Posts filed under ‘Biotechnology News and Info from Canadian Universities’

Thinking of Summer in the Cold BC Winter

A team of scientists from the University of British Columbia have genetically engineered mice that are able to withstand the wrinkle-inducing power of UV light found in the strong summer sun. It has been known for decades that prolonged exposure to the sun over one’s lifetime can cause premature aging and wrinkling of the skin. This has lead to a plethora of anti-aging skin creams and sunscreens that are designed to block out harmful UV rays in the hope of preventing sun-induced wrinkles. Now, Professor David Granville of UBC’s Department of Pathology and Laboratory Medicine has engineered mice lacking Granzyme B and found that the mice retained youthful-looking skin compared to the aged skin on normal mice. However, the benefits of Granville’s findings are not just limited to youthful looking skin.

Granzyme B (GzmB) is a serine protease that is expressed by a variety of cells and cleaves a number of extracellular membrane (ECM) proteins during inflammatory events. The breakdown of the ECM is known to be an indicator of many chronic inflammatory diseases. Thus, Granville and his team hypothesized that inhibiting the activity of GzmB may work to inhibit the breakdown of ECM during the inflammatory process. When Granville exposed GzmB deficient mice to solar-stimulated UV irradiation, they found that degradation of ECM proteins had slowed down which had manifest itself in the lack of development of expected wrinkles. Based on these findings, Granville has proposed that blocking the activity of GzmB may be an effective method for preventing other diseases associated with ECM degradation such as aneurysms and chronic obstructive pulmonary disease which are caused by the breakdown of collagen and other proteins that provide structure to blood vessels and lung passages.

Reference: Parkinson, L. G., Toro, A., Zhao, H., Brown, K., Tebbutt, S. J. and Granville, D. J. (2014), Granzyme B mediates both direct and indirect cleavage of extracellular matrix in skin after chronic low-dose ultraviolet light irradiation. Aging Cell. doi: 10.1111/acel.12298.

December 16, 2014 at 3:18 pm Leave a comment

Mount Sinai Hospital Scientist Wins World’s Largest Prize for Diabetes Research

Dr. Daniel Drucker, Senior Investigator at Mount Sinai Hospital’s Lunenfeld-Tanenbaum Research Institute, is the recipient of the world’s most valuable award for diabetes research, the 2014 Manpei Suzuki International Prize. The award, which was announced today by the Manpei Suzuki Diabetes Foundation in Tokyo, recognizes Dr. Drucker’s research in the area of gut hormones and how they control glucose and body weight, which have led to the development of two new classes of therapies for the treatment of type 2 diabetes.

“The 2014 Manpei Suzuki International Prize brings tremendous international recognition to the work that we have done for over 25 years, with my trainees and fellow scientists, both at the Lunenfeld-Tanenbaum Research Institute and at the University of Toronto,” says Dr. Drucker, who is also Professor of Medicine in the Division of Endocrinology at the University of Toronto.“We are honoured that our science has helped in the development of new medications for patients with diabetes, and delighted to have our research achievements recognized by our esteemed colleagues in Japan.”

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December 10, 2014 at 3:47 pm Leave a comment

New Advances in Next Generation RNA Sequencing

Genetic sequencing determines the precise order of the molecules that make up our DNA and RNA, which in turn are the molecular “fingerprint” of tumour cells that allow for personalized medicine for individual patients. Now, a new way of analyzing genomic data from tumours may one day allow clinicians to treat each person’s cancer as its own unique disease.
In a recent paper published by Mount Sinai researchers led by Drs. Alex Zlotta and Jeff Wrana, the team used leading-edge molecular analysis to decode the genetic makeup of a bladder cancer patient’s tumour, with will be vital to the medical decisions that are being tailored for the individual patient.
The research team established the methods to sequence all of a tumour’s RNA (whole transcriptome RNA-Sequencing) from tumours preserved in formalin. Formalin is an organic compound useful for preserving samples. Tumours are then embedded in paraffin (FFPE), which allows for samples to be solidified so that analysis can be done. When the results were compared between matched, freshly frozen tumour samples and FFPE tumour samples, the team observed similar results between the two sample types.
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December 1, 2014 at 2:40 pm Leave a comment

Largest Ever Map of Human Protein Interactions

One of the central questions in human biology is to understand how our genes determine which diseases we get and how severe they might be. Knowing just the DNA sequence, or the blueprint, is not enough. We must figure out how proteins, the genes’ products, work too.

Now an international team of researchers, jointly led by Dr. Fritz Roth (at Mount Sinai Hospital’s Lunenfeld-Tanenbaum Research Institute and the Donnelly Centre of the University of Toronto), and Dr. Marc Vidal (with the Dana-Farber Cancer Institute and Harvard Medical School in Boston), have produced the largest ever map of human protein interactions. This publicly available resource will be invaluable to anyone trying to understand complex genetic traits and develop new disease therapies.

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November 20, 2014 at 5:28 pm Leave a comment

A war between cellular defenses and ancient pathogens may contribute to cancer

In a study published by Nature Communications, researchers at the University of Ottawa’s Faculty of Medicine uncovered a novel mechanism that controls genetic change. This mechanism has possible roles in evolution, drug resistance, as well as tumor formation in a significant proportion of breast and ovarian cancers.

Cancer cells often develop resistance to drugs, a major factor preventing the cure of many types of cancers. Current evidence suggests that cancers are caused by multiple genetic changes and that continued genetic change causes tumors to develop resistance to drug treatments.

The mechanism, discovered by the research team led by Derrick Gibbings, involves an ongoing war between a cellular degradation process called autophagy and ancient pathogens known as retrotransposons. Essentially, retrotransposons create mutations within the DNA and are responsible for a quarter of the genetic differences between two individuals.

“By mutating our DNA, retrotransposons have provided us with genes vital to important functions such as the formation of placenta. In fact, almost half our genome derives from retrotransposons. However, they can also create mutations that lead to drug resistance, cancers and other diseases,” says Gibbings, assistant professor of cellular and molecular medicine. “Mammals, including humans, could not have evolved without retrotransposons. But they’re both our enemy and our friend.”

The research team discovered that autophagy degrades retrotransposons and prevents them from creating new mutations in the genome. Autophagy is known to be insufficiently active in 35% to 70% of ovarian and breast cancer tumors. Gibbings’ team is currently following up on preliminary evidence that in breast cancer patients, retrotransposons become overactive and can affect the survival rate of these women.

“We now understand that retrotransposons have an impact on the creation and growth of tumors as well as the evolution of species. Our results suggest that autophagy helps buffer these processes,” says Gibbings. “This leads us to believe that by allowing autophagy to do its job, we may be able to slow tumors and their reappearance after chemotherapy through the use of some relatively benign drugs already being used to treat other medical conditions.”

Thanks to the University of Ottawa for contributing this story.

November 10, 2014 at 3:00 pm Leave a comment

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