Learn How Cannabis Kills Cancer! Part 1: VEGF -Backed up by National Cancer Institute

[Bi0hazard]

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 @ http://cancerres.aacrjournals.org/content/64/16/5617.full.pdf

YouTube Video - Cancer Cure - Cannabis & Cannabinoids,by Robert Melamede,PhD
Youtube Link @ http://www.youtube.com/watch?v=n31Nuj_AvTg
[youtubeif]http://www.youtube.com/watch?v=n31Nuj_AvTg[/youtubeif]

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:

 

[skunkbear]

Im using this now and seems to work, well see.

 

[Bi0hazard]

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.

 

[Bi0hazard]

Straight from the National Cancer Institute's Website (Very Important article to pass around)

Full Article @ http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4

"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]

Analgesia
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]

 

[siddhartha]

thanks for putting this together
Sidd

 

[GP73LPC]

awesome, agree with sidd, thanks for the effort compiling this info...

 

[Ichabod Crane]

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?

 

[Hydro-Soil]

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!

 

[Bi0hazard]

Glioma Cancer Article: Cannabinoid Action Induces Autophagy-Mediated Cell Death Through Stimulation of ER Stress in Human Glioma Cells. (2009)

Full Article @ http://cannabisscience.com/images/downloads/cancer3.pdf

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 @ http://www.examiner.com/article/cannabinoids-inhibit-glioma-cell-invasion-brain-cancer-studies

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])

 

[Bi0hazard]

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 @ www.fasebj.org/content/20/14/2633.full.pdf

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)

Abstract: http://journals1.scholarsportal.info/details.xqy?uri=/00145793/v579i0030/6885_crlmgicdimcl.xml

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.

 

[Bi0hazard]

Pancreatic Cancer Article: Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum Stress–Related Genes (2006) Apoptosis = Cell Death (in this case of Cancer Cells only)

Full Article: http://cancerres.aacrjournals.org/content/66/13/6748.full

Abstract: Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of especial interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration (a) induced apoptosis, (b) increased ceramide levels, and (c) up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stress–related targets activating transcription factor 4 (ATF-4) and TRB3 in Δ9-tetrahydrocannabinol–induced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 expression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress–related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer.

 

[MrDude]

Most people know of reefer madness, and this is one more thing they has deceived the people with. Cancer is no oncontrolled cell growth, but a controlled cell growth.

Cancer as an overhealing wound: an old hypothesis revisited
http://www.ncbi.nlm.nih.gov/pubmed/18628784

The early hypothesis that "tumors are wounds that duo not heal" has been verrified in a large number of cellular and molecular studies

Cancer is a functional repair tissue
http://www.ncbi.nlm.nih.gov/pubmed/16290925

However, if the wound is persistent due to chronic physical (radiation, electromagnetic field, trauma, particles, etc.), chemical (carcinogens, toxic chemicals, heavy metals etc.) or biological (aging, free radicals, inflammation, nutrient deficiency, bacteria and virus infections, stress, etc.) damage, amplification of GR gene activation in surrounding cells may lead to a clinical cancer. Attempts to destroy cancer cells without healing underlying persistent wounds will allow for eventual recurrence.

The death of the cancer cell
http://www.ncbi.nlm.nih.gov/pubmed/21507929

the search for identification of a cancer cell should be abandoned


A new hypothesis for the cancer mechanism
http://www.ncbi.nlm.nih.gov/pubmed/22179983

Our proposed hypothesis is that cancer is a natural wound healing-related process


Cancers as wounds that do not heal: differences and similarities between renal regeneration/repair and renal cell carcinoma
http://www.ncbi.nlm.nih.gov/pubmed/16849569

Somatic mutation theory of carcinogenesis: why it should be dropped and replaced
http://www.ncbi.nlm.nih.gov/pubmed?term=11170258
http://www.oncoveterinaria.com.ar/co...inogenesis.pdf

The somatic mutation theory of cancer: growing problems with the paradigm?
http://www.ncbi.nlm.nih.gov/pubmed?term=15382143

Paradoxes in carcinogenesis: new opportunities for research directions
http://www.ncbi.nlm.nih.gov/pubmed?term=17683619

Inflammation and cancer: the oncogene-driven connection
http://www.ncbi.nlm.nih.gov/pubmed?term=18502035

Pathways connecting inflammation and cancer
http://www.ncbi.nlm.nih.gov/pubmed?term=18325755

The main reaseon people survives with cannabinoids it because it´s promote epithelial wound healing etc.

 

[neuroherb]

Brussel Sprouts are showing very positive results in the isophyanate killing cancer and given there is no narco effect I suppose if you were solely interestedinm edicinal effect without seeking any intoxicant pleasure then this would be a better direction than smoking cannabis or any drug.

Edit: I think the compound is Allyl Isothiocyanate, saw a few minutes about it on the embarrasing bodies program as I was flicking channels the other night.

 

[rootcap]

nice collection of great information.

 

[mr.brunch]

thanks for the info.
trouble is pharma doesn't want a cure, cos if they cure you , you wont come back for expensive treatments.
lets face it the laws are not based on whether weed is beneficial or not.
i havent seen any laws banning poisonous mushrooms, or plants that could kill you...
just ones that make you feel good. wonder why this is?
maybe because people who feel good dont feel the need to waste large sums of money on useless shite in the hope this will improve them somehow

 

[Bi0hazard]

There is definitely a battle between the pharmaceutical company and grown cannabis.

(Important) The reason they are so threatened by medical cannabis, not really synthesized cannabinoids is because companies are NOT allowed to Patent anything that grows naturally. They have to synthesize or genetically modify it in order to have intellectual property rights of a chemical/medicine to patent it. Since cannabis with many of the cannabinoids can be grown without relying on a pharma company for your supply - they realize you will be out of their profit audience during their monopoly period of medicine distribution through patenting meds. I think this is one of the main reasons the medical industry constantly hides the benefits of grown/smoked cannabis, while taking other propaganda like attacks at it.

The Pharmaceutical companies have big stakes in ensuring that medical marijuana is shut down. The main backbone of the prescription industry is the ability to patent medicine as a company. Anything that grows naturally - which hasn't been synthesized or modified (Intellectual property rights) cannot be patented. For instance, Vitamin C, D, E etc cannot be patented, just like growing cannabis. This is why they are not raiding factories producing and selling Marinol (Prescription synthetic THC) - but instead are raiding places that sell bud, edibles etc. - forms of the drug they can't patent. This also plays into a lot of the suppression of medical breakthroughs around cannabis - because it threatens the income, industry and holdings of all these companies who sell medicines for conditions that cannabis can treat as well, and usually a lot safer.

There are places in the world where they have been doing studies on Cannabis and Cannabinoids since the 70's. A lot of advancements in it's treatments have been found this way, and they have even ran some of the synthetic cannabinoid agonists on people in Phase II and Phase III trials with success. For instance, HU-211, an isomer of THC that doesn't bind to the CB1 receptor (No Psycho-active effects) but keeps much of the other medical benefits of THC intact. Is used to prevent excess damage during brain trauma or injury, after discovering that cannabinoids are naturally increase to help protect the brain during injury. This system used synthetic agonists to create an even stronger protective effect, and was able to reduced the amount of oxidation damage by over 50% in humans, and is now on-hand and used by many hospital emergency rooms around the world.

The Pharmaceutical companies ARE interested in possibly developing CB1 and CB2 medicines. It will most likely still reach some degree of resistance given how Naive most of the medical industry is to cannabis, mostly due to the distortions, unfounded discrediting, and propaganda against cannabis that exists for a multitude of reasons not to mention the stigmas being compounded since refer madness days. However, there are many places that are interested in specially targeted CB2 receptors, since they have no HIGH or psycho-active effect - and there are many also working with selective CB1 agonists as well for further research as well as many treatments.

Although it is not being covered by the mainstream there are currently 6608 Cannabinoid related patents! and the number is rising constantly. The scientific implications and results backing their efficiency are starting to become well understood by those in the medical field who are willing to look, and not to mention the other cannabinoids are drastically less toxic than THC, which by itself has no Human LD-50 (death dose). Literally one would have to consume close to 72x their body weight in cannabis (10% thc) all within 10 minutes to even reach a bodily shut down. Which is obviously beyond far fetched in it's possibility - I can't even contemplate smoking 1lb in 10 minutes, let alone 10,000+ lbs in 10 minutes. That's 1,000 pounds a minute!!! Anyone pushing that amount might want to think about taking a break for 2 weeks to get their tolerance back up =P

Current Listing of Patents using Cannabinoids: 6608
http://www.patentstorm.us/search.html?q=cannabinoid&s.x=0&s.y=0

 

[rootcap]

money money money... this is the name of the game... we all know that allready.
in the past it was a secret, but in this days, it kinda hard to hide this kind of medicine.

the only thing i cant understand is why we are sitting without doing nothing ???
if we all come out together, all over the world, black, white, green, yellow, no matter what or where and start making some noise maybe, but only maybe the medicine companies will lose in the battle...
if we just gonna share this info between us, and we already know this information then we doing nothing... think about it...

 

[neuroherb]

Hey BioHazard great read and wow to the patents list based on cannabinoids.

Whats the story with Monsanto in the states do they get a patent on the seeds they develop?

If that was the case is it not feasable in the states at least to patent crosses of landrace strains where the parentage is kept seccret until the patent is approved?

 

[Bi0hazard]

neuroherb,

To my understanding Monsanto gets a patent on seeds when they "genetically modify it" which could be changing it to be more resistant to pests or diseases - things that farmers initially wanted without all these other strings attached.

The trick is, they can't patent something that grows naturally, but as soon as they genetically modify it - the seed becomes the corporations "Intellectual Property Rights" and they can patent it and sue any other company who makes or uses their genetics without buying it.

No joke, Monsanto sued farmers who didn't use their genetically modified seeds, while having a farm near others who did. If any of the pollen from the genetically modified seeds landed on the farmers fields who weren't using it - they were being sued for having the genetically modified pollen in their fields without purchased permission! wtf... Even though they didn't want the pollen, we all know what that does to yield and other controlled breeding projects! they were still sued for having it hit their farm - when in reality it was the corporations genetics that were contaminating the farmers fields - rather than the farmers trying to use modified genetics behind their back - they never planted any GM seeds...

Also Monsanto creates seeds with Terminator genes, which makes it so all plants from their seeds will not produce their own seeds. So you can never be self sufficient with your own seeds if you buy from them, because they will never drop seeds of your own that you can keep. This way the corporation forces farmers to buy new seeds every year from them, rather than saving their own naturally as was done for thousands and thousands of years.. This goes back to the patent issue of control...

 

[neuroherb]

Yea that matchs other stories I have heard on Monsanto like accidentally mixing their natural and GM seed supply so they could go 'oh well they've been mixed you'll have to use the GM version'. That would mean in theory then instead of cross breeding for the various strains if they could identify the genetic switches that controlled the smell, taste, CBD, various THC's and terpenes and then manipulated that to achieve a medicinal effect they could possibly patent it. Switching of the ability of the plant to seed would be known science to them from what you say so wouldn't take much to figure out.

I remember a while back on here there was talk that in the US either the gov or pharma companies were going around copyrighting the names to strains and I reckon if they could legaly monetize cannabis they would already be in a position to start doing so.