Cannabis has been making a lot of noise lately. Multiple states across the United States and countries around the world have successfully legalized medical Marijuana, and the Uruguay parliament recently voted to create the world’s first legal marijuana market. This is good news as the health benefits of Cannabis are vast, with multiple medical and scientific studies that confirm them. On the other hand, arguments against the use of marijuana is usually published in Psychiatric journals, which show no scientific evidence that Cannabis is harmful to human health. All psychological evaluations from the intake of cannabis are largely based on assumptions, suggestions and observations (1). When we look at the actual science behind Cannabis, the health benefits can be overwhelming. So what does one who opposes the use of cannabis base their belief on? Nothing, not scientific evidence anyways. The negative stigmatism attached to marijuana is due to it’s supposed psychotropic effects, yet again, there is no scientific evidence to show that marijuana has any psychotropic effects. Nonetheless, cannabis has recently been the focus of medical research and considered as a potential therapeutic treatment and cure for cancer.
Cannabis is a great example of how the human mind is programmed and conditioned to believe something. Growing up, we are told drugs are bad, which is very true, however not all substances that have been labelled as “drugs” by the government are harmful. Multiple substances are labelled as a “drug” in order to protect corporate interests. One example is the automobile and energy industry, a car made from hemp is stronger than steel, and can be fuelled from hemp alone. Henry Ford demonstrated this many years ago. Hemp actually has over 50,000 uses!
Let’s take a look at the science behind Cannabis and Cancer. Although Cannabis has been proven to be effective for a large range of ailments, this article will focus mainly on it’s effectiveness in the treatment of cancer. Cannabinoids may very well be one of the best disease and cancer fighting treatments out there. Cannabinoids refer to any of a group of related compounds that include cannabinol and the active constituents of cannabis. They activate cannabinoid receptors in the body. The body itself produces compounds called endocannabinoids and they play a role in many processes within the body that help to create a healthy environment. Cannabinoids also play a role in immune system generation and re-generation. The body regenerates best when it’s saturated with Phyto-Cannabinoids. Cannabinoids can also be found in Cannabis. It is important to note that the cannabinoids are plentiful in both hemp and cannabis. One of the main differentiations between hemp and cannabis is simply that hemp only contains 0.3% THC while cannabis is 0.4% THC or higher. (Technically they are both strains of Cannabis Sativa.) Cannabinoids have been proven to reduce cancer cells as they have a great impact on the rebuilding of the immune system. While not every strain of cannabis has the same effect, more and more patients are seeing success in cancer reduction in a short period of time by using cannabis.
While taking a look at these studies, keep in mind that cannabis can be much more effective for medicinal purposes when we eat it rather than smoking it. Below are 20 medical studies that prove cannabis can be an effective treatment and possible cure for cancer. Please keep in mind that this is a very short list of studies that support the use of medicinal marijuana. Please feel free to further your research, hopefully this is a good starting point.
1. A study published in the British Journal of Cancer, conducted by the Department of Biochemistry and Molecular Biology at Complutense University in Madrid, this study determined that Tetrahydrocannabinol (THC) and other cannabinoids inhibit tumour growth. They were responsible for the first clinical study aimed at assessing cannabinoid antitumoral action. Cannabinoid delivery was safe and was achieved with zero psychoactive effects. THC was found to decrease tumour cells in two out of the nine patients.
2. A study published in The Journal of Neuroscience examined the biochemical events in both acute neuronal damage and in slowly progressive, neurodegenerative diseases. They conducted a magnetic resonance imaging study that looked at THC (the main active compound in marijuana) and found that it reduced neuronal injury in rats. The results of this study provide evidence that the cannabinoid system can serve to protect the brain against neurodegeneration.
3. A study published in The Journal of Pharmacology And Experimental Therapeutics already acknowledged the fact that cannabinoids have been shown to possess antitumor properties. This study examined the effect of cannabidiol (CBD, non psychoactive cannabinoid compound) on human glioma cell lines. The addition of cannabidiol led to a dramatic drop in the viability of glioma cells. Glioma is the word used to describe brain tumour. The study concluded that cannabidiol was able to produce a significant antitumor activity.
4. A study published in the journal Molecular Cancer Therapeutics outlines how brain tumours are highly resistant to current anticancer treatments, which makes it crucial to find new therapeutic strategies aimed at improving the poor prognosis of patients suffering from this disease. This study also demonstrated the reversal of tumour activity in Glioblastoma multiforme.
5. A study published in the US National Library of Medicine, conducted by the California Pacific Medical Centre determined that cannabidiol (CBD) inhibits human breast cancer cell proliferation and invasion. They also demonstrated that CBD significantly reduces tumour mass.
6. A study published in The Journal of Pharmacology and Experimental Therapeutics determined that THC as well as cannabidiol dramatically reduced breast cancer cell growth. They confirmed the potency and effectiveness of these compounds.
7. A study published in the Journal Molecular Cancer showed that THC reduced tumour growth and tumour numbers. They determined that cannabinoids inhibit cancer cell proliferation, induce cancer cell apoptosis and impair tumour angiogenesis (all good things). This study provides strong evidence for the use of cannabinoid based therapies for the management of breast cancer.
8. A study published in the Proceedings of the National Academy of Sciences of the United States of America (PNAS) determined that cannabinoids inhibit human breast cancer cell proliferation.
9. A study published in the journal Oncogene, by Harvard Medical Schools Experimental Medicine Department determined that THC inhibits epithelial growth factor induced lung cancer cell migration and more. They go on to state that THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers.
10. A study published by the US National Library of Medicine by the Institute of Toxicology and Pharmacology, from the Department of General Surgery in Germany determined that cannabinoids inhibit cancer cell invasion. Effects were confirmed in primary tumour cells from a lung cancer patient. Overall, data indicated that cannabinoids decrease cancer cell invasiveness.
11. A study published by the US National Library of Medicine, conducted by Harvard Medical School investigated the role of cannabinoid receptors in lung cancer cells. They determined its effectiveness and suggested that it should be used for treatment against lung cancer cells.
12. A study published in the US National Library of Medicine illustrates a decrease in prostatic cancer cells by acting through cannabinoid receptors.
13. A study published in the US National Library of Medicine outlined multiple studies proving the effectiveness of cannabis on prostate cancer.
14. Another study published by the US National Library of Medicine determined that clinical testing of CBD against prostate carcinoma is a must. That cannabinoid receptor activation induces prostate carcinoma cell apoptosis. They determined that cannabidiol significantly inhibited cell viability.
15. A study published in the journal Molecular Pharmacology recently showed that cannabinoids induce growth inhibition and apoptosis in matle cell lymphoma. The study was supported by grants from the Swedish Cancer Society, The Swedish Research Council and the Cancer Society in Stockholm.
16. A study published in the International Journal of Cancer also determined and illustrated that cannabinoids exert antiproliferative and proapoptotic effects in various types of cancer and in mantle cell lymphoma.
17. A study published in the US National Library of Medicine conducted by the Department of Pharmacology and Toxicology by Virginia Commonwealth University determined that cannabinoids induce apoptosis in leukemia cells.
18. A study published by the US National Library of Medicine results show cannabinoids are potent inhibitors of cellular respiration and are toxic to highly malignant oral Tumours.
19. A study published by the US National Library of Medicine determined that that THC reduces the viability of human HCC cell lines (Human hepatocellular liver carcinoma cell line) and reduced the growth.
20. A study published in The American Journal of Cancer determined that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumour biopsies at much higher levels than in normal pancreatic tissue. Results showed that cannabinoid administration induced apoptosis. They also reduced the growth of tumour cells, and inhibited the spreading of pancreatic tumour cells.
All sources highlighted throughout article. Click on the highlighted parts of the article to view them.
Im dyslexic, its not an excuse more an advance warning...
n 1974 researchers learned that THC, the active chemical in cannabis, shrank or destroyed tumors in test mice. But the DEA quickly shut down the study and destroyed its results, which were never replicated -- until now.
The term medical marijuana took on dramatic new meaning in February, 2000 when researchers in Madrid announced they had destroyed incurable brain tumors in rats by injecting them with THC, the active ingredient in cannabis.
The Madrid study marks only the second time that THC has been administered to tumor-bearing animals; the first was a Virginia investigation 26 years ago. In both studies, the THC shrank or destroyed tumors in a majority of the test subjects.
Most Americans don't know anything about the Madrid discovery. Virtually no major U.S. newspapers carried the story, which ran only once on the AP and UPI news wires, on Feb. 29, 2000.
The ominous part is that this isn't the first time scientists have discovered that THC shrinks tumors. In 1974 researchers at the Medical College of Virginia, who had been funded by the National Institute of Health to find evidence that cannabis damages the immune system, found instead that THC slowed the growth of three kinds of cancer in mice -- lung and breast cancer, and a virus-induced leukemia.
The DEA quickly shut down the Virginia study and all further cannabis/tumor research, according to Jack Herer, who reports on the events in his book, "The Emperor Wears No Clothes." In 1976 President Gerald Ford put an end to all public cannabis research and granted exclusive research rights to major pharmaceutical companies, who set out -- unsuccessfully -- to develop synthetic forms of THC that would deliver all the medical benefits without the "high."
The Madrid researchers reported in the March issue of "Nature Medicine" that they injected the brains of 45 rats with cancer cells, producing tumors whose presence they confirmed through magnetic resonance imaging (MRI). On the 12th day they injected 15 of the rats with THC and 15 with Win-55,212-2 a synthetic compound similar to THC. "All the rats left untreated uniformly died 12-18 days after glioma (brain cancer) cell inoculation ... Cannabinoid (THC)-treated rats survived significantly longer than control rats. THC administration was ineffective in three rats, which died by days 16-18. Nine of the THC-treated rats surpassed the time of death of untreated rats, and survived up to 19-35 days. Moreover, the tumor was completely eradicated in three of the treated rats." The rats treated with Win-55,212-2 showed similar results.
The Spanish researchers, led by Dr. Manuel Guzman of Complutense University, also irrigated healthy rats' brains with large doses of THC for seven days, to test for harmful biochemical or neurological effects. They found none.
"Careful MRI analysis of all those tumor-free rats showed no sign of damage related to necrosis, edema, infection or trauma ... We also examined other potential side effects of cannabinoid administration. In both tumor-free and tumor-bearing rats, cannabinoid administration induced no substantial change in behavioral parameters such as motor coordination or physical activity. Food and water intake as well as body weight gain were unaffected during and after cannabinoid delivery. Likewise, the general hematological profiles of cannabinoid-treated rats were normal. Thus, neither biochemical parameters nor markers of tissue damage changed substantially during the 7-day delivery period or for at least 2 months after cannabinoid treatment ended."
Guzman's investigation is the only time since the 1974 Virginia study that THC has been administered to live tumor-bearing animals. (The Spanish researchers cite a 1998 study in which cannabinoids inhibited breast cancer cell proliferation, but that was a "petri dish" experiment that didn't involve live subjects.)
In an email interview for this story, the Madrid researcher said he had heard of the Virginia study, but had never been able to locate literature on it. Hence, the Nature Medicine article characterizes the new study as the first on tumor-laden animals and doesn't cite the 1974 Virginia investigation.
"I am aware of the existence of that research. In fact I have attempted many times to obtain the journal article on the original investigation by these people, but it has proven impossible." Guzman said.
In 1983 the Reagan/Bush Administration tried to persuade American universities and researchers to destroy all 1966-76 cannabis research work, including compendiums in libraries, reports Jack Herer, who states, "We know that large amounts of information have since disappeared."
Guzman provided the title of the work -- "Antineoplastic activity of cannabinoids," an article in a 1975 Journal of the National Cancer Institute -- and this writer obtained a copy at the University of California medical school library in Davis and faxed it to Madrid.
The summary of the Virginia study begins, "Lewis lung adenocarcinoma growth was retarded by the oral administration of tetrahydrocannabinol (THC) and cannabinol (CBN)" -- two types of cannabinoids, a family of active components in marijuana. "Mice treated for 20 consecutive days with THC and CBN had reduced primary tumor size."
The 1975 journal article doesn't mention breast cancer tumors, which featured in the only newspaper story ever to appear about the 1974 study -- in the Local section of the Washington Post on August 18, 1974. Under the headline, "Cancer Curb Is Studied," it read in part:
"The active chemical agent in marijuana curbs the growth of three kinds of cancer in mice and may also suppress the immunity reaction that causes rejection of organ transplants, a Medical College of Virginia team has discovered." The researchers "found that THC slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent."
Guzman, writing from Madrid, was eloquent in his response after this writer faxed him the clipping from the Washington Post of a quarter century ago. In translation, he wrote:
"It is extremely interesting to me, the hope that the project seemed to awaken at that moment, and the sad evolution of events during the years following the discovery, until now we once again Œdraw back the veil‚ over the anti-tumoral power of THC, twenty-five years later. Unfortunately, the world bumps along between such moments of hope and long periods of intellectual castration."
News coverage of the Madrid discovery has been virtually nonexistent in this country. The news broke quietly on Feb. 29, 2000 with a story that ran once on the UPI wire about the Nature Medicine article. This writer stumbled on it through a link that appeared briefly on the Drudge Report web page. The New York Times, Washington Post and Los Angeles Times all ignored the story, even though its newsworthiness is indisputable: a benign substance occurring in nature destroys deadly brain tumors.
Boy, two, with brain cancer is 'cured' after secretly being fed medical marijuana by his father
(Daily cannabis turns you mental Mail story)
A desperate father whose son was suffering from a life-threatening brain tumour has revealed he gave him cannabis oil to ease his pain. And he has now apparently made a full recovery.
Cash Hyde, known as Cashy, was a perfectly healthy baby when he was born in June 2008 but became sick shortly before his second birthday.
At first he was misdiagnosed with glandular fever before his parents Mike and Kalli, from Missoula in Montana, were given the devastating news he had a serious brain tumour.
The little boy had to have arduous chemotherapy treatment to reduce the growth, which had drastic side effects including seizures and a blood infection.
His distraught parents were repeatedly told he was likely to succumb to the illness because the condition was so bad.
After one bout of high-dose chemotherapy, Cash was so weak he could not lift his head and was too sick to eat any solid food for 40 days.
It was at this point that Mr Hyde decided to take action and go down the route of medical marijuana to try to help his young son.
Cash's doctors refused to even discuss the option but his father went and sought authorisation elsewhere and then secretly administered it through his son's feeding tube.
He also told doctors to stop giving Cash the cocktail of anti-nausea drugs he had been taking - although he never told them what he was doing.
Mr Hyde told KXLY News that his son started looking better right away.
Mr Hyde said: 'He hadn't eaten a thing in 40 days - and, it was really incredible to watch him take a bite of a piece of cheese. It shows that he wants to live'.
He credits the cannabis oil with helping his son get through the chemo, and say Cash has now been declared cancer free by doctors.
The boy is now back and home and living the life of a typical young boy, playing with his elder brother Colty.
Medical marijuana is legal in some states, including Montana, but its use for children is poorly understood and quite rate.
The US federal government does not recognise the legality of using the drug for medical reasons and frequently clashes with states over the issue.
Mr Hyde told KXLY: 'It's very controversial, it's very scary. But, there's nothing more scary than losing your child.'
Cannabis For Infant's Brain Tumor, Doctor Calls Child "A Miracle Baby"
Medical marijuana is gaining acceptance, but could it even help kids? Dr. William Courtney has seen it happen, and on Friday, told HuffPost Live host Alyona Minkovski about it. Saying he was "quite a skeptic 5 or 6 years ago", Dr. Courtney continued that "my youngest patient is 8 months old, and had a very massive centrally located inoperable brain tumor." The child's father pushed for non-traditional treatment utilizing cannabis.
"They were putting cannabinoid oil on the baby's pacifier twice a day, increasing the dose... And within two months there was a dramatic reduction, enough that the pediatric oncologist allowed them to go ahead with not pursuing traditional therapy."
The tumor was remarkably reduced after eight months of treatment. Dr. Courtney pointed out that the success of the cannabis approach means that "this child, because of that, is not going to have the long-term side effects that would come from a very high dose of chemotherapy or radiation... currently the child's being called a miracle baby, and I would have to agree that this is the perfect response that we should be insisting is frontline therapy for all children before they launch off on all medications that have horrific long term side effects."
Tetrahydrocannabinol-Induced Apoptosis in Jurkat Leukemia T Cells Is Regulated by Translocation of Bad to Mitochondria
What is apoptosis?
Apoptosis, on the other hand, is relatively civil, even though it may not sound so at first -- it's when a cell commits suicide. How is that better than necrosis? For one thing, the cleanup is much easier. It's sometimes referred to as programmed cell death, and indeed, the process of apoptosis follows a controlled, predictable routine.
Plant-derived cannabinoids, including Δ9-tetrahydrocannabinol (THC), induce apoptosis in leukemic cells, although the precise mechanism remains unclear. In the current study, we investigated the effect of THC on the upstream and downstream events that modulate the extracellular signal-regulated kinase (ERK) module of mitogen-activated protein kinase pathways primarily in human Jurkat leukemia T cells. The data showed that THC down-regulated Raf-1/mitogen-activated protein kinase/ERK kinase (MEK)/ERK/RSK pathway leading to translocation of Bad to mitochondria. THC also decreased the phosphorylation of Akt. However, no significant association of Bad translocation with phosphatidylinositol 3-kinase/Akt and protein kinase A signaling pathways was noted when treated cells were examined in relation to phosphorylation status of Bad by Western blot and localization of Bad to mitochondria by confocal analysis. Furthermore, THC treatment decreased the Bad phosphorylation at Ser112 but failed to alter the level of phospho-Bad on site Ser136 that has been reported to be associated with phosphatidylinositol 3-kinase/Akt signal pathway. Jurkat cells expressing a constitutively active MEK construct were found to be resistant to THC-mediated apoptosis and failed to exhibit decreased phospho-Bad on Ser112 as well as Bad translocation to mitochondria. Finally, use of Bad small interfering RNA reduced the expression of Bad in Jurkat cells leading to increased resistance to THC-mediated apoptosis. Together, these data suggested that Raf-1/MEK/ERK/RSK-mediated Bad translocation played a critical role in THC-induced apoptosis in Jurkat cells. (Mol Cancer Res 2006;4(8):549–62)
Cannabinoids, the biologically active constituents of marijuana (Cannabis sativa), produce a wide spectrum of central and peripheral effects, such as alterations in cognition and memory, analgesia, anticonvulsion, anti-inflammation, and alleviation of both intraocular pressure and pain relief (1). There has been a growing interest in cannabinoids since the cloning of two subtypes of the cannabinoid receptors, CB1 (2) and CB2 (3). The CB1 receptor is mainly expressed in the central nervous system, whereas the CB2 receptor is predominantly expressed in immune cells (4). Both cannabinoid receptors are coupled to heterotrimeric Gi/o proteins and interact with the mitogen-activated protein kinases (MAPK), particularly the extracellular signal-regulated kinase (ERK; ref. 5).
At almost the same time, endogenous ligands for these receptors, capable of mimicking, to some extent, the pharmacologic actions of marijuana's psychoactive principle Δ9-tetrahydrocannabinol (THC), have been discovered (6). Numerous studies have shown that THC can modulate the functions of immune cells (7). More recently, we reported that the immunosuppressive property of THC can be attributed, at least in part, to its ability to induce apoptosis in T cells and dendritic cells through ligation of CB2 receptors and that the latter was regulated by activation of nuclear factor-κB (8), recruiting both intrinsic and extrinsic pathways of apoptosis. Interestingly, we also found that THC and other cannabinoids could induce apoptosis in transformed murine and human T cells (9), including primary acute lymphoblastic human leukemia cells, and furthermore that the treatment of mice bearing a T-cell leukemia with THC could cure ∼25% of the mice (10). These findings are consistent with studies showing that THC and other cannabinoids can induce apoptosis in a variety of tumor cell lines, thereby raising the possibility of the use of cannabinoids as novel anticancer agents (11).
The precise mechanism through which cannabinoids induce apoptosis is under active investigation and may vary based on cell type. In normal and transfected neural cells, vascular endothelial cells, and Chinese hamster ovary cells, cannabinoid treatment was shown to induce activation of ERK (12), c-Jun NH2-terminal kinase (JNK), and p38 (13, 14). In contrast, it was shown that cannabinoids were cytotoxic in leukemic cells and that they inhibited neuronal progenitor cell differentiation through attenuation of the ERK pathway (15). In glioma cells, THC was shown to induce apoptosis via ceramide generation (16). However, cannabinoids can also block ceramide-induced apoptosis of normal astrocytes (17). Together, such studies suggest that the precise signaling pathways that are evoked by cannabinoid receptor activation in normal and transformed cells may vary based on cell type and that such activation could lead to the generation of survival or death signals.
In the current study, we investigated the molecular mechanisms underlying apoptosis induced by THC, specifically addressing the role of MAPK signaling. Treatment with THC caused interruption of the MAPK/ERK kinase (MEK)/ERK signaling module that was required for apoptotic lethality, and this event possibly played an important functional role in mediating THC-induced translocation of Bad to mitochondria.
Treatment of Jurkat Cells with THC Induces Suppression of the Raf-1/MEK/ERK Cytoprotective Signaling Pathway through the Signaling of the Cannabinoid Receptors
To gain insights into the functional role of cannabinoid receptor pathway in THC-mediated lethality, Jurkat cells were pretreated with either SR141716 (CB1 antagonist) or SR144528 (CB2 antagonist) in the absence or presence of THC for a designated period (6-30 hours), after which the percentage of cells displaying the morphologic features of apoptosis was determined by the Wright-Giemsa-stained cytospin preparation. THC caused dose-dependent apoptosis in Jurkat cells (data not shown) with a very substantial increase in cell death detected at 10 μmol/L (Fig. 1A ). Time course analysis revealed that exposure to SR141716 (CB1 antagonist) or SR144528 (CB2 antagonist) individually at the concentration of 1 or 2 μmol/L were minimally toxic over 30-hour treatment interval, whereas treatment with 10 μmol/L THC alone caused ∼50% apoptosis (Fig. 1A). However, when cells were pretreated with either SR141716 or SR144528 followed by exposure to THC, there was a significant reduction in apoptosis by 6 hours and a very substantial reversal in lethality after 12 hours (Fig. 1A). Very similar results were obtained when THC-treated cells were evaluated for combined early and late apoptotic cells by Annexin V/propidium iodide (PI) analysis (Fig. 1B). In this assay, cells stained for Annexin V alone are considered to be early apoptotic cells and those stained for Annexin V and PI represent late apoptotic cells. We also analyzed the cells for loss of mitochondrial membrane potential (MMP; Δψm) as described (10) and designated them as cells with “low” 3,3-dihexyloxacarbocyanine iodide uptake (Fig. 1B). Next, we measured the levels of CB1 and CB2 receptors in Jurkat cells and compared them with other tumor cell lines, such as the T-cell lymphoma Hut78 and the glioma U251 known to express CB1 receptors. As shown in Fig. 1C, Jurkat and Hut78 but not U251 cells expressed significant levels of CB2 mRNA. In addition, when CB1 mRNA levels were analyzed, Jurkat cells were found to express low levels. Interestingly, when all cells were cultured with THC, CB1 and CB2 receptor expression was significantly increased. These data explained why in Jurkat cells not only CB2 antagonist but also CB1 antagonist were able to partially block THC-induced apoptosis.
To further characterize the downstream signaling pathways that trigger apoptosis following activation of cannabinoid receptors, Jurkat cells were pretreated with either CB1 or CB2 antagonists in the absence or presence of THC for 12 hours. As shown in Fig. 1D, THC treatment of Jurkat cells caused reduced phosphorylation of Raf-1, whereas total protein levels remained constant. In addition, exposure of cells to THC diminished the levels of phosphorylation of MEK1/2, with the total MEK1/2 expression remaining unchanged. Similarly, phosphorylation of ERK1/2 was largely decreased in THC-treated cells, but total ERK1/2 expression remained unperturbed. In contrast, when cells were pretreated with CB1 or CB2 antagonists, the effects of THC on each of these proteins were largely reduced. None of the THC concentrations tested induced alterations in phospho-p38 or phospho-JNK. In addition, no changes were observed in levels of total p38 or JNK. Consequently, we evaluated the levels of phospho-p90RSK (Thr359/Ser363), phospho-p90RSK (Ser380), phospho-p90RSK (Thr573), and total p90RSK following exposure of Jurkat cells to THC in the absence or presence of CB1/2 antagonists (Fig. 1D). THC caused a reduction in p90RSK phosphorylation involving both Thr359- and Ser363-specific phosphorylation sites. However, when cells were pretreated with CB1 or CB2 antagonist, the effects of THC on both phosphorylation sites of this protein were significantly reversed. No changes were detected in levels of total p90RSK or phospho-p90RSK on sites Ser380 and Thr573. Attempts also were made to extend ERK inactivation to other human tumor cell lines. As shown in Fig. 1E, an 18-hour exposure of Molt4, Hut78, and SupT1 cells to THC resulted in a marked reduction in the levels of phospho-ERK1/2, with the total ERK1/2 expression remaining unchanged. Finally, essentially similar results were obtained when the effects of THC were examined in kinase activity. A decrease in ERK activity was detectable in Jurkat cells after treatment with THC beginning at hour 1, and this effect was even more pronounced at 12 hours (Fig. 1F). Taken together, these data suggest that suppression of the Raf-1/MEK/ERK cytoprotective signaling pathway by THC may play an important functional role in the induction of apoptosis in Jurkat cells as well as in other tumor cell lines tested.
Antiapoptotic Effect of Phorbol 12-Myristate 13-Acetate Depends on ERK Activation
To confirm the possible role of ERK activation in THC-induced apoptosis, Jurkat cells were pretreated with 10 nmol/L phorbol 12-myristate 13-acetate (PMA), a potent activator of ERK (18, 19). Next, the cells were treated with10 μmol/L THC for a total of 12 hours or left untreated. Parallel studies were done on cells precultured with 25 μmol/L U0126, a MEK inhibitor. The extent of apoptosis was then determined by terminal deoxynucleotidyl transferase–mediated dUTP end labeling (TUNEL) assay. Treatment of cells with THC alone for 12 hours caused ∼43% apoptosis, which was partially blocked in the presence of either CB1 or CB2 antagonist, thereby confirming the involvement of CB1 and CB2 receptors in apoptosis (Fig. 3A ). In addition, THC-induced apoptosis was also partially blocked by PMA (Fig. 3A). Moreover, treatment of cells with U0126 alone caused significant levels of apoptosis consistent with our hypothesis that MEK inhibition in Jurkat cells can lead to cell death. Furthermore, the combination of THC plus U0126 caused a marked increase in apoptosis, which was more than that seen when either of these compounds was used alone. As expected, treatment with PMA plus U0126 caused a significant inhibition in apoptosis when compared with the use of U0126 alone. To characterize interaction between THC and U0126 more rigorously and over a range of drug concentrations at a fixed ratio (1:2.5), median dose effect analysis was used. When the extent of apoptosis was determined, combination index values considerably less than 1.0 were obtained (Fig. 3B), corresponding to highly synergistic interaction. These data together suggest that THC-induced ERK inactivation may play a critical role in apoptosis in Jurkat cells.
http://wakeup-world.com/…/cannabis-oil-provides-new-hope-f…/ - Very very good news, this 5 year old lad with a grade 4 brain tumour has been LEGALLY perscribed cannabis oil in thE UK by a private clinic to treat his brain cancer. You read that right he has been LEGALY prescribed it. This is fantastic news so good i could almost cry, the hard work is paying off, people are cottoning on
http://www.worthingherald.co.uk/…/grandmother-puts-faith-in… - Grandmother with soon not to be terminal cancer is using oil to stay alive, still has to hide like a criminal for interview
Article, from USA blowing the herbs trumpet and slating the authorities over criminalisation http://www.sfweekly.com/…/key-words-cannabis-oil-cure…/full/ (since this has been written its now decriminalised)
Cannaboids occur naturally in breast milk, well who would have thought it, no wonder cannabis is so good for us humans -http://www.cannabiscure.info/files/cannabis_breastmilk.htm
Cannabis oil and breast cancer -http://www.cannabiscure.info/files/breast_cancer.htm
Another article in the Mail, think the editor must have been smoking to let two positive articles through in as many weeks……Read the comments! http://www.dailymail.co.uk/…/Cannabis-oil-helped-cured-canc…
I dont know if anyone picked up on this, in todays DAILY MAIL, a grandfather who has cured his own cancer with cannabis oil, again its in the DAILY MAIL.....this is brilliant! - http://www.dailymail.co.uk/…/I-cured-cancer-CANNABIS-OIL.ht…
From September 2013, 'Cannabis oil saved my mothers life', she's 93 and took oil to treat cancer. She's gone from being in palliative care and incapable of moving to washing herself and getting herself out of bed and this was in ENGLAND.http://ukcsc.co.uk/change-view-cannabis ... d-mothers-…/
73 year old man diagnosed with stage 3B lung cancer, he'd had enough of chemo having just about survived leukaemia, unfortunately he was diagnosed with pneumonia and admitted to hospital and told he had weeks to live, in desperation he tried cannabis oil......he is now fine, not only that but he's healthier than he has ever been and he is cancer and pneumonia free. - http://www.unitedpatientsgroup.com/…/a-cannabis-cancer-sur…/
14 year old girl cures herself of cancer, the only bad side effect was the taste! - http://www.vapexhale.com/…/14543813-to-be-alive-meet-alysa-…
The video is a little tinny but the bottom line is she used oil to treat her various cancers and now she is cancer free -https://www.youtube.com/watch?v=Bskc3B5e_SQ&feature=share