cell signaling

Role of TAK1 in resident fibro/adipogenic progenitors. A Key modulator of the inflammatory milieu and a therapeuthic target in chronic diseases

In our aging society, degenerative complications of chronic diseases are on the rise and account for a significant percentage of deaths. Among these, fibrosis is the most common, and yet no therapy capable of mitigating its effects is available. Investigating and understanding the signaling pathways that influence fibrogenic progenitor (FAP) fate will not only elucidate a key component of the regenerative process but may reveal pathways that could be targeted therapeutically to prevent inflammation, fibrosis, and enhance regeneration or maintain muscle homeostasis.

Primary Investigator: 
Award Type: 
Year: 
2019

Developing new anti-cancer drugs that target abnormal signaling networks in cancer

A defining characteristic of cancer cells is their ability to grow and replicate in an uncontrolled manner. Cancer cells have altered signaling pathways that allow them to bypass checkpoints that would normally prevent their rapid growth. STAT3 protein is a master regulator of cancer cell signaling and is found to be overactive in 70 % of cancers. While healthy cells can survive without STAT3, cancer cells become addicted to overactive STAT3 and are sensitive to disruptions in this pathway.

Primary Investigator: 
Award Type: 
Year: 
2019

Tying the gut in knots: Characterizing how pathogenic E. coli transform the gut cell landscape

Diarrheal disease affects 1.7 billion people every year, killing around 760,000 children. A leading cause of this disease are bacteria like enteropathogenic Escherichia coli (EPEC). EPEC’s ability to cause disease relies entirely on creating an environment in which it can thrive. EPEC achieves this by secreting “effector” proteins directly into human host cells, which rewire the human cell, allowing EPEC to take control of cell immune signalling.

Primary Investigator: 
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Year: 
2018

Identifying oncogenic signaling pathways that mediate immune exclusion in ovarian cancer

Despite major advances in our understanding of the mechanisms behind the body’s immune response against cancer, several obstacles limit the success of immunotherapy as a cancer treatment. In particular, the physical exclusion of immune cells from tumour beds is associated with poor prognosis and a limited response to immunotherapy.

Primary Investigator: 
Award Type: 
Year: 
2018

Defining mechanisms of lineage transformation in lung cancer to combat resistance to targeted therapies

Lung cancer is the leading cause of cancer-related death in Canada. A major reason for the poor prognosis is the lack of effective drugs for treating advanced tumours.

New understanding of the mutations driving lung cancer has led to the development of targeted therapies that selectively inhibit mutated genes, leading to rapid cancer regression in specific subsets of patients. However, while these therapies improve patient survival and quality of life, they are not curative as all patients develop drug resistance.

Primary Investigator: 
Award Type: 
Year: 
2018

JAK-STAT pathway mutations in B-cell lymphomas: Implications for the tumour microenvironment and treatment failure

Lymphoma is a cancer of the lymphatic system where tumours develop from abnormal growths of white blood cells. Non-Hodgkin Lymphomas (NHL) are the fifth most common cancers diagnosed in Canada. Of those, diffuse large B-cell lymphoma (DLBCL) is the most common.

Primary Investigator: 
Award Type: 
Year: 
2018

Unraveling disparate roles of Notch-1 and Notch-2 signaling in bladder cancer

Bladder cancer is the fifth most common cancer, yet it remains understudied and we are only now making strides in understanding it's molecular make-up. Recently we and others have discovered that loss of the cell surface receptor Notch-1 drives growth of some bladder cancers, while increased Notch-2 activity drives growth of other bladder cancers. Here we aim to determine how Notch-1 and Notch-2 can lead to such differing effects on cancer growth even though they share many features. From this we aim to design a new drug to inhibit Notch-2. 

We will: 

Primary Investigator: 
Year: 
2018

Development of a novel biotherapeutic fusion protein inhibitor for treatment of advanced prostate cancer

Recent advances in targeted therapies have transformed the treatment of several types of cancer. Numerous agents, including small molecule drugs and therapeutic antibodies targeting receptor tyrosine kinases (RTKs) such as EGFR, Her-2 and MET, are currently in clinical trials or have received regulatory approval. These agents are exhibiting impressive clinical responses demonstrating that these RTK pathways are clinically validated drug targets and key drivers of multiple cancers such as breast, lung and colorectal cancers. 

Primary Investigator: 
Year: 
2017

Targeting stress granules: A novel strategy to inhibit Ewing sarcoma metastasis

Metastatic disease remains the single most powerful predictor of adverse outcomes in Ewing sarcoma (ES) and other childhood sarcomas (malignant connective tissue tumours). High risk ES appears to be characterized by uninhibited outgrowth of neoplastic clones that have acquired additional genomic or epigenomic alterations, which facilitate the spread of the cancer cells. 

Primary Investigator: 
Award Type: 
Year: 
2017
Health Category: 

Evaluation of the role of FRMP on BDNF expression and signaling

Fragile-X syndrome (FXS) is the most common form of inherited intellectual disability and is the best characterized form of autism spectrum disorder. This genetic condition is caused by a mutation in the FMR1 gene, leading to the functional loss of FMR1 protein (FMRP). Besides being important for neuronal development, this protein also exerts a strong influence on synaptic plasticity. As a matter of fact, FMRP is highly expressed in the dentate gyrus (DG) of the hippocampus, one of the few regions of the adult brain where the birth of new neurons takes place. 

Primary Investigator: 
Award Type: 
Year: 
2017

IL-37 signaling via SIGIRR: A novel mechanism to suppress intestinal epithelial cell driven inflammation and dysbiosis

Patients with Inflammatory Bowel Disease (IBD) suffer bouts of extreme gut inflammation that disrupt the population of bacteria in their intestines. Consequently, IBD patients often have fewer beneficial bacteria and suffer an overgrowth of potentially dangerous bacteria. In healthy individuals, such responses are typically prevented by SIGIRR, a protein made by the cells that line the gut. 

Primary Investigator: 
Award Type: 
Year: 
2017

Identifying the molecular mechanisms underlying sex differences in fat storage using Drosophila as a model

In Canada, metabolic diseases (e.g. cardiovascular disease, type 2 diabetes, obesity) are leading causes of death, disability, and hospitalization. Currently, more than 10 million Canadians suffer from metabolic disease, with direct and indirect costs to the economy estimated to be $20 billion each year. Approximately 40% more men than women suffer from metabolic disease. In addition, commonly prescribed drugs used to prevent and treat metabolic disease are more effective in one sex than the other (e.g. fenofibrates).

Primary Investigator: 
Award Type: 
Year: 
2017
Health Category: 

Co-targeting Hsp27 and EGFR as a strategy to improve EGFR targeted therapies in EGFR dependent solid tumors

Epidermal Growth Factor Receptor (EGFR) is a key regulator of cell proliferation and a driver oncogene in several tumors. Many cancers have constitutively activated EGFR which leads to excessive signalling. Inhibition of EGFR using erlotinib or gefitinib significantly improves survival in patients with Non Small Cell Lung Cancer (NSCLC) while panitumumab and cetuximab are currently used in colorectal and head and neck cancer.

Primary Investigator: 
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Year: 
2015

Investigating a novel target for cerebral edema during stroke

Michael Smith Foundation for Health Research/Vancouver Coastal Health Research Institute Post-Doctoral Fellowship Award

Primary Investigator: 
Award Type: 
Year: 
2015

Targeting the regulation of DNA repair by CDK12 for breast and ovarian cancer therapy

Human cells experience DNA damage every day, but DNA repair systems ensure that resulting mutation rates are extremely low. Two main pathways repair severe DNA damage in cells. The 'copying' pathway connects broken DNA ends by copying the missing sequence from the second DNA copy that is present before cells divide. The 're-joining' pathway simply re-joins the broken DNA ends irrespective of the missing sequence.

Primary Investigator: 
Award Type: 
Year: 
2015

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