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Well I make 20k a year...just starting investing in January since it was the first time I had free capital in my life.
My assets were around 5k this time last year and now nearing 20k. I know how to save money, every penny counts.
You claimed to have sold 200k shares at .11 just missed out on 2k. Damn I'd be pissed too!
Bitter you sold just before the run? Thats was the plan, get all the weak hands and disbelievers out before $CBIS breaks free. This money is for those that think cannabis will help people, not those that just want money! You will chase now, have
Fun!
$CBIS long and strong!
How are those .08s coming?
You wont regret it! CBIS is changing the world! Keep some shares long to support this awesome company.
If they dilute they do. But that is not what I meant. Longs support the share price and thus bring recognition to the company. Without us to support the price at these high levels traders would be sending it way down. Then when the company needs to dilute it is worth less and causes a further drop in pps.
Love for humanity is what this stock is all about. Greed takes it down, but love>greed and nobody can stop the truth forever.
Like a virus the thought of cannabis medicines has invades the public mind. Mostly dormant only subtle symptoms are showing. Only those in the know can see the infection. Soon it will break out into the general populace. However this thought virus will bring a new age of health to the earth.
Yes the volatility wears me down too, but we can use it to out advantage for gaining a larger long position. I haven't sold a single share yet! I could have sold at 24 and tripled by shares, but hindsight...
I will try to take some profits on the next run around .24-.42. Then it will consolidate to high teens IMO. The 200 week ma will be support in a few months, just watch!
4-6 months from now we will be heading to FDA just as the weekly golden cross is forming. Just after the elections perhaps..
Kane knows exactly how to do it everyone.
$CBIS in it to win it!
Congrats to all who held!
Everyone who sold, chase your hearts out!
$CBIS
What did I tell you? Stay strong my friend, we are part of what will become the greatest medical revolution since pharmecuticals. Longs are brining a new era of health and wellbeing to patients!
Flippers! Take heed! If you have made significant profits off this company, give back with a long term investment. You are helping to change the world, and could make huge money to boot!
Stay strong
$CBIS forever!
Can you say clinical trials?
It needed to consolidate down a bit more after the run to .17. Look after the run to .24 it dipped down one day to .08, then went back up and then back down to .08. Similarity this hit the .11s after the run to .17 and then went to .14s and now back to .11s to finish the consolidation. Give it a few days, Friday will be a huge green day, if you get my drift ;)
It is bouncing off he 50MA here. Sell if it breaks that perhaps, but it wont go much lower, maybe the 84. It is already oversold, will rally soon.
You have some good short term technical analysis. But I think you are still missing out on important fundamentals that will drive this higher in the long term. Also, investor hype should not be discounted, look at the APS plays.
Yes, bounced off the 50ma again. Should putter around here a while until the next big announcement.
Are we talking about the 100 share trade at 5c? Big $5 trade. Yes it happened, but out of sequence, the price never went below 8 for any sizable trading.
I added at .17 and .15. Don't sweat it. Still in the big green because most is from .03/.04, but Yeah It sucks.
Might drop down tomorrow and bounce off the MA (50) at 10.5 tomorrow. I don't see it going much lower than that. I suspect a big PR this week about product launch or something else which will have a strong effect on PPS.
This stock is still quite bullish on the long term, just have some patience and you will be rewarded.
Kill cancer cells by apoptosis. If you don't understand biology, then don't ask me to explain it. Do your own DD.
Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors
Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors
Nonmelanoma skin cancer is one of the most common malignancies in humans. Different therapeutic strategies for the treatment of these tumors are currently being investigated. Given the growth-inhibiting effects of cannabinoids on gliomas and the wide tissue distribution of the two subtypes of cannabinoid receptors (CB1 and CB2), we studied the potential utility of these compounds in anti–skin tumor therapy. Here we show that the CB1 and the CB2 receptor are expressed in normal skin and skin tumors of mice and humans. In cell culture experiments pharmacological activation of cannabinoid receptors induced the apoptotic death of tumorigenic epidermal cells, whereas the viability of nontransformed epidermal cells remained unaffected. Local administration of the mixed CB1/CB2 agonist WIN-55,212-2 or the selective CB2 agonist JWH-133 induced a considerable growth inhibition of malignant tumors generated by inoculation of epidermal tumor cells into nude mice. Cannabinoid-treated tumors showed an increased number of apoptotic cells. This was accompanied by impairment of tumor vascularization, as determined by altered blood vessel morphology and decreased expression of proangiogenic factors (VEGF, placental growth factor, and angiopoietin 2). Abrogation of EGF-R function was also observed in cannabinoid-treated tumors. These results support a new therapeutic approach for the treatment of skin tumors.
Part of discussion:
Nonmelanoma skin cancer is one of the most common malignancies in humans. Different types of strategies are currently being investigated as therapies for the treatment of these tumors, including cryotherapy, topical chemotherapeutic agents such as 5-fluorouracil, and photodynamics, the success of which is hampered by limitations such as the poor penetration of molecules into the skin and the difficulty of gaining access to the whole tumor (10–12). The present data indicate that local cannabinoid administration may constitute an alternative therapeutic approach for the treatment of nonmelanoma skin cancer. Of further therapeutic interest, we show that skin cells express functional CB2 receptors. The synergy between CB1 and CB2 receptors in eliciting skin tumor cell apoptosis reported here is nonetheless intriguing because it is not observed in the case of cannabinoid-induced glioma cell apoptosis (21, 22). In any event, the present report, together with the implication of CB2- or CB2-like receptors in the control of peripheral pain (40–42) and inflammation (41), opens the attractive possibility of finding cannabinoid-based therapeutic strategies for diseases of the skin and other tissues devoid of nondesired CB1-mediated psychotropic side effects.
A Population-Based Case-Control Study of Marijuana Use and Head and Neck Squamous Cell Carcinoma
A Population-Based Case-Control Study of Marijuana Use and Head and Neck Squamous Cell Carcinoma
annabinoids, constituents of marijuana smoke, have been recognized to have potential antitumor properties. However, the epidemiologic evidence addressing the relationship between marijuana use and the induction of head and neck squamous cell carcinoma (HNSCC) is inconsistent and conflicting.
Cases (n = 434) were patients with incident HNSCC disease from nine medical facilities in the Greater Boston, MA area between December 1999 and December 2003. Controls (n = 547) were frequency matched to cases on age (±3 years), gender, and town of residence, randomly selected from Massachusetts town books. A questionnaire was adopted to collect information on lifetime marijuana use (decade-specific exposures) and associations evaluated using unconditional logistic regression.
After adjusting for potential confounders (including smoking and alcohol drinking), 10 to 20 years of marijuana use was associated with a significantly reduced risk of HNSCC [odds ratio (OR)10-<20 years versus never users, 0.38; 95% confidence interval (CI), 0.22-0.67]. Among marijuana users moderate weekly use was associated with reduced risk (OR0.5-<1.5 times versus <0.5 time, 0.52; 95% CI, 0.32-0.85). The magnitude of reduced risk was more pronounced for those who started use at an older age (OR15-<20 years versus never users, 0.53; 95% CI, 0.30-0.95; OR=20 years versus never users, 0.39; 95% CI, 0.17-0.90; Ptrend < 0.001). These inverse associations did not depend on human papillomavirus 16 antibody status. However, for the subjects who have the same level of smoking or alcohol drinking, we observed attenuated risk of HNSCC among those who use marijuana compared with those who do not.
Our study suggests that moderate marijuana use is associated with reduced risk of HNSCC.
See you guys are looking at this the wrong way. It takes very little equipment to make cannabis extracts, that is the beauty of it. It is extremely easy for the company to mass produce it at low cost.
The high tech equipment used by other companies just contributes to their costs. They aren't doing any synthesis like other companies need to.
This is the beauty of cannabis medicines, need very little things to produce them.
All the high tech equipment and chemicals used in other pharmas just contribute to the destruction of the earth.
Cannabis heals the earth and people together, without the need for expensive technology or pollution in its creation.
The run from 3 started when they released a huge PR about the New COO. It bounced off 50 MA the day before, but on that day was in a strong downtrend until that PR sent it running.
How would your technical analysis have seen that coming?
They have real products and a real future to help people.
$npk has $1000 in assets and a $1000000000 market cap. That is a scam, CBIS is the real deal.
Where do you want to make money? Scamming other investors or helping heal sick people?
Seriously, learn to read...
70 million in operating loss!
Quote from 10-K:
As of December 31, 2011 we had a working capital deficit of $2,285,621.
2 million is debt, the 70 million is how much they have spent to far to build the company.
It was a hypothetical question to place your moral compass, not something based in reality...
The health of our species is more important than my personal money.
“It is health that is real wealth and not pieces of gold and silver.”
-Gandhi
The system of greed and corruption you support through your lifestyle is causing cancer, YES.
If you are not part of the solution, you are part of the problem..
So you would rather have $1 million than have cancer cured?
Who cares if millions of people are dying terrible deaths and suffering needlessly I have MONEY!
Karma will repay you one day.
He announced they would be giving away the products at the conference April 26-28. The launch will coincide with that or happen before IMO.
Seeing cannabis medicines get the recognition and use they deserve is more important to me than the money I invested in this company.
Would you rather have $1 million dollars, or have cancer cured for humanity?
There are two groups of people on this board, those who think their investment will help humanity while making them money.
And those that just want to trade to make money and could care less who is suffering with disease which could be treated so easily. Which are you?
These were hash oil extracts I believe. It will take time for the information to spread. They cannot put those products on the shelves and say they cure cancer. This is why they are doing all the documentary stuff and the OTC products. Need recognition for what their products can do before people will start buying them.
The last PR which stated that they have been getting a lot of requests for showing the movie and the treatments is a very good sign. They know that they need to use social media to their advantage and they will.
They are trying to get these products approved so they can actually help patients. Sure they want to make money, but they want to make money by actually curing disease and not treating the symptoms.
The OTC products haven't been launched yet, so of course they haven't made any revenues off the
Last quarter. I suspect the launch
Soon so it will take a while to see how they affect the revenues.
Where do you see the bottom, and will it rebound higher or do you see this as the end?
Delta 9-tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells.
Delta 9-tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells.
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.
Cannabis-derived substances in cancer therapy--an emerging anti-inflammatory role for the cannabinoids.
Cannabis-derived substances in cancer therapy--an emerging anti-inflammatory role for the cannabinoids.
Cannabinoids, the active components of the cannabis plant, have some clinical merit both as an anti-emetic and appetite stimulant in cachexic patients. Recently, interest in developing cannabinoids as therapies has increased following reports that they possess anti-tumour properties. Research into cannabinoids as anti-cancer agents is in its infancy, and has mainly focussed on the pro-apoptotic effects of this class of agent. Impressive anti-cancer activities have been reported; actions that are mediated in large part by disruptions to ubiquitous signalling pathways such as ERK and PI3-K. However, recent developments have highlighted a putative role for cannabinoids as anti-inflammatory agents. Chronic inflammation has been associated with neoplasia for sometime, and as a consequence, reducing inflammation as a way of impacting cancer presents a new role for these compounds. This article reviews the ever-changing relationship between cannabinoids and cancer, and updates our understanding of this class of agent. Furthermore, the relationship between chronic inflammation and cancer, and how cannabinoids can impact this relationship will be described.
The endocannabinoid system and cancer: therapeutic implication.
The endocannabinoid system is implicated in a variety of physiological and pathological conditions (inflammation, immunomodulation, analgesia, cancer and others). The main active ingredient of cannabis, ?(9) -tetrahydrocannabinol (?(9) -THC), produces its effects through activation of CB(1) and CB(2) receptors. CB(1) receptors are expressed at high levels in the central nervous system (CNS), whereas CB(2) receptors are concentrated predominantly, although not exclusively, in cells of the immune system. Endocannabinoids are endogenous lipid-signalling molecules that are generated in the cell membrane from phospholipid precursors. The two best characterized endocannabinoids identified to date are anandamide (AEA) and 2-arachidonoylglycerol (2-AG). Here we review the relationship between the endocannabinoid system and anti-tumour actions (inhibition of cell proliferation and migration, induction of apoptosis, reduction of tumour growth) of the cannabinoids in different types of cancer. This review will focus on examining how activation of the endocannabinoid system impacts breast, prostate and bone cancers in both in vitro and in vivo systems. The therapeutic potential of cannabinoids for cancer, as identified in clinical trials, is also discussed. Identification of safe and effective treatments to manage and improve cancer therapy is critical to improve quality of life and reduce unnecessary suffering in cancer patients. In this regard, cannabis-like compounds offer therapeutic potential for the treatment of breast, prostate and bone cancer in patients. Further basic research on anti-cancer properties of cannabinoids as well as clinical trials of cannabinoid therapeutic efficacy in breast, prostate and bone cancer is therefore warranted.
Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy.
Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy.
Hepatocellular carcinoma (HCC) is the third cause of cancer-related death worldwide. When these tumors are in advanced stages, few therapeutic options are available. Therefore, it is essential to search for new treatments to fight this disease. In this study, we investigated the effects of cannabinoids--a novel family of potential anticancer agents--on the growth of HCC. We found that ?(9)-tetrahydrocannabinol (?(9)-THC, the main active component of Cannabis sativa) and JWH-015 (a cannabinoid receptor 2 (CB(2)) cannabinoid receptor-selective agonist) reduced the viability of the human HCC cell lines HepG2 (human hepatocellular liver carcinoma cell line) and HuH-7 (hepatocellular carcinoma cells), an effect that relied on the stimulation of CB(2) receptor. We also found that ?(9)-THC- and JWH-015-induced autophagy relies on tribbles homolog 3 (TRB3) upregulation, and subsequent inhibition of the serine-threonine kinase Akt/mammalian target of rapamycin C1 axis and adenosine monophosphate-activated kinase (AMPK) stimulation. Pharmacological and genetic inhibition of AMPK upstream kinases supported that calmodulin-activated kinase kinase ß was responsible for cannabinoid-induced AMPK activation and autophagy. In vivo studies revealed that ?(9)-THC and JWH-015 reduced the growth of HCC subcutaneous xenografts, an effect that was not evident when autophagy was genetically of pharmacologically inhibited in those tumors. Moreover, cannabinoids were also able to inhibit tumor growth and ascites in an orthotopic model of HCC xenograft. Our findings may contribute to the design of new therapeutic strategies for the management of HCC.
Cannabidiol induces programmed cell death in breast cancer cells by coordinating the cross-talk between apoptosis and autophagy.
Cannabidiol induces programmed cell death in breast cancer cells by coordinating the cross-talk between apoptosis and autophagy.
Cannabidiol (CBD), a major nonpsychoactive constituent of cannabis, is considered an antineoplastic agent on the basis of its in vitro and in vivo activity against tumor cells. However, the exact molecular mechanism through which CBD mediates this activity is yet to be elucidated. Here, we have shown CBD-induced cell death of breast cancer cells, independent of cannabinoid and vallinoid receptor activation. Electron microscopy revealed morphologies consistent with the coexistence of autophagy and apoptosis. Western blot analysis confirmed these findings. We showed that CBD induces endoplasmic reticulum stress and, subsequently, inhibits AKT and mTOR signaling as shown by decreased levels of phosphorylated mTOR and 4EBP1, and cyclin D1. Analyzing further the cross-talk between the autophagic and apoptotic signaling pathways, we found that beclin1 plays a central role in the induction of CBD-mediated apoptosis in MDA-MB-231 breast cancer cells. Although CBD enhances the interaction between beclin1 and Vps34, it inhibits the association between beclin1 and Bcl-2. In addition, we showed that CBD reduces mitochondrial membrane potential, triggers the translocation of BID to the mitochondria, the release of cytochrome c to the cytosol, and, ultimately, the activation of the intrinsic apoptotic pathway in breast cancer cells. CBD increased the generation of reactive oxygen species (ROS), and ROS inhibition blocked the induction of apoptosis and autophagy. Our study revealed an intricate interplay between apoptosis and autophagy in CBD-treated breast cancer cells and highlighted the value of continued investigation into the potential use of CBD as an antineoplastic agent.
Israeli researchers say more doctors should recommend marijuana to cancer patients
Israeli researchers say more doctors should recommend marijuana to cancer patients
You know what cancer patients need to heal?
They need to eat, sleep and feel better.
What drug would you choose?
I gave the presentation in a first year biology class. The topic was biology and ethics. My presentation was about how cannabis can cure cancer and the ethical implications of police, media, and pharmaceutical companies from keeping this information and treatment from people. That's why nothing has changed since then, because these powerful interests make too much from treating cancer. Curing cancer would decrease business, they don't want that.
You are so distrusting of CBIS but believe the government and big pharma are on your side? Who's really drinking the Kool aid here?