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Chronic Inflammation Could Spur Cancer
People with a high white blood cell count -- a sign of inflammation -- are more likely to die of cancer, a new study finds.
The research points to an "important new epidemiological evidence of an essential link between inflammation and cancer mortality," conclude researchers at the National University of Singapore.
Their study included data on nearly 3,200 Australians, averaging close to 66 years of age, who were free of cancer when they were initially evaluated by researchers between 1992 and 1994. By the study's end in late 2001, 212 of the study volunteers had died of some form of cancer.
The risk of cancer death was greatest among study participants with the highest white blood cell counts, the researchers report in the Jan. 23 issue of the Archives of Internal Medicine. This was true even when the researchers controlled for other factors that might affect white blood cell count, such as smoking, diabetes and aspirin use.
The link between high white blood cell count and risk of death from cancer was especially strong for people who died of lung cancer.
"In our study, white blood cell count was associated with cancer mortality, even after adjusting for smoking status," the study authors wrote. "In subgroup analysis, the association was also present among those who never smoked, suggesting that the observed association between white blood cell count and cancer mortality is not fully explained by smoking."
The researchers also noted the risk of cancer death was higher among people with high white blood cell counts who did not take aspirin, compared to those who did take aspirin. This suggests that aspirin may provide a protective effect against cancer for people with a high white blood cell counts.
"Our findings suggest that local inflammatory processes that have long been known to be associated with tumor progression may be reflected in the systemic inflammatory maker of higher white blood cell count," the study authors wrote.
More information
The U.S. National Library of Medicine has more about white blood cell count.
Curry Spice Plus Cabbage Compound May Fight Cancer
Numerous studies have suggested the curry spice turmeric can help fight off cancer.
And new research suggests it might help protect against -- and even treat -- prostate cancer, especially when combined with a substance found in cauliflower, cabbage and other kinds of vegetables.
Researchers at Rutgers, the State University of New Jersey, found that a combination of turmeric (also called curcumin) and phenethyl isothiocyanate (PEITC) was effective against prostate cancer. PEITC is abundant in a group of vegetables that includes cauliflower, cabbage, watercress, winter cress, broccoli, Brussels sprouts, kale, kohlrabi and turnips.
"The bottom line is that PEITC and curcumin, alone or in combination, demonstrate significant cancer-preventive qualities in laboratory mice, and the combination of PEITC and curcumin could be effective in treating established prostate cancers," Ah-Ng Tony Kong, a professor of pharmaceutics, said in a prepared statement.
He and his colleagues created mice with human prostate cancer tumors to test the effectiveness of PEITC and curcumin.
"Despite convincing data from laboratory cell cultures, we knew little about how PEITC and curcumin would perform in live animals, especially on prostate cancer," Kong said. "So, we undertook this study to evaluate how effective PEITC and curcumin might be -- individually and in combination -- to prevent and possibly treat prostate cancer."
The mice were injected with PEITC or curcumin, alone or in combination, three times a week for four weeks. The injections began a day before the prostate cancer cells were placed in the mice.
The study was published in the Jan. 15 issue of Cancer Research.
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Colon Cancer
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Scientists Inflame Debate on Cancer's Genesis
No. 105; source : http://www.le.ac.uk/press/press/cancersgenesis.html
Long-term over-cooking of the immune system causing tissues to inflame and blood vessels to grow may be the single most important cause of cancer, according to a controversial report in this week's British Journal of Cancer.
Although many scientists agree that inflamed tissues may play a role in cancer, the authors go much further, arguing that long-standing over-activation of the immune system is the key event in the genesis of many forms of the disease.
Their research could herald an entirely new approach to both preventing and treating cancer, with the prospect that some existing anti-inflammatory drugs currently front-line treatments for conditions like arthritis and inflammatory bowel disease - could be used to keep cancer at bay.
According to conventional wisdom, cancer has a variety of causes, including inherited genetic errors, infections and exposure to chemicals and UV radiation. But Dr Ken O'Byrne of the University of Leicester and Prof Angus Dalgleish of St George's Hospital, London argue that many of these factors work in the same way by switching on the immune system for too long.
Dr O'Byrne says: "One of the biggest mysteries of cancer is why the body allows cells to build up cancerous mutations, when it has an immune system that ought to stop this from happening.
"But we think that when the immune system overcooks, perhaps because of long-term exposure to an infection or carcinogenic chemical, it loses its ability to fight disease and instead may actually begin to nurture and protect young cancer cells.
"If we could calm the immune system down with certain anti-inflammatory drugs, we might be able to reduce the rates of many common cancers."
Tissues become inflamed when the immune system is kicked into action by injury, infection or an allergic reaction. White blood cells and molecules involved in the immune response pour into the tissue from the blood supply and lymphatic system, while many other molecules are produced by the tissue itself.
These molecules are designed to fight off infection and to help the body heal as quickly as possible. But the same molecules that stimulate the regeneration of damaged tissues may also play a part in the birth of cancer and accelerate its growth and spread.
According to O'Byrne and Dalgleish, an immune system that is continually switched on encourages the genesis of cancer in a number of different ways:
- Paradoxically, over-activation of the immune system sometimes actually switches off the immune cells that would normally kill developing cancer cells. The immune system then fails to notice when cancer develops.
- Immunity, as well as killing viruses, bacteria and abnormal cells, is also designed to protect healthy cells, keeping them alive, encouraging them to divide and allowing them to move to areas where tissues need replenishing. But in some circumstances, an over-activated system can be perfect for looking after cancer cells too, encouraging them to grow and spread.
- As part of the healing process, the immune system stimulates the growth of blood vessels. These provide regenerating tissue with a plentiful supply of oxygen and nutrients, and are also perfect for feeding hungry cancer cells.
- Many immune system molecules are extremely chemically reactive, and may actually cause cancerous mutations by attacking DNA.
Dalgleish and O'Byrne believe that nearly all carcinogens work by over-cooking the immune system. As examples, they cite tobacco smoke and HPV, the virus that causes cervical cancer, both of which can cause long-term inflammation.
And in a final, bizarre twist, not only may inflammation cause cancer, but cancer might cause inflammation too. The researchers think that the most successful cancer cells are those that are able to exactly mimic inflammatory conditions, in order to help themselves grow and spread.
Professor Dalgleish says: "An inflamed tissue is a melting pot of cancer-causing molecules, so what better way for a cancer cell to give itself a helping hand that by learning to copy those very same conditions? Of course this means that some anti-inflammatory pills might not only help in preventing cancer, but in treating the disease too."
Dr Mary Berrington, Science Information Manager for The Cancer Research Campaign, which publishes the British Journal of Cancer, says: "This review makes a fascinating, if not novel, case for the link between exhausted immunity, chronic inflammation and cancer. It’s essential that we look at all the evidence, although much of it at the moment is circumstantial."
For media inquiries please contact Professor O'Byrne on 0116 258 7602, The Cancer Research Campaign's press office on 0207 487 3768 or mobile 07836 229 208 or mobile 07768 992 023. University of Leicester Press Office: 0116 252 3335.
New Colon Cancer Marker Found
Protein's role in stopping bacterial-induced inflammation, UCSD medical researchers show
28 Apr 2005
In findings that could have implications for autoimmune disorders and drug-resistant bacterial infections, researchers at the University of California, San Diego (UCSD) School of Medicine have identified a key protein involved in the appropriate shut-down of inflammation following an immune response to invading pathogens.
Published in the April 28, 2005 issue of the journal Nature, the study in mice and lab cultures of immune cells called macrophages showed that a protein called I-kappa-B kinase alpha (IKKa) is responsible for terminating an inflammatory response before it can damage cells and organs.
Senior author Michael Karin, Ph.D., UCSD professor of pharmacology, explained that IKKa is part of a sophisticated two-punch system that maintains a proper inflammatory response. While it is well known that IKKa's sister protein, IKK beta (IKKb), initiates the inflammatory response, little was known about the mechanism for stopping the response before it injures tissue, such as the damage that occurs in chronic bacterial and parasitic infections like tuberculosis and leprosy, or in autoimmune disorders like rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus (SLE).
Karin's team, which was the first to identify the IKK protein complex in 1996, determined in this new investigation that both IKKa and IKKb are activated at the same time following a microbial infection. While IKKb initiates the inflammatory response by causing the degradation of inhibitory proteins called IkBs, IKKa interacts with two additional proteins - RelA and C-Rel - which move into the nucleus of the cell after the IkBs are degraded. After being "tagged" by IKKa in the cytoplasm of the cell, RelA and c-Rel bind to genes that mediate the inflammatory response. But their life is limited - the IKKa-mediated "tag" ensures that RelA and c-Rel will bind to their target genes for only a short duration. Once RelA and c-Rel are removed from their target genes, the inflammatory response is terminated.
"This is very important for a proper inflammatory response in infection and immunity," Karin said. "The inflammatory response involves the production of potentially toxic mediators, so it is important that inflammation be allowed to do its work rapidly, but only transiently."
The new findings also have implications for disorders such as flesh-eating staph infections and drug-resistant bacterial infections that are difficult to treat. The researchers note that in these cases, it might be possible to develop an inhibitor of IKKa that boosts the inflammatory response to better fight these infections. However, such an inhibitor should have a short half-life, so that its potential devastating effect can be properly terminated.
The Karin lab, which has made several of the past discoveries involving IKKb's pro-inflammatory role, has also studied IKKa over the years, but they have identified roles unrelated to the primary inflammatory response. For example, in 2001, the investigators determined that IKKa was essential for formation of the skin's outer layer.* In a follow-up study, the team found clues that IKKa may be more involved in the immune response than they previously thought, but its role still appeared limited.** The current study is the first, however, to specifically show the novel mechanisms used by the protein to control the duration of an inflammatory response.
The study was funded by the National Institutes of Health. The co-first authors were Toby Lawrence, Ph.D., and Magali Bebien, Ph.D., post-doctoral fellows in the Laboratory of Gene Regulation and Signal Transduction, UCSD Department of Pharmacology. Currently, Lawrence is an assistant professor and member of the Faculty of Medicine, Imperial College London. Additional authors were George Liu, Ph.D., UCSD Division of Pediatric Infectious Diseases, UCSD School of Medicine; and Victor Nizet, M.D., associate professor of pediatrics, UCSD School of Medicine.
* UCSD Researchers Discover Protein Essential for Formation of Skin's Outer Layer health.ucsd.edu/news/2001/04_02_Karin.html
** UCSD Researchers Discover New Role For Immune-Response Enzyme health.ucsd.edu/news/2001/08_20_Karin.html
Contact: Sue Pondrom
spondrom@ucsd.edu
619-543-6163
University of California - San Diego
http://www.ucsd.edu
Cancer passes heart disease as top killer in U.S.
source: http://www.cbc.ca/story/science/national/2005/01/20/cancer-050120.html
Last Updated Thu, 20 Jan 2005 14:49:53 EST
WASHINGTON - Cancer has surpassed heart disease for the first time as the top killer of Americans under age 85, the American Cancer Society says.
More people are surviving both illnesses, but the mortality rate of heart disease is plunging faster.
"It's dropping fast enough that another disease is eclipsing it," said Dr. Walter Tsou, president of the American Public Health Association.
The cancer society's annual statistical report, released Wednesday, says that 476,009 Americans under 85 died of cancer in 2002, the most recent year for which figures are available. That's slightly more than the 450,637 who succumbed to heart disease.
The group predicts that 1.372 million Americans will be diagnosed with cancer in 2005 and more than half a million – 570,280 – will die of it. This doesn't include a million cases of two minor forms of skin cancer.
The death rate from all cancers has dropped by 1.5 per cent a year since 1993 among men and 0.8 per cent a year since 1992 among women, the report says. It now kills about one in four Americans.
The single biggest reason for the cancer death rate's decline is that fewer people are smoking, the report said. Smoking rates plummeted between 1965 to 2002, from 42 per cent to 22 per cent of the adult population.
Better screening methods and treatments have also helped keep more people alive, the report says.
According to the cancer society, smoking still causes a third of all cancer deaths and obesity, poor diet and lack of exercise cause another third – all factors that also contribute to heart disease.
"We want to send the message: Don't smoke, eat right, exercise and maintain normal weight, and see your doctor for normal checkups," said Dr. Harmon Eyre, the cancer society's chief medical officer.
In 2005, the society predicts there will be:
- 163,510 deaths from lung cancer.
- 56,290 deaths from colon cancer.
- 40,870 deaths from breast cancer.
- 30,350 deaths from prostate cancer.
- 19,200 deaths from non-Hodgkin's lymphoma.
- 7,770 deaths from melanoma.
Colon cancer is the third most common cancer found in U.S. men and women, according to the American Cancer Society (ACS). This year, there will be almost 105,000 new colon cancer cases, more than 40,000 rectal cancer cases, and more than 56,000 colorectal cancer deaths in the U.S., predicts the ACS.
Facts about Colon Cancer:
- Colorectal cancer is one of the most preventable cancers
- Both men and women are at risk for colorectal cancer
- Risk increases as we age. In fact, most cases occur in people 50 and older
- Colorectal cancer is the second leading cause of cancer related death for men and women in the U.S.
- Medicare helps pay for colorectal screening tests
- Colorectal cancer starts with no symptoms. Screening can help to detect it early, and determine what treatment works best. When colorectal cancer is detected in its earliest stage, the survival rate is 96%
- More than one-third of colorectal cancer deaths could be avoided if people over 50 had regular screening tests.
If you have any of the following symptoms, please discuss them with your Doctor immediately:
- Blood in or on the stool
- A change in bowel habits
- Stools that are narrower than usual
- General stomach discomfort
- Frequent gas pains
- Unexplained weight loss.
For more information on colorectal cancer, you may visit the following websites: www.cancer.org http://www.acg.gi.org/patientinfo/cgp/cgpvol1.html#colorectal
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