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[Sea Mac]

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

OK, Folks ... it is BACK!!!!

4 Years ago the NIH published a report on compounds in Marijuana and their effects on Cancer. A Week later the DEA Made them change the wording to reflect the "No Medical Use" line/lie: in order to keep on kicking in sick peoples doors, and confiscating EVERYTHING they Own, in Asset Forfeiture schemes.

Now that the DEA is defying federal rules - openly defying Congress - and PERSISTING in carrying forward prosecution of patients in states where MMJ is legal ... The NIH updates their PDQ on Cannabis and Cancer ONCE AGAIN: categorically stating that THC and Other compounds in Marijuana KILL Cancer Cells!!!

The following is a COPY of the PDQ as it stands on April 13th 2015:

  Cannabis and Cannabinoids (PDQ®)     

Laboratory/Animal/Preclinical Studies

Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis species (e.g., Cannabis sativa L.) .[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 (HCC) 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 invasion and metastasis.[9-12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents.[13,14] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. For example, these compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats, while they protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[9]

The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC.[15] Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC 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 [16] and breast cancer.[17]

An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic mammary cells.[18] Other studies have also shown the antitumor effect of cannabinoids (i.e., CBD and THC) in preclinical models of breast cancer.[19,20]

CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[21] In this experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation. In a subsequent study, the investigators found that the antiproliferative effect of CBD was counteracted by selective CB1 but not CB2 receptor antagonists, suggesting an involvement of CB1 receptors.[22]

Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[12] ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.

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.[23] 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.[24,25]
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.[26] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[27-30]

CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine.[31] In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells. Also, CBD together with THC may enhance the antitumor activity of classic chemotherapeutic drugs such as temozolomide in some mouse models of cancer.[13,32]

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.[33] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[34]

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.[35] 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.[36,37]

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.[38-40] One study reported that the efficacy of synthetic CB1- and CB2-receptor agonists were comparable with the efficacy of morphine in a murine model of tumor pain.[41]


References

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• National Toxicology Program: NTP toxicology and carcinogenesis studies of 1-trans-delta(9)-tetrahydrocannabinol (CAS No. 1972-08-3) in F344 rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser 446 (): 1-317, 1996. [PUBMED Abstract]
• Bifulco M, Laezza C, Pisanti S, et al.: Cannabinoids and cancer: pros and cons of an antitumour strategy. Br J Pharmacol 148 (2): 123-35, 2006. [PUBMED Abstract]
• Sánchez C, de Ceballos ML, Gomez del Pulgar T, et al.: Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor. Cancer Res 61 (15): 5784-9, 2001. [PUBMED Abstract]
• McKallip RJ, Lombard C, Fisher M, et al.: Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Blood 100 (2): 627-34, 2002. [PUBMED Abstract]
• Casanova ML, Blázquez C, Martínez-Palacio J, et al.: Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest 111 (1): 43-50, 2003. [PUBMED Abstract]
• Blázquez C, González-Feria L, Alvarez L, et al.: Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Cancer Res 64 (16): 5617-23, 2004. [PUBMED Abstract]
• Guzmán M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003. [PUBMED Abstract]
• Blázquez C, Casanova ML, Planas A, et al.: Inhibition of tumor angiogenesis by cannabinoids. FASEB J 17 (3): 529-31, 2003. [PUBMED Abstract]
• Vaccani A, Massi P, Colombo A, et al.: Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism. Br J Pharmacol 144 ( 8) : 1032-6, 2005. [PUBMED Abstract]
• Ramer R, Bublitz K, Freimuth N, et al.: Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1. FASEB J 26 (4): 1535-48, 2012. [PUBMED Abstract]
• Velasco G, Sánchez C, Guzmán M: Towards the use of cannabinoids as antitumour agents. Nat Rev Cancer 12 (6): 436-44, 2012. [PUBMED Abstract]
• Cridge BJ, Rosengren RJ: Critical appraisal of the potential use of cannabinoids in cancer management. Cancer Manag Res 5: 301-13, 2013. [PUBMED Abstract]
• Vara D, Salazar M, Olea-Herrero N, et al.: Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy. Cell Death Differ 18 (7): 1099-111, 2011. [PUBMED Abstract]
• Preet A, Qamri Z, Nasser MW, et al.: Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis. Cancer Prev Res (Phila) 4 (1): 65-75, 2011. [PUBMED Abstract]
• Nasser MW, Qamri Z, Deol YS, et al.: Crosstalk between chemokine receptor CXCR4 and cannabinoid receptor CB2 in modulating breast cancer growth and invasion. PLoS One 6 (9): e23901, 2011. [PUBMED Abstract]
• Shrivastava A, Kuzontkoski PM, Groopman JE, et al.: Cannabidiol induces programmed cell death in breast cancer cells by coordinating the cross-talk between apoptosis and autophagy. Mol Cancer Ther 10 (7): 1161-72, 2011. [PUBMED Abstract]
• Caffarel MM, Andradas C, Mira E, et al.: Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition. Mol Cancer 9: 196, 2010. [PUBMED Abstract]
• McAllister SD, Murase R, Christian RT, et al.: Pathways mediating the effects of cannabidiol on the reduction of breast cancer cell proliferation, invasion, and metastasis. Breast Cancer Res Treat 129 (1): 37-47, 2011. [PUBMED Abstract]
• Aviello G, Romano B, Borrelli F, et al.: Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer. J Mol Med (Berl) 90 ( 8) : 925-34, 2012. [PUBMED Abstract]
• Romano B, Borrelli F, Pagano E, et al.: Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol. Phytomedicine 21 (5): 631-9, 2014. [PUBMED Abstract]
• Preet A, Ganju RK, Groopman JE: Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 27 (3): 339-46, 2008. [PUBMED Abstract]
• Zhu LX, Sharma S, Stolina M, et al.: Delta-9-tetrahydrocannabinol inhibits antitumor immunity by a CB2 receptor-mediated, cytokine-dependent pathway. J Immunol 165 (1): 373-80, 2000. [PUBMED Abstract]
• McKallip RJ, Nagarkatti M, Nagarkatti PS: Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response. J Immunol 174 (6): 3281-9, 2005. [PUBMED Abstract]
• Massa F, Marsicano G, Hermann H, et al.: The endogenous cannabinoid system protects against colonic inflammation. J Clin Invest 113 ( 8) : 1202-9, 2004. [PUBMED Abstract]
• Patsos HA, Hicks DJ, Greenhough A, et al.: Cannabinoids and cancer: potential for colorectal cancer therapy. Biochem Soc Trans 33 (Pt 4): 712-4, 2005. [PUBMED Abstract]
• Liu WM, Fowler DW, Dalgleish AG: Cannabis-derived substances in cancer therapy--an emerging anti-inflammatory role for the cannabinoids. Curr Clin Pharmacol 5 (4): 281-7, 2010. [PUBMED Abstract]
• Malfitano AM, Ciaglia E, Gangemi G, et al.: Update on the endocannabinoid system as an anticancer target. Expert Opin Ther Targets 15 (3): 297-308, 2011. [PUBMED Abstract]
• Sarfaraz S, Adhami VM, Syed DN, et al.: Cannabinoids for cancer treatment: progress and promise. Cancer Res 68 (2): 339-42, 2008. [PUBMED Abstract]
• Nabissi M, Morelli MB, Santoni M, et al.: Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents. Carcinogenesis 34 (1): 48-57, 2013. [PUBMED Abstract]
• Torres S, Lorente M, Rodríguez-Fornés F, et al.: A combined preclinical therapy of cannabinoids and temozolomide against glioma. Mol Cancer Ther 10 (1): 90-103, 2011. [PUBMED Abstract]
• Mechoulam R, Berry EM, Avraham Y, et al.: Endocannabinoids, feeding and suckling--from our perspective. Int J Obes (Lond) 30 (Suppl 1): S24-8, 2006. [PUBMED Abstract]
• Fride E, Bregman T, Kirkham TC: Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood. Exp Biol Med (Maywood) 230 (4): 225-34, 2005. [PUBMED Abstract]
• Walker JM, Hohmann AG, Martin WJ, et al.: The neurobiology of cannabinoid analgesia. Life Sci 65 (6-7): 665-73, 1999. [PUBMED Abstract]
• Meng ID, Manning BH, Martin WJ, et al.: An analgesia circuit activated by cannabinoids. Nature 395 (6700): 381-3, 1998. [PUBMED Abstract]
• Walker JM, Huang SM, Strangman NM, et al.: Pain modulation by release of the endogenous cannabinoid anandamide. Proc Natl Acad Sci U S A 96 (21): 12198-203, 1999. [PUBMED Abstract]
• Facci L, Dal Toso R, Romanello S, et al.: Mast cells express a peripheral cannabinoid receptor with differential sensitivity to anandamide and palmitoylethanolamide. Proc Natl Acad Sci U S A 92 ( 8) : 3376-80, 1995. [PUBMED Abstract]
• Ibrahim MM, Porreca F, Lai J, et al.: CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids. Proc Natl Acad Sci U S A 102 ( 8) : 3093-8, 2005. [PUBMED Abstract]
• Richardson JD, Kilo S, Hargreaves KM: Cannabinoids reduce hyperalgesia and inflammation via interaction with peripheral CB1 receptors. Pain 75 (1): 111-9, 1998. [PUBMED Abstract]
• Khasabova IA, Gielissen J, Chandiramani A, et al.: CB1 and CB2 receptor agonists promote analgesia through synergy in a murine model of tumor pain. Behav Pharmacol 22 (5-6): 607-16, 2011. [PUBMED Abstract]

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• Updated: December 17, 2014

Retrieved from:  http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4 on April 13th 2015.

Once again research is published AGAINST the DEA's LIES that Marijuana has no medically approved use ... let us see if the DEA makes them change the wording of these articles once again ...

Yes, overwhelming PRELIMINARY Research has shown a noticeable increase in cancer survival rates with THC Use! (And do ANY of you know a regular pot smoker who died of cancer? Traffic accidents got most of the ones I knew ... in their OLD Age!!!!)

Pot is the ONLY recreational substance I know of that can ENHANCE your health ... instead of tearing it down!

[Sea Mac]

 

[Sea Mac]

Received by Email April 8th, 2011:

Americans for Safe Access
Monthly Activist Newsletter
April 2011    Volume 6, Issue 4

Federal Agency Recognizes Cannabis Fights Cancer
Touts Anti-Tumor Action Then Scrubs Website

It lasted less than a week, but an agency of the U.S. federal government for the first time acknowledged that cannabis can fight cancer, and said that health care providers may recommend it for that purpose. That contradicts the federal government's oft-repeated contention that cannabis has no medical value. After five days of media attention, the suggestion that cannabis may be used to combat tumors was removed.

The controversy began on March 17, when the National Cancer Institute (NCI) posted on their website a new "Physicians Data Query", or PDQ, entitled "Cannabis and Cannabinoids.". That PDQ classifies cannabis as a Complementary Alternative Medicine (CAM) and summarizes several decades of research on the potential role of cannabis and its constituent chemicals in cancer treatment, including the many studies in laboratories and animals that have demonstrated its tumor-fighting properties.

The NCI concluded that "the health care provider may recommend medicinal Cannabis not only for symptom management but also for its possible direct antitumor effect." Those antitumor effects of cannabinoids include reducing the spread of cancer cells, selectively cutting off the blood supply to tumors, and reprogramming malignant cells to die off. Researchers have demonstrated these effects both in animal models of cancers and in laboratory studies of human cancer lines, including skin, breast, bone, liver, adrenal, leukemic, and brain cancers.

Within a week, the NCI website was revised to say: "Though no relevant surveys of practice patterns exist, it appears that physicians caring for cancer patients who prescribe medicinal Cannabis predominantly do so for symptom management.".  A week later, the NCI created a new section to distance the statements from federal policy and defend the changes as clarifications.

"Manipulating science for political purposes is offensive in every context, as the Obama Administration's memo on scientific integrity makes clear," said ASA Executive Director Steph Sherer. "But patients deserve complete and accurate information from their doctors, and removing research conclusions because they don't fit an outdated policy is outrageous.

The PDQ still notes that "cannabis has been used for medicinal purposes for thousands of years", and says people living with cancer may find cannabis effective for combating nausea, stimulating appetite, relieving pain, and improving sleep. These are the same therapeutic qualities described in the Institute of Medicine's 1996 review of cannabis as medicine.

The NCI is a division of the National Institutes of Health (NIH) which is part of the Department of Health and Human Services (DHHS). DHHS calls marijuana a dangerous drug with no medical value and has to date denied attempts to reclassify it as a medicine. A petition to reschedule cannabis to make it a drug doctors may prescribe has been pending for nearly a decade with no response from the federal government.

Since that petition was filed by the Coalition for Rescheduling Cannabis, of which ASA is part, hundreds of additional scientific articles on the therapeutic potential of cannabis have been published, eight states more have passed medical cannabis laws, and the country's two largest physician groups have each called for a federal review.

Federal refusal to acknowledge the scientific consensus on the medical efficacy of cannabis is longstanding. In 1988, the Drug Enforcement Administration ignored the findings of its own Chief Administrative Law Judge, Francis L. Young, who found after extensive hearings that "marijuana has been accepted as capable of relieving the distress of great numbers of very ill people, and doing so with safety under medical supervision."

[elyusium]

The NCI are a bunch of cowards at best or are grossly distorting Science at worst considering why they exist to begin with. Even backed by solid science they tow the line of the DEA. This new research is of course excellent for the "cause" as it were. Though I can't link direct in this post there is another piece of very good news in today's release of NORML's newsletter.
peace
 

Bethesda, MD: The website of the National Cancer Institute (NCI), a component of the United States National Institutes of Health (NIH), has acknowledged the cancer-fighting properties of marijuana's active components, but stopped short of recognizing that oncologists may recommend cannabis as an anti-proliferative treatment therapy.

The agency last week added a new section to its cancer.gov website to address the issue of marijuana and cancer. The section, entitled 'Cannabis and Cannabinoids (PDQ),' provides "an overview of the use of cannabis and its components as a treatment for people with cancer-related symptoms caused by the disease itself or its treatment."

The website states that preclinical trials have shown that marijuana's active compounds may selectively target and inhibit cancer cell growth. "Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis," the site reads. "Cannabinoids appear to kill tumor cells but do not affect their non-transformed counterparts and may even protect them from cell death."

The site further states: "The potential benefits of medicinal Cannabis for people living with cancer include antiemetic effects, appetite stimulation, pain relief, and improved sleep."

However, previous language included in this section of the website stating, "In the practice of integrative oncology, the health care provider may recommend medicinal Cannabis not only for symptom management but also for its possible direct antitumor effect" was removed by site administrators on Monday, March 28.

That portion of the website has been modified to now read, "Though no relevant surveys of practice patterns exist, it appears that physicians caring for cancer patients who prescribe medicinal Cannabis predominantly do so for symptom management."

New language added to the page further states, "The U.S. Food and Drug Administration (FDA) has not approved the use of Cannabis as a treatment for any medical condition."

The NCI amended its language after several media outlets reported that their initial assessment "could have an impact on the classification of marijuana as a schedule I drug." Under federal law, cannabis is defined as a schedule I controlled substance with no recognized medical utility.

In a prepared statement, the NCI stated that its online material should not be viewed as "treatment recommendations and are not representative of any federal policy." The agency added, "In light of the attention garnered by the PDQ summary statement on 'Cannabis and Cannabinoids,' reviewers ... reexamined the recently posted statement and decided to change the wording, in order to clarify the meaning that the Board originally intended to convey and to correct several possible misinterpretations."

For several decades, preclinical studies have documented the anti-cancer activity of cannabinoids and endocannabinoids in various types of cancerous cells, including breast carcinoma, prostate cancer, colorectal carcinoma, skin carcinoma, lung carcinoma, oral cancer, and lymphoma.

United State's researchers initially documented the anti-tumor effects of cannabinoids in a 1975 study published in the Journal of the National Cancer Institute.

For more information, please contact Allen St. Pierre, NORML Executive Director, at (202) 483-5500 or Paul Armentano, NORML Deputy Director, at: paul@norml.org. NORML's literature review of cannabis' anti-cancer properties is available online at: http://www.norml.org//index.cfm?Group_ID=7002.