Archive for the ‘Nutrition and Cancer’ Category

Zebrafish ‘window on cancer’ shows birth of tumour – and body’s response

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Posted 14 Dec 2010 — by James Street
Category antiinflammatory, Educational, Immune System

15 Dec 2010
Scientists using translucent zebrafish as a “window on cancer” have been able to see in real time how tumour cells are born – and immediately attract cells from the immune system.

This inflammatory response seems to both attack and aid the cancer cells and the balance between the two provides a new therapeutic target for cancer researchers. It also links cancer to the wound healing process, which may even lead to anti-inflammatory drugs being used to treat cancer patients.

Dr Adam Hurlstone, of the University of Manchester’s Faculty of Life Sciences, explained: “This is a very exciting finding. It was a huge surprise to us to see the tumour cells detected by the immune system so quickly: a cancer cell appears, gives a signal and the body’s immune system is immediately alerted.

“The speed of the response and being able to see it so clearly in the zebrafish was very exciting.

“In addition we have established other novel aspects: that hydrogen peroxide is the signal molecule given by both wounded and transformed pre-cancerous cells to the immune system and that the carefully choreographed response can both attack and aid cancer cells at their very birth.

“This link between wound healing and cancer gives us new therapeutic targets and potential therapies such as anti-inflammatory drugs that have already undergone clinical trial.”

The study, published in PLoS Biology today (Tuesday 14 December 2010) and funded at the Manchester end by Cancer Research UK, was a collaboration between Dr Hurlstone, and the team of Professor Paul Martin, the University of Bristol, and of Dr Marina Mione, FIRC Institute of Molecular Oncology in Milan.

The team studied the onset of different cancer types, including melanoma, an extremely aggressive form of skin cancer, in zebrafish larvae. Zebrafish have been used to study embryonic development for years but it is only recently that they have become a popular species for modelling disease, and notably cancer. Mutations in their genes result in the same diseases as humans, while their transparency is extremely useful for seeing the disease’s progress.

The team found that the immune system’s leucocytes (white blood cells) home-in on sites containing only very few cancer cells. They also found that they had been attracted to the site by hydrogen peroxide produced by cancer cells and their neighbours, a molecule also used to trigger the immune system when the body is wounded. The leucocytes immediately began to work at the sites – some attacking the cancer cells, others providing stimulants to them.

Dr Hurlstone said: “We have returned to a classical concept that cancer is a wound that will not heal. We are asking, what is the significance of that? Inflammation is supposed to be a good thing – it is painful but specialist cells zoom in and eat the debris and secrete factors to heal a wound. So with inflammation in cancer, is it fighting or helping the disease? The answer is both.

“That has been addressed before but this is the first time it has been seen at the birth of cancer.

“We have now shown how quickly the immune system responds to cancer, what its role is in the progression of the disease and also made clear the parallels between cancer and wound healing (for instance, the common signal molecule hydrogen peroxide).

“This throws up some exciting leads in terms of clinical applications. We should look at inflammation again from a therapeutic perspective. Now we know the role of hydrogen peroxide in recruiting leucocytes to the area, producers and receptors of that molecule could become therapeutic targets. We could even see anti-inflammatory drugs being used for cancer. Another route is to target the immune system’s response in order to tip the balance from the leucocytes that heal to those that attack in cases of cancer.”

He added: “This study and its novel, significant findings was only possible because we used live cell imaging in the almost transparent zebrafish embryos.”
Notes for editors

Video and still images of immune system cells engulfing the area are available, along with copies of the paper ‘Live imaging of innate immune cell sensing of transformed cells in zebrafish larvae: parallels between tumor initiation and wound inflammation’.

For these or an interview with Dr Adam Hurlstone, contact Media Relations Officer Mikaela Sitford on 0161 275 2111, 07768 980942 or

Cancer adjuvant therapy

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Posted 10 Dec 2010 — by James Street
Category Alternative Therapies, Complementary Therapy, Natural Therapies, Nutrition and Cancer, Prevention

Cancer adjuvant therapy

The following compendium drawn (in part) from Beyond Aspirin (Newmark et al. 2000) underscores herbs that inhibit COX-2, an enzyme intricately involved in the cancer process. Natural compounds usually have many mechanisms of action; thus, the protective mechanisms common to the herb often extend beyond enzyme inhibition and are described herein. Because of the synergism of herbs, combinations are often of greater value than a single herb.

Berberine, strong and bitter in taste and found in various herbs, delivers anti-inflammatory properties via COX-2 inhibition (Fukuda et al. 1999). Kaempferol, a constituent of berberine, is a strikingly active inhibitor of COX-2 activity (Chen et al. 1999; Newmark et al. 2000). Berberine is unique, having the ability to inhibit COX-2 activity without involving the beneficial COX-1 enzyme.

The anti-inflammatory traits of feverfew have an ability to inhibit the COX-2 enzyme (Hwang et al. 1996). According to Newmark et al. (2000), feverfew contains a lactone, or chemical compound called parthenolide. Parthenolide, in turn, contains a variant of methylene-gamma-lactone (MGL) that interacts with macrophages. The white blood cell-lactone interaction suppresses a critical protein process, a repression that ultimately inhibits the COX-2 enzyme. In addition, feverfew contains apigenin (a flavonoid) and melatonin, both COX-2 inhibitors (Murch et al. 1997).

From the scores of biologically active components contained in ginger, some are specific for inhibiting COX-2 and others for inhibiting 5-lipoxygenase, enzymes responsible for the formation of pro-inflammatory agents (prostaglandin E2 and leukotriene B4) from AA. Ginger safely modulates COX-2 activity but also brings balance to COX-1 (an enzyme responsible for gastric mucosal integrity) in a manner vastly superior to synthetic NSAIDs (Newmark et al. 2000; Reiter et al. 2001).

Salicylic acid, the main anti-inflammatory component of aspirin, is a naturally occurring compound found in green tea, having COX-2 inhibiting qualities. The polyphenols and flavonoids contained in green tea are also COX-2 inhibitors (Noreen et al. 1998).

Anti-tumor metastatic activity of beta-glucan purified from mutated Saccharomyces cerevisiae (baker’s yeast)

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Posted 28 Nov 2010 — by James Street
Category Alternative Therapies, experimental treatments, General Cancer Research, Nutrition and Cancer

Int Immunopharmacol. 2008 Jan;8(1):36-42. Epub 2007 Oct 30.

Yoon TJ, Kim TJ, Lee H, Shin KS, Yun YP, Moon WK, Kim DW, Lee KH.

Bio-Food and Drug Research Center and Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chungju 380-701, Republic of Korea.

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The beta-glucans isolated from Saccharomyces cerevisiae (S. cerevisiae) enhance the innate immune system, but there is little evidence for its antitumor activity. To examine the antitumor and immunostimulating activities of beta-glucan (IS-2) purified from mutated S. cerevisiae, we made an experiment on innate immune response against metastasis of cancer cells by comparing with the beta-glucan from wild-type S. cerevisiae. In experimental lung metastasis of colon 26-M3.1 carcinoma or B16-BL6 melanoma cells, prophylactic administration of beta-glucan purified from mutated S. cerevisiae significantly inhibited lung metastasis in a dose-dependent manner. Furthermore, therapeutic administration of IS-2 also significantly inhibited the colon 26-M3.1 cell growth in mice. In an assay of liver and spleen metastasis produced by i.v. inoculation of L5178Y-ML25 lymphoma cells, IS-2 also significantly inhibited metastasis in CDF1 mice. Furthermore, pretreatment with IS-2 two days before tumor inoculation significantly prolonged the survival time of tumor-bearing mice. In an in vitro cytotoxicity analysis, IS-2 (up to 100 microg/ml) did not affect the growth of colon 26-M3.1 cells. In contrast, IS-2 enhanced splenocyte proliferating activity in a dose-dependent manner. Peritoneal macrophages stimulated with IS-2 produced various cytokines, such as IL-1beta, IFN-gamma, and IL-12. In addition, treatment with IS-2 (20 microg/mouse) induced tumoricidal activity of peritoneal macrophages against colon 26-M3.1 cells. In an assay for natural killer (NK) cell activity, IS-2 (20 microg/mouse, i.v.) significantly augmented NK cytotoxicity against Yac-1 tumor cells at 2 days after IS-2 treatment. The depletion of NK cells by injection of rabbit anti-asialo GM1 serum abolished the inhibitory effect of IS-2 on lung metastasis of colon 26-M3.1 cells. These data suggest that IS-2 inhibits tumor metastasis via activation of macrophages and NK cells.

PMID: 18068098 [PubMed - indexed for MEDLINE]

Immunostimulatory activities of a low molecular weight antitumoral polysaccharide isolated from Agaricus blazei Murill (LMPAB) mushroom in Sarcoma 180 ascitic tumor-bearing mice

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Posted 28 Nov 2010 — by James Street
Category Alternative Therapies, Natural Therapies, Nutrition and Cancer

Pharmazie. 2009 Jul;64(7):472-6.

Niu YC, Liu JC, Zhao XM, Su FQ, Cui HX.

The Institute of Medicine, Qiqihar Medical College, 249 Heping Road, Fula’erji District, Qiqihar 161042, China.


LMPAB is a linear beta-(1-3)-glucan we isolated from polysaccharide extract of Agaricus blazei Murill (AbM). Effects of LMPAB on splenic natural killer (NK) cell activity, splenocyte proliferation, index of spleen and thymus, IFN-gamma expression in spleen and the concentration of IL-12, IL-18 and TNF-alpha in serum of S180 ascitic tumor-bearing mice were detected. The results showed that intraperitoneal injection of LMPAB (100 mg x kg(-1) x d(-1)) significantly increased the thymus index. LMPAB augmented splenic NK cell activity in a dose-dependent manner (50-200 mg x kg(-1) x d(-1)). The concanavalin A (3 microg/ ml) stimulated splenocyte proliferation was significantly enhanced by LMPAB at dosages of 50, 100 or 200 mg x kg(-1) x d(-1). Further studies showed that LMPAB (50, 100 or 200 mg x kg(-1) x d(-1), 14d) significantly increased the production of IL-12, TNF-alpha, IL-18 and the expression IFN-gamma as determined by ELISA and immunohistochemistry, respectively. These results clearly indicate that the anti-tumor effects of LMPAB are closely associated with up-regulation of activity of NK cells, expression of IFN-gamma in spleen and the systemic level of IL-12, IL-18 and TNF-alpha in tumor-bearing mice.

PMID: 19694186 [PubMed - indexed for MEDLINE]

Battling Breast Cancer a Six Mushroom Blend

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Posted 28 Nov 2010 — by James Street
Category Alternative Therapies, Nutrition and Cancer
Bloomington : IN : USA | Nov 28, 2010

Healthy Mushrooms

Medical Mushrooms Are Being Proven Effective in Breast Cancer

Researchers from the Indiana University and Methodist Research Institute examined an unconventional approach of a medical mushroom formula to battle against breast cancer.

The findings of the study are in the December issue of the International Journal of Oncology. The results are inspiring in the battle against breast cancer.

Dr. Daniel Sliva, head researcher states that the formula prevents the growing of powerful metastatic human breast cancer cells, it also restrains the metastatic possibility of these cells. The formula which is all natural is created from a combination of six strong assortments of medical mushrooms cultivated on immune boosting and cancer battling botanicals which work jointly to give breast protection and immune system support. The conditions in which they were grown aide naturally to expand the amount biologically active ingredients in the mushrooms.

Breast cancer is among one of the most common cancers affecting women and has caused 39,840 deaths this year in the United States. Even though there has been essential advancements made in the treatment of breast cancer, treatments for advanced breast cancer still provide minimal hope. This new study demonstrates this strong mushroom formula holds a favorable possibility in the battle against highly intrusive form of breast cancer. Medical mushrooms have been greatly studied and researched for their anti-tumor and their immune modifying results. The mushrooms are vital for the maintenance of overall endurance and cellular health. Dr. Eliaz points out that the special blend of ingredients generated positive and encouraging results. The compounds support breast health through guarding cellular and immune boosting vitality. The researchers of the study acknowledge Dr. Eliaz for developing the formula.

Dr. Sliva in final comments notes that cancer metastasis is a involved development that consists of cell adhesion, migration, invasion and the stopping of some of the processes that is vital to restrain cancer metastasis. The formula the researchers studied restricts all of the processes, does not have any side effects which are linked to chemotherapy treatments.

Agaricus bisporus mushroom

The most edible and most common mushroom. Studies conducted on this mushroom at the City of Hope National Medical Center, had studied this mushroom type and its effects of halting breast cancer development.

A controlled study last year was conducted which had observed the diets in 2018 women. Half of the women did have breast cancer. The study had revealed a major decrease of occurrences of the cancer in women who had diets that consisted of consuming greater than 10 grams of fresh mushrooms each day The women in study who had consumed the fresh mushrooms each day had a less chance for the risk of developing breast cancer. It also had shown that women who not only had mushrooms in their daily diet but also had regular consumption of green tea, had a breast cancer risk decrease by almost ninety percent.

In another study in which was conducted among Korean women had discovered a strong association of the consumption of mushrooms and reduction in the risk of breast cancer.

In vivo research (research done using a living organism) has shown that the everyday common mushroom holds the possibility to stimulate the immune system. On one of the studies conducted on this mushroom to was discovered to boost dendritic cell function. In the testing, a compound was displayed in these ordinary mushrooms that has anti-cancer properties. These properties have the ability to halt the growing of the HT29 colon cancer cells, Caco-2 colon cancer cells, MCF-7 breast cancer cells. This mushroom turns out to be a unique source of combined linoleic acid and have natural antioxidants.

Agaricus Brazil Mushroom

In a little known cultural area are the persons who reside in Piepdade, which location is about 200 kilometers from Sao Paulo, the capital of Brazil. The residents of this community live long and extremely healthy lives had hardly ever endure common illnesses or diseases such as cancer, heart disease, asthma or arthritis.

Two American scientists who had visited this area some forty years prior, had discovered the persons who live there ate a type of mushroom which could not be located in Brazil or any part of the world. Their findings had been published and from their examination of the nutritional content of the mushroom it was noted in scientific journals widely.

Former President Ronald Reagan was known to take these mushrooms in his successful fight against skin cancer. Agaricus Blazei Murill become known to the world.

Studies were sped up in Japan to study the health properties of this mushroom. It was discovered to be effective as a cancer inhibitor through animal experiments. It was also noted to be one of the best medical mushrooms to battle cancer with a noted cure rate of 99% and inhibition rate of 99.4%.

At the University of Tokyo University Medical Department, the National Cancer Center Laboratory and Tokyo College of Pharmacy, mice who had cancerous tumors were fed the mushroom. These cancerous tumors were eliminated by 90% in the mice. In mice who were fed the mushroom as a protective agent, then injected with a strong cancer causing Sarcoma 180, 99.4% of the mice had shown no tumor growth.

Dr. Mamdooh Ghoneum, Ph.D, with the King Drew Medical Center of UCLA, in 1995, discovered the mushrooms can add to the total number of immune cells throughout the entire body. Also, discovered was its ability to make the cells stronger.

Dr. Ghoneum findings were presented at the San Francisco’s Ninth World’s Immunology Congress.

Mushrooms and breast cancer

Researchers from the Beckman Research Institute, had tested seven vegetable extracts for their enzyme blocking activity and discovered white button mushrooms had the strongest effects. Researchers examined ten other kinds of mushrooms and those that also halted enzyme activity were stuffing mushrooms, portobello, crimini, shiitake and baby button. Since white button mushrooms are consumed the most, the extracts from the mushroom was tested. It was found that the extract decreased the spreading of breast cancer cells in a lab dish and when fed to mice who were implanted with breast cancer cells it had halted tumor growth. Based upon amounts of extract used on the mice it was established 100 grams of mushrooms each day would be sufficient to prevent breast cancer growth.

The theory of mushrooms decreasing breast cancer is due to the immunoassay in the mushroom which halts the enzyme used by the body to create estrogen

What is the truth about medical marijuana?

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Posted 26 Nov 2010 — by James Street
Category Alternative Therapies, Cannabis, Drug Testing, Drugs, Legal, Lung Metastases, Metastases

Dr. Donald Tashkin

Stuart Richland

Department of Justice

The Marijuana Cancer Cure Cult

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Posted 25 Nov 2010 — by James Street
Category Cannabis


By Bruce Mirken, AlterNet
Posted on January 26, 2010, Printed on November 25, 2010

In his 1971 State of the Union speech, President Richard Nixon declared war on cancer, prompting passage of the National Cancer Act, aimed at making the “conquest of cancer a national crusade.” Just four years later, scientists from the National Cancer Institute published a study demonstrating that a group of compounds taken from a common, widely cultivated plant shrank lung tumors that had been implanted in mice, extending their survival.

In a world that made sense, this plant and the anticancer drugs it produced would have been rushed into further testing, and we’d have known in a few years whether they had potential as treatments for human cancers. Instead, research proceeded at a glacial pace, with almost no further progress till the 1990s. Since then, vast quantities of lab and animal data have confirmed those early findings, but studies of these plant compounds in actual human beings with cancer remain nearly nonexistent.

What got in the way was Nixon’s other war, the “war on drugs.” The plant in question was cannabis sativa — marijuana — public enemy number one in that other war, and discovering that marijuana had beneficial properties was the last thing the U.S. government wanted to do.

Dr. Manuel Guzman of Complutense University in Madrid, lead author of the only human study yet published of a cannabinoid as cancer treatment, puts it slightly more diplomatically. The lack of immediate followup to those early reports “remains a mystery to me,” he says. Guzman cites a number of obstacles to human trials, including the fact that cannabinoids are “still seen by many doctors and regulatory agencies as drugs of abuse,” as well as “lots of paperwork” and a lack of commercial interest in natural compounds that can’t be patented.

Complicating things further, the relative vacuum created by the lack of human studies and the hostility of the U.S. government to the whole question of marijuana’s beneficial effects has left the field wide open for zealots who promote cannabis as a “cure” for cancer as if it were already a proven fact rather than a possibility in desperate need of serious study.

A Protective Effect?

Instead of researching cannabinoids as anticancer drugs, federal officials have continued to falsely imply that marijuana causes lung cancer. For example, a 2002 brochure for parents, “Talk to Your Child About Marijuana,” still available on the Office of National Drug Control Policy Web site, advises, “Smoking marijuana is as least as bad as smoking cigarettes.”

In fact, the largest, most well-controlled studies have consistently failed to find an increased risk of lung cancer or other typically tobacco-related cancers among marijuana smokers. These include a 65,000-patient 1997 study conducted at Kaiser Permanente in Oakland, California and a 2006 case-control study (in which patients with cancer were matched with similar patients without cancer to compare risk factors) from the UCLA lab of Dr. Donald Tashkin, one of the world’s leading experts on the pulmonary effects of drugs.

In the UCLA study, there was a consistent trend — albeit short of statistical significance — toward lower cancer risk among even the heaviest marijuana smokers. This was a surprise to some, given that marijuana smoke contains many of the same carcinogenic compounds as tobacco smoke. The researchers wrote:

Although purely speculative, it is possible that such inverse associations may reflect a protective effect of marijuana. There is recent evidence from cell culture systems and animal models that 9-tetrahydrocannabinol, the principal psychoactive ingredient in marijuana, and other cannabinoids may inhibit the growth of some tumors by modulating key signaling pathways leading to growth arrest and cell death, as well as by inhibiting tumor angiogenesis. These antitumoral associations have been observed for several types of malignancies including brain, prostate, thyroid, lung, and breast.

In an October 2003 review in the journal Nature Reviews: Cancer, Guzman detailed the extensive body of test-tube and animal research showing that cannabinoids inhibit tumors of the lung, uterus, skin, breast, prostate and brain (including gliomas, the type of tumor that killed Sen. Edward Kennedy). He also noted: “Cannabinoids have favorable drug-safety profiles and do not produce the generalized toxic effects of conventional chemotherapies. Cannabinoids are selective antitumor compounds, as they can kill tumor cells without affecting their non-transformed counterparts.”

Such selectivity is exactly what you want in an anticancer drug. The reason chemotherapy can be so awful is that most chemo drugs aren’t selective enough; they kill cancer cells, but are also toxic to healthy cells, leading to vomiting, hair loss and other miseries.

The ‘Cure’?

Nearly all of the evidence about cannabinoids as anticancer drugs comes from lab studies using cell cultures or animals with experimentally implanted tumors. The annals of medical research are littered with drugs that looked promising in the lab but didn’t work in people. Still, that doesn’t stop some enthusiasts from touting cannabis as a cure for cancer, sometimes making even open-minded scientists and medical marijuana advocates nervous.

When I worked at the Marijuana Policy Project, we received several impassioned emails imploring us to tell Sen. Kennedy that cannabis could cure his brain tumor. Others touted Canadian Rick Simpson’s “Healing Hemp Oil” Web site, Phoenix Tears.

In a series of videos, letters and other materials on the site, Simpson — who has had repeated run-ins with law enforcement over his cannabis-related activities and was, according to a Dec. 14 posting, staying in Europe indefinitely to avoid arrest — promotes what he calls “hemp oil” as a “simple herbal cure for cancer. I have used these extracts to cure three areas of skin cancer on my own body, also, I have cured cancers for others.” Simpson also touts hemp oil for pain and a variety of other conditions.

The site includes video and written instructions for making the preparation. The procedure involves using a solvent such as naphtha or isopropyl alcohol to extract the THC from marijuana, then boiling off the solvent using a rice cooker to leave a thick oil with a high THC concentration.

Simpson warns readers away from conventional cancer treatments: “Hemp oil has a very high success rate in the treatment of cancer, unfortunately many people who come to me have been badly damaged by the medical system with their chemo and radiation etc. The damage such treatments cause have a lasting effect and people who have suffered the effects of such treatments are the hardest to cure.”

He offers numerous stories and testimonials describing seemingly hopeless cancers cured by hemp oil, but no controlled, scientific experiments.

And critics find plenty to worry about. First, they note, despite warnings and disclaimers on the site, the procedure for making the medicine is risky. Mitch Earleywine, author of Understanding Marijuana and a professor of psychology at the State University of New York at Albany, calls the do-it-yourself procedure “outrageously dangerous. Even if you don’t light yourself on fire, you may end up with leftover solvent that would slowly poison the healthiest of us.”

There’s a reason scientists don’t base conclusions on anecdotes, Earleywine explains. “Cancer remits spontaneously sometimes, which is a good thing. Unfortunately, it leads to superstitious conditioning so people think that whatever they did last must be the source of the cure. Especially with some cancers, where a great many people die, all the spontaneous recoveries associated with hemp oil get remembered while all those that don’t either get forgotten or attributed to the horrors of the disease.”

Earleywine stresses that he is not dismissing the possibility that some form of cannabis might be an effective cancer treatment. “THC killing tumors is actually true,” he says, “but we’re not at the human stage [of research].”

Simpson is dismissive of critics who cite the lack of human studies. “How are you going to do controlled studies when it is illegal in Canada to do so?” he said in an emailed response to questions.

In fact, researcher Mark Ware of McGill University in Montreal has done clinical trials of medical cannabis in Canada, including a study comparing several different cannabis preparations in use by chronic pain patients.

Simpson calls the idea of spontaneous cancer remissions “nonsense.” As for possible risks of his preparation, he argues, “It is irresponsible to give people liver toxic chemicals, chemotherapy and radiation, so if they are talking about irresponsible why do not look at their own medical system? It is not irresponsible to save peoples lives with a harmless natural, non-addictive medicine from nature. If you watch our documentary, you will see that I use a simple water purification process to get rid of solvent residue. I have been ingesting oil for over eight years and I have supplied this oil to thousands of people who also have experienced no problems with solvent residue.”

While cautious about reports that are “solely anecdotal,” Paul Armentano, deputy director and resident science wonk at the National Organization for the Reform of Marijuana Laws, lays blame for the lack of proper data at the foot of prohibition. “It is a shame that lone individuals must try and engage in the work that the medical establishment should be undertaking, yet have turned a blind eye to,” he says. “Unfortunately, what we have is speculation rather than hard science, and we only have the politicization of cannabis to blame.”

The Long and Winding Research Road

The one human study of a cannabinoid cancer treatment published thus far was conducted by Dr. Guzman and colleagues and published online in June 2006 by the British Journal of Cancer. The scientists infused a THC solution directly into the tumors of nine patients with glioblastoma multiforme, a deadly form of brain cancer, for whom standard treatments had failed. This small pilot study wasn’t aimed at proving that THC worked, simply that it was safe to administer to these otherwise doomed patients .

It proved entirely safe, with no negative effects attributed to the THC and no “overt psychoactive effects.” And while there were no miracle cures, there were glimmers of possible efficacy. In one patient with an “extremely aggressive” cancer, tumor growth was curbed for nine weeks. In another, symptoms improved, although tumor growth was not stopped. And in some cases, lab tests with cells taken from tumor biopsies showed that THC decreased the number of viable cancer cells.

Guzman and colleagues noted that THC may not be the best cannabinoid to use as a cancer treatment, as others have been shown more potent in lab tests. And while the direct infusion technique delivered a high THC concentration to specific locations, it may not have reached all parts of these large tumors.

Still, the results were positive enough that the researchers urged further tests, including studies of cannabinoids in combination with other cancer drugs. Guzman is hoping to do more studies, but notes that with all the bureaucratic, procedural and financial hurdles, “The way ahead is long and winding.”

But if more human studies aren’t happening yet, lab work continues to produce intriguing results. Just this month, the journal Molecular Cancer Therapeutics published a new study providing the first evidence that combination cannabinoid therapy is more potent than using THC or other cannabinoids as single agents.

Sean McAllister and colleagues from the California Pacific Medical Center Research Institute in San Francisco tested THC, cannabidiol (CBD) and both drugs combined on human glioblastoma cell lines. In two of the three cell lines tested, the THC/CBD combination proved the most potent — more so than would be expected by just adding the anticancer effects of the two drugs together, suggesting a synergistic action.

“Combinations, compared to individual drug treatments with specific cannabinoid-based compounds, may represent an improvement for the treatment of patients with glioblastoma and perhaps additional cancers,” McAllister says. “It is also possible that other constituents of Cannabis sativa which are not structurally related to cannabinoids could improve antitumor activity when combined.”

That leads to an obvious question: Why not use the whole plant — whether smoked, vaporized, or in some sort of extract like Simpson’s? “In regard to brain cancer, it is highly unlikely that effective concentrations of either Δ9-THC or CBD could be reached by smoking cannabis,” McAllister says. “In regard to additional cancers, I feel defined formulations and dosing will be needed in order to effectively treat patients.”

McAllister says his team is moving toward “clinical trials in both breast and brain cancer, but it is a slow process.” The next step, he says, will be to try to replicate his test-tube results in animals. “No agency in the U.S. would allow me to move forward to clinical trials without some form of proof of concept data in a relevant preclinical in vivo model.”

That may be an accurate assessment, but Armentano thinks it’s too cautious “given the long established safety of cannabinoids, including THC which is already a legal pharmaceutical, and CBD, which is non-psychoactive, is not a central nervous system depressant and has no risk of overdose.”

Not only is there abundant evidence that cannabinoids kill cancer cells, Armentano says, “Investigators now even understand the mechanism of action; in other words, they know how and why cannabinoids kill cancerous cells and halt the spread of malignant tumors.”

The question of whether these cannabis compounds can cure cancer in people, he says, “ought to have been already answered decades ago.”

Bruce Mirken is a San Francisco-based writer and media consultant who served as director of communications for the Marijuana Policy Project from 2001 to


© 2010 Independent Media Institute. All rights reserved.
View this story online at:

Marijuana and Cancer: Dr. Andrew Weil

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Posted 25 Nov 2010 — by James Street
Category Alternative Therapies, Cannabis, Drugs, experimental treatments, Lung Metastases, Prevention

Marijuana for Cancer?
I know that medical marijuana can help relieve nausea and vomiting due to chemotherapy, but recently, I’ve heard about the use of marijuana to actually treat cancer. Is this true?
You’re quite right: exciting new research suggests that the cannabinoids found in marijuana may have a primary role in cancer treatment and prevention. A number of studies have shown that these compounds can inhibit tumor growth in laboratory animal models. In part, this is achieved by inhibiting angiogenesis, the formation of new blood vessels that tumors need in order to grow. What’s more, cannabinoids seem to kill tumor cells without affecting surrounding normal cells. If these findings hold true as research progresses, cannabinoids would demonstrate a huge advantage over conventional chemotherapy agents, which too often destroy normal cells as well as cancer cells.
Related Weil Products
Dr. Weil on Healthy Aging for Cancer Support – Dr. Weil on Healthy Aging – Do you or a loved one have cancer? The Dr. Weil on Healthy Aging online guide has simple, effective preventive health information and tools including an exclusive version of Dr. Weil’s Anti-Inflammatory Food Pyramid. Join today and get 14 days free!
As long ago as 1975, researchers reported that cannabinoids inhibited the growth of a certain type of lung cancer cell in test tubes and in mice. Since then, laboratory studies have shown that cannabinoids have effects against tumor cells from glioblastoma (a deadly type of brain cancer) as well as those from thyroid cancer¸ leukemia/lymphoma, and skin, uterus, breast, stomach, colorectal, pancreatic and prostate cancers.

So far, the only human test of cannabinoids against cancer was done in Spain and was designed to determine if treatment was safe, not whether it was effective. (In studies on humans, such “phase one trials,” are aimed at establishing the safety of a new drug, as well as the right dosage.) In the Spanish study, reported in 2006, the dose was administered intracranially, directly into the tumors of patients with recurrent brain cancer. The investigation established the safety of the dose and showed that the compound used decreased cell proliferation in at least two of nine patients studied.
Marijuana for Cancer?
I know that medical marijuana can help relieve nausea and vomiting due to chemotherapy, but recently, I’ve heard about the use of marijuana to actually treat cancer. Is this true?

Answer (Published 7/23/2010)
You’re quite right: exciting new research suggests that the cannabinoids found in marijuana may have a primary role in cancer treatment and prevention. A number of studies have shown that these compounds can inhibit tumor growth in laboratory animal models. In part, this is achieved by inhibiting angiogenesis, the formation of new blood vessels that tumors need in order to grow. What’s more, cannabinoids seem to kill tumor cells without affecting surrounding normal cells. If these findings hold true as research progresses, cannabinoids would demonstrate a huge advantage over conventional chemotherapy agents, which too often destroy normal cells as well as cancer cells.
Related Weil Products
Dr. Weil on Healthy Aging for Cancer Support – Dr. Weil on Healthy Aging – Do you or a loved one have cancer? The Dr. Weil on Healthy Aging online guide has simple, effective preventive health information and tools including an exclusive version of Dr. Weil’s Anti-Inflammatory Food Pyramid. Join today and get 14 days free!
As long ago as 1975, researchers reported that cannabinoids inhibited the growth of a certain type of lung cancer cell in test tubes and in mice. Since then, laboratory studies have shown that cannabinoids have effects against tumor cells from glioblastoma (a deadly type of brain cancer) as well as those from thyroid cancer¸ leukemia/lymphoma, and skin, uterus, breast, stomach, colorectal, pancreatic and prostate cancers.

So far, the only human test of cannabinoids against cancer was done in Spain and was designed to determine if treatment was safe, not whether it was effective. (In studies on humans, such “phase one trials,” are aimed at establishing the safety of a new drug, as well as the right dosage.) In the Spanish study, reported in 2006, the dose was administered intracranially, directly into the tumors of patients with recurrent brain cancer. The investigation established the safety of the dose and showed that the compound used decreased cell proliferation in at least two of nine patients studied.
It is not clear that smoking marijuana achieves blood levels high enough to have these anticancer effects. We need more human research, including well-designed studies to find the best mode of administration.

If you want to learn more about this subject, I recommend an excellent documentary film, “What If Cannabis Cured Cancer,” by Len Richmond, which summarizes the remarkable research findings of recent years. Most medical doctors are not aware of this information and its implications for cancer prevention and treatment. The film presents compelling evidence that our current policy on cannabis is counterproductive and foolish. Another reliable source of information is the chapter on cannabinoids and cancer in Integrative Oncology (Oxford University Press, 2009), a textbook I edited with integrative oncologist Donald I. Abrams, M.D.

Andrew Weil, M.D.

The anticancer effects of vitamin K

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Posted 20 Nov 2010 — by James Street
Category Alternative Therapies, Mouse Osteosarcoma Studies, Natural Therapies, Nutrition and Cancer

Alternative Medicine Review,  August, 2003  by Davis W. Lamson,  Steven M. Plaza

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Continued from page 4.

The proto-oncogene bcl-2 has been shown to protect against apoptosis. The addition of bcl-2 to cell cultures (2B4 and FL5.12) countered the cell death imposed by the oxidative burst from K3. Bcl-2 was not able to decrease the ROS produced by K3, as measured by cyanide-resistant oxygen consumption, yet it was able to inhibit dose-related killing of the cell lines from 50 [micro]M-200 [micro]M of K3. These results suggest that ROS, acting as second messengers, signal downstream transcription factors, such as nuclear factor-kappa B (NF-kB), Fos/Jun, and others that may be protected by the antioxidant-governing activities of Bcl-2. (93) The transcription factor NF-kB is involved in stress-induced FasL expression. Fas is one of the important death receptors in the tumor necrosis factor superfamily. The gene encoding the ligand for Fas, designated as FasL, activates Fas by trimerization of the receptor. Activation-induced cell death is commonly mediated by the Fas/FasL system, and menadione induces Fas as well as FasL expression. Capriccio et al (94) found that a functional Fas/ FasL system was needed in order to induce apoptosis. Experiments showed that mutant leukemia cell lines lacking a functional Fas ligand were resistant to FasL killing by menadione. It was also found that mice lacking functional FasL or expression of Fas were also resistant to the cytotoxic effects of K3.

Vitamin K3 has been shown to inhibit growth and induce apoptosis of stomach cancer cells in a dose-dependent fashion. The inhibition was found to be due to sulfhydryl arylation of critical cystine residues that mediated protein tyrosine phosphorylation. The inhibition of cell growth by K3 induced tyrosine phosphorylation of hepatocyte growth factor receptors (c-met) and epidermal growth factor receptors (EGFR), which in turn activated the RAS signaling pathway. The addition of vitamin K3 also created a sustained phosphorylation of extracellular signal-regulated kinase (ERK), part of the mitogen-activated protein kinase (MAPK) superfamily associated with cellular signal transduction, proliferation, and apoptosis. Vitamin K3 is thought to induce both protein tyrosine kinase activation from the receptor pathway and inhibit ERK protein tyrosine phosphatases (that dephosphorylate activated kinases). ERK phosphorylation has been found to be critical to not only growth factor-induced cell proliferation, but also to K3-mediated cell death. It is thought that K3 can act without ligand binding through the inhibition of protein tyrosine phosphatases. (95)

Cell Cycle Arrest

The ability of vitamin K to induce cell cycle arrest and cell death may also be explained by the inhibition of protein kinases in association with a cyclin-dependent mechanism. Cyclins are regulatory proteins of the cell cycle that activate cellular maturation-promoting factors. Cyclins complex and modulate the protein kinase catalytic subunit of proteins such as p34CDC2, known alternately as cyclin dependent kinasel (CDK1). This protein kinase is a member of the serine/threonine protein kinase family. The designation “CDC2″ refers to “cell division cycle 2″ at the G1 to S and G2 to M transitions. Cyclins, such as cyclin B1, have no inherent enzymatic activity; rather, they act by means of cyclin-dependent kinases that phosphorylate serine and threonine residues on kinase cell cycle regulators. For example, cyclin B1 complexes with p34CDC2, forming the maturation-promoting factor, which in turn is essential in G1/S and G2/M transitions in the cell cycle. Phosphorylation and dephosphorylation act as on-and-off switches for the cell cycle. Dephosphorylation of p34CDC2 increases its activity.

K3 can inhibit CDKs. such as CDK1 (p34CDC2) (100 [micro]M for 1 hour) by hyperphosphorylating the protein. (45,96) The addition of menadione to malignant cell culture has been shown to inhibit the cell cycle at the G1/S and S/G2 phases. Concentrations in the 25-100 [micro]M range have been found to delay S/G2 in a dose-dependent manner. (45) Cell division cycle 25 (CDC25) are protein-tyrosine phosphatases critical for cell cycle progression. This family of CDC25 phosphatases is responsible for the activation of cyclin-dependent kinase CDC2 through the removal of two phosphate groups. CDC25A, required for the progression from G1 to S, has been found to be inactivated by vitamin K3, and the loss of enzymatic activity was due to modification of the active site. (97)

The addition of vitamin K3 to HepG2 cells hyperphosphorylated the CDC2 kinase, inactivating the enzyme and inhibiting the cell cycle. (98) It has been proposed that menadione modifies the active sites of the CDC25 dual specificity protein phosphatases and reduces or even abolishes the dephosphorylating activity of the enzyme. Vitamin K3 binds to active sulfhydryl groups of cysteine residues at active p34CDC2 sites. (45) This action stems from binding to the catalytic domain of CDC25 phosphatase. K3 also decreased protein-tyrosine phosphatase by 2- to 3-fold (45) and suppressed the expression of proliferating cell antigen as well as cyclin B in S phase. (99)

Vitamin K2 has also been shown to work at the level of the cell cycle, acting on cyclins to inhibit the cell cycle and initiate differentiation. It is a powerful inducer of differentiation in a number of myeloid leukemia cell lines in various stages of maturation. The mechanism of differentiation by K2 differs from retinoic acid. Vitamin K2 has not been found to bind retinoic acid receptors (RAR) alpha, beta, or gamma, or retinoid X receptor (RXR) alpha receptors. (68) This work with vitamin K2 implies there is an undiscovered nuclear receptor or mechanism for differentiation.

Researchers have proposed that the p21 gene may act with vitamin K2 as an additional factor in cellular differentiation. Previously it was thought that tumor suppressor genes such as p53 and BRCA1 induce the expression of the p21 gene. It was demonstrated that vitamin K2 can also stimulate p21 in a p53-independent manner. (100) (K2 was also shown to be unable to induce p53 in MG-63 human osteosarcoma cells, while inducing p21 gene.) MG-63 cells, shown to lack the p53 gene, were inhibited by vitamin K2 at high concentrations between [10.sup.-7] and [10.sup.-5] M/L. The elevated levels of p21 resulted in the differentiation of osteosarcoma cells.

The action of vitamin K2 in cell cycle arrest acts at the G1/S transition. When K2 transcriptionally activates the p21 protein, it complexes and inhibits the phosphorylation of G1 cyclin-dependent kinases in the cell cycle. This results in the arrest of cells in the G0/G1 phase of the cell cycle.


Vitamin K, in all its various forms, has been shown to have anticancer effects. Vitamin K cancer research has focused on two basic mechanisms to explain these effects. The older mechanism relies on an oxidative effect produced by the one-electron cycling of vitamin K3 that surpasses the oxidative capacity of the cancer cell, leading to death. Other mechanisms have been proposed due to the anticancer effect of vitamin K forms that either do not readily cycle (K1 and K2) or that are at levels that do not initiate cycling. These clues to another mechanism have led researchers to discover an alternative mechanism of action that acts at the level of protein kinases and phosphatases. Vitamin K has been found to act on proteins such as myc and fos, which in turn leads to growth arrest and death. Cell cycle arrest has also been found to be initiated by phosphatases at the level of cyclins, which are critical in the cell cycle.


The authors wish to thank Richard and Jileen Russell and the Smiling Dog Foundation for a grant supporting this project; Bastyr University for grant administration; and the Complementary Cancer Research Center for partial support.


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(2.) Furie B, Furie BC. Molecular basis of vitamin K-dependent gamma-carboxylation. Blood 1990;75:1753-1762.

(3.) Rannels SR, Gallaher KJ, Wallin R, Rannels DE. Vitamin K-dependent carboxylation of pulmonary surfactant-associated proteins. Proc Natl Acad Sci U S A 1987;84:5952-5956.

(4.) Shearer MJ. Role of vitamin K and Gla proteins in the pathophysiology of osteoporosis and vascular calcification. Curr Opin Clin Nutr Metab Care 2000;3:433-438.

(5.) Suttie JW. Synthesis of vitamin K-dependent proteins. FASEB J 1993;7:445-452.

(6.) Wu FY, Liao WC, Chang HM. Comparison of antitumor activity of vitamins K1, K2 and K3 on human tumor cells by two (MTT and SRB) cell viability assays. Life Sci 1993;52:1797-1804.

(7.) Shiraki M. Vitamin K2. Nippon Rinsho 1998;56:1525-1530. [Article in Japanese]

(8.) Douglas AS, Robins SP, Hutchison JD, et al. Carboxylation of ostcocalcin in post-menopausal osteoporotic women following vitamin K and D supplementation. Bone 1995;17:15-20.

Mounting evidence shows red wine antioxidant kills cancer

Mounting evidence shows red wine antioxidant kills cancer

March 25, 2008
PDF file of scientific study

Rochester researchers showed for the first time that a natural antioxidant found in grape skins and red wine can help destroy pancreatic cancer cells by reaching to the cell’s core energy source, or mitochondria, and crippling its function. The study is published in the March edition of the journal, Advances in Experimental Medicine and Biology.

The study also showed that when the pancreatic cancer cells were doubly assaulted — pre-treated with the antioxidant, resveratrol, and irradiated — the combination induced a type of cell death called apoptosis, an important goal of cancer therapy.

The research has many implications for patients, said lead author Paul Okunieff, M.D., chief of Radiation Oncology at the James P. Wilmot Cancer Center at the University of Rochester Medical Center.

Although red wine consumption during chemotherapy or radiation treatment has not been well studied, it is not “contraindicated,” Okunieff said. In other words, if a patient already drinks red wine moderately, most physicians would not tell the patient to give it up during treatment. Perhaps a better choice, Okunieff said, would be to drink as much red or purple grape juice as desired.

Yet despite widespread interest in antioxidants, some physicians are concerned antioxidants might end up protecting tumors. Okunieff’s study showed there is little evidence to support that fear. In fact, the research suggests resveratrol not only reaches its intended target, injuring the nexus of malignant cells, but at the same time protects normal tissue from the harmful effects of radiation.

“Antioxidant research is very active and very seductive right now,” Okunieff said. “The challenge lies in finding the right concentration and how it works inside the cell. In this case, we’ve discovered an important part of that equation. Resveratrol seems to have a therapeutic gain by making tumor cells more sensitive to radiation and making normal tissue less sensitive.”

Resveratrol is known for its ability to protect plants from bacteria and fungi. Purified versions have been described in scientific journals as potential anti-cancer, anti-inflammatory and anti-atherogenic agents, and for their ability to modulate cell growth. Other well-known antioxidants derived from natural sources include caffeine, melatonin, flavonoids, polyphenols, and vitamins C and E.

A flurry of antioxidant studies in recent years has not proven how and why they work at the cellular level. At the suggestion of a young scientist in his lab, Okunieff began studying resveratrol as a tumor sensitizer. That’s when they discovered its link to the mitochondria.