New imaging discoveries may improve physicians’ ability to diagnose and treat two serious injuries affecting football players, according to two studies presented this week at the annual meeting of the Radiological Society of North America (RSNA).

In the first study, researchers reviewed 101 magnetic resonance imaging (MRI) knee exams of 330 candidates for the 2005 professional football draft and found 57 tears of the lateral meniscus, a flat, disc-shaped ligament that supports the outer knee joint, and 26 tears of the medial meniscus, which supports the inner knee joint.

“These findings are remarkable because the authors of most previous studies have reported a predominance of medial meniscal injuries,” said Jeffrey Towers, M.D., lead author of the study and associate professor of radiology at the University of Pittsburgh Medical Center in Pennsylvania.

At first, Dr. Towers suspected that the unusually high percentage of lateral meniscal tears was associated with anterior cruciate ligament (ACL) tears. ACL tears are fairly common among elite college football players, and 80 percent of meniscal tears that occur in association with ACL tears are in the outer knee joint.

“Tackling is usually done from the outside of the knee, imparting a load that traps the lateral meniscus in addition to tearing the ACL,” Dr. Towers said.

However, the study revealed that while 18 lateral and eight medial meniscal tears were found in conjunction with ACL tears, 36 lateral and 18 medial tears were isolated injuries. The findings also included evidence of three prior lateral tears.

“What we found is that almost three-quarters of the lateral meniscal tears were not in the setting of ACL tears,” Dr. Towers said.

Dr. Towers believes that the discovery of this high incidence of lateral meniscal tears among elite athletes may have a significant impact on improving physicians’ ability to diagnose and treat this condition.

“The fact that we found a concentration of lateral meniscal tears could mean that there’s something about this sport that predisposes athletes to this injury,” Dr. Towers said. “We found the highest incidence of lateral meniscal tears in linemen and defensive secondary players. Now that we recognize this, there may be ways to address the players who are most at risk for this injury.”

In a second paper, Dr. Towers and colleagues identified for the first time an indirect sign of syndesmotic tear, a frequently misdiagnosed injury more commonly known as high ankle sprain. Currently, the condition is most commonly diagnosed by uncomfortable physical examination of the syndesmosis, a large ligament above the ankle.

“In syndesmotic tear, the biggest ligament that holds the tibia and fibula together is injured,” Dr. Towers explained. “The fibula can move away from the tibia, and the cylindrical groove which forms the ankle can widen under load. The problem is that routine x-rays may not show it, because it’s not grossly misaligned. It’s during athletic activity when the injury becomes most apparent.”

Left undiagnosed, high ankle sprain can impede an athlete’s performance and lead to arthritis. “The treatment for high ankle sprain is different and generally longer than for a typical ankle sprain,” Dr. Towers said. “If it is not recognized, and you send somebody out to play, the ligaments heal improperly, the ankle doesn’t fit as tightly as it should, and often the result is arthritis.”

The researchers used MRI and x-rays to study 18 candidates for the 2005 professional football draft who were found to have a history of high ankle sprain. Fourteen x-rays showed an abnormal growth of new bone, known as periostosis, at the lower part of the tibia, the large bone between the knee and foot. Two MRI exams revealed abnormal swelling due to fluid at the same site.

According to Dr. Towers, this periostosis provides physicians with an indirect sign of high ankle sprain that is decisive in diagnosing this difficult-to-detect injury.

“Even if I don’t have MR images that include the entire syndesmosis, which goes into the lower leg,” Dr. Towers said, “if I look at an ankle and see this posterior periostosis, I can now be fairly sure of a syndesmotic injury.”

Co-authors on both studies are Derek Armfield, M.D., James Bradley, M.D.,

John Norwig, M.E.D., from University of Pittsburgh Medical Center and Kenneth Buckwalter, M.D., from Indiana University Medical Center, which coordinates imaging for the professional football draft.

Maureen Morley
mmorleyrsna
Radiological Society of North America
rsna

Statins appear to be safe for people with fatty liver disease who could benefit from their cholesterol-lowering
capabilities, concludes a review paper published in the April 2005 issue of Hepatology, the official journal of the American
Association for the Study of Liver Diseases (AASLD). Published by John Wiley & Sons, Inc., the journal is available online
via Wiley InterScience at interscience.wiley/journal/hepatology.

Statins are a class of drugs that lower cholesterol levels by inhibiting the liver’s production of cholesterol. They have
been shown to decrease the risk of artherosclerosis and related diseases. In the United States, doctors write millions of
prescriptions for statins each year. However, commonly, patients on statins have elevations of liver enzymes. Current statin
product packaging recommends monitoring patients’ liver values over the course of their usage. This recommendation may
concern physicians whose patients also have known liver conditions, including elevated, though asymptomatic, liver enzymes.

Naga Chalasani, M.D., of Indiana University School of Medicine, thoroughly examined the literature related to statin
hepatotoxicity to better understand statins’ effects on patients. Statins, especially in increasing doses, have been
associated with asymptomatic elevation of aminotransferases, though this occurs in fewer than three percent of statin users.
Notably, this outcome has also occurred with similar frequency in placebo-treated patients in clinical trials. This “raises
the possibility that hyperlipidemic patients may have spontaneous fluctuations in transaminases whether or not they receive
statins,” Chalasani suggests. Still, there have been rare reports of significant liver injury associated with statins.

Statins are not recommended for patients with active liver disease, though the recommendations for those with nonalcoholic
fatty liver disease (NAFLD) are unclear. This group of patients is important to consider because the disease is common in
patients with high cholesterol and their liver condition may create a higher cardiovascular risk that could be addressed
through statin therapy.

“The studies examining the safety of statins in patients with NAFLD are limited, but the existing data provide some evidence
that they can be used safely,” reports the author, whose own studies recently showed that hyperlipidemic patients with
elevated baseline liver enzymes are not at a higher risk for hepatotoxicity from statins compared with hyperlipidemic
patients with normal transaminases.

The relationship between statins and cancer raises another important question. Statins have been shown to cause various
tumors in rodents, though short-term studies have revealed no carcinogenic effects in humans. Still other studies have
suggested that statins have an anti-tumor effect. Additionally, rhabdomyolysis can be a complication of statin therapy and
may be related to higher serum concentration levels of statins. Patients with decreased hepatic drug metabolizing activity
due to cirrhosis or other liver ailments may have a higher risk of muscle disease from statins, although the association has
not been studied.

Further studies should examine the long-term effect of statins on the liver in patients with NAFLD and non-alcoholic
steatohepatitis. More research is also needed to investigate if patients with those diseases show any clinically relevant
changes in the pharmacokinetics of different statins at various doses. Finally, the author suggests a reexamination of the
product labeling on statins, which currently calls for monitoring of liver biochemistries before and during usage.

“It is now evident that elevated aminotransferases are insensitive to detect underlying hepatic steatosis and patients with
advanced fibrosis and cirrhosis may have entirely normal aminotransferases,” he reports.

After considering the available literature thoroughly, Dr. Chalasani concludes, “There is no sound rationale why statins
should not be used in patients with chronic liver disease who otherwise need statin therapy.”

Article: “Statins and Hepatotoxicity: Focus on Patients with Fatty Liver,” Naga Chalasani, Hepatology; April 2005; Volume 41,
Issue 4 (Published Online: March 23, 2005).

John Wiley & Sons, Inc.
interscience.wiley

The long-held belief that older people perform slower and worse than younger people has been proven wrong. In a study
published today in Neuron, psychologists from McMaster University discovered that the ageing process actually improves
certain abilities: Older people appear to be better and faster at grasping the big picture than their younger counterparts.

“Going into the study, we knew that ageing changes the way people see the world,” says Allison Sekuler, one of the senior
authors and a Canada Research Chair at McMaster. “But these results are an unusual twist on the standard ‘ageing makes you
worse’ story, and they provide clear insight into what is changing in the ageing brain.”

Using computer-generated stimuli, the researchers monitored how much time subjects needed to process information about the
direction in which a set of bars moved. When the bars were small, or when the bars were low in contrast (light gray vs. dark
gray), younger subjects took less time to see the direction of motion. But when the bars were large, and high in contrast
(black vs. white), older subjects outperformed the younger subjects.

“The results are exciting not only because they show an odd case in which older people have better vision than younger
people, but also because it may tell us something about how ageing affects the way signals are processed in the brain” says
Patrick Bennett, the other senior author, also a Canada Research Chair at McMaster.

The results suggest that as we age, the ability of one brain cell to inhibit another is reduced. That sort of inhibition
helps young people find an object hidden among clutter, but it can make it hard to tune into the clutter itself. When the
young brain sees big, high-contrast bars, it effectively tunes out because there is no object hidden in the bars. But older
brains do not inhibit information in the same way, so they do not tune out the bars, and they can actually perform the task
better.

“As we get older, it becomes harder to concentrate on one thing and ignore everything else,” says Bennett. “It takes more
effort to tune out distractions. We’ve seen it in cognition and speech studies, and now we see it in vision. Although we
don’t know if those are all linked, we think the visual effect is due to changes in the effectiveness of inhibitory
neurotransmitters in the brain.” Neurotransmitters are chemical substances that can modify the way in which brain cells talk
to one another. Some neurotransmitters enhance brain signals, and others inhibit them.

The study, conducted in collaboration with PhD students Lisa Betts and Christopher Taylor, suggests that one type of
inhibitory neurotransmitter may not have as much effect in old brains as in young brains. However, the researchers caution
that although such a change makes older people perform better on this task, the same change likely leads to increased
difficulties in a much wider range of tasks.

“It’s critical to understand how ageing affects vision and the brain. If we can characterize what is happening to our brains
as we age, we’ll be in a better position to help seniors see better for longer,” says Sekuler.

The research was supported by funds from the Canadian Institutes of Health Research, the Natural Sciences and Engineering
Research Council of Canada, the Canada Foundation for Innovation, the Ontario Innovation Trust, and the Canada Research
Chairs program.

McMaster University, named Canada’s Research University of the Year by Research InfoSource, has world-renowned faculty and
state-of-the-art research facilities. McMaster’s culture of innovation fosters a commitment to discovery and learning in
teaching, research and scholarship. Based in Hamilton, the University has a student population of more than 20,000 and more
than 112,000 alumni in 128 countries.

For more information, please contact: Jane Christmas
Office of Public Relations
McMaster University
905-525-9140 ext. 27988
chrisjamcmaster

Jane Christmas – chrisjamcmaster
McMaster University

Argos Therapeutics announced the presentation of positive data from a Phase 2 trial that evaluated the safety, clinical response and immune response of AGS-003 treatment in newly diagnosed patients with metastatic renal cell carcinoma (mRCC). The data were discussed March 7 in a poster presentation at the ASCO Genitourinary Cancers Symposium. AGS-003 is a product of the Company’s Arcelis™ technology, and is a personalized, RNA-loaded, dendritic cell-based immunotherapy that is perfectly matched to each patient’s unique tumor burden. According to results from the study, AGS-003 induced a tumor-specific immune response, performed better than interferon-О± on a measure of progression-free survival, and was well tolerated.

“These results serve as preliminary proof-of-concept for AGS-003, demonstrating that this immunotherapy is able to induce an immune response to the very patient-specific tumor antigens that are targeted,” said Charles Nicolette, Ph.D., Chief Scientific Officer and Vice President of Research and Development of Argos Therapeutics. “This study not only demonstrates a favorable safety profile and early signs of efficacy, but the results also compare favorably to historical results with standard immunotherapy approaches in mRCC patients. These results provide a strong basis for the ongoing Phase 2 trial evaluating the therapy in combination with sunitinib.”

“Patients enrolled in this trial were a higher-risk, poorer-prognosis population with reduced expectations for clinical response and survival,” said Theodore Logan, M.D., of the Indiana University Simon Cancer Center and lead author on the poster. “Thus, the clinical benefit, excellent safety profile and immunologic responses observed in this study were quite encouraging. These results compare favorably to historical results with interferon-О± in an unfavorable risk group of patients and represent an encouraging development in the continued search for novel, well tolerated immunotherapy approaches in this patient population.”

At the study’s baseline, the majority of evaluable patients, all of which were classified as either MSKCC intermediate or poor-risk, suffered impaired cellular immunity to RCC tumor antigens; however, following AGS-003 treatment, the majority of evaluable patients experienced detectable cellular immunity to these same antigens, demonstrating that AGS-003 induced a tumor-specific immune response. Additionally, 50% of patients had restored T cell-mediated interleukin-2 and interferon-Оі responses, indicating general immune reconstitution. The median length of progression-free survival (PFS), from time of registration, was 5.6 months, in contrast to the historical median PFS for interferon-О± of 5.1 and 2.5 months for intermediate and poor-risk subjects, respectively. Forty percent of subjects experienced a clinical benefit, defined as either a partial response or stable disease. AGS-003 was well tolerated, with no drug-related serious adverse events or grade 3/4 adverse events observed.

This open-label Phase 2 trial enrolled 20 evaluable, newly diagnosed post-nephrectomy patients with clear cell mRCC. Subjects received intradermal injections of AGS-003 in the following sequence: 5 biweekly doses, 4 monthly doses, and 1 dose every 3 months until disease progression. Primary endpoints of the study included clinical and immune response, and secondary endpoints included safety, PFS and overall survival.

The poster, titled, “A Phase 1/2 Study of AGS-003, a Personalized Immunotherapeutic Evaluated in Newly Diagnosed Metastatic Renal Cell Carcinoma (mRCC) Subjects,” was authored by T. Logan, A. Amin, V. Cohen, M.K.K. Wong, V. Master, T. Monesmith, D. Healey, R. Jain, D. Plessinger, and C.A. Nicolette.

About the Arcelis™ Technology

Arcelis is Argos’ proprietary technology for personalizing RNA-loaded dendritic cell immunotherapies for HIV, other infectious diseases, and cancer. This platform is based on optimizing a patient’s own (autologous) dendritic cells to trigger a pathogen- or tumor-specific immune response. To address the challenge of the unique genetic profile of each patient’s disease and the genetic mutations of that disease, Argos loads the autologous dendritic cells with a sample of messenger RNA (“mRNA”) isolated from their disease. Through this process, dendritic cells can potentially prime immune responses to the entire antigenic repertoire, resulting in an immunotherapeutic that is customized to the patient’s specific disease.

Source
Argos Therapeutics, Inc.

CSL Biotherapies, a subsidiary of CSL Limited (ASX: CSL), one of the world’s leading manufacturers of influenza vaccine, announced that the U.S. Food and Drug Administration (FDA) has approved the company’s application for accelerated approval of its seasonal flu vaccine, Afluria® (Influenza Virus Vaccine) for use in the pediatric population aged 6 months and older. This approval also included labeling for CSL Biotherapies’ Influenza A (H1N1) 2009 Monovalent Vaccine which is an inactivated influenza virus vaccine now indicated for active immunization of persons ages 6 months and older against influenza disease caused by pandemic (H1N1) 2009 virus. This indication is based on the immune response elicited by the seasonal trivalent Influenza Virus Vaccines manufactured by CSL (Afluria®). CSL’s Influenza A (H1N1) 2009 monovalent vaccine and Afluria are manufactured by the same process. There have been no controlled clinical studies demonstrating a decrease in influenza disease after vaccination with Afluria.

“The FDA’s licensure of CSL Biotherapies’ thimerosal-free monovalent pandemic H1N1 vaccine for use in children aged 6 months and older is a critically important milestone,” said Paul Perreault, President, CSL Biotherapies. “The U.S. Centers for Disease Control has identified young children as a priority group for pandemic H1N1 vaccine administration. CSL Biotherapies is proud to now be in a position to help in protecting this most vulnerable population of Americans.”

CSL’s pandemic H1N1 vaccine is available in both thimerosal-free (i.e., preservative-free), single-dose, pre-filled syringes and multi-dose vial (thimerosal containing) formulations, as directed by the U.S. government. The thimerosal-free formulation is available in two dosages:

• A 0.25 mL single-dose, pre-filled syringe for use in children 6-35 months of age;
• A 0.5 mL single-dose, pre-filled syringe for use in persons 36 months of age and older

About CSL’s Influenza A (H1N1) 2009 Monovalent Vaccine

CSL’s pandemic H1N1 vaccine was licensed by the FDA for active immunization of adults on September 15, 2009. CSL’s Influenza A/H1N1 2009 vaccine is manufactured by a process identical to the one used in manufacturing CSL’s FDA-licensed trivalent seasonal influenza vaccine. CSL’s pandemic H1N1 influenza vaccine is a purified, inactivated, monovalent influenza virus propagated in embryonated chicken eggs.

CSL Biotherapies is conducting clinical trials in the U.S. of its monovalent H1N1 vaccine in children using a thimerosal-free (i.e., preservative-free) formulation. The studies were designed to determine the safety of CSL’s vaccine and its ability to elicit an immune response (also referred to as immunogenicity) in children. The studies will also evaluate the incidence of adverse events up to six months after first injection. The clinical studies are sponsored by CSL Biotherapies and funded in whole or in part with Federal funds from the U.S. Office of the Assistant Secretary for Preparedness and Response, Biomedical Advanced Research and Development Authority.

Important Safety Information

CSL’s Influenza A (H1N1) 2009 monovalent vaccine is an inactivated influenza virus vaccine indicated for active immunization of persons ages 6 months of age and older against influenza disease caused by the pandemic (H1N1) 2009 virus. The indication is based on the immune response elicited by the seasonal trivalent influenza virus vaccine manufactured by CSL (Afluria). CSL’s Influenza A (H1N1) 2009 monovalent vaccine and Afluria are manufactured by the same process. CSL’s H1N1 vaccine should not be administered to individuals with hypersensitivity to eggs, neomycin, polymyxin or anyone who has had a life-threatening reaction to previous influenza vaccination. Vaccination with the H1N1 vaccine may not protect all individuals. Immunocompromised persons may have a diminished immune response. If Guillain-Barr-syndrome has occurred within six weeks of receipt of prior influenza vaccine, the decision to give the H1N1 vaccine should be based on careful consideration of the potential benefits and risks. In adults, the most common injection-site reactions were tenderness, pain, redness and swelling. The most common systemic adverse reactions were headache, malaise and muscle aches. In children, the most common local (injection-site) adverse reactions observed in a clinical study with Afluria were pain, redness and swelling. The most common systemic adverse reactions observed were irritability, rhinitis, fever, cough, loss of appetite, vomiting/diarrhea, headache, muscle aches and sore throat. Full prescribing information can be found at cslbiotherapies-us.

About Influenza and the Novel Influenza A/H1N1 Virus

The emergence of the novel H1N1 flu, which was first detected in humans in April 2009, has proven to be very contagious, spreading worldwide, and has led to the World Health Organization declaring a pandemic on June 11, 2009.

CSL Biotherapies has developed and produced its monovalent Influenza A/H1N1 2009 vaccine drawing on four decades of experience with its proven vaccine production processes.

Source
CSL Biotherapies

We are all familiar with the fact that cognitive function declines as we get older. Moreover, recent studies have shown that the specific kind of daily activities we engage in during the course of our lives appears to influence the extent of this decline. A team of researchers from Technische Universität Berlin are studying how division of labour among honey bees affects their learning performance as they age. Surprisingly, they have found that, by switching their social role, aging honey bees can keep their learning ability intact or even improve it. The scientists are planning to use them as a model to study general aging processes in the brain, and they even hope that they may provide some clues on how to prevent them. Dr. Ricarda Scheiner, leader of the research team, presented these findings at the Society of Experimental Biology Annual Meeting in Glasgow.

The oldest bees in a colony are the foragers – a task that demands a high amount of energy. With increasing foraging duration, their capacity for associative learning was found to decrease. On the other hand, no decline was observed in nurse bees that remain inside the hive taking care of the brood and the queen, even though their age was the same as that of their foraging sisters. When the scientists artificially forced a subset of these foragers to revert to nursing tasks, they discovered that they learning performance improved again, demonstrating a remarkable plasticity in their brain circuits.

“The honey bee is a great model”, explains Dr. Scheiner, “because we can learn a lot about social organisation from it and because it allows us to revert individuals into a ‘younger’ stage. If we remove all of the nurse bees of a colony, some of the foragers will revert to nursing behaviour and their brains become ‘young’ again. We thus hope to study the mechanisms responsible for age-dependent effects, like oxidative damage, and also to discover new ways to act against these aging processes.”

Source:
Cristian C. A. Bodo

Society for Experimental Biology

Results of a study show an increased prevalence of atrial fibrillation (AF) among patients with idiopathic central sleep apnea in the absence of congestive heart failure. The study compared 60 idiopathic central sleep apnea (CSA) patients with control groups of 60 obstructive sleep apnea patients and 60 patients without a sleep-related breathing disorder, matched for age, sex and body mass index.

The study shows that the prevalence of AF in idiopathic CSA patients (27 percent) is significantly higher than the prevalence among those with either obstructive sleep apnea (1.7 percent) or no sleep apnea (3.3 percent). AF, which leads to decreased pumping efficiency of the heart, is the most common chronic arrhythmia in North America, according to background information in the article.

“The present study is the first to demonstrate a relationship between AF and CSA in the absence of congestive heart failure,” the authors write. “Our results complement recent reports suggesting that cardiac overdrive pacing may improve CSA in patients with bradyarrhythmias, many of whom had AF.”

SLEEP is the official journal of the Associated Professional Sleep Societies, LLC, a joint venture of the American Academy of Sleep Medicine and the Sleep Research Society.
Go online to journalsleep.

Medical Services
International Inc. (Pink Sheets: MSITF) wishes to announce that interest in
its West Nile rapid test kit is increasing. The season for mosquitoes that
carry the West Nile is about to start and regulatory authorities in several
countries have approached the Company through its distributors to get test
data and samples. This year is expected to be an active year for mosquitoes
carrying West Nile. This corresponds to the increase in VScan rapid test
kits for Dengue Fever and Malaria.

All countries with hot climates that have mosquitoes are taking a pro
active approach to these diseases. Currently laboratories are so backed up
that it is often a month before results are obtained. With rapid test kits
that are as accurate as the VScan rapid test kit, early diagnosis helps to
control these diseases in an area. Early diagnosis and treatment can also
reduce the severity of these diseases in the individual.

About VScan

The VScan rapid test kit is a single use, disposable, accurate, cost
effective, easy to use, test for the screening of HIV 1&2, Hepatitis B&C,
Tuberculosis (TB), Dengue Fever, West Nile, Syphilis, and Prostate Cancer.
The kits cannot be sold in Canada.

Medical Services International Inc. trades in the United States on the
NQB Pink Sheets under the symbol “MSITF”

NOTE: Certain statements in this press release are “forward-looking
statements” within the meaning of the Private Securities Act of 1995. Such
statements involve known and unknown risks, uncertainties and other factors
that may cause results to differ materially. Such risks, uncertainties and
other factors include but are not limited to new economic conditions, risk
in product development, market acceptance of new products and continuing
product demand, level of competition and other factors described in Company
reports and other filings with regulatory bodies.

Medical Services International Inc.
medicalservicesintl

Cancer researchers led by Dr. John Dick at Ontario Cancer Institute (OCI) have developed a method to convert normal human blood cells into “human” leukemia stem cells. The converted cells, when transplanted into special mice that permit the growth of human cells, can replicate the entire disease process from the very moment it begins. The findings are published in the journal Science.

Dr. Dick, Senior Scientist at OCI, the research arm of Princess Margaret Hospital, and a Professor in the Department of Molecular Genetics, University of Toronto, said: “Most human leukemia research involves studying a patient’s diseased cells or a cell line grown from those cells. However, since cancer takes many months or years to develop, just studying the cells at the end of the process does not let you know what the series of changes were that caused the cells to become leukemic, and when they happened.

“With the method we developed, we have duplicated the natural process every step of the way. The method we developed opens the pathway generally to understanding the process of how cancer begins.”

The scientific team of Frederic Barabe, James Kennedy and Kristin Hope introduced a specific leukemia gene into normal human stem cells and injected the genetically altered cells into mice that lacked immune systems. The result? 100% of the mice developed fatal leukemia that displayed the same characteristics and patterns of human disease.

For the past 20 years, said Dr. Dick, leukemia research has focused mainly on human cells where the disease already exists or by studying leukemia created in mouse cells. This study flipped it around to focus on asking which are the normal cells within which the disease arises and then how it evolves and progresses, all within the context of human cells.

“So what we are building is a new approach and way of studying how leukemia arises in the first place. We found that with the leukemia gene we were using, the disease only arose from immature stem and progenitor cells. The leukemic stem cells that were created seemed to change as the human leukemia was grown for longer times in a series of transplanted mice. Our findings of how these leukemic stem cells functioned could explain several features of the leukemia in children and adults that also contain the same leukemia gene, MLL-ENL.”

In 1994, Dr. Dick identified the first cancer stem cell in leukemia, following on the original discovery in 1962 of the blood stem cell by two other renowned OCI scientists, Drs. Ernest McCulloch and James Till — a discovery that formed the basis of all current stem cell research. Dr. Dick, who holds the Canada Research Chair in Stem Cell Biology and is also Senior Scientist at the Toronto General Research Institute and at the McEwen Centre for Regenerative Medicine, University Health Network, recently published other findings showing that colon cancer arises from stem cells specific to the tumour.

###

This research was financially supported by grants and fellowships from the Canadian Institutes for Health Research, Ontario Institute for Cancer Research, Genome Canada through the Ontario Genomics Institute, the Leukemia and Lymphoma Society, and the National Cancer Institute of Canada with funds from the Canadian Cancer Society and the Terry Fox Foundation.

Princess Margaret Hospital and its research arm, Ontario Cancer Institute, have achieved an international reputation as global leaders in the fight against cancer. PMH is a member of the University Health Network, which also includes Toronto General Hospital and Toronto Western Hospital. All three are research and teaching and research hospitals affiliated with the University of Toronto. For more information, go to uhn/

Contact: Jane Finlayson

Princess Margaret Hospital

UroToday – In the online edition of Prostate Cancer Prostatic Diseases, a group of investigators including Dr. Peter Albertsen reports on costs associated with care for prostate cancer (CaP). The goal of the study was to use the SEER database to calculate the long-term costs by cancer stage. SEER is a cancer registry linked to Medicare claims and represents 26% of the US population between 1991 and 2004.

The study cohort included men with a primary diagnosis of CaP between 1991 and 2002. To determine background medical costs for men without CaP, a 5% sample from the Medicare database was randomly selected and matched in 5-year age groups to the study population. The investigators used a phase-based model to estimate monthly treatment costs. The time periods from diagnosis to death were divided into 3 phases of care: initial, continuing and terminal care. The total average monthly cost of care was calculated for each patient by adding the payment data on each Medicare claim for each treatment phase and then dividing by the total number of follow-up months patients contributed to each phase. The differences between CaP case costs and non-cancer control costs were determined to be CaP costs. Long-term costs were calculated by combining survival data from SEER with phase-specific monthly cost estimates.

One-third of patients did not receive initial active therapy. Radical prostatectomy was greatest for stage III CaP and lowest for stage I, while radiotherapy and brachytherapy were more common among lower versus higher stage patients. The data indicated that cost outliers were driving up the mean monthly costs for each treatment phase and inflating long-term estimates. When patients in the 95-100th percentile of costs were excluded from the analysis, model-based estimates of long-term costs were more consistent with actual mean Medicare payments. The largest difference in monthly costs between CaP patients and controls was in the initial phase with an incremental difference averaging $1,857. This difference increased with increasing disease stage. Monthly terminal care costs for stages I-III were similar to non-cancer patients, but stage IV CaP patients had terminal costs over $1,000 higher versus stages I-III. Regarding survival, 61%, 56%, 55%, and 18% of stages I, II, III, and IV patients were still alive 120 months after diagnosis. Average long-term costs were $57,691 for stage IV patients and decreased to $40,969 for stage I. CaP costs were a significant part of total costs making up 40.5%, 36.2%, 33%, and 43.3% of total costs for stages I, II, III, and IV, respectively.

Stokes ME, Black L, Benedict A, Roehrborn CG, Albertsen P

Prostate Cancer Prostatic Dis. 2010 Mar 9. Epub ahead of print
doi:10.1038/pcan.2010.5

UroToday Contributing Editor Christopher P. Evans, MD, FACS

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