Marijuana a cancer preventer?

[battleweb]

This article describes how the federal governent funded research to link Lung cancer and marijuana to strengthen it's arguement against legalizing marijuana. The doctor performing the research not only found that there is absolutely no connection between lung cancer and marijuana, but he also discovered that marijuana seemed to act as a cancer preventer and European studies showed that if the cannabinoids are present when a cancer cell goes defective, the cell dies every time. To me, this is huge because in my eyes, cancer patients are the most qualified patients for medical cannabis and to find out that it not only treats symptoms of cancer and chemo-therapy, but also may prevent the spread of cancer is huge. Plus if scientists can find a controlled way to cause cancer cells to go defective and then administer cannaboids afterwards they just might find the cure to cancer.

Article:

Recent studies have reached the interesting conclusion that marijuana is a cancer preventer. One was done in California, funded by the government, designed to link marijuana and lung cancer. The government's hope was that if it were proved that marijuana causes lung cancer, then it could argue that we certainly should not legalize it. But the study showed that even after heavy use there was absolutely no connection between marijuana and lung cancer. The doctor conducting the study also concluded that marijuana seemed to act as a cancer preventer.

Other studies done at European universities have reached the conclusion that among many cancer cell lines, if the cannabinoids in marijuana are present when a cell goes defective, the cell dies every time. Simple cancer is a defective cell, not dying as it should, but replicating. A German study published in the Jan. 2 issue of the Journal of the National Cancer Institute said cannabinoids were found to slow the spread of lung and cervical cancer tumors and may also have an anti-cancer effect.

The Drug Enforcement Administration, not too long ago, was reprimanded by its own law judge for continually rejecting the application of a New England professor for the marijuana to do real research. Last I checked he had been waiting six years for an approval, and I think he is still waiting.


So, is it possible that the DEA is culpable in the deaths of cancer patients ever since they first rejected an honest request for marijuana to do research? Are our legislators using the war on drugs to scare the people to get re-elected? Would the government ignore the welfare of its own citizens to continue this wasteful and misguided policy?

Americans need to start demanding the answers to these questions now! The cure for cancer could be in our hands. When do you think the DEA will allow us to find out?

Resource: http://news.enquirer.com/apps/pbcs.d...0314/1090/EDIT

[LarryBuddz]

thanks a lot man. + rep

just used this for my health current event due tomorow

[Moto823]

I wouldn't doubt it one bit.

Weed fixes everything else...cancer too!
If it can be proven to cure cancer, it HAS to be legalized. How could the gov actually deny its useful/safe?

[Mr. Bunglesmith]

I am currently fighting cancer, and marijuana has been very helpfull to me. It's the reason I can actually eat after chemotherapy sessions (once I was out, and I lost 10 pounds in 2-3 days cause I couldn't keep anything down). The fact that it slows/prevents cancer cell growth is just an added benefit for me

[Salvial]

Originally Posted by Mr. Bunglesmith

I am currently fighting cancer, and marijuana has been very helpfull to me. It's the reason I can actually eat after chemotherapy sessions (once I was out, and I lost 10 pounds in 2-3 days cause I couldn't keep anything down). The fact that it slows/prevents cancer cell growth is just an added benefit for me

Right on man, I'm glad you found mj to help you along! When you beat cancer tell everyone how much it helped you.

[Mr. Bunglesmith]

Originally Posted by Salvial

Right on man, I'm glad you found mj to help you along! When you beat cancer tell everyone how much it helped you.

Thanks bro. I sure as hell will.

[dwfblitz]

Steve Kubby (http://en.wikipedia.org/wiki/Steve_Kubby) who's a 2008 libertarian presidential candidate and helped pass prop 215 in California, has had adrenal cancer for decades, and wasn't expected to survive 5 years. He's a cannabis user, and attributes this to his continued survival.

[Talventaivas]

I usually take secondary sources with a grain of salt, but here is an abstract of an article I found which supports the claim. I could not reproduce the entire article here, but for those interested, I have cited the source:

International Journal of Cancer 121(10):2172-80, 2007 Nov 15
121(10):2172-80, 2007 Nov 15

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.

Basically what this means is that in certain cancers (ones which express CB1/2 receptors), THC both blocks signals telling the cancer cells to proliferate (and continue being cancer), and also activates pathways resulting in cell death.

I am a cell biologist, I love this stuff and would love to research it myself...

Be it okay with the community, I'll bring more stuff like this into this thread

[partnooneicular]

Originally Posted by Talventaivas

Be it okay with the community, I'll bring more stuff like this into this thread

Please

[Rhythm of Life]

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. Methods and results. Administration of Delta(9)-THC to glioblastoma multiforme (GBM) cell lines results in a significant decrease in cell viability. Cell cycle analysis showed G(0/1) arrest and did not reveal occurrence of apoptosis in the absence of any sub-G(1) populations. Western blot analyses revealed a THC altered cellular content of proteins that regulate cell progression through the cell cycle. The cell content of E2F1 and Cyclin A, two proteins that promote cell cycle progression, were suppressed in both U251-MG and U87-MG human glioblastoma cell lines, whereas the level of p16(INK4A), a cell cycle inhibitor was upregulated. Transcription of thymidylate synthase (TS) mRNA, which is promoted by E2F1, also declined as evident by QRT-PCR. The decrease in E2F1 levels resulted from proteasome mediated degradation and was prevented by proteasome inhibitors. Conclusions. Delta(9)-THC is shown to significantly affect viability of GBM cells via a mechanism that appears to elicit G(1) arrest due to downregulation of E2F1 and Cyclin A. Hence, it is suggested that Delta(9)-THC and other cannabinoids be implemented in future clinical evaluation as a therapeutic modality for brain tumors.

Department of Laboratory Medicine, Divison of Pathology, F46, Karolinska Institutet and Karolinska University Hospital Huddinge, SE 141 86 Stockholm, Sweden.

Endogenous arachidonic acid metabolites with properties similar to compounds of Cannabis sativa Linnaeus, the so-called endocannabinoids, have effects on various types of cancer. Although endocannabinoids and synthetic cannabinoids may have pro-proliferative effects, predominantly inhibitory effects on tumor growth, angiogenesis, migration and metastasis have been described. Remarkably, these effects may be selective for the cancer cells, while normal cells and tissues are spared. Such apparent tumor cell selectivity makes the endocannabinoid system an attractive potential target for cancer therapy. In this review we discuss various means by which the endocannabinoid system may be targeted in cancer and the current knowledge considering the regulation of the endocannabinoid system in malignancy.

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.

Hebrew University, Pharmacy School, Department of Medicinal Chemistry and Natural Products, Israel. natalya@md.huji.ac.il

Marijuana has been used in medicine for millennia, but it was not until 1964 that delta9-tetrahydrocannabinol (delta9-THC), its major psychoactive component, was isolated in pure form and its structure was elucidated. Shortly thereafter it was synthesized and became readily available. However, it took another decade until the first report on its antineoplastic activity appeared. In 1975, Munson discovered that cannabinoids suppress Lewis lung carcinoma cell growth. The mechanism of this action was shown to be inhibition of DNA synthesis. Antiproliferative action on some other cancer cells was also found. In spite of the promising results from these early studies, further investigations in this area were not reported until a few years ago, when almost simultaneously two groups initiated research on the antiproliferative effects of cannabinoids on cancer cells: Di Marzo's group found that cannabinoids inhibit breast cancer cell proliferation, and Guzman's group found that cannabinoids inhibit the growth of C6 glioma cell. Other groups also started work in this field, and today, a wide array of cancer cell lines that are affected is known, and some mechanisms involved have been elucidated.

__________________________________________________ ______________

Just to name a few.