Melizzard

OK, so I've read all these wonderful studies about how many healing properties cannabinoids have and what promise they have in slowing cancer, etc. Well, I've been using MMJ for Stage IV breast cancer because I have no appetite. Without it, I don't eat. But then I uncovered these studies ... anyone have an opinion on this? What a catch 22 ... if I smoke/vape to eat, it grows cancer, but if I don't ... I starve ... WTH?

{Delta}-9-Tetrahydrocannabinol Enhances Breast Cancer Growth and Metastasis by Suppression of the Antitumor Immune Response -- McKallip et al. 174 (6): 3281 -- The Journal of Immunology
The Journal of Immunology, 2005, 174: 3281-3289.
Copyright © 2005 by The American Association of Immunologists
{Delta}-9-Tetrahydrocannabinol Enhances Breast Cancer Growth and Metastasis by Suppression of the Antitumor Immune Response1
Robert J. McKallip2,*, Mitzi Nagarkatti* and Prakash S. Nagarkatti{dagger}

Departments of * Microbiology and Immunology, and {dagger} Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA 23298

In the current study, we tested the central hypothesis that exposure to {Delta}-9-tetrahydrocannabinol ({Delta}9-THC), the major psychoactive component in marijuana, can lead to enhanced growth of tumors that express low to undetectable levels of cannabinoid receptors by specifically suppressing the antitumor immune response. We demonstrated that the human breast cancer cell lines MCF-7 and MDA-MB-231 and the mouse mammary carcinoma 4T1 express low to undetectable levels of cannabinoid receptors, CB1 and CB2, and that these cells are resistant to {Delta}9-THC-induced cytotoxicity. Furthermore, exposure of mice to {Delta}9-THC led to significantly elevated 4T1 tumor growth and metastasis due to inhibition of the specific antitumor immune response in vivo. The suppression of the antitumor immune response was mediated primarily through CB2 as opposed to CB1. Furthermore, exposure to {Delta}9-THC led to increased production of IL-4 and IL-10, suggesting that {Delta}9-THC exposure may specifically suppress the cell-mediated Th1 response by enhancing Th2-associated cytokines. This possibility was further supported by microarray data demonstrating the up-regulation of a number of Th2-related genes and the down-regulation of a number of Th1-related genes following exposure to {Delta}9-THC. Finally, injection of anti-IL-4 and anti-IL-10 mAbs led to a partial reversal of the {Delta}9-THC-induced suppression of the immune response to 4T1. Such findings suggest that marijuana exposure either recreationally or medicinally may increase the susceptibility to and/or incidence of breast cancer as well as other cancers that do not express cannabinoid receptors and are resistant to {Delta}9-THC-induced apoptosis.

Delta(9)-Tetrahydrocannabinol enhances MCF-7 cell ...[Toxicology. 2008] - PubMed Result
Delta(9)-Tetrahydrocannabinol enhances MCF-7 cell proliferation via cannabinoid receptor-independent signaling.
Takeda S, Yamaori S, Motoya E, Matsunaga T, Kimura T, Yamamoto I, Watanabe K.

Organization for Frontier Research in Preventive Pharmaceutical Sciences, Hokuriku University, Ho-3 Kanagawa-machi, Kanazawa 920-1181, Japan.

We recently reported that Delta(9)-tetrahydrocannabinol (Delta(9)-THC) has the ability to stimulate the proliferation of human breast carcinoma MCF-7 cells. However, the mechanism of action remains to be clarified. The present study focused on the relationship between receptor expression and the effects of Delta(9)-THC on cell proliferation. RT-PCR analysis demonstrated that there was no detectable expression of CB receptors in MCF-7 cells. In accordance with this, no effects of cannabinoid 1/2 (CB1/2) receptor antagonists and pertussis toxin on cell proliferation were observed. Although MCF-7 cell proliferation is suggested to be suppressed by Delta(9)-THC in the presence of CB receptors, it was revealed that Delta(9)-THC could exert upregulation of living cells in the absence of the receptors. Interestingly, Delta(9)-THC upregulated human epithelial growth factor receptor type 2 (HER2) expression, which is known to be a predictive factor of human breast cancer and is able to stimulate cancer cells as well as MCF-7 cells. Actinomycin D-treatment interfered with the upregulation of HER2 and cell proliferation by cannabinoid. Taken together, these studies suggest that, in the absence of CB receptors, Delta(9)-THC can stimulate the proliferation of MCF-7 cells by modulating, at least in part, HER2 transcription.

PMID: 18249480 [PubMed - indexed for MEDLINE

http://www.ncbi.nlm.nih.gov/pubmed/19428940?ordinalpos=1&itool=EntrezSystem2.PEntrez. Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.P ubmed_Discovery_RA&linkpos=1&log$=relatedarticles& logdbfrom=pubmed
Modulation of Delta9-tetrahydrocannabinol-induced MCF-7 breast cancer cell growth by cyclooxygenase and aromatase.
Takeda S, Yamamoto I, Watanabe K.

Organization for Frontier Research in Preventive Pharmaceutical Sciences, Hokuriku University, Ho-3 Kanagawa-machi, Kanazawa 920-1181, Japan.

Delta(9)-Tetrahydrocannabinol (Delta(9)-THC), a major constituent of marijuana, has been shown to stimulate the growth of MCF-7 breast cancer cells through cannabinoid receptor-independent signaling [Takeda, S., Yamaori, S., Motoya, E., Matsunaga, T., Kimura, T., Yamamoto, I., Watanabe, K., 2008. Delta(9)-Tetrahydrocannabinol enhances MCF-7 cell proliferation via cannabinoid receptor-independent signaling. Toxicology 245, 141-146]. Although the growth of MCF-7 cells is known to be stimulated by 17beta-estradiol (E(2)), the interaction of Delta(9)-THC and E(2) in MCF-7 cell growth is not fully clarified so far. In the present study, by using E(2)-sensitive MCF-7 cells that have expressed cyclooxygenase-2 (COX-2) and cytochrome P450 19 (aromatase), we studied whether or not COX-2 and aromatase are involved in Delta(9)-THC-mediated MCF-7 cell proliferation. It was shown that Delta(9)-THC-induced MCF-7 cell growth was inhibited by COX-2 inhibitors and was stimulated by arachidonic acid (a COX substrate). However, the growth of MCF-7 cells induced by Delta(9)-THC was not stimulated by PGE(2), and the expression of aromatase was not affected by COX-2 inhibitors, arachidonic acid, and PGE(2), suggesting that there is a disconnection between COX-2 (PGE(2)) and aromatase in Delta(9)-THC-mediated MCF-7 cell proliferation. On the other hand, Delta(9)-THC-induced MCF-7 cell growth was elevated by two kinds of aromatase inhibitors. Taken together with the evidence that Delta(9)-THC-induced MCF-7 cell proliferation was interfered with testosterone (an aromatase substrate) and exogenously provided E(2), it is suggested that (1) the growth stimulatory effects of Delta(9)-THC are mediated by the product(s) of COX-2 except for PGE(2), (2) the action of Delta(9)-THC is modulated by E(2), and (3) COX-2 and aromatase are individually engaged in the proliferation of MCF-7 cells induced by Delta(9)-THC.

Your thoughts???

Melissa

sterbo

Bottom line?
I'd rather use marihuana (as have others for thousands of years) and revel in the many benefits it has brought to my life than suffer through the migraine that I got from reading through and trying to interpret the medical double speak presented in these excerpts from the original studies...


.

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toothfairy420

All that study "proves" is that when you take human breast cancer, and implant it into a mouse, thc causes growth...it's a total Frankenstein theory, and until full human testing is approved by the government, we will have nothing but Frankenstein theories which mean absolutely nothing.

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Melizzard

OK, let me ask you this ... if any of you HAD breast cancer ... especially Stage IV, would you be willing to take that chance? Especially since I've seen the physical manifestation (ascites) of this cancer grow since starting MMJ?

Also, there is a reason they use mice to study for humans ... more than just the fact they can't Frankenstein on us at first.

Melissa

nornerator

I will go through these more thoroughly later.

It is important to note that the government ONLY allows for studies to be done if the intent is to look for negative consequences of using cannabis. The fact that we have so many studies showing positive results is a true testament to the healing power of cannabis.

As far as the first abstract goes I think it is important to mention those cells are mice breast cancer cells, not cultured human breast cancer cells.

Why wouldn't they just use cultured human cells rather than mice cells? Usually mice are used as live test-subjects because using humans would be unethical. However we are only talking about cell cultures here, why not use human cell cultures, which would be much more relavent than using mice cells.


More importantly it has been determined that THC is infact a potent anti-carcinogen that causes a cell to commit apoptosis (cellular suicide) by awakening the mitochondria..
More later..

toothfairy420

by Frankenstein, I am referring to the fact that they are taking a human cancer and implanting it into a mouse...who knows what kinds of cell changes can be caused just by doing that. Yes, if I had stage IV breast cancer, I would be smoking all the weed I could get my hands on, exactly for the reasons that nornerator stated above, there have been many more studies that prove marijuana's cancer killing benefits (dating back to the 1970's) than there have been studies that prove a detriment.

Melizzard

Well, it kind of makes sense to me that, without cannabinoid receptors, it could cause it to grow. It's the cannabinoid receptors that make it effective. I can't stop using it at lunch and dinner or I won't eat. But I was also using THC hemp oil, and I have stopped that until I determine whether or not I have those receptors or not.

xxoo
Melissa

Buzzby

Unless you're a mouse or a petri dish, I wouldn't worry too much. Mouse and in vitro studies tell us very little about how something works in the human body. This is the same kind of "science" that tells us that marijuana causes lung cancer when a study of 60,000 real live human beings tells us that it does not and may suppress lung cancer caused by tobacco.

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Ygdonmir

Yeah I don't think mice have the same form of THC receptor network that humans do. Tons of other studies have said that THC reduces cancer growth in humans because of the amount of receptors in our body. Based on that I'd say you're fine. If you find an unbiased doctor I'd ask him about it I suppose, but mice are different creatures altogether than humans.

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Jared_320

Besides, when was the last time you saw mickey and minnie at the park smoking a spliff