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Old 04-21-2012, 11:23 PM
Bi0hazard Bi0hazard is offline
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Learn How Cannabis Kills Cancer! Part 1: VEGF -Backed up by National Cancer Institute

I thought it would be important to start putting up legit scientific studies showing how cannabis treats and outright kills Cancer - I'll try to simply what is going on as well as provide the more technical sources and articles.

One way cannabinoids kills cancer:
Essentially a lot of upcoming research in cancer treatment is being done around reducing the signal protein VEGF (Vascular endothelial growth factor). VEGF is what lets cancer cells get food/protein and grow. Many attempts are being made to create medicines that reduce VEGF levels with little success, while cannabinoids have always been able to do this effectively enough to kill cancer.

Here is the how it works IN A NUTSHELL:

Blocking VEGF -> Stops Cancer growth -> Left over cancer has no way to get food and dies.

Cannabinoids like CBD and many others were able to stop the tumors ability to receive their proteins needed to grow and was able to stop tumor growth in it's tracks. While - the continued blocking of VEGF prevents the tumor from even maintaining itself, at which point the tumors begin to die! This is one of the most important breakthrough in understanding cannabis and it's ability to outright kill cancer - while protecting the cells around the cancer (which many therapy's like chemo cannot achieve - hence the loss of hair and attack on the rest of the body that big pharmas cancer medicines inflict.)

Please spread this far and wide, Imagine if they had shown this scientific evidence on American Weed or Weed Wars as proof, rather than relying on personal opinions on it from either side!

Article: Cannabinoids Inhibit the Vascular Endothelial Growth Factor Pathway in Gliomas (2004)
Full Article @

YouTube Video - Cancer Cure - Cannabis & Cannabinoids,by Robert Melamede,PhD

Youtube Link @
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There are so many of these, I'm trying not to flood the forum with them all at once, I'll post them over time as the conversation on the subject moves forward:

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Old 05-16-2012, 06:19 PM
skunkbear skunkbear is offline

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Im using this now and seems to work, well see.
Old 05-29-2012, 06:01 PM
Bi0hazard Bi0hazard is offline
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Cannabinoids and Cancer: Some brief overviews of different forms of cancer

(Overview from 2008 - Many new discoveries involving cannabinoids and medical issues have been made since then)

(Click on the Numbers after each finding to see the full Scholarly Primary Article)

Cannabinoids and Gliomas

Glioblastoma multiforme is one of the most dreadful forms of cancer and the most frequent class of malignant primary brain tumors. Antitumor action of two cannabinoid receptor agonists, Δ(9)-tetrahydrocannabinol and WIN-55,212-2 (a mixed CB1/CB2 agonist), was shown to be mediated through accumulation of ceramide, which resulted in sustained activation of extracellular signal-regulated kinase (ERK1/2; ref. 2 and references therein). It was also reported that cannabinoids down-regulated phosphoinositide 3-kinase (PI3K), protein kinase B (Akt), and ERK signaling pathways, and activated proapoptotic function of Bad protein, leading to the induction of apoptosis ( 9). It has also been shown that that selective activation of the CB2 receptor by JWH-133 mediates apoptosis in glioma cells via enhanced ceramide synthesis de novo (ref. 4 and references therein). In addition, a role for stress-regulated protein p8 (also designated as candidate of metastasis-1) and its downstream targets such as activating transcription factor-4 (ATF-4), CAAT/enhancer binding protein homologous protein, and cell death–inducible kinase (TRB3) was shown as a mechanism of the antitumor action of cannabinoids ( 2). A phase I clinical trial in nine patients with recurrent glioblastoma multiforme reported a fair safety profile of Δ(9)-tetrahydrocannabinol together with antiproliferative action on tumor cells ( 10). Contrary to these findings, Massi et al. ( 11) showed that cannabidiol treatment induces apoptosis in glioma cells in vitro and tumor regression in vivo through activation of caspases and reactive oxygen species via receptor-independent manner. Although there are few contradictory studies on the mechanism of action of cannabinoids, they all underline the importance of cannabinoids for the treatment of cancer. Hence, further studies are needed to elucidate the mechanism of action of cannabinoids in cancer treatment.

Cannabinoids and Prostate Cancer
The presence of cannabinoid receptors was shown in the prostate tissue and in prostate cancer PC-3 cells. However, it was shown that treatment of PC-3 cells with Δ(9)-tetrahydrocannabinol induced apoptosis via a receptor-independent manner ( 12). Interestingly, another study from the same group reported that activation of cannabinoid receptors in PC-3 cells stimulated the PI3K/Akt pathway with sequential involvement of Raf-1/ERK1/2 and nerve growth factor induction (ref. 13 and references therein). We have recently shown that the expression levels of both cannabinoid receptors CB1 and CB2 are significantly higher in human prostate cancer cells compared with normal prostate epithelial cells. Based on this observation, LNCaP cells were treated with WIN-55,212-2, which resulted in inhibition of cell growth and induction of apoptosis (ref. 4 and references therein) with an arrest of the cells in the G0-G1 phase of the cell cycle. This WIN-55,212-2–induced cell cycle arrest was associated with a sustained activation of ERK1/2 ( 4). To establish in vivo relevance of our in vitro findings, we showed that in CWR22Rν1 xenograft model, WIN-55,212–treated mice exhibited significant inhibition in the tumor growth with remarkable reduction of prostate-specific antigen secretion in the serum ( 14). Nithipatikom et al. ( 13) showed that increasing endogenous 2-arachidonoylgl and its stable analogue noladin ether inhibited invasion of androgen-independent prostate cancer PC-3 and DU-145 cells. Antiproliferative and apoptotic effects of endogenous cannabinoids anandamide in human prostate cancer cell lines LNCaP, DU145, and PC3 were found to be mediated through down-regulation of epidermal growth factor receptor (EGFR) and accumulation of ceramide ( 15). Interestingly, anandamide analogue (R)-methanandamide was shown to have a mitogenic effect on LNCaP cells at very low doses ( 16).

Cannabinoids and Breast Cancer
It has been shown that anandamide, potently and selectively, inhibited proliferation of human breast cancer cells. This antiproliferative activity of anandamide was accompanied by a reduction of cells in the S phase of the cell cycle and suppression of prolactin receptor (ref. 5 and references therein). Ligresti, Moriello, and colleagues ( 5) have shown antitumor activities of five natural cannabinoids, cannabidiol, cannabigerol, cannabichromene, cannabidiol acid, and Δ(9)-tetrahydrocannabinol, and suggested that cannabidiol was the most potent inhibitor of breast cancer cell growth. Both cannabidiol and the cannabidiol-rich extract also inhibited the growth of MDA-MB-231 breast carcinoma cells in athymic nude mice. In another study, (R)-methanandamide reduced the number and size of metastatic nodes, and this effect was reversed by CB1 receptor antagonist SR141716A. (R)-methanandamide–treated cells also showed decreased phosphorylation of focal adhesion–associated protein kinase and Src, and tyrosine kinases involved in migration and adhesion, suggesting that CB1 receptor activation might represent a novel therapeutic strategy to slow down the growth of breast carcinoma and to inhibit its metastatic diffusion in vivo ( 17). Contrary to these findings, McKallip et al. ( 18) have earlier shown that Δ(9)-tetrahydrocannabinol enhanced breast cancer growth and metastasis specifically in cells expressing low levels of cannabinoid receptors by suppressing the antitumor immune response, suggesting that cannabinoid exposure may increase the incidence of breast cancer as well as other cancers that do not express cannabinoid receptors.

Cannabinoids and Lung Cancer
Lung cancer survival figures argue powerfully for new approaches to control this disease by agents that could reverse, suppress, or completely halt tumor development. Guzman (ref. 1 and references therein) reported for the first time that Lewis lung adenocarcinoma growth was retarded by the p.o. administration of Δ(9)-tetrahydrocannabinol, and based in vitro studies, inhibition of DNA synthesis was identified as a mechanism for these effects. Another study showed that concentrations of Δ(9)-tetrahydrocannabinol comparable with those detected in the serum of patients after Δ(9)-tetrahydrocannabinol administration accelerate proliferation of lung cancer cells (ref. 8 and references therein). Treatment of lung carcinoma cell line NCI-H292 with nanomolar concentrations of Δ(9)-tetrahydrocannabinol led to accelerated cell proliferation that was dependent on EGFR-mediated activation of ERK1/2 as well as PKB/Akt signaling (ref. 8 and references therein). Recently, it has been shown that Δ(9)-tetrahydrocannabinol treatment inhibited epidermal growth factor–induced phosphorylation of ERK1/2, c-Jun-NH2-kinase1/2, and Akt in A549 human lung cancer cell line as well as suppression of metastasis and s.c. tumor growth in severe combined immunodeficient mice ( 8).

Cannabinoids and Skin Cancer
Melanoma is responsible for the greatest number of skin cancer–related deaths worldwide. It was reported that CB1 and the CB2 receptors are expressed in normal skin and skin tumors of mice and humans. In vitro studies showed that activation of cannabinoid receptors induced the apoptotic death of tumorigenic epidermal cells, without affecting the nontransformed epidermal cells. Administration of WIN-55,212-2 or the selective CB2 agonist JWH-133 was shown to result in growth inhibition of malignant tumors in nude mice (ref. 6 and references therein). Another study showed that activation of these receptors decreased tumor growth, angiogenesis and metastasis of melanomas in mice, and inhibited proliferation via inhibition of Akt pathway and hypophosphorylation of retinoblastoma in melanoma cells ( 6). These two studies offer an exciting opportunity to further explore the use of cannabinoids for the treatment and management of melanoma.

Cannabinoids and Pancreatic Cancer
Pancreatic cancer ranks as one of the most fatal forms of cancer, and therefore, new strategies aimed at improving the prognosis of this deadly disease are warranted. Recently, it was shown that cannabinoid administration leads to apoptosis of pancreatic tumor cells via CB2 receptor and ceramide-dependent up-regulation of p8 and ATF-4 and TRB3 stress–related genes ( 7). Another study showed that CB1 receptor antagonist AM251–induced cell death in pancreatic MIAPaCa-2 cells occurred via receptor-independent manner ( 19). Although the two studies describe contrasting mechanism of action of cannabinoids, both underline the importance of cannabinoids for the treatment of pancreatic cancer. In depth studies are therefore warranted to identify the mechanism of action of cell death induced by cannabinoids in pancreatic cancer.

Cannabinoids and Lymphoma
Studies show that exposure of murine lymphoma tumors EL-4, LSA, and P815 to Δ(9)-tetrahydrocannabinol in vitro led to a significant reduction in cell viability and an increase in apoptosis, and EL-4 tumor–bearing mice led to a significant reduction in tumor load, increase in tumor-cell apoptosis, and increase in survival of tumor-bearing mice (ref. 20 and references therein). Similar observations were made by Flygare et al. ( 20) who treated mantle cell lymphoma (MCL) cells with cannabinoid receptor ligands and found a decrease in cell viability, whereas control cells lacking CB1 were not affected. Recently, Gustafsson et al. ( 3) reported that cannabinoid receptor–mediated apoptosis induced by (R)-methanandamide and WIN-55,212-2 in MCL was associated with ceramide accumulation and p38. These data suggest that targeting CB1 and CB2 receptors by their agonists may have therapeutic potential for the treatment of lymphoma.
Old 05-29-2012, 06:02 PM
Bi0hazard Bi0hazard is offline
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Straight from the National Cancer Institute's Website (Very Important article to pass around)

Full Article @

"Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects."

"Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death." Unlike Chemo which kills nearby healthy cells and hair etc.

Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis sativa and Cannabis indica species.[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.

Antitumor Effects
One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5-8]

Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis.[9-11] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[12]

The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in hepatocellular carcinoma (HCC).[13] Both agents reduced the viability of hepatocellular carcinoma cells in vitro and demonstrated antitumor effects in hepatocellular carcinoma subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma[14] and breast cancer.[15]

In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[16] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[17,18]

In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation.[19] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[20-23]

Appetite Stimulation
Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[24] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[25]

Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in regions of the brain that regulate nociceptive processing.[26] CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[27,28]

Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.[29-31]
Old 06-06-2012, 02:24 AM
siddhartha siddhartha is offline

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thanks for putting this together
Old 06-06-2012, 04:06 AM
GP73LPC GP73LPC is offline
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awesome, agree with sidd, thanks for the effort compiling this info...
Old 06-06-2012, 07:05 AM
Ichabod Crane Ichabod Crane is online now
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I am not very good at the medical aspects of this. It states that it was given by gavage. Does it say how much and was it activated by heating first then given it to the mice? Also was some kind of carrier used such as a oil?
Old 06-06-2012, 07:59 AM
Hydro-Soil Hydro-Soil is offline

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You're going to find that most of these studies are flawed.

Flawed in that they're mainly using snythetic or extracted THC only. Flawed in that they're only using a portion of the medicinal qualities of the plant.

Flawed in that no... they're not properly heat treating this stuff before testing. Come on... you really think these docs know anything about simpson oil and real world testing on patients?

Bottom line.... cannabis is way more medicinal than even these studies suggest. The proper preperation and application of cannabis is just as important as the cannabis itself, if not more. When the docs begin to figure that one out properly... we'll see some significant studies being done. Not that it will change anything... the truth doesn't seem ot matter in the case of cannabis prohibition.

Stay Safe!
Old 06-06-2012, 04:58 PM
Bi0hazard Bi0hazard is offline
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Glioma Cancer Article: Cannabinoid Action Induces Autophagy-Mediated Cell Death Through Stimulation of ER Stress in Human Glioma Cells. (2009)

Full Article @

Autophagy can promote cell survival or cell death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that Δ9-tetrahydrocannabinol (THC), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy. Our data indicate that THC induced ceramide accumulation and eukaryotic translation initiation factor 2α (eIF2α) phosphorylation and thereby activated an ER stress response that promoted autophagy via tribbles homolog 3–dependent (TRB3-dependent) inhibition of the Akt/mammalian target of rapamycin complex 1 (mTORC1) axis. We also showed that autophagy is upstream of apoptosis in cannabinoid-induced human and mouse cancer cell death and that activation of this pathway was necessary for the antitumor action of cannabinoids in vivo.

These findings describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.

Glioma Cancer Article: Cannabinoids inhibit glioma cell invasion in brain cancer studies (2010)

Full Write up and Primary Article @

Researchers in Spain publish juicy studies such as this one: Cannabinoids, the active components of Cannabis sativa L. and their derivatives, inhibit tumor growth in laboratory animals by inducing apoptosis of tumor cells and impairing tumor angiogenesis.

Leukaemia and Breast Cancer Article: Cannabidiol inhibits tumour growth in leukaemia and breast cancer in animal studies (2006)

Italian researchers investigated the anti-tumour effects of five natural cannabinoids of the cannabis plant (cannabidiol, cannabigerol, cannabichromene, cannabidiol-acid and THC-acid) in breast cancer. Cannabidiol (CBD) was the most potent cannabinoid in inhibiting the growth of human breast cancer cells that had been injected under the skin of mice. CBD also reduced lung metastases deriving from human breast cancer cells that had been injected into the paws of the animals.

Researchers found that the anti-tumour effects of CBD were caused by induction of apoptosis (programmed cell death). They concluded that their data "support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer."

These observations are supported by investigations of US scientists who found out that exposure of leukaemia cells to CBD led to a reduction in cell viability and induction of apoptosis. In living animals CBD caused a reduction in number of leukaemia cells. The scientists noted that CBD "may be a novel and highly selective treatment for leukemia."

(Sources: Ligresti A, Schiano Moriello A, Starowicz K, Matias I, Pisanti S, De Petrocellis L, Laezza C, Portella G, Bifulco M, Di Marzo V. Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. J Pharmacol Exp Ther. 2006 May 25; [electronic publication ahead of print]; McKallip RJ, Jia W, Schlomer J, Warren JW, Nagarkatti PS, Nagarkatti M. Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression. Mol Pharmacol. 2006 Jun 5; [electronic publication ahead of print])
Old 06-06-2012, 05:01 PM
Bi0hazard Bi0hazard is offline
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Melanoma Cancer Article: Cannabinoid receptor-1 modulation induces apoptosis of human melanoma cells (2008) Apoptosis = Cell Death (in this case of Cancer Cells only)

Full Article @

ABSTRACT Melanoma causes the greatest number of skin cancer-related deaths worldwide. Despite intensive research, prevention and early detection are the only effective measures against melanoma, so new therapeutic strategies are necessary for the management of this devastating disease. Here, we evaluated the efficacy of cannabinoid receptor agonists, a new family of potential antitumoral compounds, at skin melanoma. Human melanomas and melanoma cell lines express CB1 and CB2 cannabinoid receptors. Activation of these receptors decreased growth, proliferation, angiogenesis and metastasis, and increased apoptosis, of melanomas in mice. Cannabinoid antimelanoma activity was independent of the immune status of the animal, could be achieved without overt psychoactive effects and was selective for melanoma cells vs. normal melanocytes. Cannabinoid antiproliferative action on melanoma cells was due, at least in part, to cell cycle arrest at the G1-S transition via inhibition of the prosurvival protein Akt and hypophosphorylation of the pRb retinoblastoma protein tumor suppressor. These findings may contribute to the design of new chemotherapeutic strategies for the management of melanoma.

Lymphoma Cancer Article: Cannabinoid receptor ligands mediate growth inhibition and cell death in mantle cell lymphoma. (2005)


We have earlier reported overexpression of the central and peripheral cannabinoid receptors CB1 and CB2 in mantle cell lymphoma (MCL), a B cell non-Hodgkin lymphoma. In this study, treatment with cannabinoid receptor ligands caused a decrease in viability of MCL cells, while control cells lacking CB1 were not affected. Interestingly, equipotent doses of the CB1 antagonist SR141716A and the CB1/CB2 agonist anandamide inflicted additive negative effects on viability. Moreover, treatment with the CB1/CB2 agonist Win-55,212-2 caused a decrease in long-term growth of MCL cells in culture. Induction of apoptosis, as measured by FACS/Annexin V-FITC, contributed to the growth suppressive effect of Win-55,212-2. Our data suggest that cannabinoid receptors may be considered as potential therapeutic targets in MCL.

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