Topic: Devcoin Cancer Treatment Fund (Read 1193 times)

Not in a petri dish. LOOK UP RICK SIMPSON. Cannabis cures tumors and cancers IN HUMANS

Here we go:

Tramèr et al, Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review.  BMJ 2001; 323 doi: http://dx.doi.org/10.1136/bmj.323.7303.16 (Published 7 July 2001)
http://www.bmj.com/content/323/7303/16

Objective: To quantify the antiemetic efficacy and adverse effects of cannabis used for sickness induced by chemotherapy.

Design: Systematic review.

Data sources: Systematic search (Medline, Embase, Cochrane library, bibliographies), any language, to August 2000.

Studies: 30 randomised comparisons of cannabis with placebo or antiemetics from which dichotomous data on efficacy and harm were available (1366 patients). Oral nabilone, oral dronabinol (tetrahydrocannabinol), and intramuscular levonantradol were tested. No cannabis was smoked. Follow up lasted 24 hours.

Results: Cannabinoids were more effective antiemetics than prochlorperazine, metoclopramide, chlorpromazine, thiethylperazine, haloperidol, domperidone, or alizapride: relative risk 1.38 (95% confidence interval 1.18 to 1.62), number needed to treat 6 for complete control of nausea; 1.28 (1.08 to 1.51), NNT 8 for complete control of vomiting. Cannabinoids were not more effective in patients receiving very low or very high emetogenic chemotherapy. In crossover trials, patients preferred cannabinoids for future chemotherapy cycles: 2.39 (2.05 to 2.78), NNT 3. Some potentially beneficial side effects occurred more often with cannabinoids: “high” 10.6 (6.86 to 16.5), NNT 3; sedation or drowsiness 1.66 (1.46 to 1.89), NNT 5; euphoria 12.5 (3.00 to 52.1), NNT 7. Harmful side effects also occurred more often with cannabinoids: dizziness 2.97 (2.31 to 3.83), NNT 3; dysphoria or depression 8.06 (3.38 to 19.2), NNT 8; hallucinations 6.10 (2.41 to 15.4), NNT 17; paranoia 8.58 (6.38 to 11.5), NNT 20; and arterial hypotension 2.23 (1.75 to 2.83), NNT 7. Patients given cannabinoids were more likely to withdraw due to side effects 4.67 (3.07 to 7.09), NNT 11.

Conclusions: In selected patients, the cannabinoids tested in these trials may be useful as mood enhancing adjuvants for controlling chemotherapy related sickness. Potentially serious adverse effects, even when taken short term orally or intramuscularly, are likely to limit their widespread use.

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Jatoi et al. Dronabinol Versus Megestrol Acetate Versus Combination Therapy for Cancer-Associated Anorexia: A North Central Cancer Treatment Group Study. JCO January 15, 2002 vol. 20 no. 2 567-573
http://jco.ascopubs.org/content/20/2/567

PURPOSE: To determine whether dronabinol administered alone or with megestrol acetate was more, less, or equal in efficacy to single-agent megestrol acetate for palliating cancer-associated anorexia.

PATIENTS AND METHODS: Four hundred sixty-nine assessable advanced cancer patients were randomized to (1) oral megestrol acetate 800 mg/d liquid suspension plus placebo, (2) oral dronabinol 2.5 mg twice a day plus placebo, or (3) both agents. Eligible patients acknowledged that loss of appetite or weight was a problem and reported the loss of 5 pounds or more during 2 months and/or a daily intake of less than 20 calories/kg of body weight.

RESULTS: Groups were comparable at baseline in age, sex, tumor type, weight loss, and performance status. A greater percentage of megestrol acetate-treated patients reported appetite improvement and weight gain compared with dronabinol-treated patients: 75% versus 49% (P = .0001) for appetite and 11% versus 3% (P = .02) for ≥ 10% baseline weight gain. Combination treatment resulted in no significant differences in appetite or weight compared with megestrol acetate alone. The Functional Assessment of Anorexia/Cachexia Therapy questionnaire, which emphasizes anorexia-related questions, demonstrated an improvement in quality of life (QOL) among megestrol acetate–treated and combination-treated patients. The single-item Uniscale, a global QOL instrument, found comparable scores. Toxicity was also comparable, with the exception of an increased incidence of impotence among men who received megestrol acetate.

CONCLUSION: In the doses and schedules we studied, megestrol acetate provided superior anorexia palliation among advanced cancer patients compared with dronabinol alone. Combination therapy did not appear to confer additional benefit. 

Of relevance:



Molecular biologist by trade. Heard of the effects of cannabinoids, but as always double blinded RCT evidence is lacking. There had been a few studies looking at the effects against CINV (chemotherapy induced nausea/vomiting) though, have to look them up.

Thought this was relevant :p

Also,

As soon as I get paid for writing on Devtome in June, I will be making an invention that cuts down on 2nd hand smoke
I've already made and tested the prototype

The invention will be open source, and a tutorial of how to make it yourself will be on YouTube.

I think it's good advertising.
You know they have Cannabis rallies in about every state that have HUGE attendance, and same in Canada and the UK.

Plus, if we can document curing people that is good for MJ and DVC on an international level. And it actually makes the "drug user"/"silk road" side of Bitcoin look a little better.

So you're going to grow weed and then say it's sponsored by DevCoin. ._.

Even if it is good for treating cancer, I don't think that's the best advertisement, lol.

Naples, Italy: Compounds in marijuana inhibit cancer cell growth in animals and in culture on a wide range of tumoral cell lines, including human breast carcinoma cells, human prostate carcimona cells, and human colectoral carcinoma cells, according to preclinical trial data published in the May issue of the Journal of Pharmacology and Experimental Therapeutics.

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 invasion and metastasis.[9-12] One review summarizes the molecular mechanisms of action of cannabinoids as antitumor agents.[13] 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.[14]

The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in hepatocellular carcinoma (HCC).[15] 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 [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]

CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[19] In the 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.

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.[20] 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.[21,22]

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

I'd be really interested in reading some of these studies, because I haven't yet seen anything specifically about cannabinoids inhibiting cancer growth.  I know that in some Canadian provinces, marijuana (and/or synthetic cannabinoids) is given to cancer patients, but it's used for other reasons than as an actual treatment for the disease (pain, nausea, etc.).  I'm not disparaging its use or saying that it doesn't work, just that I was previously unaware of it being used in this way.

I wish you the very best of luck in your treatment, man.

Well then you are 100% wrong.

If I meant smoking, I'd have said it myself. Thanks though 

Do you have cancer?

Ok, I could believe maybe SMOKE caused cancer, but not cannabis itself in any way. But that's why you smoke hash, and eat/vape buds

That is TOTALLY wrong. I don't know where you read that, but it's not true at all.

Cannabinoids have been proven to INHIBIT cancer cells. You can't inhibit cancer an cause it at the same time. That's like saying the drunker you get the more sober you are.

Im over 21 and in a neighboring state, when can I come get a free oz?

Fix'd

There are studies for everything. Several actually link cannabis to cancer.

Thanks

nice - good idea

Yes it is.
As proven by people all over the state. Cannabis inhibits cancer cells.