2010 Research Grants

Name of person or group
Dr. Yves Fradet
CHUQ - Hotel-Dieu de Quebec
 
Name of program or research project
Characterization of MAGE-A11 for immunotherapy of prostate cancer  Translational Research (Therapeutics/Prevention)
 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project
When prostate tumors are discovered early and are confined to the prostate gland, they can be treated effectively with surgery or radiation therapy.  However, if the tumor spreads outside of the prostate (‘metastasizes’), other treatments such as hormone therapy or radiation therapy, are necessary.  Unfortunately, these treatments often have significant unwanted side effects, and tumors may eventually stop responding to these therapies.  For these reasons, there is a need to develop new treatments that are both more effective and have fewer side effects than existing therapies.  A possible strategy is to identify genes that are uniquely turned on in prostate cancer cells but not in normal cells, and then to ‘train’ the body’s immune system to hunt down and kill only those cells that have the gene turned on.  Dr. Fradet’s group will study one such possible gene called MAGE-A11, which is turned on in prostate cancers that have been treated with hormone therapy.  Dr. Fradet’s research team will develop an antibody against MAGE-A11 and then use this antibody to examine MAGE-A11 levels in human prostate cancers and in normal prostate glands.  Once these initial pilot studies are complete, Dr. Fradet’s goal is to test the MAGE-A11 antibody in a clinical trial, with the hope of developing a prostate cancer vaccine.

Name of person or group

Dr. Frank van Veggel
University of Victoria 
 
Name of program or research project
Early detection of prostate cancer with antibody-nanoparticle conjugates by MRI – Basic Research (Early Detection)
 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project
Prostate cancer is highly treatable when it is discovered early and has not spread outside of the prostate gland.  However, once the cancer spreads beyond the prostate (‘metastasizes’), the disease is generally incurable.  Unfortunately, nearly half of men diagnosed with prostate cancer already have some cancer cells that have metastasized.  For these reasons, it is important to develop new strategies for identifying small pockets of prostate cancer cells outside of the prostate, in the hopes that these can be more effectively targeted by new therapies.  Dr. Van Veggel’s team is researching new strategies for improving magnetic resonance imaging (MRI) to detect prostate cancer.  Specifically, Dr. Van Veggel will develop tiny ‘nanoparticles’, which are attached to antibodies that detect proteins on the surface of prostate cancer cells.  His team will then test whether these nanoparticles can be detected by MRI, which may allow oncologists to detect very small regions of cancer cells outside of the prostate.  It may also be possible to load these nanoparticles with radioactive particles and use them to treat prostate cancer.  This research may open up new avenues for detecting tiny pockets of prostate cancer cells outside of the prostate, which may ultimately help to improve the prognosis for men diagnosed with metastatic prostate cancer.

Name of person or group
Dr. Eric Levesque
CHUQ – Hotel-Dieu de Quebec, Universite Laval
 
Name of program or research project
Inherited Genetic Variations and Prostate Cancer Recurrence after Prostatectomy – Translational Research (Diagnostics)
 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project

Not all prostate cancers are life-threatening; in fact, many prostate cancers do not require aggressive treatment at all.  Unfortunately, current tools do not allow oncologists to easily determine whether a given prostate cancer is likely to threaten a man’s life or not.  Because the standard treatments for prostate cancer can cause serious side-effects, including impotence and incontinence, a test that would allow oncologists to better define which men need to be treated aggressively and therefore reduce the number of men who have to deal with these side-effects.  Oncologists believe that subtle variations in genes that are involved in the production or function of male sex hormones (‘androgens’) may determine whether or not a prostate cancer progresses and becomes life-threatening.  Dr. Levesque’s research team will look for specific genetic variations in prostate cancers taken from over 1800 men, and will then look to see whether certain genetic variations occur more frequently in those men whose cancers progressed more quickly.  It is hoped that by identifying which men have prostate cancers that are more likely to become life-threatening, oncologists will be able better tailor treatments to individual patients, thus reducing the number of prostate cancers that are treated aggressively.
 


 Name of person or group

Dr. Jacques Lapointe
McGill University 
 
Name of program or research project
Role of PDK1 in prostate cancer progression (Translational Research-Diagnostics)
 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project
While some prostate cancers are likely to spread outside of the prostate gland (i.e. metastasize) and thus require aggressive treatment, others will remain confined to the prostate and do not require aggressive treatment; oncologists refer to these latter cancers as ‘indolent’.  Unfortunately, current tools do not allow oncologists to easily differentiate between indolent and aggressive prostate cancers, and this result in many men with indolent prostate cancer being treated with unnecessarily aggressive therapies, resulting in severe side-effects.  Dr. Lapointe’s research group is studying a specific gene called PDK1, which may be involved in increasing the ability of a prostate cancer to metastasize.  Dr. Lapointe will use state-of-the-art techniques to turn the PDK1 gene on or off in an experimental model of prostate cancer, and then test whether this affects the ability of the cells forming the tumor to spread.  Dr. Lapointe’s team will then examine whether men with prostate cancer in which the PDK1 gene turned on are more likely to have cancer metastasized outside of the prostate than men who’s cancers have the PDK1 gene turned off.  If this is indeed the case, Dr. Lapointe’s research may help to give oncologists a better tool to discriminate between cancers that require aggressive treatment and those that do not, which will help to prevent unnecessary treatments.

Name of person or group

Dr. Tarek Bismar
University of Calgary-Calgary Laboratory Services
 
Name of program or research project
miRNA Predictors of Lethal Hormone Refractory Prostate Cancer   (Translational Research-Diagnostics)
 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project

Oncologists know that certain genes can be turned on or off (‘regulated’) inappropriately in many prostate cancers, and that inappropriate regulation of these genes can cause a more aggressive disease.  Micro-RNA (miRNA) are small molecules that can turn other genes on or off, and it is believed that miRNA can play a role in prostate cancer progression by inappropriately regulating other genes.  Two genes that are known to be very important for the progression of prostate cancer are called ERG and PTEN; it is believed that prostate cancers that have these genes altered are more aggressive and more likely to be lethal.  Dr. Bismar’s research team will investigate whether certain miRNA molecules are turned on or off in prostate cancers that have alterations in the ERG and PTEN genes versus those prostate cancers in which the ERG and PTEN genes are normal.  These studies will increase our basic understanding of how prostate cancers develop and progress, and will allow oncologists to better predict which patients are at the highest risk of lethal disease, and thus require more aggressive treatments. 


Name of person or group

Dr. Juan Ausio
University of Victoria
 
Name of program or research project
Role of histone H2A.Z in androgen receptor dependent and independent signaling in prostate cancer  (Basic Research-Therapeutics)
 
Investment and period of investment
$119,130 from 2010 to 2012
 
Outline of program or project

The genetic material (DNA) within a cell is supported by proteins known as histones.  Scientists now know that histone proteins can be chemically modified in response to environmental factors such as diet, and that these modifications can alter whether specific genes are turned on or off.  Unlike DNA mutations, however, chemical modifications of histone proteins are potentially reversible.  The progression of prostate cancer is highly influenced by the actions of male sex hormones (‘androgens’), and researchers have found that a specific histone protein called H2A.Z can influence the actions of androgens, and thus may have an important role to play in the development of prostate cancer.  Dr. Ausio’s research team will study if and how H2A.Z can modify the actions of androgens, and whether H2A.Z can alter the progression and survival of prostate cancer cells.  Dr. Ausio’s group will also study whether H2A.Z is altered in different ways in prostate cancers cells that have stopped responding to androgens.  Dr. Ausio’s research may open up new potential avenues for the treatment of prostate cancer, especially for men for whom androgen therapy has stopped working.  


Name of person or group

Dr. Cheryl Helgason
British Columbia Cancer Agency
 
Name of program or research project
Mechanism of Immune Privilege Used by Prostate Cancer Stem Cells (Basic Research-Therapeutics)
 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project

Many scientists now believe that prostate cancers arise from a very small collection of cells termed cancer ‘stem’ cells and that in order to eradicate a tumor, these stem cells must be killed.  Unfortunately, it is also believed that these stem cells possess special properties that make them resistant to killing by traditional therapies, and very little is known about why this is the case.  One possible explanation is that prostate cancer stem cells have developed mechanisms to avoid being detected by a man’s immune system.  If this is the case, then it may be possible to better identify these stem cells and ultimately to develop strategies to better target these cells.  Dr. Helgason’s research team will examine whether specific immunity genes are turned off in prostate cancer stem cells and whether prostate cancer stem cells from tumors located inside the prostate gland have different immunity genes turned on or off than prostate cancers that have spread outside of the prostate gland (‘metastasized’).  Dr. Helgason’s work will shed light on the role of prostate cancer stem cells in the progression and spread of prostate cancer, and on why prostate cancer stem cells are resistant to therapies.
 


 
Name of person or group

Dr. Simone Chevalier
McGill University
 
Name of program or research project
Validation of novel prostate cancer progression markers and investigation of their potential as therapeutic targets (Translational Research-Therapeutics)
 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project
When it is confined to the prostate gland, prostate cancer is very often curable.  In some cases, however, current therapies fail and the cancer spreads beyond the prostate gland (‘metastasize’), at which point it is incurable.  Unfortunately, very little is known about why certain tumors respond to treatment while others do not.  If scientists could identify why specific cancers do not respond to treatment, they may be able to design new strategies for treating these cancers more effectively.  Dr. Chevalier’s research group will study a gene called FER, which may be turned on in prostate cancer cells but off in normal prostate cells, and which is known to alter the function of other genes that are important for the progression and spread of prostate cancer.  Specifically, Dr. Chevalier’s team will develop tools to investigate whether FER is turned on more frequently in prostate cancers that failed treatment and metastasized outside of the prostate versus those in which treatment was successful.  The group will then use advanced computer modeling techniques to develop new drugs that interact with FER and turn it off.  It is hoped that Dr. Chevalier’s work will give oncologists a new tool to identify tumors that are more or less likely to respond to therapy, and may result in the development of a new class of drugs that could be used to treat aggressive prostate cancer.
 

Name of person or group

Dr. Richard Austin
McMaster University and St. Joseph’s Health Care 
 
Name of program or research project
Signaling through cell surface GRP78 induces tissue factor expression/procoagulant activity: Implications in prostate cancer growth and metastasis (Basic Research -Therapeutics)
 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project
Men with prostate cancer have an increased risk of having blood clots, which can be life-threatening.  While this phenomenon is unexplained, one possibility is that prostate cancer patients have increased levels of a protein known as Tissue Factor (TF), which activates the normal processes involved in blood clotting.  Scientists also believe that TF can promote the development and progression of prostate cancer, as well as the spread of cancer outside of the prostate gland (‘metastases’).  However, the reasons that TF levels become increased in prostate cancer are not clear.  Dr. Austin’s research team is investigating a gene called GRP78, which they believe promotes the actions of TF.  Their research will examine if and how GRP78, when turned on, promotes the development prostate cancer by turning on TF.  For these studies, Dr. Austin’s team will use a model of prostate cancer that allows them to monitor the development and spread of cancer cells and to manipulate the function of GRP78.  These studies will shed light on the role of GRP78 on the development and progression of prostate cancer, and will help to establish whether drugs that act on GRP78 could be of use to treat prostate cancer.

Name of person or group
Dr. Laurent Azoulay

McGill University 
 
Name of program or research project
Androgen Deprivation Therapy and the Risk of Stroke in Patients with Prostate Cancer (Clinical Research -Disease Management)
 
Investment and period of investment
$85,000 from 2010 to 2012
 
Outline of program or project

Male sex hormones (‘androgens’) are important for the development and progression of prostate cancer.  Androgen deprivation therapy (ADT), which involves treating men with drugs that block the production or function of androgens in prostate cancer cells, has traditionally been used only for men with advanced prostate cancer, but is now often used for men with less aggressive disease.  It has been known for some time, however, that ADT increases the risk of a man developing cardiovascular side effects, including coronary heart disease and heart attack.  There is also concern that ADT may increase the risk of stroke.  Dr. Azoulay’s team will evaluate a database of nearly 44,000 men with prostate cancer, who either did or did not receive ADT, and will attempt to establish whether or not ADT increases the risk of stroke.  This large research study will establish whether ADT increases the risk of stroke, and if so, will help oncologists better structure treatments for men who are already at high risk for stroke.
 


 Name of person or group

Dr. Vasundara Venkateswaran 
Sunnybrook Health Sciences Centre

 
Name of program or research project
Utilizing metformin to enhance the efficacy of androgen deprivation therapy in prostate cancer (Translational Research -Therapeutics)

 
Investment and period of investment
$119,966 from 2010 to 2012
 
Outline of program or project
Obese men have a significantly worse prognosis following a diagnosis of prostate cancer than non-obese men.  It is believed that this is due to the fact that obese men have higher levels of the hormone insulin in their blood.  Metformin is a drug that is commonly prescribed for people with type II diabetes, and there is evidence that metformin can also be effective against prostate cancer.  Dr. Venkateswaran’s research group will investigate whether metformin prevents the progression of prostate cancer in an experimental model, and whether specific genes that are important for cancer progression are turned on or off by treatment with metformin.  Because metformin is often added to other traditional treatments, such as androgen deprivation and radiation therapies, Dr. Venkateswaran’s group will also investigate whether adding metformin to these treatment programs enhances their anti-cancer effects.  Metformin is already approved and in use for the treatment of type II diabetes.  Therefore, if Dr. Venkateswaran’s research demonstrates that metformin reduces or prevents the progression of an experimental model of prostate cancer, it may be possible to quickly move to clinical testing of this drug in men with prostate cancer.

 


Name of person or group

Dr. Damu Tang 
McGill University 

 
Name of program or research project
ABCC2 confers chemo resistance to docetaxel in hormone refractory prostate cancer (Basic Research-Therapeutics)

 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project

When prostate cancer is confined to the prostate gland, it can often be cured by surgery or by radiation therapy.  When it has spread outside of the prostate (‘metastasized’), however, it is often treated with drugs that block the effects of male sex hormones (‘androgen deprivation therapy’; ADT).  Unfortunately, resistance to ADT eventually develops, at which point men can only be treated with a drug called docetaxel, though resistance to docetaxel eventually develops.  Dr. Tang’s research team will investigate the mechanisms that cause docetaxel resistance, which may help to improve treatments for men with ADT-resistant prostate cancer.  Specifically, Dr. Tang will investigate a gene called ABCC2, which functions as a molecular ‘pump’, removing docetaxel from the cancer cell.  ABCC2 appears be turned on only in prostate cancer ‘stem’ cells, which are a small group of cells that are believed to be where prostate cancers originate.  Dr. Tang’s group will examine the levels of ABCC2 in different prostate cancers and determine whether ABCC2 levels are higher in more aggressive prostate cancers.  In addition, Dr. Tang’s group will use molecular tools to turn the ABCC2 gene on or off in prostate cancer cells and evaluate whether this affects the ability of docetaxel to kill the cells.  The results of Dr. Tang’s research may open up new avenues for treating prostate cancers that have become resistant to ADT and to docetaxel. 


Name of person or group

Dr. George Yousef
St. Michael's Hospital 

 
Name of program or research project
Discovery of new markers for prostate cancer relapse through miRNA profiling: moving into the era of personalized medicine (Translational Research-Diagnostics)

 
Investment and period of investment
$115,518 from 2010 to 2012
 
Outline of program or project

One of the major challenges faced by oncologists is to identify men with prostate cancers that are likely to re-occur after surgery.  Scientists believe that by studying the genetic makeup of prostate cancers, they may be able to identify molecular ‘biomarkers’ that could predict which cancers are destined to re-occur.  Micro-RNAs (miRNAs) are a newly discovered class of small molecules that turn off specific genes, and it is thought that the pattern of miRNAs that are present in different tumors may predict for different outcomes.  Dr. Yousef’s research team will use state-of-the-art molecular techniques to profile the pattern of miRNAs that are present in prostate cancers taken from men who had either early, intermediate, or no relapse.  In follow-up experiments, Dr. Yousef’s group will determine whether these miRNA can alter the growth, survival, and progression of prostate cancer cells.  These studies will help to identify men who are at the highest risk of reoccurrence, which may ultimately allow oncologists to better tailor their treatments to individual men 


Name of person or group

Dr. Ivan Robert Nabi
University of British Columbia 

 
Name of program or research project
Identification of Caveolin-1 Associated Regulatory Proteins in Prostate Cancer  (Basic Research-Diagnostics)

 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project
One of the major goals of cancer researchers is to identify genes and proteins that, when turned on, cause the disease to progress more extensively or more rapidly, or to become resistant to the various therapies that are employed by oncologists to treat the disease.  Of particular importance is identifying genes that are involved in regulating the ability of prostate cancer cells to spread outside of the prostate gland (‘metastasize’), since metastatic prostate cancer is incurable.  Dr. Nabi’s research group has identified that a gene called caveolin-1 is often turned on in metastatic prostate cancer cells.  However, very little is known about if and how caveolin-1 actually contributes to prostate cancer metastasis.  Using state of the art molecular techniques, Dr. Nabi’s team will examine how caveolin-1 interacts with other genes that regulate the ability of prostate cancer cells to metastasize, and how these genes in turn affect the function of caveolin-1.  Identification of these genes may allow oncologists to better treat aggressive prostate cancers.

 
Name of person or group
Dr. Jan Jongstra 
University Health Network

 
Name of program or research project
The Role of IL-6 and STAT3 in Clonogenic Prostate Cancer Cell Growth (Basic Research-Therapeutics)

 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project
Many scientists now believe that prostate cancer arises from a small population of cells that are distinct from the other cells that form a tumor.  These cells, termed prostate cancer stem cells, may also be responsible for the reoccurrence of tumors after therapy and for the spread of prostate cancer beyond the prostate gland (‘metastasis’).  Scientists have learned that certain genes may be turned on uniquely in prostate cancer stem cells, and that these cells may have special properties that could be specifically targeted by new anti-cancer drugs.  Dr. Jongstra’s research group has identified that prostate cancer stem cells have high levels of a gene called CD44, and that these cells are highly sensitive to a new drug developed in Dr. Jongstra’s laboratory, called M-110.  Dr. Jongstra will test this drug on cells that express high or low levels of CD44, and using advanced molecular techniques, will identify other genes that modify the sensitivity of these cells to the M-110 drug.  This study may increase the understanding of how prostate cancer stem cells can be specifically targeted using new anti-cancer drugs, and this may allow oncologists to more effectively target those cells that are the biological ‘root’ of prostate cancer.
 

 

Name of person or group
Dr. Mario Chevrette 
McGill University & the Research Institute of the McGillUniversity Health Centre 

 
Name of program or research project
The Role of CD9 in Establishing Prostate Cancer Bone Metastasis (Basic Research -Therapeutics)

 
Investment and period of investment
$120,000 from 2010 to 2012
 
Outline of program or project

 

Many men diagnosed with prostate cancer will die from the disease; as a result of the cancer having spread (‘metastasized’) outside of the prostate gland, usually to bone.  Unfortunately, very little is currently known about why some prostate cancers metastasize while others remain confined to the prostate where they are curable.  Normal adult bone is constantly remodeled, with old bone being replaced by new bone through the actions of two types of cells: osteoclasts, which are responsible for removing old bone, and osteoblasts, which are responsible for building new bone.  One important gene that plays a role in the remodeling of bone is called CD9, and Dr. Chevrette’s research group previously demonstrated that CD9 is turned on in prostate cancer cells and that this may be important for their ability to metastasize to bone.  In the current project, Dr. Chevrette’s team will evaluate the role of CD9 in the formation of prostate cancer bone metastases using an experimental model in which they can manipulate the levels of CD9 in prostate cancer cells and then test the ability of these cells to metastasize to bone.  Since there are drugs that are currently used to decrease the ability of prostate cancer cells to metastasize to bone (called ‘bisphosphonates’), Dr. Chevrette’s team will also examine whether alterations in the levels of CD9 can affect the sensitivity of prostate cancer cells to these drugs.  This research will shed light on the role of the CD9 gene in prostate cancer bone metastasis, and help to define whether it may be possible to reduce the occurrence of bone metastasis by designing drugs that specifically block the function of CD9. 




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