Brain cancer study shocks scientists, reveals genetic disruption in DNA

cancer cells
Scientists who scoured the DNA of brain tumours, searching gene by gene for bad actors, were puzzled. The cancers had none of the mutations in growth-causing genes that are typical of other tumours, yet they grew quickly, with no brakes. The question was why — what had altered their genetic instructions to lead to runaway cell division?

The surprising answer, researchers reported Wednesday in the journal Nature, is that the three-dimensional structure and organization of the DNA had been disrupted. As a result, two genetic neighbourhoods that are normally separated, as if they are two gated communities, were merged. The effect was to allow a powerful snippet of DNA from one neighbourhood into the one next door, where it woke up a near-dormant growth gene. And the cells took off.

This is an entirely new way for cells to become cancerous, researchers said, and most likely is not unique to the brain cancers, low- and intermediate-grade gliomas, that were the subject of the new study. The study’s lead author, Dr. Bradley E. Bernstein, a member of the Broad Institute in Cambridge, Mass., and a pathology professor at the Massachusetts General Hospital, says he has already found a similar phenomenon in about a dozen other tumours. And, he says, the discovery suggests a potential treatment with an existing chemotherapy drug that restores the walls separating the DNA sections.

“It’s really exciting,” said Dr. Peter Dirks, a brain cancer expert at the Hospital for Sick Children in Toronto, adding that at least with gliomas, the suggested treatments could be tested in clinical trials very soon.

The finding was surprising, others said.

“What this tells me is that I know a lot less than I did before,” said Dr. Jeremy Rich, a brain cancer expert at the Cleveland Clinic.

Gliomas are the most common type of malignant brain tumour in adults — about 18,000 are diagnosed each year in the United States. The most aggressive gliomas, known as glioblastomas — the type of cancer that killed Senator Edward Kennedy — usually strike older people and have an average survival time of 18 months. The lower-grade ones tend to strike younger adults, and survival times can be much longer. Yet despite extensive study of gliomas, doctors have made little progress in treating them. Doctors usually remove the lower-grade tumours and treat patients with radiation and chemotherapy. But the tumours return, often as aggressive glioblastomas that resist cancer therapies.

“We are desperate in this disease,” Dirks said.

The researchers did, however, notice one puzzling feature in up to 80 per cent of low- and moderate-grade gliomas — a common gene that seemed to have no particular relevance to cancer often was mutated. The gene, isocitrate dehydrogenase, or IDH, had long been considered humdrum, a so-called housekeeping gene that directs cells to make an enzyme used in energy production.

“It was really surprising,” Bernstein said. “Why would a metabolism gene cause cancer?”

But then again, why was it mutated so often?

“That frequency is just shockingly high,” said Dr. Ingo K. Mellinghoff, a brain cancer expert at Memorial Sloan Kettering Cancer Center. “It makes you think it must be important.” And, he said, the mutation is one of the very first changes in the cancer cells.

There was one intriguing clue. When the IDH gene was mutated, the cancer cells’ DNA became studded with chemical tags known as methyl groups. Bernstein and his colleagues focused on those tags, asking how they might be disrupting the three-dimensional structure of the DNA.

It has long been known that human DNA is tightly packaged in cells. If all the DNA in a human cell were spread out in a line, it would be 6 1/2 feet long. Instead, it forms about 10,000 loops, like those of a shoelace. Each loop is an autonomous gated neighbourhood. The walls between the loops are made by a protein called CTCF. The extra methyl tags, Bernstein and his colleagues found, remove the CTCF walls. Now, suddenly, neighbourhoods merge.

Two merged loops in particular seemed important. One loop contains a gene, PGDFRA, that makes cells grow and is rarely turned on. But when the loop with that gene merges with an adjacent loop, the gene comes under the control of a different DNA segment that turns the gene on constantly. The cells starts to divide, and a cancer is underway.

Bernstein and his colleagues tested their hypothesis by growing glioma cells in petri dishes and adding a rarely used first-generation chemotherapy drug, 5-Azacytidine, that dissolves methyl groups. The loops re-formed in the DNA; the gates to each neighbourhood swung shut. And the growth gene turned off because now it was properly controlled by the DNA segment that kept it mostly quiet.

The research suggests that treating gliomas early, as soon as they are detected, with a drug like 5-Azacytidine can restore DNA loops, Bernstein said. The same method should apply to the growing list of other cancers with excessive numbers of methyl tags on their DNA, he added. They include liver cancers, sarcomas, colon cancers, bladder cancers and leukemia, Bernstein said.

What is needed now is a diagnostic test to detect the presence of methyl tags and thus the breaking of loops. And that, Bernstein said, is simple. And it should lead to a clinical trial to treat people early on, before the tumours get uncontrollable.

“I am biased, obviously,” Bernstein said. But, he added, “I am really optimistic about the potential of this information.”

Alternative Cancer Treatments in Mexico : Hope or Fraud?


About alternative cancer treatments in Mexico

If you search the internet, you will find more than 35 alternative care clinics and hospitals in northern Mexico, along the US border. Most of these are near Tijuana. They offer a wide range of cancer treatments that they describe as effective and curative. Some of these treatments are very difficult to find in any other country. The clinics are placed along the border so that wealthy US patients can get to them relatively easily.

For many years the US medical system has been trying to convince people that many of the alternative therapies offered in Mexico are dangerous. For many of them there is no scientific evidence to say that they are safe or even work. But some people with cancer still choose to go there and use them.

The laws that govern the Mexican health care system are very different to those in countries such as the USA and Europe. Mexico is far less strict in their regulations than other countries. So clinics can offer alternative cancer treatments that have not been scientifically proven to work. This is a serious problem and for some cancer patients may cause them a lot of harm.

The internet has become a major source of information for both patients and health professionals. It can be an easy and effective way of finding information about cancer therapies. But anyone can write information or advertise treatments about healthcare on the internet. So if someone feels like writing about using an unproven alternative cancer therapy in Mexico instead of conventional medical treatment, they can.

Types of alternative cancer treatment offered in Mexico

There are many different types of alternative therapy clinic in Mexico. We don’t have exact details of all the therapies they offer. A few examples of those advertised on the internet or in the media include

Issels treatment
Nutritional therapy such as the Gerson diet
High dose vitamins and dietary supplements
Metabolic therapy – a program developed to train the immune system to get rid of your cancer
Oxygen therapies
Hyperthermia (high temperature therapy)

Many of the clinics in Mexico offer a package of care that may involve using a combination of treatments. Often the package of care sounds very attractive because it is advertised as relaxing and caring. You will have individual care and the clinic will usually say that they can help you.

There are reports of people with cancer leaving these clinics in Mexico very happy with their care and claiming that the treatment did cure their cancer. But we have no evidence to prove this. There are also many reports of people who have had severe and life threatening side effects from the treatments. People with advanced cancers are most at risk of not being able to cope with side effects of the treatments. Many go to the clinics in a poor state of health and desperate for help. Some of these alternative cancer clinics in Mexico have no medical facilities available on site to cover emergencies that could arise.

The cost of alternative cancer treatments in Mexico

Many of the alternative cancer treatments offered in Mexico cost a lot of money. Remember that you will have to pay for flights and accommodation as well as the treatment. The treatment costs can sometimes be thousands of pounds per month.

From individual patient reports and advertisements on the internet, costs range from $3,000 to well over $30,000. The actual costs will depend on the type of alternative treatment you have and on how long you carry on with it.

What to remember

We are concerned that these alternative therapy treatments are often sold for a great deal of money. And people with cancer can be very vulnerable. It is understandable that patients or their relatives will try anything if they think it might work. But some of these treatments are just money making businesses targeting people who are ill and very vulnerable. We consider this to be very wrong.

Our message is

Be careful
Make sure you look into all available information
Talk to your own cancer doctor before you buy anything

Check out this report from Aljazeera on the subject:

Phytochemicals in Cancer Prevention

food basket phytochemicals
In the past ten years scientists have been actively studying phytochemicals that have an influence on human health. From this research we have learned much about prevention and treatment of cancer. The recent Dietary Supplement Health Education Act passed in 1994 has enabled food products to make health claims if they are substantiated by scientific research. This has caused an explosion of supplements available in health food stores and the advent of the nutraceutical industry. Although many of these nutraceuticals have some evidence of preventing certain diseases, one should beware of the lack of regulation in this area.

Phytochemicals can act at almost every step of carcinogenesis, usually to improve the outcome, but sometimes as a carcinogen.

These dietary components act as desmutagens in each stage of carcinogenesis by acting as carcinogen inactivators, enzymatic inducers, scavengers or antioxidants. Later in the process they may inhibit tumor growth by acting as suppressors.

Chemical Carcinogenesis

Cancer occurs when a cell loses its normal patterns of replication and begins to grow uncontrolled. The process of carcinogenesis is multistep, requiring mutations in several genes affecting cell growth. There is usually a long latency period from when the disease first begins until it is diagnosed, making treatment difficult. The process can be described by three phases: initiation, promotion and progression. Initiation is the time when the DNA of a cell is first damaged by a carcinogen and not repaired in the normal way. This step is affected by formation of DNA adducts, DNA repair, and mutation and deletions in the DNA. During promotion, the cell transforms into a premalignant phase, which is still reversible. This stage involves alterations in gene expression and cell proliferation. In the last step, progression, the mass becomes an invasive malignant mass through a variety of genetic mechanisms. This step is considered irreversible and eventually leads to metastasis.

Drug Metabolism

Exogenous agents that enter the body, including carcinogens, are metabolized by the body in an attempt to make them more soluble and thus more easily excreted. This metabolism is done by two categories of enzymes, phase I and phase II, both of which are present in high levels in the liver. Phase I enzymes include the cytochrome P-450 enzymes and generally act by exposing a polar functional group or adding a hydroxyl group. Although this reaction is aimed at making the drug more polar, it can also alter a carcinogen into a strong electrophile making it more reactive and thus a stronger carcinogen.

For instance, polycyclic aromatic amines such as benzo[a]pyrene, are considered pro-carcinogens which are converted to more active carcinogens by phase I enzymes. While many phytochemicals have been identified that inhibit these enzymes, many environmental pollutants such as tobacco smoke can induce these enzymes, thus altering the rates of drug metabolism.

Phase II reactions involve further modifications to make an agent more polar by conjugation with glucuronic acid, sulfuric acid, acetic acid or an amino acid. One example is the conjugation of glutathione to nitro groups on the drug by the enzyme GSH-S-transferase.

If a reactive foreign agent enters the nucleus of the cell it can interact with the DNA forming adducts which can interfere with replication, thus leading to mutations or deletions in the DNA. This phase of carcinogenesis is termed initiation and is reversible if DNA repair mechanisms are active. The promotion phase of carcinogenesis occurs when sufficient DNA damage has occurred to affect gene expression and cellular proliferation. This can be due to mutations in the genes that affect cell growth and signal transduction. A cell may sense abnormalities in cell growth and opt to undergo apoptosis, or cell death. At this point, apoptosis can save the entire organism by the removal of one abnormal cell. If this does not occur, tumor progression follows, which may be due to mutations in tumor suppressor genes or genes involved in apoptosis.

Oncogenic Signaling

Proteins involved in cell growth and the formation of cancer are known as oncogenes and anti- oncogenes. Oncogenes were originally defined as genes that contribute to neoplastic transformation when introduced into a normal cell. They were later found to be proteins involved in cell cycle progression. When expression of an oncogene is amplified, uncontrolled cell growth can result, leading to cancer. Anti-oncogenes, also called tumor-suppressor genes, are recessive genes responsible for slowing the uncontrolled growth, essentially the brakes of the cell cycle. If a tumor suppressor protein is missing or not functional due to mutation, then uncontrolled growth can occur.

Cell growth stimuli normally occur by the binding of a growth factor to its receptor, either on the plasma membrane or in the cell nucleus. In the case of a plasma membrane receptor, this message is then transferred to the interior of the cell and to the nucleus by signal transduction molecules. In the nucleus, transcription factors are activated that result in DNA synthesis and cell growth. Some cancers are hormone sensitive, such as breast cancer, and grow as a result of hormone binding to a nuclear receptor where it then stimulates cell growth.

One signal transduction molecule that has been associated with a multitude of cancers including colon and lung cancer, is the small G protein ras, associated with the inner face of the plasma membrane. Mutations in the ras protein result in loss of GTPase activity. Through post translational modification, 15 or 20 carbon lipid molecule (farnesyl) is added to the ras protein. This isoprenylation allows ras to associate with the plasma membrane and is essential for its activity. When activated, ras ultimately activates transcription factors such as myc and fos, thus altering gene expression. Inhibition of ras isoprenylation may result in anti-tumor activity.

Tumor suppressors differ from oncogenes in that they are recessive genes necessary for halting cell growth if mistakes in the DNA are identified. Either inherited mutations or random mutations can inactivate tumor suppressor genes leading to uncontrolled cell growth. Examples of tumor suppressors are; APC, DCC, p53 and Rb. Some of these tumor suppressor genes also play a role in apoptosis. Apoptosis is the last chance a defective cell has in limiting tumor growth before its uncontrolled growth puts the entire organism at risk. Cancer cells lose the ability to undergo apoptosis.

Carcinogenesis can be stopped or at least slowed at several stages including; alteration of phase I or phase II enzymes to decrease toxicity of the carcinogen, inhibition of DNA adduct formation, repair of mutation, alteration of signal transduction molecules that affect growth, or induction of cellular apoptosis. Much drug research centers on inhibition of signal transduction proteins, and we now know that many phytochemicals are able to affect these processes also. For instance, phytochemicals have been identified that can affect the following steps in carcinogenesis:

1. Modifying activation of carcinogens by inhibiting phase I enzymes.

2. Modify detoxification of carcinogens by activating phase II enzymes.

3. Scavenging DNA reactive agents.

4. Suppressing the proliferation of early, precancerous cells.

5. Stimulating the process of apoptosis in damaged cells.

6. Inhibiting other properties of cancer cells.

Who is at Risk for Developing Cancer?

The process of developing cancer is length and there are no established early markers as there are for heart disease, making it difficult to associate a cause. However, we know that one of the major contributors to cancer is cigarette smoke, and not just for lung cancer. Cigarette smoke can stimulate biotransformation enzymes making other carcinogens more active. There also appears to be a connection between the amount of red meat in the diet to an increased incidence of colon and prostate cancer, but that connection is unclear. Obesity and lack of exercise can also increase the risk of developing cancer. High fat diets may increase the risk of developing cancer, especially of the colon, rectum, and prostate. Many cancers also have a hereditary risk such as breast cancer and colon cancer. Any patient with a previous diagnosis of cancer is also at risk of developing a second cancer.

Foods and Herbs for Cancer Prevention

There has been an explosion of research to examine the cancer chemopreventive effects of food and food components. This is a brief survey of foods, herbs, and isolated components of them that have substantiated effects in chemoprevention in preclinical, epidemiological and some clinical settings. There is current disagreement as to whether isolated compounds extracted from food or the whole food is more important in chemoprevention. Although research is easier done on isolated components, in many cases it would appear that the whole food or herb is more potent. This may be due to a variety of active components that act additively or even synergistically and to the presence of agents that can decrease the toxicity of other phytochemicals present.

Research in the area of chemoprevention can be difficult for many reasons. First, research is done on a healthy individual and the time it takes to develop cancer in lengthy, making studies long, sometimes more than a lifetime. Finding a large enough body of compliant patients is also difficult. Researchers are looking for biomarkers that can serve as early signs of cancer. Most of the work reviews here is done in animals, and although we can never be sure exactly how that work translates to effects in humans, it is still relevant. Included below are only those foods and phytochemicals in which an overwhelming amount of preclinical, animal or epidemiological evidence exists regarding these chemopreventive effects. Hundreds of other phytochemicals are still in the earliest phases of investigation and not ready for clinical evaluation yet.

As there have recently been deaths that have occurred in patients after being injected with various herbal treatment, a word of caution must be made. These agents are meant as foods, to be taken orally by consumption, never by injection. Injections are typically not safe for many reasons.

Cruciferous Vegetables

In a review of 25 studies published in the literature prior to 1994, 20 showed a statistically significant inverse relationship between colorectal cancer and consumption of at least one vegetable group. The relationship being less striking for fruits. Vegetables contain a variety of anticarcinogens including carotenoids, ascorbates, tocopherols, selenium, folate, fiber, dithiothiones, indoles, thiocyanates, sterols, protease inhibitors and coumarins. More specifically, cruciferous vegetables such as broccoli, cauliflower and watercress, which contain high levels of indole-3-carbinol (I3C) and phenethyl isothiocyanate (PEITC), have been linked to a decrease in a variety of cancers. The American Cancer Society, as well as the American Dietetic Association, recommends 5 cup servings of vegetables per day to promote good health.

I3C can induce multiple cytochrome P450 enzymes as well as phase II metabolic enzymes and can decrease the binding of carcinogen to DNA. I3C can also act as an anti-estrogen by decreasing the level of estrogen receptor and affecting estrogen metabolism (estradiol 2-hydroxylation), making it effective in the prevention of breast and prostate cancer. It has been shown to inhibit the formation of chemically induced mammary tumors in mice when given orally during either the initiation phase alone or the initiation and promotion phases. In rats, doses of 50-100 mg/day, 5x/week were non-toxic. In humans, doses of 0.7 umol/kg-bw/day were found to increase estradiol 2-hydroxylation, and doses as high as 0.04 mmol/kg-bw/day have been used. Clinical trials to investigate the role of I3C in preventing breast cancer are currently planned.

PEITC is a naturally occurring sulfur compound found in cruciferous vegetables in the form of gluconasturtin. When the plant is crushed glucosinolate releases PEITC. PEITC inhibits certain cytochrome P450 enzymes which probably accounts for its chemopreventive effects. There is evidence for its use in preventing cancer of the lung, esophagus, forestomach and hepatocellular adenomas. In toxicity studies, PEITC was shown to have adverse effects on the GI tract as well as some genotoxicity. Although a safe or effective dose has not yet been established for humans, based on animal data, an effective dose would be 0.033 umol/kg-bw/day, or 40 mg PEITC or 1.4 g of watercress. Other isothiocyanates may also be effective in chemoprevention. Phase I studies are expected to begin soon to determine safety and pharmacokinetics of PEITC using a daily dose of 10 mg and up in chronic smokers.


Several epidemiological studies have shown that the ingestion of garlic is associated with decreased levels of various cancers. Garlic contains several sulfur compounds including S-allyl cysteine (SAC) and diallyl disulfide (DADS) which can inhibit phase I enzymes and induce phase II enzymes, thus acting as cancer preventing agents. Extracts of garlic, both odorized and deodorized reduce the transformation of precarcinogens to carcinogens by the P450 enzymes. In rats, DADS inhibits DNA damage and tumor formation, most specifically mammary tumor formation. It was found to be more potent when mixed with vitamin A and selenium. Sulfur containing compounds may also stimulate DNA repair and inhibit DNA and protein synthesis, thus making it potent in protecting against cancer. Onions and leeks are also high in these sulfur containing compounds.

Results from the Iowa Women’s Health Study showed that women who consumed more than one garlic head per week had a 32% reduction in the risk of colorectal cancer compared to those who did not eat garlic. Garlic and onions also contain antioxidant activity as well as selenium which contributes to its chemopreventive activity.

The application of oil-soluble constituents of garlic and onion (diallyl sufide and diallyl disulfide) were shown to inhibit the formation of skin papillomas on mice when administered topically.

Garlic administration has also been used as an adjuvant therapy to reduce the side effects of chemotherapy. This is probably due to its beneficial effects on the cardiovascular system.


A large case control study showed that patients who regularly ingested fresh ginseng extracts had a decreased risk for cancers compared with nonintakers, especially cancers of the oral cavity, esophagus, stomach, colon/rectum, liver, lung and pancreas. Recently, a study showed the effectiveness of a topical, alcohol extract of ginseng towards skin cancer in mice. Researchers applied 1-4 mg of ginseng extract per mouse prior to application of the carcinogen phorbol ester and saw a decrease in both tumor incidence and multiplicity.


Grains contain both dietary fiber and selenium, both of which contribute to chemoprevention. Dietary fiber refers to the components of plant tissue that are resistant to digestion by humans. It acts in many ways to protect against cancer: by increasing stool bulk, the contact time for carcinogens in the colon decreases; by binding with bile acids and other potential carcinogens, it reduces the concentration of free carcinogens; by lowering the fecal pH, fiber inhibits the bacterial degradation of food to potential carcinogens; and, through the production of sodium butyrate, by bacterial fermentation of dietary fiber. Sodium butyrate can induce apoptosis in colonic tumor cell lines and may be involved in inhibiting human colorectal cancer. This may explain the beneficial effect of dietary fiber in colon cancer.

Inorganic forms of selenium are converted by plants into organic selenium analogs of sulfur compounds. Since most studies on selenium use inorganic forms, and bioavailability may differ between organic and inorganic selenium, it is difficult to clearly understand the chemopreventive activity of ingesting selenium. However, low blood selenium levels are associated with a higher cancer mortality and selenium supplementation inhibits DMBA-induced mammary tumorigenesis in rats and mice. Organic selenium can be obtained through grains, vegetables and seafood, the toxicity of inorganic selenium is unknown. Selenium acts by altering carcinogen metabolism, affecting immune function, protecting against oxidant stress, and inhibiting cell proliferation.

In a recent trial to examine the role of selenium to inhibit skin cancer, patients were given 200 micrograms of selenium per day for 4.5 years. Patients were followed up for 6.4 years, and although there was not a decrease in skin cancer, there was a decrease in prostate, colorectal and lung cancers. Selenium has also been found to inhibit chemically induced and spontaneous tumor development in the mammary gland. Selenium is particularly important in the Eastern Coastal US because selenium levels in the soil and thus in the crops is very low. The high hepatoma rate in one area of China, is related to low levels of selenium in the local grain.


Monoterpenes are 10 carbon isoprenoids (5-carbon units) that are secondary products of mevalonic acid metabolism in plants. In animals the mevalonic acid pathway leads to the formation of cholesterol. These monoterpenes were first identified for their activity in controlling cholesterol biosynthesis in animals, but now over 50 monoterpenes have been found to have substantial anti-carcinogenic activity in many models. In addition to their ability to inhibit carcinogenesis, they also demonstrate the ability to induce regression of mammary, liver and pancreatic tumors in rats and have anti-tumor effects in various cell lines. Thus, they have both a chemopreventive as well as a chemo-therapeutic role. Monoterpenes are found in the essential oil fraction of many fruits, herbs and spices, as well as barley oil, rice bran oil, olive and palm oil, and wine. Lesser amounts can be found in dairy products and eggs.

Monoterpenes act at various levels to prevent and inhibit cancer growth:

1. Inhibition of protein isoprenylation, including the cell-growth associated proteins, thus inactivating .

2. Inhibition of the cholesterol pathway, which may play a role in growth inhibition.

3. Inducing apoptosis in tumor cells.

4. Inducing the expression of the liver enzymes glutathione-S-transferase and uridine diphosphoglucuronosyl transferase, thus increasing urinary excretion of carcinogen metabolites and decreasing formation of DNA adducts.

Dietary levels of isoprenoids support chemoprevention, whereas pharmacological doses are chemotherapeutic. Human studies indicate that 0.5 mmol of isoprenoids will significantly lower serum cholesterol and that 10 mmol per day provides chemoprevention.

The two most researched monoterpenes, d-limonene and perillyl alcohol are both undergoing clinical trials for the treatment of advanced stage cancers. Other important monoterpenes with anti-tumor effects are geraniol, menthol, and tocotrienol.

D-limonene is a monoterpene found primarily in the essential oil fraction from orange peel and is often used as a flavor enhancer in drinks and foods. Dietary orange peel oil (1-5%) was found to inhibit the promotion and progression of chemically initiated mammary carcinogenesis in mice and subsequently promote the regression of these tumors. Limonene has been found to decrease the incidence of many tumor types in animals including lung adenomas, skin, liver, mammary tumors and stomach tumors. Currently, limonene is under investigation as a treatment for breast cancer in humans as an alternative to tamoxifen.

A second monoterpene, perillyl alcohol, is found in the essential oil fraction of mints, lavender, and cherries. It is the hydroxylated derivative of d-limonene and is five times as potent as limonene. By selectively inhibiting isoprenylation of small guanine nucleotide-binding proteins (G proteins) by interacting with protein:prenyl transferases, perillyl alcohol can decrease the activity of the protein. The protein has a significant role in cell growth and has been identified as an oncogene in many cancers. Perillyl alcohol can also inhibit cell growth by regulating the synthesis of cholesterol and ubiquinone, as well as inducing differentiation and increasing TGF-beta receptor activated apoptosis as well as TGF-beta levels.

Perillyl alcohol has potential to inhibit colon and small intestine cancer, liver, pancreatic, mammary and prostate cancer. Currently, the NCI is carrying out phase I clinical trials for the use of perillyl alcohol for the treatment of advanced breast cancer in humans. Using a dose of 2 grams per day, there appears to be only slight renal and gastrointestinal toxicities associated with perillyl alcohol. Due to promising results, additional studies are scheduled.


Rosemary has recently been found to contain potent anti-cancer activity, particularly for breast cancer. Rosemary contains anti-oxidants that are more potent than the typical food additives BHT and BHA (tert-butyl-4-hydroxytoluene and tert-butyl-4-hydroxyanisol). Additionally, rosemary has anti-inflammatory activity shown by its ability to reduce the amount of nitric oxide production in mice cells. Nitric oxide released during inflammation, is a free radical that can damage DNA. Active constituents of rosemary include carnosol, carnosic acid, ursolic acid, betulinic acid, rosmaridiphenol and rosmanol, most of which are present in the essential oil fraction.

Besides acting as an anti-inflammatory and antioxidant, rosemary contributes to chemoprevention by preventing the binding of carcinogens to DNA and affecting metabolic enzymes. Researchers have found that whole rosemary extracts and its purified component, carnosol, in the diet of rats was able to prevent binding of the carcinogen, 7,12-dimethylbenz[a]anthracene, (DMBA) to DNA in breast cells. Ironically, the whole extract was more potent than the isolated component, carnosol, with another component, ursolic acid, being ineffective. Similar results were seen in the development of breast tumors in these rats with both rosemary and carnosol decreasing tumor formation by 37%, while the groups receiving ursolic acid showed little reduction in the amount of tumors formed.

Another study showed that rats fed 1% rosemary in their diet for two weeks prior to the administration of DMBA had 76% fewer DNA adducts compared to rats fed a control diet, even when excess fat was added to the diet which increases the number of DNA adducts. High fat diets are known to be associated with a higher risk for breast cancer. Significant effects were also seen with only 0.5% rosemary in the diet. Similar results have been found using human bronchial cells and liver cells. In these experiments the DNA binding of the carcinogens aflatoxin and benzo(a)pyrene were also shown to be inhibited by rosemary extract.

Besides acting by preventing binding of carcinogens to the DNA, rosemary can also affect the metabolism of some carcinogens in a way that decreases their toxicity. Enzymes found in the liver, known as P450, (GSH), and (QR) can affect the toxicity of some chemicals. Although the main role of the liver P450 enzymes is to detoxify compounds, the aromatic hydrocarbons such as DMBA are actually activated into much more potent carcinogens. Thus, DMBA, benzo[a]pyrene and aflatoxin are considered pro-carcinogens rather than direct acting carcinogens. The second group of enzymes, GSH and QR, act by detoxifying these active carcinogenic metabolites and thus protect against cancer.

When rats were fed diets containing whole rosemary extract, the phase II enzymes glutathione S-transferases and quinone reductases were increased significantly. Animals fed carnosol alone however, did not have an increase in these liver enzymes. Similar experiments using human bronchial cells and liver cells in tissue culture have shown that rosemary extract, carnosol and carnosic acid were all able to reduce the levels of P450 enzymes after treatment with benzo(a)pyrene or aflatoxin B1. In bronchial cells, rosemary extract, carnosol and carnosic acid were able to stimulate both glutathione S-transferase and quinone reductase after treatment with benzo(a)pyrene.

Although the anti-cancer properties of rosemary have been clearly demonstrated in animal studies, these have not yet led to human trials. Whole rosemary seems to be as beneficial or more beneficial than its isolated components.

Soy Products

Epidemiological studies have long shown an inverse association between the occurrence of hormone-dependent cancers (mainly breast and prostate) and the traditional soy-rich Asian diet. This anti-cancer activity has been attributed to the presence of phytoestrogens in soy. These phytoestrogens actually act as anti-estrogens by binding to the estrogen receptor and inhibiting the action of estrogen. Several types of cancer including breast cancer and prostate cancer grow in response to estrogen. Soy products have been shown to decrease a woman’s circulating estrogen levels and lengthen her menstrual cycle, lower serum 17 beta-estradiol levels, suppress FSH and LH surges and lower luteal phase prostaglandins. This results in a longer follicular phase of the cycle which is the time of lowest breast cell division, again, giving less stimulation to the breast tissue may result in a lowered risk of cancer. Vegetarian women lower their risk of getting breast cancer by 37%, possibly due to the increased ingestion of phytoestrogens. In post-menopausal women however, soy products have estrogenic effects such as increasing the cell lining of the vagina.

Phytoestrogens also have antioxidant activity. Although the most widely known source of phytoestrogens are soy products which include tofu, roasted soybeans, tempeh and soy milk and soy cheese. They also include lignans found in flaxseed, cereal bran, vegetables, legumes and fruits, and isoflavones found in soybeans, chick peas and other legumes. The flowers from red clover (Trifolium pratense) contain high levels of phytoestrogens also as well as burdock root (Arcticum lappa) which has a long folk history of use in the prevention of cancer. A bonus here is that phytoestrogens can also decrease your risk of heart disease, osteoporosis, and menopausal symptoms. Epidemiological studies indicate that as little as four ounces of tofu per day can reduce a woman’s risk of cancer, with fermented forms such as tempeh, having more bioavailability. Soy consumption has also been associated with a decrease in colorectal cancer.

The most extensively studied isoflavone in soy is genistein, a phytoestrogen found in soy beans and forage plants. Genistein has been found to inhibit breast and skin cancer in animal models. It binds to the estrogen receptor, preventing the binding of estrogen, which seems to promote breast cancer. Genistein is currently under clinical investigation by the NCI as a chemopreventive agent for breast and prostate cancer.


Both black and green tea (Camellia sinensis) contain polyphenols which have anti-cancer activity. This is partially due to polyphenols that are rapidly absorbed and spread through the body, acting as antioxidants. There are three basic types of tea: Green tea, from the fresh leaves of Camellia sinensis, contains catechins including epicatechin, epicatechingallate, epigallocatechin and epigallocatechin gallate; black tea, made by fermentation of green tea, contains theaflavins, and thearubigins; and oolong, which is partially fermented and so retains some, but not all, of the catechins.

Epidemiological evidence suggests that tea consumption protects against cancers of the breast, colon, liver, lung, pancreas, stomach and uterus in humans. The eight year Iowa study of postmenopausal women showed that those who drank two or more cups of black tea per day had a decreased risk of cancers of the digestive tract and urinary tract. Melanoma, and cancers of the pancreas, lung, breast, uterus and ovary were not affected however. There are inconsistencies between various studies, possibly due to comparing risks between different cultures which may have additional variables. Studies of lung and colon are the most inconclusive, with some studies showing an inverse relationship and others not. One study showing that heavy tea drinking (seven or more cups per day) may actually increase the risk of cancer. Animal studies and other pre-clinical experimentation, however, are convincing that green tea and probably black tea too, decrease the risks for several cancers, especially prostate and breast cancers.

A component of tea, epigallocatechin-3 gallate (EGCG), inhibits urokinase-type plasminogen activator (u-PA). This was proposed based on computer simulations, and found to be true in laboratory studies. Since higher urokinase levels are associated with tumors (especially more aggressive ones) and urokinase breaks down protein in tissue and blood, it is thought that urokinase activity contributes to the growth and metastasis of tumors. Inhibiting this enzyme may thus decrease tumor growth and metastasis. Both green and black tea extracts have been shown to inhibit both the initiation and promotion steps of carcinogenesis. The mechanisms include elevation of phase II metabolic enzymes such as glutathione-s-transferase, decrease in phase I enzymes and decrease in the formation of DNA adducts. Tea also inhibits 5 alpha-reductase, an enzyme in the estrogen pathway and thus may play a special role in hormone dependent cancers.

Another recent experiment showed that oral administration of green or black tea inhibited ultraviolet light induced cancer of the skin in mice. When the decaffeinated variety of green or black tea was administered however, the cancers were not inhibited, indicating that caffeine may be an active ingredient. Oral as well as topically applied tea was also effective.

The Chemopreventive Branch of the National Cancer Institute is proceeding with clinical studies to examine the use of tea in the prevention of stomach, lung, and skin cancer.


Turmeric (Curcuma longa), used extensively in curries and mustards, contains curcumin, a yellow pigment with an historical use as an anti-inflammatory and pain reliever. Some human studies have been conducted using curcumin for the treatment of inflammation, atherosclerosis and HIV. Curcumin is also an antioxidant, and found to be useful in preventing tumors of the colon, duodenum, forestomach, mammary gland, oral cavity and skin. Curcumin constitutes approximately 3% of turmeric. Rats that were given up to 2.0% curcumin in their diet for eight weeks showed no toxicity. Humans given a dose of 2,100 mg curcumin orally for 5-6 weeks showed no side effects.

Additional studies have shown that curcumin decreases chemically induced colon adenomas in rats and stimulates apoptosis as effectively as the anti-inflammatory drug sulindac which is commonly used as a chemopreventative drug for colon cancer. Doses were in the range of 2000 ppm or 0.3 mmol/kg-bw/day.

A topical administration of 0.01-2 mmol was effective against skin and oral cavity tumors in mice. Studies done with rodents have also shown that curcumin can inhibit colon, breast, and stomach cancers, at doses ranging from 0.3 to 17.4 mmol/kg-bw/day. Curcumin acts as an anti-inflammatory and an antioxidant, as well as inhibiting phase II metabolic enzymes. Curcumin may also have hormonal and antiviral effects. Because of this, the NCI is considering phase II clinical trials using curcumin, given in 50 mg doses mixed in orange juice, for dysplastic oral leukoplakia patients. Curcumin is also currently in clinical trials in AIDS patients.

There are other active ingredients to turmeric besides curcumin. A water soluble extract of turmeric, not containing curcumin, has been found to decrease forestomach tumor multiplicity and incidence in mice given benzo[a]pyrene.


Vitamins have been suggested by many both in the prevention and the treatment of cancer. In vitro experiments show vitamins E, A, and C having clear chemoprotective effects, but epidemiological and clinical studies are not as clear.

Vitamin A, or retinol, plays a key role in epithelial cell differentiation, decreasing cell proliferation and stimulating angiogenesis. Because deficiencies in vitamin A have been associated with an increased risk of cancer, it has received much attention in chemoprevention. Retinoic acid is effective at inhibiting rat mammary tumorigenesis and optimizing the efficacy of tamoxifen as a chemopreventive agent. Clinical trials are ongoing to determine the role of retinoic acid as a chemopreventive agent for breast cancer, head and neck cancer and prostate cancer, but there is also evidence that it reduces the risk of bladder cancer. The maximum tolerated dose for humans of 9-cis-RA is 100-140 mg/m2. Natural analogues of retinoids have been found to be less toxic than synthetic retinoids. Care should be taken for the pregnant patient however, since large amounts of retinoids can be teratogenic.

Some carotenoids can be converted into vitamin A and are abundant in green leafy vegetables, orange vegetables, dandelion leaves and stinging nettle. Beta-carotene may inhibit cancer by acting as an antioxidant, by modulating the immune system and by modifying enzymatic activation of carcinogens. In a study examining the protective effects of vitamins E, C, and A, high intake of carotinoids in the form of fruits and vegetables was shown to reduce the risk of lung cancer. Several studies suggest that the ingestion of a variety of retinoids and carotenoids are more beneficial than vitamin A alone in preventing cancer. Lycopene, found in tomatoes, ruby red grapefruit and red peppers has been shown to protect against prostate and cervical cancer.
Vitamin C

Vitamin C or ascorbic acid, is a powerful, water soluble, and non-toxic antioxidant. Its presence in fruits and vegetables, may account for some of the beneficial effects of these foods. Epidemiological studies support the benefits of vitamin C in the prevention of cancer, while animal studies do not. Ascorbate can block the formation of carcinogens such as nitrosamines. In a 19 year study examining lung cancer incidence (First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study) which examined 3,968 men and 6,100 women, vitamins C, E, and carotinoid intake were associated with a reduced risk of lung cancer in smokers and non-smokers. Smoking, of course, attenuated the protective effect somewhat.
Vitamin E

Tocopherols (vitamin E) occur in polyunsaturated vegetable oils and in the germ of cereal seeds (wheat germ) and palm oil. Again, vitamin E acts as an antioxidant as well as a blocker of nitrosamine formation. The literature regarding vitamin E is also inconsistent and not convincing for its use in chemoprevention.
Vitamin D

Vitamin D (alpha-(OH)D3) – has been shown to inhibit rat mammary tumors. Due to the potential imbalance that vitamin D may cause in calcium metabolism however, further studies need to be done to establish the role for vitamin D in chemoprevention.

Folate or folic acid. This water soluble B vitamin complex cannot be synthesized by mammals and must be supplied in the diet by liver, leafy green vegetables, legumes and cereals. Folate is necessary for methylation reactions and synthesis of DNA nucleotides. DNA methylation is involved in gene regulation and is necessary for inhibiting gene transcription. Hypomethylation of genes has been identified in colorectal cancers and an inverse association with folate is observed in this cancer. Overall, the effects of folic acid on carcinogenesis are complex and not fully understood, however, the NCI is proceeding with clinical development of folic acid as a chemopreventive agent.

Wine contains resveratrol, also common in mulberries and peanuts. This compound shows early evidence of inhibiting initiation, promotion and progression of cancer in vitro experiments. In mice studies, resveratrol was able to inhibit chemically induced skin tumors when applied to the skin at doses of 1-25 umol. Wine grapes also contain ellagic acid, which is an antioxidant and has been found to decrease the rate of esophageal tumors in rats. Ellagic acid is also found in berries and nuts.

Omega-3-fatty acids – may reduce cancer risk, especially for breast and gastrointestinal cancers. Its inhibitory action on cancer is related to its ability to inhibit prostaglandin synthesis. The best source of omega-3-fatty acids is fish oil but plants high in this oil include borage and flax seed.

Antioxidants – antioxidants scavenge active oxygen species such as hydroxyl radical, superoxide anion, and singlet oxygen. They can also interfere with lipid peroxidation, xanthine oxidase activity and nitrite/nitrogen oxide production. Oxidant stress has been linked to both the initiation and post-initiation stages of carcinogenesis, thus antioxidants are often found to be chemopreventive. Most herbs (see rosemary) are found to contain potent antioxidants.

Antioxidants may also have an effect on phase I and/or phase II biotransformation enzymes and can affect carcinogen metabolism. These antioxidants include phenols, alcohols, and lactones.

Anti-inflammatories – anti-inflammatory agents can decrease arachidonic acid release and metabolism by diminishing activity of phospholipases A2 and Cgamma1, cyclooxygenase and lipoxygenase. Prostaglandin biosynthesis has been linked to both the initiation and postinitiation stages of carcinogenesis. Thus, anti-inflammatories are often found to be chemopreventive agents as is evidenced by the recent advice for those at risk of colon cancer to take an aspirin each day and by the development of new non-steroidal anti-inflammatory agents (e.g., Sulindac) for the prevention of colon cancer. Many herbs (see rosemary) are found to contain potent anti-inflammatories.
Complementary Herbs to Chemotherapy

Most patients after being diagnosed with cancer, opt to undergo chemotherapy, which can have devastating side effects. This is an area where herbs can be used both to counteract some of the side effects as well as increase the efficacy of the chemotherapy. Although rigorous clinical trials have not been performed on these agents, they have a long history or efficacy and low toxicity. This is a list of some herbs that may provide relief.
Gastrointestinal tract problems and emesis

Although many improvements have been made to control emesis associated with chemotherapy, it remains a problem that most patients fear. Native Americans used Holly, (Ilex vomitoria) and Spurge (Euphorbiae) to control emesis. In addition, Catnip (Nepeta cataria), Chamomile (Matricaria chamomilla), Ginger (Zingiber officinalis), and Red Raspberry (Rubus spp.) can help comfort nausea caused by chemotherapy. Care should be taken with ginger however as it can also inhibit blood clotting. If a patient is already losing blood clotting ability due to chemotherapy, ginger can worsen that.
Stimulating the immune system

Maintaining a strong immune system is important, both to minimize the cancer and to counteract the suppressive effects chemotherapy has on the immune system. Two important immune stimulants are Echinacea (Echinacea purpurea or pallida) and Astragalus (Astragalus membranaceus). Many studies have shown the positive effects of Echinacea on the immune system and its ability to enhance the function of mononuclear white blood cells. The root, upper parts or whole plant, expressed as a juice or as an alcohol extract are all effective. Astragalus has also been documented to improve the immune system and its use might also reduce the risk of getting cancer or having a recurrence of cancer. These herbs can also be taken prior to surgery to reduce the risk of infection.
Stimulating blood components

Dose limiting effects of chemotherapy include reduction of platelet and red blood cell number. Although very few scientific studies have been interested in these aspects, there is some evidence that Agrimony (Agrimonia pilosa) can stimulate blood clotting, and Angelica (Angelica archangelica) can activate the spleen and tone the blood. Nettle infusion may also promote blood clotting.
Liver protection

As a powerful toxin itself, chemotherapy can damage the liver. Using a tincture of Milk Thistle (Carduus marianum) or an extract of its active ingredient silymarin prior to chemotherapy may help liver function and possibly increase efficacy of the cancer therapy.

Cancer patients often find themselves weakened by both the cancer itself and its treatment. An extract of Ginseng can help restore energy. In fact, in Russia, Siberian Ginseng (Eleutherococcus senticosus) is sometimes given along with chemotherapy. To decrease restlessness that may lead to a lack of sleep, skullcap (Scutellaria lateriflora) and valerian (Valerian officinalis) can help.

There is ongoing research to find drugs that can improve the effectiveness of chemotherapy, allowing a lower dose to be used and improving the quality of life in patients. Some of these agents are from herbs, such as curcumin, and compounds from Nigella. Mistletoe extracts such as Iscador or Eurixor, which are used by injection, have been shown to enhance the immune system of breast cancer patients, and may even have a negative effect on the cancer itself. Hopefully, there will be advances made in this area soon.
Patient Recommendations

For patients interested in how to decrease their risk of developing cancer by using foods, the following is general advice:

1. Eat a wide variety of foods, fruits, vegetables, legumes and whole grains.

2. Eat 5 servings of fruit and vegetables per day.

3. Season your food with a variety of herbs, and drink herb teas, especially herbs high in antioxidants.

4. Avoid obesity.

For patients concerned about the development of specific cancers, the following lists agents with chemoprotective ability towards specific cancers.

Breast Cancer – Patients concerned about the development of breast cancer should be advised to increase their consumption of cruciferous vegetables, and garlic and possibly supplementing with indole-3-carbonol. Because of the promising results of monoterpenes such as perillyl alcohol, perhaps patients could be referred to cookbooks that use essential oils.

Lung Cancer – Patients concerned about the development of lung cancer should first off, quit smoking. Increasing the consumption of cruciferous vegetables is important for the isothiocyanates they contain. Selenium, which can be found in grains and seafood has also demonstrated chemoprotective ability in lung cancer.

Prostate Cancer – Oftentimes prostate cancer is hormone dependent and thus the consumption of additional soy products can decrease the risk of prostate cancer. Both selenium and tea have been shown to provide chemoprotection for prostate cancer.

Gastrointestinal Cancer – The most important factor in decreasing the risk of gastrointestinal cancer, specifically colorectal cancer is to decrease the consumption of fat and increase the consumption of fiber. Selenium may also provide some protection as well as herbs high in antioxidants. The increased consumption of fruit and vegetables is also inversely related to the incidence of rectal cancer.

Skin Cancer – Skin cancer is one of the most rapidly increasing cancers in terms of incidence. Some herbs taken internally have been shown to provide protection from skin cancer such as tea, and silymarin from milk thistle. These compounds may also provide protection when used topically along with a sunscreen.

Stomach Cancer – Increased acidity in the stomach by ingestion of vitamin C can decrease the incidence of stomach cancer. Increased fruit and lettuce associated with a lowered risk of stomach cancer, as well as garlic consumption.

Head and Neck Cancer – Increasing the consumption of fruit and vitamin A is associated with decreased risk of head and neck cancer.

Toxic clouds confirmed over Canada Tar Sands region

toxic clouds over alberta

Analyses of the air quality in one of the largest petrochemical regions of Canada revealed the presence of concentrated toxic clouds according to a “Nobel Prize” laboratory at the University of California, Irvine laboratory. These analyses reflect the results that had already been obtained confirming the presence of carcinogenic substances in the northeast of Edmonton. Although only a sample was collected, the results are “not due to random”, according to the head of the laboratory, Donald Blake. Researchers visited the region known as the “industrial heart of Alberta” in June 2012, which includes more than 40 petrochemical companies. 96 air samples were collected in the vicinity and in rural areas upstream of the wind. The majority of the results are below safe limits for Alberta. But between the 8th and 12th of July of this year, researchers detected significant increases in the levels of benzene, a carcinogenic substance that has no safe level, during three days. One sample indicated the presence of 11 parts per billion (ppb) of benzene, another 24 ppb, and a third, 156 ppb. Alberta recommends that the rate of benzene does not exceed 9 ppb during an average of an hour . According to Mr. Blake, “If this is something that the wind brings in a home and the home receives five to 20 parts per billion benzene all the time, it starts to worry me,” he said. It was the third visit by the laboratory in the Alberta industrial heartland. In 2008 and 2010, results, reviewed by peers and published, revealed the presence in the air of chemical substances that cause smog at levels comparable – and sometimes even superior – to the largest cities and the largest industrial centers of the world. At least 10 toxic products detected in the clouds were substances carcinogenic either known, or suspected. The researchers also found that the prevalence of blood cancer in men between 1997 and 2006 in the three counties surrounding the area was significantly higher than in neighboring counties. A causal relationship has however never been established. A spokesman for the Alberta Department of the Environment said that the recommended air quality standards followed by the agency’s monitoring of industrial heartland were established by a group made up of representatives of the government,industry and environmentalists. However, she declined to comment on the results of the California laboratory.

New study shows how to reprogram cancer cells back to normal

Viotox reports on a study published in Nature Cell Biology in which researchers detailed a way to reprogram cancer cells back to normal, opening the door to new treatments for cancer.

cancer cells
Viotox reports researchers found that when they restored normal miRNA signals in cancer cells, they could reverse the process that makes cells grow uncontrollably.
Cancer is like a complex software program of life that has got out of control; instead of the code for normal cells, a code for making abnormal cells is executed. Now, a new study in Nature Cell Biology suggests there may be a way to change the code so that cancer cells revert back to normal cells.

The study shows that when normal cells come together, a specific group of miRNAs suppresses genes that encourage cell growth. But, for some reason, this is disrupted in tumor cells, and growth becomes uncontrolled – the hallmark of cancer.

The researchers found when they restored normal miRNA signals in cancer cells, they could reverse the process and control growth.

MicroRNA and Cancer

MicroRNAs or miRNAs represent an important class of small regulatory RNAs that are intrinsic to post-transcriptional gene control. They are approximately 22 nucleotides in length and regulate the expression of as much as 30% of all mammalian protein-encoding genes.

Experimental approaches have shown that some miRNAs act as tumor suppressors, and other ones as oncogenes; hence they have important roles in cancer development, progression of the disease and its prognosis. Dysregulation of miRNAs is linked to the development of cancer.

The Death of the “Dust Lady” : A terrible reminder of the health consequences of 9/11.

When the Twin Towers collapsed to the ground on September 11, 2001, a massive cloud of smoke, dust and debris released hazardous asbestos fibers, toxins and toxic substances into the air. Asbestos fireproofing materials from 20 stories of the towers came showering down on New York City. According to reports from the EPA, the implosion from the towers “pulverized asbestos to ultra-fine particles.”

lady dust
Lady Dust

The World Trade Center Health Registry estimates about 410,000 people were exposed to a host of toxins including asbestos during the rescue, recovery and clean-up efforts that followed 9/11. Lady Dust who recently died from stomach cancer was one of the victims. But some of the people most affected at Ground Zero were those assigned to rescue survivors. These workers were among the first on the scene and the last to leave the wreckage. Search and rescue workers and others responsible for cleaning up the debris in the months after the towers collapsed were also exposed to asbestos.


More than 1,100 people who worked or lived near the World Trade Center on 9/11 have been diagnosed with cancer, according to the Centers for Disease Control and Prevention.


911 toxins

9/11 and the Asbestos Lung Cancer Danger.

Asbestos lung cancer is a rare type of lung cancer, which is the most common cause of cancer death in the United States. An estimated 4,800 deaths a year are linked to this illness, a number that represents about 4 percent of all U.S. fatalities connected to cancer of the lungs. The overwhelming majority of other deaths — about 90 percent — are linked to smoking.

Medical researchers first made a probable causal relationship between exposure to asbestos and lung cancer in 1935. Seven years later, a member of the National Cancer Institute confirmed asbestos as a cause of lung cancer. Study after study continued to show the cause-effect relationship of asbestos and lung cancer. The Occupational Safety and Health Administration (OSHA) in 1986 proclaimed lung cancer as the greatest risk for Americans who worked with asbestos.

Like mesothelioma, another asbestos-related cancer, lung cancer associated with asbestos is typically diagnosed at a late stage of development because of the long latency period of development and the onset of symptoms.

Similarities and Differences of Mesothelioma and Asbestos Lung Cancer: Both take decades to develop, but only months to spread to distant organs. They have similar diagnostic procedures and treatment techniques; however, the diseases differ in physical characteristics and non-asbestos risk factors. .

Exercise Needs to Be Part of the New Standard for Cancer Prevention


Most cancers are caused by lifestyle factors — not genes.

The second most important action you can take to help guard against many types of cancer – after dieting and food choices – is exercise. Up to one-third of cancer-related deaths are due to obesity and a sedentary lifestyle, including two of the most common cancers in the world, breast and colon cancer.

But the benefits of exercise are not limited to prevention alone. It can also help you recuperate faster and help prevent recurrence of cancer. A report issued by the British organization Macmillan Cancer Support  just last year argues that exercise really should be part of standard cancer care. It recommends that all patients getting cancer treatment should be told to engage in moderate-intensity exercise for two and a half hours every week, stating that the advice to rest and take it easy after treatment is an outdated view.

Advice for fighting and preventing cancer with exercise:

Exercise reduces the risk of breast-cancer.
The relationship between physical activity and breast cancer incidence has been extensively studied, with over 60 studies published in North America, Europe, Asia, and Australia. Most studies indicate that physically active women have a lower risk of developing breast cancer than inactive women.

Exercise plays an important role in reducing the risk of cancer of the colon and rectum.
Colorectal cancer has been one of the most extensively studied cancers in relation to physical activity, with more than 50 studies examining this association. Many studies in the United States and around the world have consistently found that adults who increase their physical activity, either in intensity, duration, or frequency, can reduce their risk of developing colon cancer by 30 to 40 percent relative to those who are sedentary regardless of body mass index (BMI), with the greatest risk reduction seen among those who are most active.

Exercise reduces the risk of endometrial cancer.
About 20 studies have examined the role of physical activity on endometrial cancer risk. The results suggest an inverse relationship between physical activity and endometrial cancer incidence. These studies suggest that women who are physically active have a 20 percent to 40 percent reduced risk of endometrial cancer, with the greatest reduction in risk among those with the highest levels of physical activity.

Exercise reduces the risk of lung cancer risk.
At least 21 studies have examined the impact of physical activity on the risk of lung cancer. Overall, these studies suggest an inverse association between physical activity and lung cancer risk, with the most physically active individuals experiencing about a 20 percent reduction in risk.

Exercise may reduce the risk of liver cancer.
Research results announced at the 2013 International Liver Congress found that mice who exercised on a motorized treadmill for an hour each day, five days a week for 32 weeks, experienced fewer incidents of liver cancer than sedentary mice.

Your Lifestyle Has Tremendous Influence Over Your Health and Cancer Risk:

In light of the evidence supporting the notion that lifestyle changes, such as exercise, have a profound impact on the risk of cancer, it would be foolish in the extreme to ignore such advice. In fact, it is surprising that most oncologists will not expressly recommend exercise as a standard for cancer prevention and treatment.
exercise-30 minutes to prevent cancer
How much exercise do you need to help prevent cancer?

According to national activity guidelines, a good goal is to exercise at least 30 minutes a day on most days of the week. To get the most benefit, though, aim for about an hour a day. Moderate-intensity activities such as brisk walking may be sufficient, although there is more benefit with increased intensity.

9/11 Lady Dust Dies From Cancer

lady dust

A survivor of the attacks of 11 September 2001 in New York, immortalized in an iconic photo taken during the event, died of stomach cancer at the age of 42, her family said on Facebook.

At the time of the attacks, Marcy Borders was 28 and had worked for a month for the Bank of America, in one of the twin towers of the World Trade Center.

When one of the two towers collapsed, she had taken refuge in a nearby building, where Stan Honda, AFP photographer, took a picture of her that went around the world.

Ms. Borders appeared completely covered with a thick layer of ash, which earned her in the United States and the world, the nickname “Dust Lady” (“Lady dust”).

On the photograph, Marcy Borders, recovering from the attacks, was wrapped in a cloud of dust and seemed back lit by a disturbing yellow light.

After the attacks, Marcy Borders sank into a long spiral of unemployment, depression, alcohol and drug use, from which she had finally managed to recover from in 2011.

Since September 11, she has spent most of her time in a very modest apartment in New Jersey, not far from Manhattan and locations of the attacks, without psychological or financial support, she told AFP in 2012. She said she “always lived in fear” and rarely left her home, unable to imagine going back “in these targets, bridges, tunnels, stations (subway).”

Marcy Borders had started a treatment for cancer a year ago, suggesting that her illness may have been linked to chemical pollutants emitted during the collapse of the World Trade Center.

Can X-Rays Cause Cancer?


Some studies have estimated the risk of radiation exposure from imaging tests based on the risks from similar amounts of radiation exposure in the studies of the atomic bomb survivors. Based on these studies, the US Food and Drug Administration (FDA) estimates that exposure to 10 mSv from an imaging test would be expected to increase the risk of death from cancer by about 1 chance in 2000.

It can be difficult to study cancer risks from imaging studies that use radiation. In order to see small risks (such as 1 in 2000), a study would have to look at 10s or 100s of thousands of people. Information about other exposures that could be cancer risk factors would be needed, to see if it was likely that the cancer came from the radiation exposure. Since cancers from radiation take years to develop, the study would need to follow the patients for many years.
radiation induced cancer enlarged

Often, scientists use questionnaire studies to look for possible causes of cancer. These studies compare exposures among people who have a certain cancer to those who don’t. They may instead compare people who had a certain exposure (like to radiation) to those who didn’t. However, this is difficult to do for diagnostic radiation exposure since many people cannot accurately recall information about things that happened many years before (such as in childhood) and information about all the imaging tests that were done is often not available. There is also a concern that people with cancer tend to over report exposures that they worry may have caused their cancers.

radiation induced cases of cancer pre yesr

Studies that have found increased risk of cancer after imaging tests that use x-rays often involve people who had multiple tests or high dose procedures, including:


Studies of women who had been imaged many times with fluoroscopy as a teenager or young woman during treatment for tuberculosis have found an increased risk of breast cancer years later.

Spine x-rays

Teenagers and young women who had many x-rays of the spine to monitor scoliosis have been found to have an increased risk of breast cancer later on.

Dental x-rays

A study compared a group of people with meningioma (a brain tumor that is most often benign) with a group without the tumors. It found that the people who had the tumors were more likely to have had a type of dental x-ray called a bite-wing, and to have had bite-wing or Panorex x-rays every year.

CT scans

A study in England of exposure to radiation from CT scans found that children who received a dose of at least 30 mGy (the same as 30 mSv) to the bone marrow had 3 times the risk of leukemia compared to those who received a dose of 5 mGy or less. For brain tumors, a dose of 50 mGy or more to the brain was linked to more than 3 times the risk.

A study in Australia of exposure to radiation from CT scans in childhood and adolescence found that after an average of about 9 ½ years, those who had a CT scan had a 24% higher risk of cancer overall. The risk of cancer was higher the more CT scans the person had, and it was also higher the younger the person was at the time of the CT scan. Still, the overall risk of cancer was still low.

A study from Taiwan found that children and teens who had a CT scan of the head did not have a higher risk of brain cancer or leukemia, but were more likely to be diagnosed with a benign brain tumor.

Can Marijuana Cure Cancer?

can marijuana cure cancer

Is It Time to Acknowledge That Marijuana Can Cure Cancer?

US Surgeon General Vivek Murthy in an interview with CBS This Morning, said, “We have some preliminary data showing that for certain medical conditions and symptoms, marijuana can be helpful.” His statement echoes a growing sentiment in the medical and scientific communities that the health benefits of marijuana should no longer be ignored.

Research conducted by a team of scientists at St. George’s University of London, found the two most common cannabinoids in marijuana, tetrahydrocannabinol (THC) and cannabidiol (CBD), weakened the ferocity of cancer cells and made them more susceptible to radiation treatment. The study, which was published last year in the medical journal Molecular Cancer Therapies, details the “dramatic reductions” in fatal variations of brain cancer when these specific cannabinoids were used in conjunction with radiation therapy.

“We’ve shown that cannabinoids could play a role in treating one of the most aggressive cancers in adults,” wrote lead researcher Dr. Wai Liu, in a November 2014 op-ed for The Washington Post. “The results are promising… it could provide a way of breaking through glioma [tumors] and saving more lives.”

In his medical practice, Dr. Frankel treats a wide variety of patients with medical cannabis, which has become his specialty. Despite the many claims of cannabis performing miracles, he’s reluctant to think of it as a cure for anything. Occasionally, however, patients will experience very dramatic results. For example, he has seen tumors virtually disappear in some patients using no other therapy except taking 40 to 60 milligrams of cannabinoids a day. The most common thing he sees in cancer patients, however, are tumors shrinking, or a metastasis disappearing. Sometimes tumors will shrink or vanish, only to reemerge in other areas, months later, and then shrink or vanish again…

Check out this video on marijuana research:

19 Medical Studies That Show Cannabis Can Be A Potential Cure For Cancer

Brain Cancer

1. A study published in the British Journal of Cancer, conducted by the Department of Biochemistry and Molecular Biology at Complutense University in Madrid, determined that Tetrahydrocannabinol (THC) and other cannabinoids inhibit tumour growth. They were responsible for the first clinical study aimed at assessing cannabinoid antitumoral action. Cannabinoid delivery was safe and was achieved with zero psychoactive effects. THC was found to decrease tumour cells in two out of the nine patients.

2. A study published in The Journal of Neuroscience examined the biochemical events in both acute neuronal damage and in slowly progressive, neurodegenerative diseases. They conducted a magnetic resonance imaging study that looked at THC (the main active compound in marijuana) and found that it reduced neuronal injury in rats. The results of this study provide evidence that the cannabinoid system can serve to protect the brain against neurodegeneration.

3. A study published in The Journal of Pharmacology And Experimental Therapeutics already acknowledged the fact that cannabinoids have been shown to possess antitumor properties. This study examined the effect of cannabidiol (CBD, non-psychoactive cannabinoid compound) on human glioma cell lines. The addition of cannabidiol led to a dramatic drop in the viability of glioma cells. Glioma is the word used to describe brain tumour. The study concluded that cannabidiol was able to produce a significant antitumor activity.

4. A study published in the journal Molecular Cancer Therapeutics outlines how brain tumours are highly resistant to current anticancer treatments, which makes it crucial to find new therapeutic strategies aimed at improving the poor prognosis of patients suffering from this disease. This study also demonstrated the reversal of tumour activity in Glioblastoma multiforme.

Breast Cancer

5. A study published in the US National Library of Medicine, conducted by the California Pacific Medical Centre, determined that cannabidiol (CBD) inhibits human breast cancer cell proliferation and invasion. They also demonstrated that CBD significantly reduces tumour mass.

6. A study published in The Journal of Pharmacology and Experimental Therapeutics determined that THC as well as cannabidiol dramatically reduced breast cancer cell growth. They confirmed the potency and effectiveness of these compounds.

7. A study published in the journal Molecular Cancer showed that THC reduced tumour growth and tumour numbers. They determined that cannabinoids inhibit cancer cell proliferation, induce cancer cell apoptosis, and impair tumour angiogenesis (all good things). This study provides strong evidence for the use of cannabinoid based therapies for the management of breast cancer.

8. A study published in the Proceedings of the National Academy of Sciences of the United States of America (PNAS) determined that cannabinoids inhibit human breast cancer cell proliferation.

Lung Cancer

9. A study published in the journal Oncogene, by Harvard Medical Schools Experimental Medicine Department, determined that THC inhibits epithelial growth factor induced lung cancer cell migration and more. They go on to state that THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certainlung cancers.

10. A study published by the US National Library of Medicine by the Institute of Toxicology and Pharmacology, from the Department of General Surgery in Germany, determined that cannabinoids inhibit cancer cell invasion. Effects were confirmed in primary tumour cells from a lung cancer patient. Overall, data indicated that cannabinoids decrease cancer cell invasiveness.

11. A study published by the US National Library of Medicine, conducted by Harvard Medical School, investigated the role of cannabinoid receptors in lung cancer cells. They determined its effectiveness and suggested that it should be used for treatment against lung cancer cells.

Prostate Cancer

12. A study published in the US National Library of Medicine illustrates a decrease in prostatic cancer cells by acting through cannabinoid receptors.

13. A study published in the US National Library of Medicine outlined multiple studies proving the effectiveness of cannabis on prostate cancer.

14. Another study published by the US National Library of Medicine determined that clinical testing of CBD against prostate carcinoma is a must. That cannabinoid receptor activation induces prostate carcinoma cell apoptosis. They determined that cannabidiol significantly inhibited cell viability.

Blood Cancer

15. A study published in the journal Molecular Pharmacology recently showed that cannabinoids induce growth inhibition and apoptosis in mantle cell lymphoma. The study was supported by grants from the Swedish Cancer Society, The Swedish Research Council, and the Cancer Society in Stockholm.

16. A study published in the International Journal of Cancer also determined and illustrated that cannabinoids exert antiproliferative and proapoptotic effects in various types of cancer and in mantle cell lymphoma.

17. A study published in the US National Library of Medicine conducted by the Department of Pharmacology and Toxicology by Virginia Commonwealth University determined that cannabinoids induce apoptosis in leukemia cells.

Oral Cancer

18. A study published by the US National Library of Medicine shows that cannabinoids are potent inhibitors of cellular respiration and are toxic to highly malignant oral tumours.

Liver Cancer

19. A study published by the US National Library of Medicine determined that THC reduces the viability of human HCC cell lines (Human hepatocellular liver carcinoma cell line) and reduced their growth.
Pancreatic Cancer