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Tag Archives: University of Toronto

Friday Science Review: March 11, 2011

Insulin + Pancreatic Stem Cells, Proof of Life

University of Toronto ♦ Published in Cell Stem Cell, Mar. 4, 2011

The origin of insulin-producing pancreatic β-cells has been a matter of contentious debate. Some research groups have produced findings that would suggest β-cells duplicate themselves and that new β-cells do not arise from the differentiation of a more primitive pancreatic progenitor. Other groups have proven the existence of pancreas-derived multipotent progenitors (PMPs) that are capable of giving rise to a spectrum of cells from both the pancreatic and neural lineage. So where do β-cells come from?

New results from the lab of Dr. Derek van der Kooy point in the direction of PMPs. Lineage labeling experiments in mice showed that PMPs originate from the embryonic pancreas, as opposed to the neural crest, which has often been cited as the source of pancreatic progenitors. These findings are in conflict with previous studies which could not provide evidence of pancreatic progenitors in the developing embryo or the adult. Convincingly, Dr. van der Kooy’s group was able to show that PMPs express insulin in vivo, an attribute that has often been considered prerequisite for the production of β-cells.

Analysis of human islet tissue showed that PMPs also exist in humans, and, similar to the mouse PMPs under observation, were capable of differentiation to both the pancreatic and neural lineages. Both mouse and human PMPs were able to alleviate diabetic conditions in mice and may provide another avenue to explore in the pursuit of therapeutic cells for transplantation therapy.

Selective Pressures Shape the Genomic Integrity of Human iPS Cells During Reprogramming

Samuel Lunenfeld Research Institute ♦ Ontario Institute for Cancer Research ♦ The Hospital for Sick Children ♦ University of Toronto

Published in Nature, Mar. 3, 2011

Coercing fibroblasts to revert to an embryonic stem cell-like state places a good deal of stress on the genome. The consequences of reprogramming can affect the development of safe populations of cells for therapeutics, which is why researchers at the Samuel Lunenfeld Research Institute have been interested in understanding how the reprogramming process affects genomic integrity. The integrity of a genome can be measured using copy number variation (CNV) within a population of cells. CNVs arise from deletions or duplications in DNA; as variation increases, the integrity of the genome declines.

In this study supervised by Dr. Andras Nagy and Dr. Timo Otonkoski, researchers characterized the CNV content of 22 human iPS cell lines and 17 human ES cell lines using Affymetrix SNP arrays. Induced pluripotent cell lines were created by way of retroviral transduction or with the use of a transposon known as piggybac. The number of CNVs in iPS cells was roughly twice that found in ES cells on average and many CNVs found in iPS cells were undetectable in ES cells suggesting that CNVs are generated during the reprogramming process. To the surprise of the group the number of CNVs in iPS cells was greatest at early stages, and decreased as cells were passaged in culture.

Researchers hypothesized that the reduction in copy number variation could be the result of two things, firstly, a DNA repair mechanism that corrects deletions and additions as the cells grow and divide in vitro, or mosaicism in early cultures followed by selection of iPS cells that have lower variation and greater genomic stability; a survival of the fittest in a way. It is unlikely that a DNA repair mechanism could operate fast enough to account for the rapid reduction of CNVs observed in iPS cells in culture and indeed, after using fluorescence in situ hybridization (FISH), it was confirmed by the lab group that mosaicism did exist in early cultures of iPS cells. In order to prove that selection was driving the decrease in CNVs researchers focused on deletions that cannot be corrected by DNA repair mechanisms. They found that several of these deletions were selected against during passaging of iPS cell lines. This pressure was bidirectional however, as some CNVs were selected for, not against.

CIITA, A Promiscuous Partner in Lymphoid Cancers

Centre for Translational and Applied Genomics ♦ BC Cancer Agency ♦ University of British Columbia

Published in Nature, Mar. 2, 2011

Chromosomal translocation events are a common abnormality leading to the development of cancer but few have been described as contributors to the development of lymphoid cancers. A new chromosomal translocation event has been implicated in the development of Hodgkin lymphoma and primary mediastinal B-cell lymphoma (PMBCL). Large scale mutations of this nature occur when non-homologous chromosomes transiently stick together and cause breakages that lead to the exchange of genetic information. If genes are placed next to one another following the translocation event, fusion transcripts are created which can lead to cellular abnormalities and malignant expansion.

Genome-wide mapping of translocation events can be carried out using paired-end sequencing of expressed transcripts. Researchers used such a platform to analyze two Hodgkin lymphoma cell lines. Analysis uncovered a highly expressed gene fusion between the MHC class II complex (CIITA) and an uncharacterized gene. Further analysis of 263 B-cell lymphoma cell lines went on to show that the CIITA translocation was highly recurrent in PMBCL (38%) and Hodgkin lymphoma (15%). The genetic event appears to be quite specific to PMBCL as it was observed in only 3% of diffuse large B-cell lymphoma cell lines.

Researchers note that although certain translocation events of very specific rearrangements are key contributors to some B-cell lymphomas, resulting in unique clinopathological features, many well characterized B-cell lymphomas still lack identifiable translocations that define the disease. Translocations in B-cell lymphomas are a rare occurrence, and until the publication of this research, no translocations had ever been reported in PMBCL.

Friday Science Review: February 11, 2011

Cardiac Differentiation: A Customized Approach

McEwen Centre for Regenerative Medicine ♦ University of Toronto ♦ SickKids

Published in Cell Stem Cell, Feb. 4, 2011

Dr. Gordon Keller of the McEwen Centre for Regenerative Medicine has been a pioneer in the stem cell world and was the first researcher to produce functioning cardiomyocytes from embyronic stem cells. These cells form clusters in the petri-dish that beat in unison, a rather marvelous sight to behold. The efficient differentiation of embryonic stem cells to cardiac cells requires monitoring the very earliest stages of their development. Monitoring the expression of one gene, Flk-1, has been instrumental in recognizing the formation of cardiac mesoderm, an early step in the developmental path of cardiomyocytes. A problem that remains however, is that Flk-1 is expressed in different forms of mesoderm, not all of which lead to the cardiac lineage. A second gene, PdgfR-α, can be used to separate cardiac and hematopoietic lineages when monitored in conjunction with Flk-1. Fractions of differentiating cells that coexpress the two genes have greater cardiomyocyte potential. Keller’s lab group used these two genes to study the stage-specific effects that Activin/Nodal and BMP signaling have on the development of cardiomyoctyes. They found that very small changes in the amount of Activin/Nodal or BMP had profound effects on the proportion of Flk-1+/PdgfR-α+ cells that appeared early on in the differentiation protocol, and that optimization of these concentrations in cultures of human pluripotent stem cells could give rise to structures that contain more than 50% Flk-1+/PdgfR-α+ cells. A major finding by Keller’s team is that different mouse and human pluripotent stem cell lines required unique optimization to produce maximal results, stressing the importance of using differentiation protocols that are in effect customized to individual pluripotent stem cell lines.

β-Catenin Maintains Pluripotency of Stem Cells with Two Divergent Signaling Cascades

Stem Cell and Cancer Research Institute ♦ McMaster University ♦ University of Guelph

Published in Cell Stem Cell, Feb. 4, 2011

It is widely assumed that β-catenin, a key molecule in the Wnt/β-catenin signaling pathway, helps sustain pluripotency through its interaction with TCL/LEF transcription factors. However, recent research shows that β-catenin also promotes pluripotency by complexing with and stabilizing Oct-4, a key member of the transcriptional network that maintains the pluripotent nature of stem cells. Glycogen synthase kinase-3 (GSK-3) has emerged as an important regulatory of pluripotency, in part because β-catenin is one of its primary substrates. After GSK-3 phosphorylates β-catenin it is degraded, which encourages stem cells to exit the pluripotent state and differentiate to other cell types. Dr. Bradley Doble and his colleagues previously showed that mouse embryonic stem cells (mESCs) that are entirely deficient in GSK-3 express very high levels of β-catenin and exhibit a severe impairment in their capacity to differentiate into the three germ layers. In this recent work, Doble and his team hypothesized that hyperactivated β-catenin/TCF was responsible for the pluripotent “lock” that was imposed on mESCs lacking GSK-3 expression. To the surprise of researchers, GSK-3α/β double knock out mESCs still maintained pluripotency even when they stably expressed a dominant negative form of the TCF transcription factor. How were they doing this? Apparently β-catenin can maintain pluripotency independent of functioning TCF. Researchers showed that β-catenin promotes the maintenance of pluripotency by interacting with Oct-4 in a divergent signaling cascade.

Next Generation Gene Therapy for Hemophilia A: Pre-clinical Progress

Queen’s University ♦ Published in Molecular Therapy, Feb. 1, 2011

Researchers pursuing therapies for Hemophilia A have turned to gene therapy for answers but have struggled to provide convincing pre-clinical results. Patients with the disorder have vastly decreased plasma concentrations of FVIII, a clotting factor that prevents blood loss after injury. Although viral vectors can produce the protein following system injection into animal models, its efficacy is compromised by the introduction of neutralizing anti-FVIII antibodies. Researchers hypothesized that the development of neutralizing antibodies was the result of transgene expression in the antigen presenting cells of mice. The solution to this problem was to “hide” the transgene by placing it under the control of a liver-specific promoter. This approach worked in normal mice, however researchers studying mice with hemophilia B still found that an anti-FVIII immune response was mounted in the presence of the new tissue-specific promoter. As a second layer of defense against this response researchers incorporated target sequences into the transgenic construct that had perfect complementarity to hematopoietic-specific miRNA sequences. These target sequences led to suppression of the transgene specifically in hematopoietic cells, including antigen expressing cells, limiting the neutralizing response. Dr. David Lillicrap and his team at Queen’s University have now used a similar approach to produce some very promising results in a mouse model of hemophilia A. A combination of a liver-restricted promoter, a miRNA regulated FVIII transgene, and a pseudotyped viral envelope seemed to do the trick.

Friday Science Review: January 28, 2011

Cancer’s Byzantine Architecture – The Plot Thickens

Campbell Family Institute for Cancer Research ♦ Ontario Cancer Institute ♦ University of Toronto

Published in Nature, 20 Jan., 2011

In the mid 90s one of Canada’s foremost stem cell researchers, John Dick, made the rather shocking discovery that not all cancer cells are equivalent. Based on his eloquent work we were able to formulate our current thinking on cancer biology, which has it that only a small sub-population of cells within tumours support malignant expansion, while the majority of cancer cells — although dividing — can only divide so many times before they hit cell cycle arrest and begin to senesce. Therefore, to completely eradicate a population of cancer cells, this minority of “cancer stem cells” must be targeted and destroyed. Our historical view on transformation was that single cells accumulate mutations over time, and in a step-wise fashion their genetic contents slowly mutates to the point that the cell itself loses control over its proliferation. Under this model each clone, or descendant of the original transformant, is linearly related. However, recent genomic work in the area indicates that this view is all too simple. It is now apparent that the architecture, the “framework” upon which cancer supports itself, is in fact a complex and branching network of sub-clones that each have the capacity to support tumour growth. Working with human BCR-ABL lymphoblastic leukemia cell lines, John Dick and his colleagues found that many diagnostic patient samples had several genetically distinct leukemia-initiating clones. DNA copy number alteration (CNA) profiling allowed them to reconstruct an evolutionary map of these clones. Transplantation of clones into xenograft models revealed that the predominant diagnostic clone, sometimes, but not always, was associated with the most aggressive growth properties. In some cases, interestingly, minor subclones proved to be the most potent leukemia-initiating cells. Next generation cancer therapeutics are being targeted to cancer stem cells, but now it appears — for these to be effective — they must target not only the dominant cancer stem cell clone, but all of the minor subclones that may be equally, if not more, vicious.

Freeing Systems Biology Data from the Shackles of the 2D Realm

University of Toronto ♦ Published in PLoS ONE, Jan. 10, 2011

One of the great challenges of systems biology will be to integrate multiple data sets, of widely differing scales, into an interactive and visual interface for human interpretation. Visualization is an important element in elucidating the connections between diverse data sets. Only in recent times have platforms existed that have the capacity to weave together large quantities of data into meaningful 3D representations. Historically, visualizations of biological data have been limited to 2D outputs that fail to do justice to the underlying connections between different biological processes. The need for 3D visualization tools is essential. We as humans have lived and evolved in a 3D environment and as a result have adapted a profound capacity to reason and conceptualize along three axes. In addition, biological processes occur within 3D environments, so carrying out analysis of biological data sets in three dimensions is logical. As a solution to this challenge, a group of researchers at the University of Toronto led by Dr. Nicholas Provart have created an open-source template that integrates and visualizes systems biology data as  interactive 3D representations on the world wide web. The group applied their template to the model plant organism Aribidopsis thaliana and have dubbed it ePlant. The platform incorporates proteome-scale protein structure prediction and annotation along with existing -omics scale data, and allows users to evaluate protein structure and function, protein-protein interactions, protein subcellular locations (great visual display here), gene expression patterns, and genetic variation. The result is a program that integrates systems biology data found on the nanoscale with genetic variation found on the kilometer-scale. The open-source nature and flexibility of the ePlant framework circumvents one of the major limitations of current computational systems biology tools — accessibility. ePlant does not require users to download specific data visualization and analysis software to their specific operating system, reducing the learning curve required to grasp the program. Software development on the world wide web also allows for community-driven expansion of systems biology software like that of ePlant, allowing for continued growth and refinement.

Friday Science Review: January 7, 2011

Symmetry Saves the Day

University of Toronto ♦ Published in Stem Cells, Dec. 29, 2010

One of the hallmarks of stem cells is their ability to maintain the stem cell pool indefinitely through the process of asymmetric division. When they divide they give rise to one slightly more differentiated cell and one daughter stem cell identical to the original. By carrying out cell division in this manner, stem cell populations, at least in theory, are capable of living indefinitely. David Piccin and Cindi Morshead — researchers at the Donnelly Centre for Cellular and Biomolecular Research — discovered that the Wnt (pronounced ‘wint’) signaling pathway is involved in damage response in neural stem cells found in the brain. Using a mouse model Piccin and Morshead show that when neural stem cells sense it is time to replenish the stem cell population, for example during the period following a stroke, Wnt signaling contributes to a signaling cascade that promotes symmetric division. When stem cells divide symmetrically they produce two identical daughter stem cells rather than one daughter stem cell and a differentiated progenitor, ensuring that the stem cell pool does not become depleted.

H5N1 Vaccine Derived from Tobacco Plants Shows Results in the Clinic

Medicago Inc. ♦ Published in PLoS ONE, Dec. 22, 2010

Egg-based vaccine manufacturing failed to live up to its promise of rapidly producing large quantities of live vaccine for control of viral outbreaks. During the recent H1N1 influenza pandemic only 3 million doses of live vaccine had been produced by the 5 month mark, when 60 million had been expected. Canadian biotechnology company Medicago Inc. has come up with an all together different approach that could make fast and efficient vaccine production a reality — a plant-based manufacturing technology that produces influenza vaccines using Nicotiana benthamiana. At the core of the vaccine technology is something known as a “Virus-Like Particle” (VLP). VLPs are small entities containing the hemagglutinin protein of H5N1, and are produced by infecting tobacco plants with an Agrobacterium inoculum containing an H5 expression cassette. VLPs are then harvested from the aerial portions of the plant. Although a VLP resembles a viral particle, it lacks the genetic content within, thus is replication defective and non-infectious. Another aspect differentiating Medicago’s approach is that the technology only requires the genetic sequence of the virus, not an actual sample, as is the case with technologies using inactivated virus in vaccines. In a preclinical study led by Medicago’s Dr. Louis Vezina, researchers show that a VLP vaccine could induce cross-reactive antibodies in ferrets. After challenging the animals with lethal doses of H5N1 researchers observed reduced pathology and suppressed viral loads in vaccinated animals. The paper also reports on clinical results: a phase 1 trial of the H5 VLP vaccine in healthy adults between the ages of 18 and 60 revealed that the plant-derived vaccine was tolerated well at all doses and had strong immunogenicity as detected by microneutralization assays. These results taken together hold promise for Medicago’s plant-based manufacturing technology. Another plus? The vaccine can be produced in 3 weeks of sequence release! This is no doubt why DARPA made a non-repayable contribution of $21 million to Medicago back in August to build a 90,000 square foot cGMP facility in North Carolina for VLP vaccine production.

Friday Science Review: December 17, 2010

I’ll begin the FSR this week with a few comments regarding some investigational work coming from the McLaughlin-Rotman Centre for Global Health.   Professors Dr. Peter Singer and Dr. Abdallah Daar, and PhD student Ken Simiyu, traveled to Africa to better understand why commercialization in the biotechnology and healthcare industry has been so poor of late.

Stagnant Technologies Need Stimulus

University of Toronto ♦ Published in Science, Dec. 10, 2010

After visiting some 23 academic institutions in six countries and interviewing 39 scientists, researchers have dug up some of the underlying issues preventing Africa’s biotechnological innovations from migrating to commercial success. Although previous studies in Africa have analyzed health innovation at the country level there has never been a systematic evaluation highlighting the troubles of specific technologies. Some of the technologies identified in the study include traditional plant products, new chemical entities, diagnostics, vaccines, and medical devices. In their travels the group came across some very interesting technologies indeed; researchers at the University of Ghana are developing a visually readable point of care diagnostic that uses monoclonal antibodies to detect the malaria parasite in urine; other work from Tanzania’s National Institute for Medical Research is being invested in the development of novel extraction techniques, specifically those to extract and purify artemisinin from the plant Artemisia annua for the preparation of derivatives to fight artemisinin resistance in malarial therapy. So why aren’t these technologies making a move towards market? A number of reasons. The mindsets of many researchers interviewed were simply not commercially oriented, with most scientists focusing on teaching and publishing to disseminate knowledge. Finding funding for validation studies of early stage technologies is another issue. African scientists need support from institutional investors but there are very few African funds in existence that support the biotechnology and healthcare space. Other issues identified by interviewees included a lack of commercially oriented government policy, poorly understood intellectual property regimes, and regulatory red tape. Peter Singer previously identified three areas that would help spur technology development in Africa: proof-of-concept funds, networks to link scientists and entrepreneurs together, and innovation centres that provide shared research infrastructure. Some have proposed establishing ‘Life Sciences Innovation Centres’ throughout Africa. These would serve a similar purpose as MaRS, here in Toronto, and the newly proposed Clerk-Maxwell Centres in the UK, with the goal of uniting researchers, industry, and entrepreneurs to accelerate commercial development of life science assets. This integrative approach is catching on, and could be the ingredient that will remedy the static nature of Africa’s commercial environment in the life sciences sector.

RD3 at the Root of Congenital Blindness

University of British Columbia ♦ Published in PNAS, Dec. 7, 2010

The protein RD3, previously of unknown function, has been implicated in the development of Leber Congenital Amaurosis Type 12 (LCA12). The disease is characterized by rapid degeneration of the photoreceptor cells during fetal development leading to blindness at birth or in the first year of life. Dr. Robert Molday and his team at the Centre for Macular Research show that RD3 interacts with two different forms of guanylate cyclase, GC1 and GC2, mediating their export from the endoplasmic reticulum. GC1 and GC2 are essential for the production of cGMP — a secondary messenger of phototransduction — and in their absence cGMP production is impaired. Dr. Molday believes that LCA12 may be caused by cGMP deficiency which leads to constitutive closure of cGMP gated calcium channels. Proper gradients of calcium across the membranes of photoreceptor cells is likely required for their long-term survival.

New Target for Chronic Pain Unveiled

University of Toronto ♦ Published in Science, Dec. 3, 2010

Synaptic plasticity is the ability of neural connections to vary in strength based on the extent of use or disuse of a neural pathway. This characteristic of the nervous system is key to the process of learning and memorizing sensory experiences, and it is also believed to play a role in pathological pain. Most researchers have focused on proteins that lead to synaptic plasticity as opposed to those that maintain synaptic plasticity over the long-term. A new study led by Dr. Min Zhuo implicates protein kinase M zeta (PKMξ) in the maintenance of chronic pain. Peripheral damage in a mouse model upregulated PKMξ in the anterior cingulate cortex, a region of the brain known to be involved in the onset of chronic pain. Zhou went on to show that microinjections of a PKMξ inhibitory peptide ZIP into the anterior cingulate cortex dampened synaptic potentiation and behavioural sensitization. This research uncovers an excellent target for chronic pain.

Trends Update — Social Media Reshaping Healthcare: Twitter as a Public Health Surveillance Tool for the 21st Century

We have been following innovative uses for social media in the biotech and healthcare industry here on the blog. Recently, a comprehensive paper was published in PLoS ONE outlining the use of “infoveillance” tools on the web to track the public response to the H1N1 epidemic. Dr. Gunther Eysenbach and Cynthia Chew, both researchers at Toronto’s Centre for Global eHealth Innovation, mined and archived over 2 million Twitter posts between May 1 and December 31, 2009. After carrying out an in depth analysis of these “tweets”, they validated Twitter as an effective medium to capture real-time content, sentiment, and public attention trends. Infoveillance methods include data mining, aggregation, and categorizations of online text and together form the toolkit for the new study of “infodemiology”. In the paper, Eysenbach points out that Twitter is particularly amenable to textual mining and analysis due to the concise nature of tweets that users share with their respective followers.

The concept of infodemiology began to crop up in the early 2000s when several different researchers began playing with the idea of using Internet health-related searches to provide epidemiological data that could be used to inform public health. In 2004, Eysenbach became interested in tracking flu-related searches using online syndromic surveillance. Historically, syndromic surveillance systems have typically relied on data from patient encounters with health professionals. But what if we could track the health concerns of citizens before they ever see a physician? It turns out we can. The study of infodemiology on the World Wide Web has the potential to provide automatic, continuous, and virtually real-time snapshots of public opinion and behavioural trends. In the context of public health this means capturing public health concerns at their earliest stages and even predicting major influenza pandemics weeks before they happen.

In 2006 Eysenbach published findings from a rather clever experiment he had completed over the 2004/2005 flu season. In order to track the number of people in Canada that were searching for either “flu” or “flu symptoms” he created an ad “campaign” through the keyword-triggered advertising program Google AdSense. For the purposes of optics the flu keywords led searchers to an advertisement that linked them to a generic patient education website after a click. Eysenbach then gathered FluWatch data, including influenza cases, positive lab test results, and influenza-like illness reported by sentinel physicians (“ILI-SPR”) around the country, and correlated these disease surveillance metrics with his Google advertisement data. Incredibly, Eysenbach found that clicks on the flu advertisement he had created correlated more strongly and in a more timely fashion (statistically significant on both accounts) with influenza cases and positive lab test results than did the ILI-SPR data. In a nutshell, his online experiment was more accurate at predicting rises in influenza cases than was the nation-wide sentinel physician program.

Three years later in 2009 a research paper funded by Google was published in Nature describing an influenza surveillance system piggy-backing on the popularity of certain Google search queries. The model underlying the surveillance system was generated by processing hundreds of billions of previous individual Google searches stored in web search logs. (Despite Eysenbach’s earlier work being cited in the Google paper, most journalists failed to recognize that Google’s idea wasn’t entirely new). Today Google Flu Trends can be accessed online to follow worldwide estimates of influenza-like activity. Google may have to go back to the drawing boards and refine its model however, as a new study published this past summer shrouds the accuracy of the system in some doubt. Researchers at the University of Washington evaluated Google Flu Trends against the gold standard positive influenza virus infection and its accuracy came up short – about 25% short.

The new H1N1 Twitter study reaffirms Eysenbach’s status as a visionary in the field of infodemiology. With “Web 2.0” upon us, and tsunamis of user-generated content flooding the web, the Internet “has made measurable what was previously immeasurable” in Eysenbach’s words. What we could not measure 10 years ago due to the (comparatively) static nature of the Internet, is now readily measurable with infoveillance tools. In the context of H1N1 Eysenbach says:

“H1N1 marks the first instance in which a global pandemic has occurred in the age of Web 2.0 and presents a unique opportunity to investigate the potential role of these technologies in public health emergencies.”

To carry out analysis of tweet content in the H1N1 study Chew and Eysenbach used an open-source infoveillance system known as Infovigil (Eysenbach’s own creation) that automatically and continuously dissects textual information from Twitter. They created a “codebook” with three primary variables: 1) tweet content, 2) mode of expression, and 3) type of link posted, if any. Each of these categories had several subcategories allowing for good separation of different tweet “types”. The study had some interesting findings. Over the duration of the study the relative proportion of tweets using “H1N1” increased from 8.8% to 40.5%, indicating that the public gradually began to adopt the WHO-recommended terminology as opposed to “swine flu”. With respect to tweet content, personal accounts of H1N1 increased over time while humorous content declined, indicating that the public’s perception of the subject became more serious. The public attention was aroused in certain instances, especially following the WHO pandemic level 6 announcement on June 11, 2009, which gave rise to a large spike in tweets. Only 4.5% of tweets were identified as misinformation.

Overall the study is a nice proof of concept and displays the fact that Twitter is a rich source of public opinion for the health authorities. Infoveillance can be used in the future not only for capturing sentiment, experiences, and behavioural trends, but importantly for tracking misinformation and identifying the informational needs of the human population. More studies of this kind should elucidate the value that social media will have for knowledge translation research and help refine the precision and accuracy of infoveillance tools for future infodemiology studies.

Friday Science Review: December 3, 2010

It’s all about microscopic machinery this week with two articles in Molecular Cell (Cell Press) and a third in Nature Cell Biology.

The MMS22L-TONSL Complex to the Rescue: A Sine Qua Non for Genome Integrity

Samuel Lunenfeld Research Institute ♦ University of Toronto

Published in Molecular Cell, November 24, 2010

In order for DNA replication to occur smoothly, a large complex of DNA polymerases and other proteins must work in harmony and navigate their way down the length of double-stranded DNA to synthesize daughter strands. This machinery, known as the ‘replisome’, frequently stumbles upon genomic glitches and other impediments that have the potential to hinder its progress. As a result, the cell has evolved a basket of mechanisms to ensure that the replisome avoids stalling and the replication fork continues to move. In a study led by Dr. Anne-Claude Gingras of the Samuel Lunenfeld Research Insitute, scientists use an RNAi screen to identify MMS22L-TONSL — a complex that appears to rescue the replisome during times of replicative stress. The newly identified complex exerts its rescue effects by interacting with single-stranded DNA (ssDNA) during end processing or in regions where the replication fork has stalled. After seeking out ssDNA MMS22L-TONSL goes to work catalyzing the repair of faulty DNA lesions, opening a path forward for the replisome.

MicroRNA Families Modulate Embryonic Messenger Transcripts

McGill University

Published in Molecular Cell, November 24, 2010

It appears microRNA (miRNA) controls expression of messenger RNA targets at the embryonic stage. These special RNA molecules originate in the nucleus, much like mRNA, but are subsequently modified by the enzyme RNaseIII and then exported to the cytoplasm. It is here that they are cleaved and manipulated into their mature form by the enzyme Dicer. After being processed miRNAs are incorporated into silencing complexes that then sort through the mRNA content of the cytoplasm, silencing specific transcripts as they go.  Dr. Thomas Duchaine and his colleagues utilized a C. elegans model to show that two embryonic miRNA families contribute to a natural RNAi process by suppressing expression of target mRNAs. The group also shows that silencing, achieved through epigenetic modification of targets, occurs in a target-specific manner with a unique modification pattern provided to each mRNA target.

Molecular Maintenance of Centromeres, GTPase Pulls the Switch

University of Montreal

Published in Nature Cell Biology, November 21, 2010

The central region of the chromosome has the responsibility of controlling chromosomal separation during cellular division. Like almost all parts of the genome, this region, known as the centromere, is subject to epigenetic regulation. The specialized H3 histone CENP-A is found exclusively at centromeres and is believed to be the epigenetic label of the region. Dr. Paul Maddox and his team at the University of Montreal have recently discovered new agents that maintain the assembly of CENP-A following its addition to the centromere region. A GTPase activating protein interacts with a CENP-A factor to recruit a number of auxiliary proteins that play an essential role in stabilizing newly added CENP-A. This stabilization process early on in the cell cycle is critical in ensuring that each new chromosome receives a sufficient quantity of CENP-A following cell division.

Friday Science Review: November 26, 2010

Ivermectin Nails Neurotransmission in Brugia malayi

McGill University

Published in PNAS, November 16, 2010

Well over 100 million people are currently infected with Brugia malayi, a microscopic nematode that causes lymphatic filariasis. Infection can eventually lead to the chronic inflammatory disease known as elephantiasis. In an effort to better understand this parasitic creature Dr. Timothy Geary and his team in the Institute of Parasitology at McGill University took a closer look at its glutamate-gated chloride channels (GluCls). These channels are localized to a very specific muscle structure surrounding an excretory vesicle in B. malayi and are essential for controlling protein release. Researchers show that ivermectin, a broad-spectrum anti-parasitic medication commonly deployed to reduce B. malayi infection, directly interferes with GluCl function preventing excretion of proteins from this excretory site. As protein excretion is known to be a very important aspect of the parasites survival system, allowing it to evade the immune system of the host it colonizes, researchers attribute the effectiveness of ivermectin to its ability to interfere with neurotransmission at GluCls. Screening for additional compounds that interact with GuCls could provide new treatment paradigms for B. malayi infection in the future.

Prion Disease: A Sticky Situation

University of Toronto ♦ University of British Columbia

Published in PNAS, November 16, 2010

Prion diseases include the infamous mad-cow disease (bovine spongiform encephalopathy), fatal familial insomnia, and the human disease ‘kuru’. The latter of these, believe it or not, being caused by human cannibalism and documented in small tribes located in Papua New Guinea that partake in strange funeral rituals following the deaths of relatives (I’ll spare you the details). These neurodegenerative diseases are often terminal and are caused by proteins, known as a prions, that have a propensity to aggregate together forming dangerous plaques that ultimately destroy neural tissue. Not all prion proteins are bad however, their behaviour depends on structural state. A switch from the α-helical conformation to the pathological β-form leads to rogue prion proteins that ‘stick’ to one another. Researchers at the University of Toronto were curious as to why animals of different sizes have different susceptibilities to prion diseases. In this study led by Dr. Avijit Chakrabartty, scientists used X-ray crystallographic structure analysis and a rabbit model to identify cellular mechanisms that explain the rabbit’s relative immunity to prion diseases. A helix-capping motif found in rabbits prevents folding of prion proteins into the pathological state. Findings like these, elucidating the underlying mechanisms driving transformation to the pathological state, should help us brainstorm future therapies for these deadly diseases.

Friday Science Review: November 12, 2010

Although I already commented on the stem cell discovery that came out of McMaster earlier this week, I felt that a more detailed look at the methods section would be needed to do justice to the science. After all, the true value of this discovery is in the protocol utilized to make it.

On Fibroblasts and Blood: Just to recap, Dr. Mick Bhatia and his colleagues at McMaster University published findings in Nature earlier this week explaining how they have managed to convert human skin cells to various cellular components of blood. In order to do this they first cultured human fibroblasts in a regular mix of cell culture media atop a thin layer of extracellular matrix protein known as matrigel. By supplementing the media with two growth factors essential for early hematopoiesis, FLT3LG (FMS-like tyrosine kinase 3 Ligand) and SCF (stem cell factor), and transfecting the cells with a lentivirus carrying the stem cell gene OCT4, they were able to stimulate formation of a multipotent hematopoietic progenitor expressing the lineage marker CD45+. This cell type could then be coerced into different blood cells with the addition of a few more hematopoietic cytokines; after which Dr. Bhatia observed the formation of three distinct cell types – monocytes, granulocytes, and myeloid cells, all expressing unique lineage markers. Amazingly, the monocytes could be grown in the presence of M-CSF (macrophage-colony stimulating factor) and IL-4 (interleukin-4) to produce macrophages that actually engulfed FITC-labelled beads. To produce red blood cells, EPO (erythropoietin) had to be added during the initial step of the protocol along with FLT3LG and SCF, upon which enucleated red blood cell-like cells emerged expressing the erythroblast marker CD71. The next step is figuring out how a single efficient differentiation protocol can produce the full spectrum of blood components in one shot, which will be a challenge, but one I’m sure the team at McMaster’s Stem Cell and Cancer Research Institute are up to.

Bacterial Immune System: Some bacteria have their own micro-immune system in the form of the CRISPR/Cas locus. After bacteria are infected with viruses this immune locus takes up small pieces of viral DNA known as ‘spacer’ DNA. These provide a mode of protection by allowing the bacteria to recognize and destroy foreign viral DNA upon subsequent infections. In a recent Nature study, researchers discovered that bacteria are also able to incorporate spacer DNA from plasmids that contain antibiotic resistance genes. Bacteria that do so inadvertently lose antibiotic resistance by destroying the plasmid, and as a result, are unable to pass these genes on to other bacteria. Exploitation of the CRISPR/Cas locus could allow for the generation of safer bacterial strains with greater resistance to bacteriophages and less antibiotic resistance. This study was led by Dr. Sylvain Moineau of the Department of Biochemistry at Laval University.

A Hidden Hotspot: Scientists at the University of British Columbia have recently solved the crystal structure of the ryanodine receptor found within the endoplasmic and sarcoplasmic reticulum – cellular organelles that surround the nucleus. Mutations in the receptor, which governs the release of calcium ions in muscle cells, have led to serious cardiac and skeletal diseases in humans. Several mutation ‘hotspots’ were identified in the hidden cytoplasmic domain of the receptor, explaining why scientists were previously unable to find any. The findings of Dr. Filip Van Petegem and his team, published in Nature, will allow for the development of new methods to target abnormalities in ryanodine receptors.

Robotic Precision: A new feat from the Department of Mechanical and Industrial Engineering at the University of Toronto – single cell manipulation and patterning with a robotic system. Dr. Yu Sun and his team developed motion control algorithms and integrated this with computer ‘vision’ to allow a robot to track cells in real time, pick single cells up, and then drop them off at precise locations. The machine uses a glass pipette, similar to those used in manual manipulation of cells, and can carry out its daily job at a rate of 15 seconds per cell with a 95% success rate. The device is expected to greatly bolster the speed of single-cell studies, and should prove useful for any studies requiring fine manipulation. Find the study in PloS ONE.

Friday Science Review: November 5, 2010

A Deadly Competitor: The marine bacterium Vibrio cholerae has built-in mechanisms that may allow it to compete with other species of bacteria and better colonize its host. Researchers recently discovered a secretion system (T6SS) in V. cholerae allowing it to inject toxic substrates directly into the cytoplasm of prey. Now a group at the University of Alberta, led by Dr. Stefan Pukatzki, has shown that this strain of bacteria aggressively competes against a number of gram-negative bacteria including Escherichia coli and Salmonella and was able to reduce E. coli survival by 100,000-fold. It would be interesting to see whether the disruption of T6SS could be used as a tool to put a damper on cholera outbreaks and/or increase the time between outbreaks. Find the study published in PNAS.

Signature of Kidney Disease: The most common form of glomerular-based kidney disease is IgA nephropathy (IgAN). Roughly 40% of patients suffering from the disease will experience kidney failure in 10 years. The strongest predictor of clinical outcome in IgAN is proteinuria, or elevated levels of protein in the blood – often albumin. Researchers at the University of Toronto have identified what appears to be a genetic signature of the disease. An in vitro model of proteinuria was created by exposing primary human kidney tubular epithelial cells to high levels of albumin. Gene expression in these cells was then measured with a microarray to derive a panel of 231 “albumin-regulated genes” that were upregulated or repressed as a result of albumin exposure. Researchers then translated this to the clinic by analyzing biopsy samples from patients with IgAN. What they found is that they were able to perfectly segregate biopsy samples from control samples. Convincingly, the panel could be reduced to 11 genes and be used to distinguish any form of primary glomerulonephritis from control, suggesting that this signature could have great utility in predicting clinical outcome in glomerular-based kidney disease in the future. This study included researchers from the University of Toronto, University of Michigan, and University Hospital Zurich in Switzerland. Find it here in PLoS ONE.

Thyroid On the Move: The congenital endocrine disorder hypothyroidism results from improper differentiation, migration, or growth of thyroid tissue. In a majority of cases (~80%), incomplete migration leads to ectopic thyroid tissue. Previous studies with identical twins suggest that the disease is almost certainly caused by somatic mutations or epigenetics as in some cases there have been discordance rates of up to 92%. In a recent study published in PLoS ONE, scientists used microarray analysis to uncover 1011 genes that were either induced or repressed by a factor of 2-fold in ectopic thyroid nodules. Grouping of these genes into gene ontology groups using DAVID (Database for Annotation, Visualization, and Integrated Discovery) identified several clusters of genes related to development and organogenesis. After validating many of these genes, 19 were isolated as being exclusively related to thyroid ectopy. Genes involved in embyronic development (TXNIP) and the Wnt pathway were among those that contributed most to formation. Further work on a larger cohort of patients may allow for elucidation of the molecular mechanisms behind defective thyroid migration during early embryogenesis.

Friday Science Review: October 22, 2010

Some great research to touch on this week in top-notch journals including Science, Cell, and NEJM. The first publication really emphasizes the strength of collaborative research projects around the globe.

Understanding Endometriosis: Ovarian clear-cell carcinomas are less common than high-grade serous carcinomas (12% and 70% of total respectively), but still remain the second leading cause of death from ovarian cancer. It is important that the mechanisms behind the formation of this rare subtype are elucidated because it is not responsive to conventional platinum-taxane chemotherapeutic regimes that are currently the first-line treatment for ovarian cancer. In a comprehensive study published in The New England Journal of Medicine, researchers sequence the entire transcriptomes of 18 ovarian clear-cell carcinomas  and identify frequent somatic mutations in the tumor suppressor gene ARID1A (the AT-rich interactive domain 1A). ARID1A encodes the protein BAF250a which in turn is part of the chromatin remodeling complex SWI-SNF that regulates a diversity of cellular processes including DNA repair and tumor suppression. Interestingly, the mutation appears specific to the clear-cell and endometrioid subtypes. After identifying the ARID1A mutation, researchers carried out targeted re-sequencing in a mutation-validation cohort consisting of an additional 210 carcinoma samples from all subtypes. Combining the discovery cohort and validation cohort, the ARID1A mutation was found in 55 of 119 clear cell carcinomas (46%), 10 of 33 endometrioid  carcinomas (30%), but not one of 76 high-grade serous ovarian carcinomas. These findings strongly implicate ARID1A mutation in the early transformation of endometriosis into cancer and the genesis of clear-cell and endometrioid ovarian carcinomas. This exhaustive work was carried out by some 45 researchers in a dozen or so institutions found in Canada, the United States, and Australia.

Danger Signaling: Physical injury to tissue leads to cell necrosis and the release of special patterning molecules, including proteins, nucleic acids, extra-cellular matrix proteins, and various lipids as a complex milieu of chemotaxic signals. Neutrophils are able to use these unique signals to guide themselves to the site of a wound, and play an important role in recycling debris from dying cells. In a study published in Science, led by Dr. Paul Kubes of the Immunology Research Group at the University of Calgary, researchers used a mouse model of sterile injury and an in vivo imaging technique known as spinning disk confocal microscopy to observe the kinetics of eGFP-expressing neutrophils in response to thermal induced necrotic injury. Experiments revealed that necrotic cells activated a multistep hierarchy of cues that lured neutrophils to the site of danger. Another interesting finding of the study is that neutrophils appear to travel to the site of injury intravascularly as opposed to taking the most direct route through tissue. The group proposes that danger sensing and recruitment mechanisms may have evolved to prioritize intravascular travel in order to reduce the collateral damage incurred if neutrophils were to migrate directly through healthy tissue.

In Pursuit of Perfection: The fundamental limit of minimally invasive surgery is at the level of the single cell. In principal, lasers are capable of operating at this spatial resolution however efforts to achieve this have been limited by thermal and shock wave induced collateral damage to surrounding tissue. The long-held promise of a fine surgical laser has been delivered by two investigators in the Toronto research community with the creation of a novel laser source – the Picosecond IR Laser (PIRL). As a cutting modality the PIRL has a shorter pulse duration than conventional surgical lasers, vaporizing tissue on the picosecond timescale rather than burning on the nanosecond, and exploits a new cutting mechanism that selectively energizes water molecules. Researchers created full thickness wounds in CD1 mice using PIRL to demonstrate that it caused neither cavitation or any associated shock wave induced damage, and also showed that PIRL greatly reduced scar formation by comparison to conventional surgical laser or scalpel. The technology is expected to be useful in surgical procedures where scarring is particularly debilitating. Dr. Benjamin Alman, Head of the Division of Orthopedic Surgery at Sick Kids, and Dr. Dwayne Miller, in the Department of Chemistry at the University of Toronto, were co-principal investigators in this study published in PloS ONE.

At the Junction: The RAS/MAPK signaling pathway contributes to a number of important cellular processes including proliferation, differentiation, and survival. In its most basic form the pathway is regulated by the small GTPase RAS, and the three core kinases RAF, MEK, and ERK/MAPK. Like most signaling pathways, the RAS/MAPK pathway is controlled by a diversity of post-translational modifications but much less is known about regulation of its core protein components at the mRNA stage. Using a genome-wide RNAi screen in Drosophila S2 cells, researchers set out to identify other proteins involved in the pathway that could modulate MAPK protein levels. In doing so they identified the Exon Junction Complex (EJC) as a regulator of mapk transcripts. The complex is believed to contribute to the regulation of exon definition and suggests that the EJC has a key role in early regulation the RAS/MAPK pathway. This study, published in Cell, was led by Dr. Marc Therrien at the University of Montreal.


Monday Biotech Deal Review: October 18, 2010

Despite the short week, it was a busy one in the Canadian biotech sector. Read on to learn about the Labopharm / Paladin licensing deal, Ondine’s new facelift (and 15:1 equity liposuction), and various other biotech updates and news. 

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Friday Science Review: October 9, 2009

Breast cancer, genomics and two cover stories in prestigious journals…

Cancer Evolution and Progression:  Scientists at the BC Cancer Agency have sequenced and compared the entire cancer genome of a metastatic tumour versus the primary breast tumour that originated nine years earlier.  They used next generation DNA sequencing technology to reveal 32 mutations in the metastatic cancer but surprisingly only five of these were present in the original tumour.  Six mutations were present at lower frequencies in the primary tumour, 19 were not detected and 2 were undetermined.  These differences may provide clues about how cancer becomes resistant to therapy or how a tumour switches to aggressive metastasis that spreads to other sites in the body.  The study demonstrated that cancers evolve and that there may be significant heterogeneity within the tumours.  These findings emphasize the importance of ongoing research efforts to sequence all cancer genomes and buttress arguments in favour of personalized medicine.

The study was lead by Dr. Samuel Aparicio at the BC Cancer Agency and appears as the cover story in the latest edition of Nature.

Honey, I shrunk the lab: The “lab-on-a-chip” concept has been in use for a number of years but Dr. Aaron Wheeler’s Microfluidics Laboratory at the University of Toronto has designed a new module for use in breast cancer detection and care.  The hand-held sized device can extract and quantify estrogen in a very small sample size – as little as a 1 microliter sample of tissue or blood – by using electrical charges to move liquids around in a precise manner over a microchip.  Current methods require a much larger sample, about the size of a penny, which is often impractical to obtain.  Since elevated estrogen levels are associated with breast cancer risk and pathogenesis, this new device could be used at point-of-care to screen at-risk patients or to monitor therapies and provide results within minutes instead of days.

Dr. Wheeler collaborated with Dr. Robert Casper (University of Toronto and Samuel Lunenfeld Research Institute) on this project, which garnered the inaugural cover story in the new journal, Science Translational Medicine.

Genome Map Upgrade: Researchers have generated a comprehensive structural map of the human genome in identifying and marking regions that are duplicated or deleted, the so-called copy number variation (CNV).  Genetic variation is what makes us different and certain areas of the genome reflect these differences whereas other genetic regions show very little variation and are likely essential function genes.  It also provides important clues to understanding evolution and provides the foundation for future research in developing personalized medicine.   The international study was co-lead by Dr. Stephen Scherer at The Centre for Applied Genomics (Hospital for Sick Children, Toronto) and provides the following comments:

“The scale of this current project is 100 times the scale of all others.”

“Previous work in this field would be like a paper fold-up map; this advancement is like a GPS that takes you where you need to go. It allows you to navigate the landscape of the genome, from its peaks where there is vast genetic variation, to its valleys devoid of it.”

“Variation is indeed the spice of life and we now know that nature buffers this variation by using CNVs. We are harnessing this knowledge to fight disease.”

Dr. Scherer is also involved in maintaining the Database of Genomic Variants, which provides researchers around the world access to a curated catalog of CNVs.  Details of the research report appear in the advanced on-line edition of Nature.

Congratulations to McGill University alumni Jack Szostak and Willard Boyle for winning the 2009 Nobel Prize in their respective disciplines.

Dr. Jack Szostak started at McGill when he was 15 years old and graduated in 1972, specializing in cell biology.  This was the start of a brilliant research career where he co-discovered how telomeres and telomerase protects chromosomes from losing genetic material during cell division.  He shares the 2009 Nobel Prize for Medicine.

Dr. Willard Boyle completed his BSc (1947), MSc (1948) and PhD (1950) from McGill.   He shares the Nobel Prize for Physics for the 1969 co-invention of the charged-couple device (CCD) that is used in today’s digital photography technology.

Friday Science Review: October 2, 2009

Prostate cancer and H1N1 updates…

Nanotechnology is Coming:  A research study by a group of University of Toronto engineers, nanoscientists, and pharmaceutical specialists has garnered a lot of media attention this week describing the use of nanomaterials in microchip technology to create a highly sensitive biosensor.  In the more technical report published in Nature Nantotechnology this week, they describe a special nanostructuring technique arranged in an array architechture to expand the dynamic range and sensitivity of the system for nucleic acid and protein biodetection.  The microchip is small, fast, and super sensitive.

In an earlier publication in ACS Nano, they applied their nanotechnology to detect prostate cancer biomarkers.  They demonstrated the accuracy, sensitivity and speed of the non-invasive test, which they are trying to package into a small hand-held device that can readily conduct testing at the point-of-care.  Of course, the application of this technology goes far beyond prostate cancer and can be adapted to detect other cancer biomarkers, HIV and other diseases.   Nanomaterial, nanotechnology, nanomedicine – these are hot words that you will hear about more frequently in the near future.

The research was lead by University of Toronto scientists, Drs. Shana Kelley and Ted Sargent.  A spinoff company based on the molecular diagnostic platform, tentatively called GenEplex, is in the works with the support of the Ontario Institute for Cancer Research’s Intellectual Property Development and Commercialization Program.  Also, the Ontario Genomics Institute is funding a microRNA application of the technology to the tune of almost $1 million.

In other prostate cancer research news:

Targeting IGF-1R:  Researchers targeted the Insulin-like growth factor-1 receptor (IGF-1R) with antisense technology to suppress IGF-1R expression in prostate cancer cells.  They found that by inhibiting IGF-1R signaling activity, the cancer cells grew more slowly but also increased their rate of cell death.  This is the first preclinical proof-of-principal that antisense therapy targeting IGF-1R in prostate cancer may be a viable treatment route and warrants further investigation.

The study was conducted by Dr. Michael Cox at the Vancouver Prostate Centre and published in this week’s editon of The Prostate.

Fatty Acids Promote Prostate Cancer: The hormone androgen, and its androgen receptor partner, have been shown to contribute to prostate cancer progression.  In this research report, researchers at the University of British Columibia suggest that elevated fatty acid (arachadonic acid) levels in the tumors may lead to increased activation of steroid hormone synthesis and contribute to the progression of the cancer.  Therefore, they recommended that fatty acid pathways should also be targeted as part of a therapeutic approach to treating prostate cancer.

Dr. Colleen Nelson led the research team at the Vancouver Prostate Centre and published the report also in this week’s edition of The Prostate.

H1N1 Update: Following last week’s “seasonal flu vs. swine flu” vaccination story, the Public Health Agency of Canada reviewed their own data and soon declared their position on the yet unpublished study saying that “there is no link between having a seasonal flu shot and developing a severe bout of pandemic flu.”  More to follow on this as the controversial study should become public next week.

In other H1N1 news:

Big Pharma gets Immunity: As increasing H1N1 cases emerge and Health Canada is being encouraged to expedite the approval of H1N1 vaccines, the Public Health Agency of Canada is following other countries in stating that they will protect GlaxoSmithKline, the maker of the vaccine, from any lawsuits arising from potential side effects.

Surgical Masks are Adequate: Healthcare workers should be encouraged by a study comparing standard surgical masks versus N95 respirator in protecting against flu viruses (swine included).  In the randomized controlled study, conducted by flu expert Dr. Mark Loeb at McMaster University, 446 nurses from eight hospitals in Ontario were equally distributed to wear either sugical masks or fit-tested N95s.  The results showed that there was an insignificant difference (23.6%, surgical mask vs. 22.9%, N95) in the number who contract the ‘flu’ during the course of the season.  However, this study is sure to raise more debate within the healthcare community as unpublished work in China found that N95 masks can cut the risk of catching the flu virus by 75% while surgical masks offer no protective effect.  Dr. Loeb’s study is published in the early edition of JAMA.   A commentary on this issue is also provided by the U.S. Centers for Disease Control and Prevention.

Benefits of Handwashing? And if you are not confused enough about how to avoid catching the virus, consider this article in CMAJ questioning the benefits, due to lack of scientific evidence, of hand washing in preventiing the transmission of influenza viruses.

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Canada — and MaRS — Draw Notice on List of Biotechnology Clusters

world_map_2002A report at Genetic Engineering and Biotechnology News, picked up today by FierceBiotech, discusses emerging biotechnology clusters.  It’s worth excerpting the whole bit on Canada:

Both Toronto and Vancouver have good, small companies, but they’re struggling for capital. They have the benefit of government support and strong universities, particularly the University of Toronto, the University of Guelph, and the University of British Columbia. Entrepreneurship skills need to be honed, however.

In the heart of Toronto, the MaRS Center incubates a host of companies within about a mile of five teaching hospitals, the University of Toronto, the provincial parliament, and the financial district. The local government takes a close interest in the Center’s success, and several promising research projects are moving toward commercialization.

Vancouver, on Canada’s west coast, consistently ranks as a fast-growing cluster, attracting more than 90 companies, some with late-stage trials. The University of British Columbia has an active tech-transfer department that has spun out several companies.

The report also discusses innovative activity in China and India, among others, that fits with the trend we have observed.  Read the whole report here.

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Friday Science Review: February 27, 2009

Cool Canadian science developments this week:

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