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Old 04-22-2012, 07:47 PM   #16
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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])
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Old 04-22-2012, 07:53 PM   #17
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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 @ 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.—
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Old 04-22-2012, 08:03 PM   #18
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Lymphoma Cancer Article: Cannabinoid receptor ligands mediate growth inhibition and cell death in mantle cell lymphoma. (2005)

Abstract: http://journals1.scholarsportal.info...lmgicdimcl.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.
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Old 04-22-2012, 08:05 PM   #19
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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/co...6/13/6748.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.
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Old 04-29-2012, 08:04 PM   #20
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Originally Posted by Hash Zeppelin View Post
I smoked pure high quality bho at a heavy rate after i got burns on my face, and scars that were supposed to be there for a year are not there at all. second degree burns. no scars. the doctor is shocked!
I wonder what the CDN levels were on your BHO..

“CBN” = cannabinol – Formed when CBNA is heated (or exposed to UV light). Sedative, antibacterial(MRSA), Treats Burns, psoriasis, breast cancer
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Old 04-30-2012, 05:17 AM   #21
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BiOhazard, Great information! Thank you for making this thread! Sweet stuff! monkey5
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Old 04-30-2012, 05:37 AM   #22
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http://www.jci.org/articles/view/37948 - Journal of Clinical Investigation

Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid, Spain

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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.
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Old 04-30-2012, 11:48 PM   #23
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Originally Posted by Bi0hazard View Post
I wonder what the CDN levels were on your BHO..

“CBN” = cannabinol – Formed when CBNA is heated (or exposed to UV light). Sedative, antibacterial(MRSA), Treats Burns, psoriasis, breast cancer
Probably quite high. It was made from 8 week indicas I let go 9 weeks for chron's meds.
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Old 05-01-2012, 07:27 AM   #24
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maybe im missing it.... is the adminstered dose by way of smoking or ingesting or topical through oils? what method are they using throughout the studies?
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