Archive for June, 2009

ATLANTA, GA — The recent release of two large randomized trials suggests that if there is a benefit of screening, it is, at best, small, says a new report in CA: A Cancer Journal for Clinicians. Authored by Otis W. Brawley, M.D. of the American Cancer Society and Donna Ankerst, Ph.D. and Ian M. Thompson, M.D. of the University of Texas Health Science Center at San Antonio, the review says because prostate cancer is virtually ubiquitous in men as they age, it is clear that a goal of “finding more cancers” is not acceptable. Instead, public health principles demand that screening must reduce the risk of death from prostate cancer, reduce the suffering from prostate cancer, or reduce health care costs when compared with a non-screening scenario. The authors suggest prostate cancer screening has yet to reach one of these standards to date.

No major medical group, including the American Cancer Society, currently recommends routine prostate cancer screening for men at average risk. In the United States, prostate cancer will affect one man in six men during his lifetime. Since the mid-1980s, screening with the prostate–specific antigen blood test has more than doubled the risk of a prostate cancer diagnosis. The review says a decrease in prostate cancer death rates has been observed since that time, but the relative contribution of prostate–specific antigen testing as opposed to other factors, such as improved treatment, has been uncertain.

The report says a computer modeling study using National Cancer Institute’s Surveillance, Epidemiology, and End Results registries estimated that more than one in four cancers detected in whites (29 percent) and nearly half of cancers detected in blacks (44 percent) were overdiagnosed cancers. A similar model using data from Europe estimated a 50 percent overdiagnosis rate. The authors say patients who are diagnosed with clinically insignificant tumors are subject to unnecessary diagnostic tests and unneeded treatment and suffer psychosocial harms. They are also labeled “a cancer patient,” which can have negative economic consequences. Also, say the authors, overdiagnosis significantly affects 5–year survival statistics, making them uninformative in demonstrating progress in cancer control.

The report says the future of prostate cancer will include better screening tests, better methods to assess a man’s risk of prostate cancer, and prevention strategies, including the use of finasteride, a drug currently used for the treatment of urinary symptoms related to prostate enlargement.

In a separate but related editorial, Peter Boyle, Ph.D., D.Sc., of the International Prevention Research Institute, Lyon, France and report co-author Dr. Brawley say “the real impact and tragedy of prostate cancer screening is the doubling of the lifetime risk of a diagnosis of prostate cancer with little if any decrease in the risk of dying from this disease.” They say in 1985, before prostate–specific antigen screening was available, an American man had an 8.7 percent lifetime risk of being diagnosed with prostate cancer and a 2.5 percent lifetime risk of dying from the disease. Twenty years later, in 2005, an American man had a 17 percent lifetime risk of being diagnosed with prostate cancer and a 3 percent risk of dying from the disease. They add that even in the best case scenario, applying the findings of a European trial that found PSA led to a 20 percent reduction in the risk of death, the average man who chooses screening decreases his risk of prostate cancer death from a lifetime risk of 3 percent to a lifetime risk of 2.4 percent. In exchange, he doubles the chances of becoming a prostate cancer patient, his risk of diagnosis rising from about nine percent to at least 17 percent.

They conclude that “men should discuss the now quantifiable risks and benefits of having a prostate–specific antigen test with their physician and then share in making an informed decision,” and that “the weight of the decision should not be thrown into the patient’s lap.”

- MFP Wire Services
- 6-30-2009

LONDON, UK – Scientists at Queen Mary, University of London have discovered that an ingredient in human breast milk protects and repairs the delicate intestines of newborn babies.

The ingredient called pancreatic secretory trypsin inhibitor, or PSTI, is found at its highest levels in colostrum – the milk produced in the first few days after birth.

The lining of a newborn’s gut is particularly vulnerable to damage as it has never been exposed to food or drink. The new study* highlights the importance of breastfeeding in the first few days after the birth.

The researchers found small amounts of PSTI in all the samples of breast milk they tested but it was seven times more concentrated in colostrum samples. The ingredient was not found in formula milk.

The researchers examined the effects of PSTI on human intestinal cells in the lab. When they inflicted damage to the cells they found that PSTI stimulated the cells to move across the damaged area forming a natural protective ‘plaster’. They also found that PSTI could prevent further damage by stopping the cells of the intestine from self-destructing. Additional research suggests that PSTI could reduce damage by 75 per cent.

PSTI is a molecule which is normally found in the pancreas where it protects the organ from being damaged by the digestive enzymes it produces. Research suggests that it plays a similar protective role in the gut.

The team at Queen Mary have also found that PSTI is produced in the breast but until now they did not know exactly why.

Professor Ray Playford of Barts and the London School of Medicine and Dentistry, part of Queen Mary, University of London led the study.

He said: “We know that breast milk is made up of a host of different ingredients and we also know that there are a number of health benefits for babies who are breast-fed.

“This study is important because it shows that a component of breast milk protects and repairs the babies delicate intestines in readiness for the onslaught of all the food and drink that are to come.

“It reinforces the benefits of breast feeding, especially in the first few days after birth.”

- MFP Wire Services
- 6-30-2009

PITTSBURGH, PA – The current H1N1 swine flu strain has genetic roots in an illness that sickened pigs at the 1918 Cedar Rapids Swine Show in Iowa, report infectious disease experts at the University of Pittsburgh Graduate School of Public Health in the New England Journal of Medicine. Their paper, published online today and slated for the July 16 print issue, describes H1N1’s nearly century-long and often convoluted journey, which may include the accidental resurrection of an extinct strain.

“At the same time the 1918 flu pandemic was rapidly spreading among humans, pigs were hit with a respiratory illness that closely resembled symptoms seen in people,” said senior author Donald S. Burke, M.D., dean, University of Pittsburgh Graduate School of Public Health. “Early experiments confirmed that this 1918 swine virus and a human strain emerged about the same time. Since then, this ancestor virus has re-assorted genetically with other influenza strains at least four times, leading to the emergence of the new 2009 strain, which has retained some similarities to the original virus.”

In the paper, Dr. Burke and lead author Shanta M. Zimmer, M.D., assistant professor, University of Pittsburgh School of Medicine, describe the temporary “extinction” of the H1N1 virus from humans in 1957 and its subsequent re-emergence 20 years later. They note a small 230-person outbreak of H1N1 in 1976 among soldiers in Fort Dix, New Jersey that did not extend outside the military base. Then, H1N1 influenza re-emerged in 1977 among people in the former Soviet Union, Hong Kong and northeastern China. Careful study of the genetic origin of the 1977 strain showed that it was not the Fort Dix strain, but, surprisingly, was related closely to a 1950 human strain. Given the genetic similarity of these strains, re-emergence was likely due to an accidental release during laboratory studies of the 1950 strain that had been preserved as a ‘freezer’ virus, they said.

The authors hypothesize that concerns about the Fort Dix outbreak stimulated a flurry of research on H1N1 viruses in 1976, which led to an accidental release and re-emergence of the previously extinct virus a year later. The re-emerged 1977 H1N1 strain has continued to circulate among humans as seasonal flu for the past 32 years.

Although originally traced to Mexico, the exact physical origins of the 2009 H1N1 pandemic virus are unknown. Because the current strain shares common ancestry with older flu strains, it is possible that portions of the population may have partial immunity to the new pandemic virus.

The authors also go on to explain that the danger posed by a virus isn’t based solely on its lethality, but also on its transmissibility, which is the ability to jump from animals to humans and to survive by mutating to adapt to its new human host. H1N1 influenza viruses have demonstrated this ability throughout their history.

“Studying the history of emergence and evolution of flu viruses doesn’t provide us with a blueprint for the future, but it does reveal general patterns, and this kind of information is critical if we are to be as prepared as possible,” said Dr. Burke.

- MFP Wire Services
- 6-30-2009