Pharma Notes

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of pathology, $366,171 over three years, to identify new mechanisms for controlling cancer resistance.

This work may lead to new approaches to effectively treat breast cancer by activating a protein that helps to trigger cancer cell death. • Wei Xiao, professor of microbiology and immunology, was awarded with

U of S co-investigator Ron Geyer, professor of pathology, $375,000 to determine how the Uev1 gene plays its role in promoting breast cancer and develop reagents specifically targeting the longer form of the gene for breast cancer diagnosis and treatment.

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NEWS CELLULAR TAIL LENGTH TELLS DISEASE TALE

Simon Fraser University molecular biologist Lynne Quarmby’s adventures in pond scum have led her and four student researchers to discover a mutation that can make cilia, the microscopic antennae on our cells, grow too long. When the antennae aren’t the right size, the signals captured by them get misinterpreted. The result can be fatal.

Quarmby and her team’s work was published in the science journal Current Biology. The researchers discovered that the regulatory gene CNK2 is present in cilia and controls the length of these hair-like projections. This discovery is important because cilia, or flagella, dangle from all of our cells. Their ability to propel some cells, such as sperm, and allow molecular communication in others, for example cellular responses to hormones, determines how we develop from embryos and how our bodies function in adulthood.

When cilia are too short or too long they cause various human hereditary diseases and deformities, such as too many fingers or toes, blindness and Polycystic Kidney Disease, which affects one in 600 people.

Quarmby and her doctoral student Laura Hilton—senior and lead authors, respectively, on this paper are among the few scientists globally who study cilia-disassembly as opposed to assembly.

A crucial part of all cells’ lifecycle is their cilia’s disassembly before cell division and assembly after it. The gene LF4 is a known assembly regulator and prior to this study, scientists thought that assembly speed controlled cilia’s ultimate length or shrinkage. But Quarmby and Hilton have discovered that disassembly speed is also important, and that the regulatory gene CNK2 plays a key role in controlling it.

Similar to how a balance between water pressure and gravity determines the height of a fountain’s stream, a balance of assembly and disassembly speed determines cilia’s length. When growing and shrinking happen simultaneously, cilia length remains constant.

The focus of their study of algae cilia was on those with defective CNK2 and

SFU cell biologist Lynne Quarmby’s years of mucking about in pond scum are paying off. She’s made a major cellular discovery about cilia. Photo Courtesy of SFU Public Affairs and Media Relations.

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NEW RESEARCH SHEDS LIGHT ON ABNORMAL HEART MUSCLE THICKENING AND POTENTIAL TREATMENT While most people would consider discovery that proteins involved in cell a big heart to be a good thing, for death also play a key role in abnormal heart disease experts, it is often a heart muscle thickening. sign of serious disease. Specifically, The research, published in the online it often occurs in people with high edition of Proceedings of the National blood pressure, diabetes, heart Academy of Sciences (PNAS), could failure and certain genetic condi- lead to new treatments for certain tions. Now, Dr. Lynn Megeney of forms of heart disease. Several years the Ottawa Hospital Research In- ago, Dr. Megeney noticed that heart stitute and the University of Ottawa muscle cells undergoing this kind (uOttawa) has made the surprising of abnormal growth had many similarities with cells that are beginning to undergo an orderly form of cell suicide called programmed cell death. In the current research paper, Dr. Megeney and his team showed that blocking the proteins that control this form of cell death also blocks abnormal heart muscle thickening. The procedure included exposing rats to a number of different drugs that each induce abnormal heart muscle thickening. The rats were then given a form of experimental gene therapy to block cell suicide proteins in the heart. Three weeks later, the rats that received the experimental therapy had much smaller heart muscle cells (37 per cent smaller than those that did not receive the therapy), and smaller hearts overall. In fact, the disease model rats that received the experimental therapy seemed just as healthy as normal rats. “This research is very important scientifically, and potentially clinically as well,” said Dr. Duncan Stewart, a practicing cardiologist who is also CEO and scientific director of the Ottawa Hospital Research Institute, vice-president of research at The Ottawa Hospital and a professor at uOttawa. “This research is particularly applicable to certain genetic forms of heart disease, as well as to hypertension, which affects about 40 per cent of the adult population.” “An important observation from our work is that proteins from the caspase family, which play a key role in cell suicide, are also activated early in the process of cardiac cell hypertrophy,” added Dr. Pasan Fernando, a co-author on the paper who is also a scientist at Nordion and the University of Ottawa Heart Institute and an assistant professor at uOttawa. “By blocking one or several of these proteins, we may be able to not only reduce cardiac disease but also prevent it from even occurring.” This research was funded by the Ontario Research Fund, the Heart and Stroke Foundation of Canada, the Canadian Institutes of Health Research, the Mach Gaensslen Foundation and The Ottawa Hospital Foundation.

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