BreakThrough Digest Medical News |
| University of Montreal researchers discover how drug prevents aging and cancer progression Posted: 25 Mar 2013 09:00 PM PDT University of Montreal researchers have discovered a novel molecular mechanism that can potentially slows the aging process and may prevent the progression of some cancers. In the March 23 online edition of the prestigious journal Aging Cell, scientists from the University of Montreal explain how they found that the antidiabetic drug metformin reduces the production of inflammatory cytokines that normally activate the immune system, but if overproduced can lead to pathological inflammation, a condition that both damages tissues in aging and favors tumor growth.
“Cells normally secrete these inflammatory cytokines when they need to mount an immune response to infection, but chronic production of these same cytokines can also cause cells to age. Such chronic inflammation can be induced, for example by smoking” and old cells are particular proficient at making and releasing cytokines says Dr. Gerardo Ferbeyre, senior author and a University of Montreal biochemistry professor. He adds that, “We were surprised by our finding that metformin could prevent the production of inflammatory cytokines by old cells “. In collaboration with Michael Pollack of the Segal Cancer Centre of the Jewish General Hospital, McGill University, Dr. Ferbeyre and his team discovered that metformin prevented the synthesis of cytokines directly at the level of the regulation of their genes. “The genes that code for cytokines are normal, but a protein that normally triggers their activation called NF-?B can’t reach them in the cell nucleus in metformin treated cells”, Dr. Ferbeyre explained. “We also found that metformin does not exert its effects through a pathway commonly thought to mediate its antidiabetic effects”, he added. “We have suspected that metformin acts in different ways on different pathways to cause effects on aging and cancer. Our studies now point to one mechanism”, noted lead authors of the study Olga Moiseeva and Xavier Deschênes-Simard. Dr. Ferbeyre emphasized that, “this is an important finding with implications for our understanding on how the normal organism defends itself from the threat of cancer and how a very common and safe drug may aid in treatment of some cancers and perhaps slow down the aging process. He adds, “It remains that determining the specific targets of metformin would give us an even better opportunity of profit from its beneficial effects. That’s what we want to figure out next”. ### Notes: The University of Montreal is known officially as Université de Montréal. The research involved in the study “Metformin inhibits the senescence-associated secretory phenotype by interfering with IKK/NF-B activation” was financed by Prostate Cancer Canada and the Canadian Institutes of Health Research (MOP-82887). Contact: William Raillant-Clark |
| Better treatment for stroke patients on horizon Posted: 25 Mar 2013 09:00 PM PDT Two molecules may provide, for the first time, an indication of which stroke patients will suffer a further, long-term neurological deficit, allowing doctors to tailor treatment more effectively. Subarachnoid haemorrhage (SAH), a form of stroke, affects around half a million people worldwide each year. Nearly 50 per cent of patients who survive the initial haemorrhage die within 30 days, with survivors likely to suffer permanent disability.
A study by Dr Sanjaya Kuruppu and Professor Ian Smith of Monash University and clinicians at Harvard Medical School, Dr Mingming Ning and Dr Sherry Chou, has shown that there may be a way to predict the sub-group of SAH patients that will suffer severe long-term disability. By assessing the cerebrospinal fluid of SAH patients, the researchers discovered that in the three days immediately following the stroke, an enzyme, endothelin converting enzyme-1 (ECE-1) and its substrate big endothelin-1 (BigET-1) were elevated in patients that suffered a disability that severely impacted on their capacity to self-care. Dr Sanjaya Kuruppu, of the Monash Department of Biochemistry and Molecular Biology said the discovery was a breakthrough in treating a deadly and unpredictable condition. “This is the first time doctors have had an early and accurate indication that disability will occur, giving them time to focus appropriate and aggressive therapies on this group of patients,” Dr Kuruppu said. “More importantly, it provides families with information required to make crucial decisions about subsequent long-term care.” As cerebrospinal fluid is routinely monitored following SAH, testing for elevated levels of ECE-1 and BigET-1 would have no negative impact on patients. Professor Ian Smith, Pro Vice-Chancellor (Research and Research Infrastructure) was the lead researcher on the project at Monash. “The next step in bringing this breakthrough to a clinical setting is to develop the technology to enable rapid diagnosis in a hospital setting and we’re currently making progress on this,” Professor Smith said. The Monash researchers, again in collaboration with Harvard, are planning a larger clinical study in the near future. They aim to determine the exact threshold level of the molecules required to classify a patient as being at high risk of developing long-term disability. ### The discovery is protected by a provisional patent filed jointly with Massachusetts General Hospital/Harvard Medical School. The research was funded by Monash University, the National Health and edical Research Council of Australia, and the National Institute of Health (USA). Contact: Emily Walker |
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