabinoids. Therefore, endocannabinoids appear to be a powerful tool for investigation in the development of drugs and treatments against advanced Prostate cancer.
Download the .pdf: Here

Cannabinoids, Endocannabinoids and Cancer
“Cannabinoids exert a number of interesting effects that are dependent on the cell line or tumour type. Synthetic (and phyto) cannabinoids and the endocannabinoid system are implicated in inhibiting cancer cell proliferation and angiogenesis, reducing tumour growth and metastases, and inducing apoptosis”
Download the .pdf: Here

Cannabinoids inhibit prostate carcinoma growth in vitro and in vivo
“In conclusion, the in vitro data presented here allow us to suggest that non-THC cannabinoids, and CBD in particular, retard proliferation and cause apoptosis of PCC via a combination of cannabinoid receptor-independent, cellular and molecular mechanisms. Our data, however, do not argue against the previously suggested role of CB1 and CB2 receptors in prostate carcinoma although they do exclude the participation of these receptors in the effects of non-THC cannabinoids. Indeed, the effects reported here, together with previously reported cannabinoid receptor-mediated effects of THC on PCCs, might encourage clinical studies on cannabinoids and Cannabis extracts as a therapy for human prostate carcinoma, either as single agent or in combination with existing compounds”
Download the .pdf: Here

Rhabdomyosarcoma, (RMS), is an aggressive and malignant type of cancer and it is generally considered to be a disease in children as the vast majority of cases occur in those below the age of 18. Despite being a relatively rare cancer, it accounts for approximately 40% of all recorded soft tissue sarcomas and RMS can occur in any site on the body, but is primarily found in the head, neck, genitals, and extremities.

Chico Ryder
Chico was diagnosed with Rhabdomyosarcoma, a rare soft tissue cancer in December 2012. It all began with one very large swollen tonsil.
He was 10 years old, a normal kid who enjoyed life to the full, he loved skateboarding, dirt biking and soccer, playing at club level for a local team. He had moved to the USA with his now 14-year-old brother Sonny and mum and dad from his native Manchester, England, four years before and quickly made friends, first at Topanga Elementary School, then Lupin Hill Elementary in Calabasas where he had just entered the 5th grade.
At first the doctors thought he had a regular throat infection, but it didn’t clear up, then a swelling started to appear on the side of his neck. The doctors were worried that it might be lymphoma, so he had surgery to remove the swollen tonsil in early December 2012, but the biopsy results came back clear. Just as everyone was beginning to breathe a sigh of relief, and prepare for Santa’s arrival, on December 20th 2012 he went to UCLA where his doctor had decided to send him for a second opinion. The specialist there took one look at his scan and immediately called in the paediatric oncologists and admitted him into the hospital for further tests.
By this time the swelling in the back of his throat had grown much bigger, as had the swelling on his neck. The doctors told his parents that they thought he only had 10 more days before the swelling would completely block his airways. His heart rate was very irregular as the growth was also pushing onto his carotid artery. The doctors said there was a chance it was a rare infection, but the more likely scenario that it was a cancerous growth.
Chico was getting more and more poorly and by the time Christmas Day came, he didn’t even have the energy to open his presents. The doctors didn’t want to start treatment until they were sure of what kind of cancer they were dealing with, but time was running out. On December 28th 2012, the doctors were finally able to reveal that Chico had a very rare form of cancer called Rhabdomyosarcoma. Because of the location of the tumour, surgery to remove it was deemed too risky, so as time was of the essence, that very day he received his first dose of chemotherapy of a harsh regimen that was to last for 43 weeks. A week later he received his second dose of chemotherapy – on his 11th birthday.
Also in his treatment plan were 28 radiation sessions over a 6 week period which he completed in March 2013.
Chico received chemotherapy for ten months between December 2012 and October 2013 and spent most of that period in the hospital. He had a very rough time throughout his treatment. The chemo caused virtually permanent nausea and vomiting and 13 times out of 14 rounds of chemo he ended up being hospitalised for fevers and neutropenia. He got concurrent fungal and bacterial bloodstream infections, C-Difficile and had to be fed first intravenously and then through a stomach tube. The side effects from the harsh chemo landed him in a wheelchair due to damage to the nerves in his legs and feet and of course like many other cancer patients, he lost his hair, eyebrows and eyelashes.
BUT after 10 long months of tortuous treatment, Chico finally, finally finished in October 2013 and was declared to be in remission from the cancer! HOORAY!!!
He is currently working on returning to being a normal kid again. His hair has grown back, he is beginning to eat again and has been able to have his feeding tube removed. He still has walking issues but is having intensive physical therapy which in time should enable him to walk properly again. His wheelchair is no longer needed!
Chico used a range of integrative therapies alongside the conventional treatment, including cannabis oil (which is legal in his home state of California), mistletoe, acupuncture, a range of supplements including medicinal mushrooms, IP6 and a whole host of others. He continues to use these integrative therapies to help prevent relapse and is committed to helping spread the word, particularly about the benefits for cancer patients of cannabis oil and is actively campaigning for it to be more widely available to all cancer patients, particularly in his native UK. He has been instrumental in kick-starting research into cannabis oil and paediatric cancers, which is about to start at UCLA, where he was treated. Chico has lost too many friends to this monster of a disease to sit back and do nothing.
It has been a long, long haul and the work is not over yet, but Chico, throughout, has retained his cheeky sense of humour and has been forever touched by the kindness of the messages and support he has received, particularly from his Facebook page. He has been bowled over by all the donations from kind people who have helped contribute towards the cost of his treatment and by the many gifts and cards he’s received from everyone.
Chico’s family are very humbled and touched by the outpouring of love and support from their many friends both in the USA and UK (and Canada and Ireland and other far-flung places!).
Please show your support by liking and sharing Chico’s Facebook page: Here

CB1 is a potential target for treatment of translocation-positive rhabdomyosarcoma
“show that HU210 has tumour grow inhibiting properties in vivo. This could represent one possible novel treatment strategy that might improve outcome in this paediatric tumour”

Download the .pdf: Here

Skin Cancer
Non-melanoma skin cancer is one of the most common malignancies in humans.
Inhibition of skin tumour growth and angiogenesis by activation of cannabinoid receptors
“Here we report that CB1 and CB2 cannabinoid receptors are expressed in normal epidermis and in skin tumors and that both receptors are functional in the induction of apoptosis of skin tumour cells and the regression of skin carcinomas. It is therefore plausible that apoptosis of tumor cells and tumor regression are two causally related events. Nonetheless, our data indicate that cannabinoid anti-tumoral action may also rely on the inhibition of tumor angiogenesis”
Download the .pdf: Here