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Emotional Bonds to Cigarettes Make It Hard To Quit Smoking

February 15, 2012 By Leave a Comment

A new study shows that nearly 90% of heavy smokers say that even though they know smoking is dangerous, they still consider cigarettes their “friend.” Researchers say that emotional bond may help explain why smokers have such a hard time quitting, even with the help of nicotine-replacement therapies. “The danger of losing a friend was more threatening to them that the dangers of smoking, and they worried what would take the place of cigarettes emotionally,” write researcher Beti Thompson, PhD, of the Fred Hutchinson Cancer Research Center in Seattle, and colleagues. “They use smoking to comfort themselves not only in trying situations but also in situations that many people find relatively inconsequential.”

 

For the study, published in the December 2003 issue of Nicotine & Tobacco Research, researchers interviewed 51 heavy smokers (most were white men who smoked more than 25 cigarettes per day) about their attitudes about smoking and attempts to quit. Nearly two-thirds reported that they were physically addicted to cigarettes and more than half said the smell and taste of tobacco affected their decision to smoke. Participants also said they felt many social pressures to smoke, including pressure from the tobacco companies, family members, and smoking buddies. More than half also said that smoking relieved emotional problems and was a means to cope with stress, reduce anger, or withdraw from people or situations.

 

Others said social triggers got in the way of attempts to quit smoking. For example, they wondered how they could go out for a drink without smoking or couldn’t imagine giving up a cigarette at the end of a meal. On the plus side, a whopping 94% said they thought quitting would lead to improved health, but they saw giving up cigarettes as a nearly unattainable goal. “Although heavy smokers know they need to stop smoking, they feel angry that this source of physical pleasure should be taken from them,” write the researchers. “They see themselves as victims who have been duped into smoking and continued smoking.”

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Study Links Hormone Replacement Therapy To Elusive Tumors

February 15, 2012 By Leave a Comment

The suspected breast cancer risk associated with post-menopausal hormone replacement therapy may involve a type of tumor that can be hard to detect, researchers reported on Tuesday. The report from the Fred Hutchinson Cancer Research Center, Group Health Cooperative and the University of Washington, Seattle, looked at 705 women between the ages of 50 and 74. It found the incidence of all types of breast cancer in the group was increased by 60 to 85 percent by replacement therapy and that long-term users had a higher risk for lobular breast cancer.

 

“We found an elevated risk of invasive breast cancer among post-menopausal women who were long-term, recent users of oral estrogen, either alone or in combination with progestin,” said the study published in this week’s Journal of the American Medical Association. “These results are generally consistent with the results from other case-control and cohort studies and (a) recent collaborative analysis,” it added. “Two prior studies have observed a two to three-fold increase risk of lobular breast cancer associated with current combination therapy, and we found similarly large risks of lobular cancer associated with current combination therapy and longer duration of all formulations of hormone replacement therapy,” it said. If there really is an increased risk for lobular breast cancer, it added, that “could have implications for screening, because lobular carcinomas are relatively more difficult to palpate (feel) and more difficult to diagnose by mammography.

 

However, until more is known about the costs and benefits of different screening modalities for women using hormone replacement therapy, it would be premature to use our results as a basis for modifying early detection activity in them.” About 38 percent of U.S. women between the ages of 50 and 74 are on hormone replacement therapy, according to medical literature. The therapy replaces estrogen which the ovaries cease to produce at menopause — a change that can cause mood swings, vaginal dryness, lowered libido, hot flashes and insomnia. The replacement therapy also is believed to have the potential to prevent heart disease and ward off osteoporosis. Risks associated with the treatment include breast cancer and blood clots.

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Designer virus attacks cancer cells

February 15, 2012 By Leave a Comment

An Ottawa cancer researcher has engineered a virus able to kill many types of cancer cells while leaving normal cells healthy. He hopes to begin trials in human patients in just over a year. Tests in live mice have been so successful that in some 80 per cent of cases the virus killed all the human cancer cells carried by the mice. Dr. John Bell, of the Ottawa Regional Cancer Centre, has been working on the designer virus for years. In 2000, he engineered an early version of the same virus — one so successful that most cancer cells were “completely blown away.” But there was a catch: It only worked in combination with a hormone treatment. The latest version works by itself. While the history of cancer research has seen many treatments that work in mice but not in humans, Bell’s new virus has been so outstanding that he’s hopeful it will have a bright future. As well, he has been testing human cancer cells injected into mice.

 

While these are nourished by the animals’ blood, they keep their human DNA and are still human cells, a more valuable research tool than ordinary mouse tumours. The medical research journal Cancer Cell has made the findings the cover story of today’s edition. A separate review of Bell’s work calls it “a breakthrough” and “a promising new therapeutic oncolytic (cancer-killing) viral candidate.” The anti-cancer weapon is a genetically engineered version of vesicular stomatitis virus (VSV), an animal virus that in Canada mainly causes minor infections in cattle. “We’ve been engineering it to make it so that it kills tumour cells more specifically,” Bell said. “In some of the ways we administered it, 100 per cent of the animals were cured. So it’s pretty effective,” he said.

 

“In the paper we analysed 60 different samples from cancer patients — and about 80 per cent of the samples we looked at were killed. So it’s a broad spectrum of cancers.” He believes cancer cells have a structural weakness normal cells do not. Identifying this flaw was the crucial first step toward finding a virus that would infect them. Once inside the cancer cell, the virus starts to make thousands of copies of itself. “So it’s like a little parasite. It takes over all the machinery inside the cell and turns it to its own use. So it basically turns the cell into a bag, a virus-producing cell. The result of that is you make lots of viruses and the cell just dies.”

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Indirect Harm of Quackery

February 15, 2012 By Leave a Comment

Some of the worst quackery-related tragedies result from delay or failure to act. An example of a needless death involved an Oregon man who treated his basal cell carcinoma of the mouth with a mail-order remedy for 15 years. What makes this case especially tragic is that since this type of cancer almost never metastasizes, he had many years in which to correct his folly. Although badly disfigured by the growing tumor, he continued self-treatment. Overreliance upon dietary treatment is a common means by which indirect harm kills cancer sufferers. The appeal of dietary remedies is connected to folk medicine. Nearly every culture, beginning with the ancient Egyptians, has believed in the half-truth “you are what you eat.” This implies that diseases are caused by faulty diet and, conversely, can be cured by eating the “right” foods. Publicity given to epidemiological speculations about “cancer-prevention diets” encourages the belief that diet holds great promise for both prevention and treatment of cancer.

 

The fact is that, although nutrient deficiencies can cause some diseases and dietary excesses can cause or aggravate several others, the vast majority of diseases do not have a nutritional cause. One food-as-medicine approach that is popular today is macrobiotics, which received widespread publicity when Anthony Sattilaro, M.D., a Philadelphia physician, concluded that the diet had helped him overcome prostatic cancer. National magazine articles, a book and television appearances spread the belief that macrobiotics had cured his cancer. Although Sattilaro had also undergone conventional therapy, macrobiotics seemed to fulfill some emotional need unmet by regular therapy. He eventually died of his disease, but this fact was not mentioned in the macrobiotic press. The macrobiotic diet bears some resemblance to currently recommended cancer-prevention diets.

 

However, because of its rigidity, low-fat content, negligible use of simple sugars, and exclusive reliance upon vegetable rather than animal protein, it is a poor one for cancer patients undergoing radiation or chemotherapy. These patients need a high-quality, nutrient-dense diet because the ability of their intestine to absorb nutrients is impaired. “Natural” treatments that can delay proper care are often advocated by well-meaning friends and relatives who are culturally conditioned to believe in their value. This thinking is deeply rooted in many cultures and is as old as written records themselves. The Book of Job, said to be the oldest in the Bible, is a drama aimed at dispelling the notion that victims are responsible for their own diseases. Job is a good man who suffers terribly. His friends plead with him to confess his wrongdoings, but he is innocent. The message is clearly that the presence of disease does not mean the sufferer is a sinful person. However, moralistic approaches that blamed victims for their diseases were prevalent until Pasteur proved the existence of germs that can strike the innocent and immoral alike.

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A third of hardcore smokers think their health is completely unaffected by smoking

February 15, 2012 By Leave a Comment

Many elderly smokers are hardcore addicts who have no intention of giving up, according to a new study. Cancer Research UK scientists found that the proportion of hardcore smokers greatly increased with age. Nearly a third of smokers over the age of 65 were categorised as hardcore smokers, compared with only 5 per cent of those aged 16-24. The increase with age may reflect a false sense of security after years of smoking with few perceived negative health effects, the researchers say. The study found that a third of hardcore smokers thought their health was completely unaffected by smoking, and would remain so in the future.

 

Smoking was cited as the main pleasure in life by 31 per cent of those questioned an attitude similar to that of the character Dot Cotton in the soap opera EastEnders, leading the scientists to coin this type of attitude Dot Cotton syndrome. Researcher Professor Martin Jarvis said, As smokers get older more of them develop entrenched attitudes. Some just give up hoping they can ever succeed in quitting, and some are lulled into a false sense of security simply by having survived so far. The reality is that by quitting cigarettes they can add years to their life. Despite the health benefits of quitting, the study found that hardcore smokers actively defy pressure to quit 56 per cent resent social pressure to give up and 40 per cent do not think their smoking influences children.

 

However, public health messages can help, Professor Jarvis says. In California smoking is less socially acceptable. An intensive anti-smoking campaign has run for a decade a statewide public smoking ban, TV campaigns, and targeted health messages have all helped people understand the health risks of smoking in a clear and vivid way. This has resulted in less smokers but also a lower proportion of hardcore smokers many are in the process of trying to give up.

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WHO raises death rate from 4.2 million to 4.9 million per year

February 15, 2012 By Leave a Comment

Experts have blasted a study purportedly from the World Health Association that suggests second-hand smoke does not cause lung cancer. “This is simply not sound science,” said David Sweanor, the Ottawa-based lawyer for the Non-Smokers’ Rights Association. “The only place we have seen this kind of garbage is from the tobacco industry.” Jim Repace of Maryland, author of more papers on second-hand smoke than anyone in the world, describes the study as “propaganda, not science.” The study was said to have been commissioned by the World Health Organization, long known for its belief second-hand smoke causes cancer. The seven-country European study was co-ordinated by the International Agency for Research on Cancer in Lyon, France. It was described as “one of the largest ever to look at the link between passive smoking and lung cancer, and eagerly awaited by medical experts and anti-tobacco groups.” Researchers compared 650 lung-cancer patients with 1,542 healthy people.

 

Their data were said to suggest there not only is no connection between second-hand smoke and lung cancer, but that second-hand smoke might even have a slight protective anti-cancer effect. If you were surprised to find such a conclusion coming from study instigated by the World Health Association, so too was the acting chief of the UN organization’s tobacco program. “This was certainly nothing done in my office,” said Neil Collishaw, who works in the WHO’s Geneva offices. Mr. Collishaw described the International Agency for Research on Cancer as a “sister” agency. “But if my organization, as you say, commissioned it, it’s strange I haven’t heard of it,” he said. “Particularly strange, since it’s said to have been ‘eagerly awaited.’ ” As for the study being one of the largest ever on the topic, Mr. Collishaw snorted. “This is certainly untrue. One of the earliest studies, conducted in Japan, followed hundreds of thousands of people — and there are other studies in that category.” He said all the larger studies bringing together the data from smaller studies have agreed that passive smoking is a cause of lung cancer.

 

Mr. Repace, a retired U.S. Environmental Protection Agency scientist who has written 50 papers on second-hand smoke, was even more emphatic. “The data linking passive smoking and lung cancer are simply overwhelming. This conclusion is shared by every organization of the U.S. federal government with a purview over public health. The American Medical Association and the American Association of Cancer Research agree. “And the most recent study — by the California State Environmental Protection Agency — not only links second-hand smoke with lung cancer, but with nasal sinus cancer, as well.” Not all studies find a causal link between second-hand smoke and lung cancer, Mr. Repace acknowledges. But of the 30 studies that had been done by 1992, 24 did. The remaining six were either neutral, flawed by distorting factors, or had only slight statistical significance. “So we had 24 studies that were positive,” he said.

 

“If passive smoking has no effect on lung cancer, what’s the probability of this result? Only six in 10,000.” Fourteen of the 30 studies looked at “dose response” to determine whether exposure to second-hand smoke increased the likelihood of developing lung cancer. Ten of them established — each with a 95-per-cent confidence level — that there indeed was a dose response. And the chances of that happening, if passive smoking and lung cancer are unconnected, is one in 10 billion, Mr. Repace said. Since even the tobacco companies now concede that smoking causes lung cancer, the suggestion that second-hand smoking has no connection with lung cancer is “awfully fishy on the intuitive level,” he said.

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Glucarate Supplements Aid in Ex-Smokers’ Fight Against Cancer

February 15, 2012 By Leave a Comment

Supplementing one’s diet with glucarate, a compound occurring naturally in the body and also found in fruits and vegetables, may reduce ex-smokers’ risk of lung cancer by blocking cancer-causing agents, binding with them and removing them from the body, according to recent studies.* This is good news for the approximately 12 million Americans getting ready to quit smoking on November 20 as part of the American Cancer Society’s Great American Smokeout. One of the country’s leading cancer researchers, Thomas J. Slaga, Ph.D., chair of the Center for Causation and Prevention at the AMC Cancer Research Center in Denver, believes that glucarate supplementation is an important preventive measure for people who have an increased risk of cancer from smoking.

 

“I would recommend glucarate to ex-smokers as well as anyone at a higher-than-average risk of developing cancer,” said Slaga, who was previously thedirector of Cancer Cause and Prevention at the University of Texas, M.D.Anderson Cancer Center Science Park–Research Division for fifteen years. “Studies suggest that stopping smoking alone does not reduce the risk of lung cancer to the level of someone who has never smoked. Anyone who is concerned about developing lung cancer can reduce their risk by quitting smoking, eating a healthy diet rich in fruits and vegetables and taking glucarate supplements,” added Slaga.

 

The protective function of glucarate in the body’s natural cancer prevention mechanisms has long been established. Now, a new study partially funded by the National Institutes of Health and the American Cancer Society and published in “Cancer Detection and Prevention” indicates that glucarate supplementation amplifies these processes by increasing the removal of carcinogens from the body. Other recent studies indicating the potential use of glucarate in boosting the body’s detoxification processes include those published in “Cancer Letters”, “Nutrition Research” and “Anticancer Research.”

 

For example, a study published in “Anticancer Research” found there was a 50% decrease in tumor incidence when glucarate was given to laboratory animals with induced cancer. Glucarate is found in abundance in fruits and vegetables and, in fact, may be partially responsible for their much touted cancer-preventive characteristics. The compound affects different detoxification pathways than those acted upon by antioxidants, which also are found in fruits and vegetables and also have been shown to have anti-cancer properties. Therefore, glucarate can be taken in conjunction with antioxidants for maximum protection against cancer.

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Charting The Creation Of Some Breast Cancer Cells

February 14, 2012 By Leave a Comment

A slow-motion movie of the changes inside a breast cell as it becomes a particularly stubborn type of cancer cell would show a process very much like that depicted for the first time in a new study by researchers at Dana-Farber. The investigators, led by Debajit Biswas, D.Sc., in the laboratory of Arthur Pardee, Ph.D., of Dana-Farber’s Cancer Biology department, have charted the chain of events by which breast cancer cells known as estrogen receptor-negative (or ER-negative) cells are formed. Because such cells do not need the female hormone estrogen to grow and proliferate, conventional drugs like tamoxifen that block estrogen from acting on breast cells are generally ineffective against ER-negative tumors. About 30 percent of all breast cancers are ER-negative. “The discovery of the steps involved in the creation of ER-negative breast cancer cells means scientists now have an array of targets for drugs that may be able to stop the process in its tracks, providing the first specific therapy for patients with ER-negative breast tumors,” Biswas says.

 

Thus far, the studies have been conducted in laboratory samples of cells only. The study, published in the most recent issue (July 18) of the Proceedings of the National Academy of Sciences, focuses on what happens after ER-negative cells have been stimulated to grow. The on-off switch for growth in ER-negative cells is a “receptor” on the cell surface. When the receptor meets a substance called epidermal growth factor (EGF), it signals the cell to begin dividing uncontrollably. In the new laboratory study, Biswas and his colleagues map out some of the key stages in the process of ER-negative cells’ becoming cancerous. One involves a protein complex called nuclear factor kappa B (NF-kB), which is activated when EGF docks at the cell.

 

In its active form, NF-kB serves as an “ignition switch” for cell division. The activation of NF-kB by EGF is itself a complex process, involving several stages and at least three different enzyme systems. Biswas’ team has shown those stages in detail — and, just as importantly — shown that one of them can be blocked by a compound called Go6976. The compound essentially short-circuits the growth signals within cancerous ER-negative cells and causes them to die. Biswas and his associates have been carrying out this study with support from the Massachusetts Department of Public Health Breast Cancer Research Program.

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Cannabis extract shrinks brain tumours

February 14, 2012 By Leave a Comment

Cannabis extracts may shrink brain tumours and other cancers by blocking the growth of the blood vessels which feed them, suggests a new study. An active component of the street drug has previously been shown to improve brain tumours in rats. But now Manuel Guzmán at Complutense University, Spain, and colleagues have demonstrated how the cannabis extracts block a key chemical needed for tumours to sprout blood vessels – a process called angiogenesis. And for the first time, the team has shown the cannabinoids impede this chemical in people with the most aggressive form of brain cancer – glioblastoma multiforme. Cristina Blázquez at Complutense University, and one of the team, stresses the results are preliminary. “But it’s a good point to start and continue,” she told New Scientist.

 

“The cannabinoid inhibits the angiogenesis response – if a tumour doesn’t do angiogenesis, it doesn’t grow,” she explains. “So if you can improve angiogenesis on one side and kill the tumour cells on the other side, you can try for a therapy for cancer.” “This research provides an important new lead compound for anti-cancer drugs targeting cancer’s blood supply,” says Richard Sullivan, head of clinical programmes, at Cancer Research UK. The team tested the effects of delta-9-tetrahydrocannabinol in 30 mice. They found the marijuana extract inhibited the expression of several genes related to the production of a chemical called vascular endothelial growth factor (VEGF).

 

VEGF is critical for angiogenesis, which allows tumours to grow a network of blood vessels to supply their growth. The cannabinoid significantly lowered the activity of VEGF in the mice and two human brain cancer patients, the study showed. The drug did this by increasing the activity of a fat molecule called ceramide, suggests the study, as adding a ceramide inhibitor stifled the ability of the cannabinoid to block VEGF. Small and pallid “We saw that the tumours [in mice] were smaller and a bit pallid,” adds Blázquez. The paleness of the cancer reflected its lack of blood supply as a result of the treatment. In the human patients, she says: “It seems that it works, but it’s very early.”

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Prostate Specific Ets factor

February 14, 2012 By Leave a Comment

Prostate Specific Ets factor is a recently identified transcriptional activator that is overexpressed in prostate cancer. To determine whether this gene is overexpressed in breast cancer, we performed a virtual Northern blot using data available online at the Cancer Genome Anatomy Project website. Ninety-five SAGE libraries were probed with a unique sequence tag to the Prostate Specific Ets gene.

 

The results indicate that Prostate Specific Ets is expressed in 14 out of 15 breast cancer libraries (93%), nine out of 10 prostate cancer libraries (90%), three out of 40 libraries from other cancers (7.5%), and four out of 30 normal tissue libraries (13%). To determine the possibility that the Prostate Specific Ets gene is a novel marker for detection of metastatic breast cancer in axillary lymph nodes, quantitative real-time RT-PCR analyses were performed. The mean level of Prostate Specific Ets expression in lymph nodes containing metastatic breast cancer (n=22) was 410-fold higher than in normal lymph node (n=51).

 

A receiver operator characteristic curve analysis indicated that Prostate Specific Ets was overexpressed in 18 out of 22 lymph nodes containing metastatic breast cancer (82%). The receiver operator characteristic curve analysis also indicated that the diagnostic accuracy of the Prostate Specific Ets gene for detection of metastatic breast cancer in axillary lymph nodes was 0.949. These results provide evidence that Prostate Specific Ets is a potentially informative novel marker for detection of metastatic breast cancer in axillary lymph nodes, and should be included in any study that involves molecular profiling of breast cancer.

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