Anthrax as a cancer treatment

Scientists have used a version of the anthrax toxin to kill tumours in mice. The toxin was so effective that after just one treatment, tumours were reduced in size by up to 92%. The technique has been developed by researchers from the US National Institutes of Health. It works by targeting a protein called urokinase which is produced in high levels by cancerous cells. The researchers genetically altered the structure of the anthrax toxin so it only invaded cells that produced high levels of urokinase. Different tumour types The toxin effectively killed several types of tumour cells, without causing any apparent damage to normal tissue. Tumour cells began dying just 12 hours after the first treatment. Two treatment cycles were enough to completely obliterate 88% of a type of tumour called a fibrosarcoma. It also knocked out 17% of a second type of tumour called a melanoma.

 

However, the toxin did not damage skin cells or hair follicles surrounding the tumour – suggesting that the toxin is highly selective, and may not lead to the severe side effects sometimes associated with alternative treatments. The researchers stress that further research is needed to determine if the engineered anthrax toxin will have similar effects in humans. Lead researcher Dr Steve Leppla told BBC News Online: “The fact that our cytotoxin can successfully kill several different solid tumours suggests it may be even better on leukemias, where the toxin has an easier time reaching every tumour cell. “We are testing that now.” Dr Elaine Vickers, of Cancer Research UK, described the research as very interesting, but warned that it was still at an early stage.

 

She said more work was needed to discover whether the technique worked in humans, and to confirm that it did not damage healthy cells. “Molecules that are over-produced by cancer cells are very interesting as targets for developing new cancer treatments, hopefully with fewer of the side-effects associated with more conventional therapies. “However, it is essential that the molecule targeted by the treatment is exclusively over-produced by cancer cells to avoid damage to healthy tissue. “This is particularly important if a potent toxin, such as the anthrax toxin being investigated in this research, is being used to kill the cancer cells.” The research is published in the Proceedings of the National Academy of Sciences.

Teen smokers risk breast cancer

In 1998, the International Agency for Research on Cancer (IARC), cancer research branch of the World Health Organization (WHO), published a seven-country study that found a 16-17% increase in lung cancer risk associated with secondhand smoke. This finding is consistent with the rest of the scientific literature. Before the study was published, on March 8, 1998, the London Sunday Telegraph reported, incorrectly, that WHO was withholding the study because not only did it fail to show secondhand smoke caused lung cancer, but suggested that Secondhand smoke could even reduce lung cancer risk.

 

These “astounding results are set to throw wide open the debate on passive smoking health risks.[and] are certain to be an embarrassment to the WHO,” said the newspaper story, quickly picked up from Australia to the U.S. to Zimbabwe. British American Tobacco (BAT), was suspected of fuelling the Sunday Telegraph story. Dr. Chris Proctor, a scientific spokesman for BAT Industries, was quoted: ‘If this study cannot find any statistically valid risk you have to ask if there can be any risk at all.” It is longtime tobacco industry practice to distort the meaning of “statistical significance.” The World Health Organization immediately released a strong denial, titled “Passive Smoking Does Cause Lung Cancer, Do Not Let Them Fool You.”

 

It said the study results were not being withheld but, according to accepted scientific practice, had been sent to a reputable scientific journal for peer review before publication. The results of this study, which have been completely misrepresented in recent news reports, are very much in line with the results of similar studies both in Europe and elsewhere: passive smoking causes lung cancer in non-smokers. Long before the WHO/IARC study was released, Philip Morris had prepared a strategy to discredit it. From the company’s September 1993 “Action Plan”:

Smoking gives addicts a deadly high

Smoking, one of the world’s major killers, draws in its victims by offering a subtle but compelling high, scientists say. On Thursday, the U.S.-based cigarette manufacturer Liggett Group made the astonishing move of admitting that smoking damages health and is addictive. Tobacco companies have denied this for years. But doctors and anti-smoking campaigners can cite volumes of evidence that details just how smoking not only damages the body, but tricks it into begging for more. “The evidence that it is powerfully addictive is absolutely overwhelming,” said Dr Martin Jarvis, an addiction expert for the Imperial Cancer Research Fund, a British charity. Of more than 61,000 people surveyed by the U.S. Centres for Disease Control, 79.6 percent of daily cigarette smokers said they could not cut down. Only 66 percent of daily cocaine users said they could not. “It’s a kind of stimulant drug, a bit like amphetamine. One of the thoughts about why cigarettes are so addictive is the route of administration,” Jarvis said. “When you inhale it in smoke you are getting the drug hitting the brain within seven to 10 seconds, which is actually faster than if you injected it. It is also cleared from the body very rapidly so you have to keep getting yourself a hit to keep levels up.”

 

Scientists are beginning to understand the effects of nicotine on the brain. It seems literally to excite brain cells. One brain chemical that smoking affects is dopamine, an important neurotransmitter, or chemical that carries messages between brain cells. “It has something to do with reward mechanisms in the brain,” said Leslie Iversen, a pharmacologist at England’s Oxford University. “It seems to be a final common pathway that is activated by a whole series of drugs that people seem to like using and that includes nicotine, cocaine, alcohol, marijuana and heroin.” Researchers at Brookhaven National Laboratory in Upton, New York, found last year that smokers had less of an enzyme called monoamine oxidase (MAO), which breaks down dopamine, than ex-smokers or people who do not smoke. This would mean more dopamine was available to their brains. Drugs such as cocaine and heroin have a similar effect.

 

Other research has shown that nicotine locks on to areas in the brain that release acetylcholine, another neurotransmitter that sets off electrical impulses in nerve and muscle cells. Yet others have found it causes nerve cells to send out a larger-than-normal amount of glutamate, an excitory transmittor which, as the name implies, excites or stimulates cells. Experts say about three million people die each year from smoking-related illness in developed countries, representing 20 percent of all deaths. Eight different types of cancer, from lung cancer to leukaemia, are linked with smoking and smoking is the single biggest risk factor for heart disease. “Tobacco smoke contains a large number of chemicals that are known to cause cancer by damaging the DNA of cells,” said Dr David Phillips, a research scientist specialising in molecular carcinogenesis at the Institute of Cancer Research in London.

Top 10 Cancer-Fighting Foods

1. Tomatoes -These tasty spheres are bursting with the powerful antioxidant vitamin C and lycopene. Vitamin C bolsters the immune system and fends off cancer-causing free radicals, and lycopene is instrumental in cutting the risk of stomach, mouth, bladder, cervical, colon and prostate cancer. 2. Cruciferous Vegetables- Broccoli, red cabbage, cauliflower, kale, red beets and brussels sprouts all belong to this veggie family. All are amply fortified with cancer-fighting phytochemicals, including sulforaphane, beta-carotene and indolcarbinol. 3. Spinach-Popeye knew his nutrition. This dark, leafy vegetable is chock-full of antioxidants such as glutathione, vitamin C, beta-carotene, folic acid and carotenoids. Bright orange carrots are also an excellent source of beta-carotene and carotenoids — chemicals known to curb various cancers. 4. Beans- Beans, beans, they’re good for … beating digestive and breast cancer! Soybeans are stocked with protease inhibitors that don’t let cancer cells invade the body, and also contain isoflavones instrumental in protecting against breast cancer. Fava beans fight carcinogens, reducing the risk of cancer in the digestive tract.

 

5. Hot red peppers -Biting into these zesty peppers may set off a fire in your mouth, but the capsaicin inside snuffs out harmful carcinogens emitted by cigarettes and some foods. These hot numbers are number one in protecting against lung cancer. 6. Garlic -This member of the onion family isn’t only powerful in flavor and scent. Garlic effectively thwarts carcinogens with organosulfides and allicinthus, helping to protect the body from breast cancer. 7. Oranges -Jam-packed with cancer-fighting bioflavonoids and immune system-boosting vitamin C, oranges also contain 170 photochemicals, including carotenoids. In addition, limonoids found in oranges and other citrus fruits fuel the immune system to fight cancer 8. Berries -Strawberries, blueberries, cranberries, raspberries, blackberries and red and purple grapes boast more than a sweet taste. These bite-sized fruits get their dark hue from anthocyanins that can neutralize carcinogens. Plus, berries are bursting with flavonoids, a powerful group of cancer-fighting antioxidants.

 

9. Fiber-Rich Foods -Foods full of fiber, such as whole wheat, grains, fortified cereals and apples, protect the body from pancreatic and stomach cancer while also helping to flush toxins from the body. And apples provide an additional cancer kicker with their ample supply of ellagic acid. Ellagic acid inhibits cancer cell division, thus thwarting the growth process of breast, pancreatic, esophageal, skin, colon and prostate cancer — confirming that apples truly do keep the doctor away. 10. Green and Black Tea -Long heralded for their health benefits, black and green tea are teeming with antioxidants known as polyphenols, the most potent called catechin. Whether you drink them cold or hot, green and black tea can help you fight cancer.

CANCER Hair today – Gone Tomorrow

Professor Veronica James has been involved in the research of breast cancer for decades. Despite her research having been published in many scientific journals and known throughout the scientific community, she remains admirably modest. She has an incredible lack of ostentation for someone who has developed a breast cancer detection technique that offers a more effective, accessible and pain free alternative to mammography. Her house in the Sydney suburb of Kenthurst is a domestic laboratory of scientific practicalities. An intriguing glass cylinder filled with water sits on the mantelpiece – a thermometer that determines the temperature through the changing viscosity of the water; there are clocks that line the walls of the house, each based on a different scientific principle. In the kitchen the peeled and sliced apples we eat with our pork was sliced and peeled with a vintage contraption collected from overseas.

 

There is even a pulley system that enables the fish at the bottom of the garden to be fed without physically making the steep walk. Her unique collection reflects the scintillating mind that developed a technique where, from a single hair, it can be determined whether a person will develop breast cancer. “Hair from people with breast cancer has a different intermolecular structure to hair from healthy people. We are able to see it early…the best part about it, if anyone who has ever had a mammography test, taking a single hair is not in anyway invasive, it’s not painful…Mammography has a 30 percent error rate. My success rate was coming out at about 99.7 percent. So it is far more reliable at getting the result”, said Professor James. Since 1978 Professor James has had to overcome great obstacles such as a lack of funding, equipment, an understanding of the physics of her work by critics and also the patriarchal nature of the scientific community, to develop this technique. But her greatest obstacle has only just arrived. There is a high price to pay to protect scientific research and breakthroughs. An international patent was taken out by Professor James in 1999 to protect her research and technique. To hold the patent it must be lodged into each country and translated separately into the different languages. As you can imagine this process is not cheap.

 

Approximately $80,000 in fact. “My present problem is my patent. I took out a patent to ensure that my technique would be available to women across the world at a price they can afford. I felt that that would help all the women who have helped me. Come July 10, if I haven’t gone ahead with the patent’ it will fall then anyone can take up this work. I could see it being bought and killed or other people buy it and charge a mint for it, but they don’t have to buy it, they’ ll just take it” said Professor James, her modesty fails to hide the worried and disappointed look on her face. The research is in its final stages, the worst time if any to be experiencing funding difficulties. Clinical trials and further sample testing is all that is left. This includes giving lectures and attending many meetings to help the scientific and the medical communities understand this technique.

Why Chemo Doesn’t Work

Dr. Ralph Moss has written the book, Questioning Chemotherapy, which documents the ineffectiveness of chemotherapy in treating most cancers. On November 19, 1977, he was fired for telling the public the truth. At a press conference on November 18th, he and the Second Opinion working group released a well-documented 48-page report that stated the top officials of the Memorial Sloan-Kettering Cancer Center had lied about the results of a study performed at the center regarding “Laetrile”–(a natural, alternative cancer treatment). Dr. Moss has gained credibility by writing eight books, including his most recent work, Cancer Therapy: The Independent Consumer’s Guide to Non-Toxic Treatment. He also wrote The Cancer Industry, a documented research work telling of the enormous financial and political corruption in the “cancer establishment”. He indicates that the motivating forces in cancer research and treatment are often power and money, and not the cure of cancer patients. He also writes, The Cancer Chronicles, a newsletter reporting on new cancer treatments and preventive measures.

 

Dr. Moss’ work documents the ineffectiveness of chemotherapy on most forms of cancer. However, he is fair in pointing out that there are the following exceptions: Acute Iymphocytic leukemia, Hodgkin’s disease, and nonseminomatous testicular cancer. Also, a few very rare forms of cancer, including choriocarcinoma, Wilm’s tumor, and retinoblastoma. But all of these account for only 2% to 4% of all cancers occurring in the United States. This leaves some 96% to 98% of other cancers, in which chemotherapy doesn’t eliminate the disease. The vast majority of cancers, such as breast, colon, and lung cancer are barely touched by chemotherapy. However, there is another category where chemotherapy has a relatively minor effect–The most “successful” of these is in Stage 3 ovarian cancer, where chemotherapy appears to extend life by perhaps eighteen months, and small-cell lung cancer in which chemotherapy might offer six more months.

 

Effective cancer treatment is a matter of definition. The FDA defines an “effective” drug as one which achieves a 50% or more reduction in tumor size for 28 days. In the vast majority of cases there is absolutely no correlation between shrinking tumors for 28 days and the cure of the cancer or extension of life. When the cancer patient hears the doctor say “effective,” he or she thinks, and logically so, that “effective” means it cures cancer. But all it means is temporary tumor shrinkage.

Starve a Tumor, or Feed a Tumor?

Within a tumor, chaos reigns: Nutrients are scarce, and healthy tissue is muscled out by cancerous tissue so aggressive that the tumor even sacrifices parts of itself to continue its relentless expansion. It’s in this rough-and-tumble environment, controlled by a dizzying array of molecular signals, that researchers at the James P. Wilmot Cancer Center are grappling with a conundrum: Starve a tumor of oxygen, and the tumor should die .

 

But without oxygen, pretty much all of today’s anti-cancer weapons are useless. Feeding the tumor may actually be better for the patient. “It’s like a two-headed beast,” says Edith Lord, Ph.D., professor of Oncology in Microbiology & Immunology at the University of Rochester’s cancer center. “If you cut off the blood vessels, the tumor doesn’t grow, but it’s also harder to treat with current therapies.” Five years ago the dawn of a new era in cancer research — the pursuit of anti-angiogenesis, or the cutting off or prevention of blood vessel growth — was hailed as a new way to knock out tumors by starving them of oxygen.

 

But progress has been slow and spotty, and scientific results inconsistent. There have been a few clinical trials of the new medicines, but none is yet approved for widespread use. Now doctors are coming more to terms with the negative complications of starving tumors of oxygen. “The crucial role that oxygen plays in killing tumors has been under appreciated,” says Bruce Fenton, Ph.D., associate professor of radiation oncology at the Wilmot Cancer Center.

Multiple effects of green tea

The polyphenols present in green tea help prevent the spread of prostate cancer by targeting molecular pathways that shut down the proliferation and spread of tumor cells, as well as inhibiting the growth of tumor nurturing blood vessels, according to research published in the December 1 issue of Cancer Research. A team of researchers from the University of Wisconsin, Madison, Wis., and Case Western Reserve University, Cleveland, Ohio, documented the role of green tea polyphenols (GTP) in modulating the insulin-like growth factor-1 (IGF-1)-driven molecular pathway in prostate tumor cells in a mouse model for human prostate cancer. “Consumption of GTP led to reduced levels of IGF-1,” said Hasan Mukhtar, Ph.D., Department of Dermatology at the University of Wisconsin, the senior author of the paper.

 

“GTP also led to increased levels of one of the binding proteins for IGF-1, the insulin growth factor binding protein-3. These observations bear significance in light of studies that indicate increased levels of IGF-1 are associated with increased risk of several cancers, such as prostate, breast, lung and colon.” GTP modulation of cell growth via the IGF-1 axis coincides with limited production or phosphorylation of key cell survival proteins, including PI3K, Akt and Erk1/2, the research indicated. The PI3K molecular pathway in cells, which includes Akt and Erk1/2, works to promote cell survival, rather than programmed cell death, also known as apoptosis. GTP also caused reduced expression of proteins known to be associated with the metastatic spread of cancer cells.

 

GTP inhibited the levels of urokinase plasminogen activator as well as matrix metalloproteinases 2 and 9, cellular molecules linked to the metastasis. The green tea polyphenols contributed to minimizing tumor development by governing the amount of vascular endothelial growth factor (VEGF) in the serum of the prostate cancer mouse model. The reduction of VEGF may result from GTP-induced suppression of IGF-1 levels. VEGF functions to recruit and develop new blood vessels that carry nutrients to developing tumors. By reducing the amount of VEGF, GTP works to minimize nutrients flowing to and supporting tumor growth.

DNA double-strand breaks and aging

Humans and animals undergo ageing, and although their primary cells undergo cellular senescence in culture, the relationship between these two processes is unclear. Here we show that gamma-H2AX foci (gamma-foci), which reveal DNA double-strand breaks (DSBs), accumulate in senescing human cell cultures and in ageing mice. They colocalize with DSB repair factors, but not significantly with telomeres. These cryptogenic gamma-foci remain after repair of radiation-induced gamma-foci, suggesting that they may represent DNA lesions with unrepairable DSBs. Thus, we conclude that accumulation of unrepairable DSBs may have a causal role in mammalian ageing. Folate deficiency causes massive incorporation of uracil into human DNA (4 million per cell) and chromosome breaks.

 

The likely mechanism is the deficient methylation of dUMP to dTMP and subsequent incorporation of uracil into DNA by DNA polymerase. During repair of uracil in DNA, transient nicks are formed; two opposing nicks could lead to chromosome breaks. Both high DNA uracil levels and elevated micronucleus frequency (a measure of chromosome breaks) are reversed by folate administration. A significant proportion of the U.S. population has low folate levels, in the range associated with elevated uracil misincorporation and chromosome breaks. Such breaks could contribute to the increased risk of cancer and cognitive defects associated with folate deficiency in humans. Folate deficiency significantly increases uracil content and chromosome breaks (as measured by micronucleated cells) in human leukocyte DNA.

 

Folate supplementation reduces both the uracil content of DNA and the frequency of micronucleated cells, indicating that uracil misincorporation may play a causative role in folate deficiency-induced chromosome breaks. A calculation is presented to explain how the levels of uracil found in DNA could cause chromosome breaks. Based on this calculation, the frequency of uracil repair events that might result in double-strand DNA breaks increases by 1752-fold. These results are consistent with clinical and epidemiological evidence linking folate deficiency to DNA damage and cancer.

Link between carbohydrate intake and hormonal cancers

Carb-conscious dieters may be lowering their risk of breast cancer while they¹re shedding pounds, based on the findings of research published in this month¹s edition of the journal Cancer Epidemiology, Biomarkers & Prevention. In a case-control study of 1,866 women in Mexico, those who derived 57 or more percent of their total energy intake from carbohydrates incurred a risk of breast cancer 2.2 times higher than women with more balanced diets. Dietary patterns in Mexico are characterized by higher consumption of carbohydrates and lower intake of fat and animal protein than those in more affluent western countries. The team of researchers from the Instituto de Salud Pblica in Cuernavaca, Mexico, and the Harvard School of Public Health in Boston, suggests that the association between carbohydrates and breast cancer may be related to elevated levels of insulin and insulin-like growth factor binding proteins in the blood. Scientists have long suspected that diet was among the factors contributing to breast cancer, said study co-author Walter Willett, M.D., M.P.H., Dr.P.H, the Fredrick John Stare Professor of Epidemiology and Nutrition at the Harvard School of Public Health.

 

Now, with studies like ours, we are beginning gradually to understand what elements of diet specifically are associated with the disease, and to grasp the chemical and biological processes that contribute to it at the cellular level. Of all the carbohydrate compounds, sucrose and fructose demonstrated the strongest association with breast cancer risk in the study. Sucrose is derived from sugar cane, sorghum and the sugar beet; it is most commonly found in table sugar and sweetened prepared foods and beverages. Fructose is a component of sucrose and is also found in fruit. Eating sweets and starches causes a rapid rise in the body¹s blood sugar levels, which in turn cues the production of insulin and triggers a biological process that ultimately can influence carcinogenesis by causing cells to proliferate.

 

Insulin and an insulin-like growth factor also may contribute to higher circulating levels of biologically active estrogens, a risk factor for breast cancer in pre-menopausal women. Ninety percent of breast tumors are insulin-receptor positive and over-express the insulin-like growth factor. The prevalence of type 2 diabetes, often associated with obesity, reflects an underlying insulin resistance in the Mexican population generally. Among urban Mexicans, nearly one-third of women between the ages of 12 and 49 are overweight. Yet when the research team took into account body mass index and other such potentially confounding factors as socioeconomic status, age at first birth, number of children, and family history of breast cancer, the relationship between carbohydrate intake and breast cancer remained the same.