November marks the sixth anniversary of Techna, UHN’s youngest research institute. In that time Techna has grown its Technology Development Team to over 40 technical project managers, engineers, developers and more.
Techna was designed to accelerate the development of technology and to help deploy it into the healthcare system, and has had a number of successes in its short tenure. Partnerships with over 40 industry partners and the management of over 30 high-impact projects have helped Techna generate 10 patents, 29 licencing opportunities, 7 licensed products and 5 start-ups. Globally, Techna’s technologies and innovations now impact the treatment or management of over 3,000 patients daily.
In addition, Techna has moved toward self-sustainability with fee-for-service offerings to help develop and “productize” medical technology. Read more about their service offerings here.
Happy birthday, Techna!
The Techna Institute was established with the generous support of The Princess Margaret Cancer Foundation, FDC Foundation, Myron and Berna Garron and Agnico Eagle.
Maintaining work-life balance. Eating a healthy diet. Balance is something that our minds and bodies are constantly striving for.
For example, when the lungs are damaged by cigarette smoke or infections, the body sets to work, trying to repair the damage. Underlying this process is a type of cell known as the myofibroblast, which are recruited to the site of injury to orchestrate would-healing responses, including scar formation.
The problem is that, just as we sometimes fail at balancing our lifestyles, the body can get it wrong. In the case of repeated injury to the lung, myofibroblasts can become over-active; this promotes the formation of excessive scar tissue—so much so that the organ becomes inflexible, resulting in a serious condition known as pulmonary fibrosis. As fibrosis worsens, individuals with pulmonary fibrosis find it harder and harder to breathe and the transport of oxygen into the bloodstream becomes insufficient—causing respiratory failure and death.
It is not exactly known how myofibroblasts are activated to promote organ scarring. To address this issue, a team led by Krembil Senior Scientist Dr. Mohit Kapoor and co-lead investigators Dr. David Lagares and the late Dr. Andrew Tager (both from Harvard University) initiated a study to explore the molecular signals that activate myofibroblasts in people with pulmonary fibrosis.
In the study, the researchers compared lung myofibroblasts isolated from people with or without pulmonary fibrosis, and found that the level of Ephrin-B2, a protein on the surface of cells, was higher in myofibroblasts from fibrotic lungs. Using a series of experimental models, they discovered that an enzyme called ADAM10 causes part of Ephrin-B2 to be cleaved from the surface of the cell. The released piece, called sEphrin-B2, instructs myofibroblasts to migrate to the site of injury, generate scar tissue and promote fibrosis.
The team also found that administering sEphrin-B2 protein under the skin caused skin fibrosis, further implicating this molecule as a key player in the formation of excessive scar tissue. Moreover, by blocking the activity of ADAM10, they found that less sEphrin-B2 was released, resulting in reduced activation of myofibroblast cells and reduced fibrosis.
“Our study provides the first proof of concept that the ADAM10-sEphrin-B2 pathway drives organ fibrosis,” explains Dr. Lagares. Dr. Kapoor adds, “These results provide new targets for the development of therapies to prevent organ failure by preventing fibrosis—not only in the lungs and skin, but also in other tissues affected by fibrosis such as joints, the heart, the liver and the kidney.”
This work was supported by Université de Montréal, the American Thoracic Society Foundation, the Pulmonary Fibrosis Foundation, the Scleroderma Foundation, the National Institutes of Health, the Scleroderma Research Foundation and the Toronto General & Western Hospital Foundation.
Lagares D, Ghassemi-Kakroodi P, Tremblay C, Santos A, Probst CK, Franklin A, Santos DM, Grasberger P, Ahluwalia N, Montesi SB, Shea BS, Black KE, Knipe R, Blati M, Baron M, Wu B, Fahmi H, Gandhi R, Pardo A, Selman M, Wu J, Pelletier JP, Martel-Pelletier J, Tager AM, Kapoor M. ADAM10-mediated ephrin-B2 shedding promotes myofibroblast activation and organ fibrosis. Nat Med. 2017 Oct 23. doi: 10.1038/nm.4419.
UHN was ranked number one on the 2017 list of Canada’s Top 40 Research Hospitals, released by RE$EARCH Infosource Inc.
The annual rankings compare research hospitals across Canada according to their research funding data. Funds that were considered included grants, contributions and contracts from all internal and external government and non-government sources.
UHN research expenditures totaled $332 million in the 2016 fiscal year, a value that earned the UHN the top rank for the seventh year in a row. In comparison to last year, UHN research expenditure funding increased by 5%.
Within the “Large Hospitals” category (total hospital spending >$1B), UHN also led in terms of research hospital intensity, which is defined as the percent of research spending versus total hospital spending. Within the same category, UHN came in fourth in terms of research intensity (dollars spent per appointed researcher), with London Health Sciences Centre in the lead.
Other hospitals that ranked among the top five for total research expenditure included The Hospital for Sick Children in Toronto ($201.4M), McGill University Health Centre in Montreal ($178.8M), Hamilton Health Sciences ($171.4M) and the Provincial Health Services Authority in Vancouver ($161.9M).
To view the complete list of Canada’s Top 40 Research Hospitals, click here. To see the Spotlight on Hospital Research Activity within the large hospitals category, click here.
RE$EARCH Infosource Inc. reports on research across Canada, and releases other annual lists, including the Top 50 Research Universities and Top 50 Research Colleges.
Rick Hansen is a Canadian icon who changed our perception of spinal cord injury (SCI). As a teenager, he sustained an SCI that paralyzed him below the waist. Despite his disability, he embarked on a trek across the world in his wheelchair. He performed this amazing feat as part of his ‘Man in Motion World Tour’ to raise funds for SCI research and promote the potential of all people living with disabilities.
The spinal cord consists of a thin column of nerve tissue that extends from the base of the brain to the lower back. It serves as the main pathway through which the brain and the rest of the body communicate. This two-way communication is dependent on the millions of nerve cells and the fibers that extend from them and comprise the spinal cord. Damage to the spinal cord can kill nerve cells or impair their function, leading to pain, paralysis and loss of sensation in different parts of the body. Presently, there are no treatments to repair the damage from SCI.
Researchers have shown that a molecule known as RGMa is involved in nerve tissue injury. RGMa is produced in nerve tissue, prevents the growth of damaged nerve fibers and is detected at high levels in tissues affected by diseases such as multiple sclerosis and Alzheimer disease.
In light of these observations, a team of Krembil researchers examined the potential role of RGMa in SCI. This team was led by Drs. Charles Tator, Philippe Monnier and Andrea Mothe.
The researchers found that damaged spinal cord tissue from patients and an experimental model of SCI contained high levels of RGMa, suggesting that the molecule was produced in response to damage. Importantly, they showed that inhibiting RGMa activity in the SCI model produced several positive effects: not only did it promote the survival of nerve cells and the growth of their fibers near the site of injury, but it also improved movement, coordination and mobility. Moreover, the inhibition of RGMa also alleviated the pain that typically follows SCI.
These findings highlight the therapeutic potential of targeting RGMa to promote recovery after SCI. If RGMa inhibition continues to produce promising results in the lab, clinical trials will be conducted to establish whether it benefits patients with SCI.
This work was supported by the Rick Hansen Institute, the Canadian Institutes of Health Research, AbbVie, Spinal Cord Injury Ontario and the Toronto General & Western Hospital Foundation.
Mothe AJ, Tassew NG, Shabanzadeh AP, Penheiro R, Vigouroux RJ, Huang L, Grinnell C, Cui YF, Fung E, Monnier PP, Mueller BK, Tator CH. RGMa inhibition with human monoclonal antibodies promotes regeneration, plasticity and repair, and attenuates neuropathic pain after spinal cord injury. Sci Rep. 2017 Sep 5. doi: 10.1038/s41598-017-10987-7.
There are many rites of passage in life: driving a car at 16, voting at 18… and screening for colon cancer at 50. Though it can sound uncomfortable, this one is just as important as life’s other milestones: according to the National Cancer Institute, regular colonoscopies can reduce your risk of dying from colorectal cancers by up to 70%.
For people with a higher risk of developing colon cancer, guidelines often call for increased screening with colonoscopies, starting at a younger age. However, for young cancer survivors there are no clear guidelines in place.
Cancer therapies such as radiation therapy are known to increase the risk of developing cancer years later. When this happens, these cancers are sometimes referred to as ‘secondary cancers’. But in order to create guidelines for screening for secondary cancers, evidence is needed to show that these cancers can be detected at early stages and that screening with colonoscopies would actually help.
To address this issue, PM Cancer Centre’s Dr. David Hodgson and colleagues recruited a group of 35 to 49 year-old cancer survivors who had received radiation therapy to the abdomen in the past. They were then screened with a standard colonoscopy.
The team found that despite their younger age, the cancer survivors had abnormal growths (polyps) in their colons that were comparable to what would be found in people age 50 or older. And the prevalence of a certain type of polyp (adenomatous polyps) was similar to that found for patients known to be at high risk of developing colon cancer.
“This study provides the first evidence that early-onset colorectal cancer in people who received prior radiation therapy does have a preclinical phase that can be detected with colonoscopy screening,” said Dr. Hodgson. “The prevalence of polyps found here is comparable to other groups for whom screening is recommended. This bolsters the case for the creation of guidelines for cancer survivors that initiate screening at younger ages.”
This work was supported by the Canadian Cancer Society Research Institute, the Pediatric Oncology Group of Ontario and The Princess Margaret Cancer Foundation.
Daly PE, Samiee S, Cino M, Gryfe R, Pollett A, Ng A, Constine LS, Hodgson DC. High prevalence of adenomatous colorectal polyps in young cancer survivors treated with abdominal radiation therapy: results of a prospective trial. Gut. 2017 Oct. doi: 10.1136/gutjnl-2016-311501.