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Hundreds of people have been writing in asking where they can get some of the THC/Cancer Research!
Of course we want everyone to have as much information as possible in order to make the best decision for their own treatment.
You may simply be curious to see the results of these studies.
Either way, you can find a wealth of scientific studies on this page.

Please check out any link that is of interest to you. Below you will find the links and a brief description of what you will find at these sites.
To locate some of the medical journal results you may be required to search for a code - (provided with the websites below).

Google THC Cancer for your OWN results!




www.sethgroup.org

- SETH stands for Scientists Exploring Truth in Healing. We are an interdisciplinary team of scientists seeking to develop new models for cancer research based on compassion and open mindedness. Paying attention to what people with cancer are experiencing, our group focuses on ways to test promising new therapies that could be integrated with conventional treatments. Our goal is to find the evidence and act quickly to publish it in peer-reviewed scientific journals to make the information, positive or negative, available to the public.

On THC: "...No chemotherapy can match this nontoxic anti-cancer action. The implication is that this plant compound could be a safe medicine against brain tumors, without the side effects of chemotherapy. These exciting results may be just the tip of the iceberg, however, because DELTA9-THC is only one of many active compounds in medicinal cannabis. Other active constituents of the Cannabis plant (called cannabinoids) are also likely to have a nontoxic anti-cancer action."

(SEE THC KILLING BRAIN TUMOR CELLS WITHOUT DAMAGING HEALTHY BRAIN CELLS!)
(Requires Apple:QuickTime)

- EVIDENCE FOR SELECTIVE ANTI-TUMOR ACTIVITY OF THC TO BE PUBLISHED IN PRESTIGIOUS NEURO-ONCOLOGY JOURNAL (posted 3.9.05) (more)




www.msnbc.msn.com

Doctors group backs medical marijuana -
American College of Physicians urges government to rethink prohibition

The policy statement said, "ACP encourages the use of nonsmoked forms of THC (the main psychoactive element in marijuana) that have proven therapeutic value." It also backed research into additional therapeutic uses of marijuana. The government should review marijuana's status as a so-called schedule I controlled substance, alongside such drugs as LSD and heroin, given scientific evidence of its safety and efficacy for some medical conditions, the doctors group said. It called for exempting doctors who prescribe or dispense medical marijuana in accordance with state law from federal criminal prosecution and other actions. It also urged protection from criminal penalties for patients who use medical marijuana as permitted under state laws.








17934890 <<< COPY AND PASTE THIS REFERENCE CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"

Delta9-Tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells.
Galanti G, Fisher T, Kventsel I, Shoham J, Gallily R, Mechoulam R, Lavie G, Amariglio N, Rechavi G, Toren A.
The Mina and Everard Goodman Faculty of Life Science, Bar-Ilan University, Ramat-Gan, Israel.

Background. The active components of Cannabis sativa L., Cannabinoids, traditionally used in the field of cancer for alleviation of pain, nausea, wasting and improvement of well-being have received renewed interest in recent years due to their diverse pharmacologic activities such as cell growth inhibition, anti-inflammatory activity and induction of tumor regression. Here we used several experimental approaches, which identified delta-9-tetrahydrocannabinol (Delta(9)-THC) as an essential mediator of cannabinoid antitumoral action.

PMID: 17934890 <<< COPY AND PASTE THIS CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"
[PubMed - as supplied by publisher]







17952650 <<< COPY AND PASTE THIS REFERENCE CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"

Cannabinoids and gliomas.
Velasco G, Carracedo A, Bl��zquez C, Lorente M, Aguado T, Haro A, S��nchez C, Galve-Roperh I, Guzm��n M.
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.

Cannabinoids, the active components of Cannabis sativa L., act in the body by mimicking endogenous substances--the endocannabinoids--that activate specific cell surface receptors. Cannabinoids exert various palliative effects in cancer patients. In addition, cannabinoids inhibit the growth of different types of tumor cells, including glioma cells, in laboratory animals. They do so by modulating key cell signaling pathways, mostly the endoplasmic reticulum stress response, thereby inducing antitumoral actions such as the apoptotic death of tumor cells and the inhibition of tumor angiogenesis. Of interest, cannabinoids seem to be selective antitumoral compounds, as they kill glioma cells, but not their non-transformed astroglial counterparts. On the basis of these preclinical findings, a pilot clinical study of Delta(9)-tetrahydrocannabinol (THC) in patients with recurrent glioblastoma multiforme has been recently run. The good safety profile of THC, together with its possible growth-inhibiting action on tumor cells, justifies the setting up of future trials aimed at evaluating the potential antitumoral activity of cannabinoids.

PMID: 17952650 <<< COPY AND PASTE THIS CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"
[PubMed - indexed for MEDLINE]







17931597 <<< COPY AND PASTE THIS REFERENCE CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"

Cannabinoid receptor agonists are mitochondrial inhibitors: a unified hypothesis of how cannabinoids modulate mitochondrial function and induce cell death.
Athanasiou A, Clarke AB, Turner AE, Kumaran NM, Vakilpour S, Smith PA, Bagiokou D, Bradshaw TD, Westwell AD, Fang L, Lobo DN, Constantinescu CS, Calabrese V, Loesch A, Alexander SP, Clothier RH, Kendall DA, Bates TE.
School of Biomedical Sciences, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK.

Time-lapse microscopy of human lung cancer (H460) cells showed that the endogenous cannabinoid anandamide (AEA), the phyto-cannabinoid Delta-9-tetrahydrocannabinol (THC) and a synthetic cannabinoid HU 210 all caused morphological changes characteristic of apoptosis (programed cell death). Janus green assays of H460 cell viability showed that AEA and THC caused significant increases in OD 595 nm at lower concentrations (10-50 microM) and significant decreases at 100 microM, whilst HU 210 caused significant decreases at all concentrations. In rat heart mitochondria, all three ligands caused significant decreases in oxygen consumption and mitochondrial membrane potential. THC and HU 210 caused significant increases in mitochondrial hydrogen peroxide production, whereas AEA was without significant effect. All three ligands induced biphasic changes in either mitochondrial complex I activity and/or mitochondrial complex II-III activity. These data demonstrate that AEA, THC, and HU 210 are all able to cause changes in integrated mitochondrial function, directly, in the absence of cannabinoid receptors.

PMID: 17931597 <<< COPY AND PASTE THIS CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"
[PubMed - indexed for MEDLINE]






17621270 <<< COPY AND PASTE THIS REFERENCE CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"

Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo.
Preet A, Ganju RK, Groopman JE.
Division of Experimental Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

Delta(9)-Tetrahydrocannabinol (THC) is the primary cannabinoid of marijuana and has been shown to either potentiate or inhibit tumor growth, depending on the type of cancer and its pathogenesis. Little is known about the activity of cannabinoids like THC on epidermal growth factor receptor-overexpressing lung cancers, which are often highly aggressive and resistant to chemotherapy. In this study, we characterized the effects of THC on the EGF-induced growth and metastasis of human non-small cell lung cancer using the cell lines A549 and SW-1573 as in vitro models. We found that these cells express the cannabinoid receptors CB(1) and CB(2), known targets for THC action, and that THC inhibited EGF-induced growth, chemotaxis and chemoinvasion. Moreover, signaling studies indicated that THC may act by inhibiting the EGF-induced phosphorylation of ERK1/2, JNK1/2 and AKT. THC also induced the phosphorylation of focal adhesion kinase at tyrosine 397. Additionally, in in vivo studies in severe combined immunodeficient mice, there was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls. Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC. Our study suggests that cannabinoids like THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers.

PMID: 17621270 <<< COPY AND PASTE THIS CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"
[PubMed - indexed for MEDLINE]







17583570 <<< COPY AND PASTE THIS REFERENCE CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"

The cannabinoid delta(9)-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells.
Greenhough A, Patsos HA, Williams AC, Paraskeva C.
Department of Cellular and Molecular Medicine, Cancer Research UK, Colorectal Tumour Biology Group, School of Medical Sciences, University of Bristol, University Walk, Bristol, United Kingdom.

Deregulation of cell survival pathways and resistance to apoptosis are widely accepted to be fundamental aspects of tumorigenesis. As in many tumours, the aberrant growth and survival of colorectal tumour cells is dependent upon a small number of highly activated signalling pathways, the inhibition of which elicits potent growth inhibitory or apoptotic responses in tumour cells. Accordingly, there is considerable interest in therapeutics that can modulate survival signalling pathways and target cancer cells for death. There is emerging evidence that cannabinoids, especially Delta(9)-tetrahydrocannabinol (THC), may represent novel anticancer agents, due to their ability to regulate signalling pathways critical for cell growth and survival. Here, we report that CB1 and CB2 cannabinoid receptors are expressed in human colorectal adenoma and carcinoma cells, and show for the first time that THC induces apoptosis in colorectal cancer cells. THC-induced apoptosis was rescued by pharmacological blockade of the CB1, but not CB2, cannabinoid receptor. Importantly, THC treatment resulted in CB1-mediated inhibition of both RAS-MAPK/ERK and PI3K-AKT survival signalling cascades; two key cell survival pathways frequently deregulated in colorectal tumours. The inhibition of ERK and AKT activity by THC was accompanied by activation of the proapoptotic BCL-2 family member BAD. Reduction of BAD protein expression by RNA interference rescued colorectal cancer cells from THC-induced apoptosis. These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells. The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy. (c) 2007 Wiley-Liss, Inc.

PMID: 17583570 <<< COPY AND PASTE THIS CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"
[PubMed - indexed for MEDLINE]







17202146 <<< COPY AND PASTE THIS REFERENCE CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"

Cannabinoids induce glioma stem-like cell differentiation and inhibit gliomagenesis.
Aguado T, Carracedo A, Julien B, Velasco G, Milman G, Mechoulam R, Alvarez L, Guzm��n M, Galve-Roperh I.
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.

Glioma stem-like cells constitute one of the potential origins of gliomas, and therefore, their elimination is an essential factor for the development of efficient therapeutic strategies. Cannabinoids are known to exert an antitumoral action on gliomas that relies on at least two mechanisms: induction of apoptosis of transformed cells and inhibition of tumor angiogenesis. However, whether cannabinoids target human glioma stem cells and their potential impact in gliomagenesis are unknown. Here, we show that glioma stem-like cells derived from glioblastoma multiforme biopsies and the glioma cell lines U87MG and U373MG express cannabinoid type 1 (CB(1)) and type 2 (CB(2)) receptors and other elements of the endocannabinoid system. In gene array experiments, CB receptor activation altered the expression of genes involved in the regulation of stem cell proliferation and differentiation. The cannabinoid agonists HU-210 and JWH-133 promoted glial differentiation in a CB receptor-dependent manner as shown by the increased number of S-100beta- and glial fibrillary acidic protein-expressing cells. In parallel, cannabinoids decreased the cell population expressing the neuroepithelial progenitor marker nestin. Moreover, cannabinoid challenge decreased the efficiency of glioma stem-like cells to initiate glioma formation in vivo, a finding that correlated with decreased neurosphere formation and cell proliferation in secondary xenografts. Gliomas derived from cannabinoid-treated cancer stem-like cells were characterized with a panel of neural markers and evidenced a more differentiated phenotype and a concomitant decrease in nestin expression. Overall, our results demonstrate that cannabinoids target glioma stem-like cells, promote their differentiation, and inhibit gliomagenesis, thus giving further support to their potential use in the management of malignant gliomas.

PMID: 17202146 <<< COPY AND PASTE THIS CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"
[PubMed - indexed for MEDLINE]







17065222 <<< COPY AND PASTE THIS REFERENCE CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"

Cannabinoid receptors as novel targets for the treatment of melanoma.
Bl��zquez C, Carracedo A, Barrado L, Real PJ, Fern��ndez-Luna JL, Velasco G, Malumbres M, Guzm��n M.
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.

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.

PMID: 17065222 <<< COPY AND PASTE THIS CODE INTO THE SEARCH FIELD AT NCBI AND PRESS "GO"
[PubMed - indexed for MEDLINE]

(ASK YOURSELF: IF CANNABINOIDS WORK SO WELL KILLING CANCER, WHY IS IT BEING MIXED WITH CHEMOTHERAPY??)
OF COURSE, THE ANSWER IS SIMPLE... $$$!!!







Cannabis compound stops spread of breast cancer: researchers
Last Updated: Monday, November 19, 2007 | 11:52 AM ET CBC News

California Pacific Medical Center Research Institute

...Cannabis compound CBD could provide a non-toxic alternative to chemotherapy for cancer treatments. Previous research has shown the compound can block human brain cancers, and recent lab experiments have shown it may be able to do the same for breast cancer. "Right now we have a limited range of options in treating aggressive forms of cancer. Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients," said researcher Dr. Sean McAllister in a release. "This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects." CBD works by blocking the activity of gene Id-1, which is associated with metastasis �� the spread of cancer cells away from the original tumor site. The compound does not share marijuana's psychoactive properties. "We know that Id-1 is a key regulator of the spread of breast cancer," said senior author Dr. Pierre-Yves Desprez in a release. "We also know that Id-1 has also been found at higher levels in other forms of cancer. So what is exciting about this study is that if CBD can inhibit Id-1 in breast cancer cells, then it may also prove effective at stopping the spread of cancer cells in other forms of the disease, such as colon and brain or prostate cancer." Researchers stressed that they were not encouraging cancer patients to smoke pot, adding that it would be highly unlikely for patients to receive an effective concentration of the compound in that way. The team's findings were published in the journal Molecular Cancer Therapeutics.








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