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  • Agenda posted for TFRI's BC Node 2018 Day

    by Peter Mothe | Nov 14, 2018
    BCNode


    THE TERRY FOX RESEARCH INSTITUTE'S BC NODE will host its annual Node Day on Friday, Nov. 23, 2018 at the Sheraton Wall Centre in Vancouver.

    This year's conference will be held as part of the BC Cancer Summit, and will see a number of TFRI-funded researchers presenting their work. The keynote speech for the event, titled The Road Ahead for Precision Oncology, will be given by TF4CN member Dr. Lillian Siu (BC Cancer). 

    TFRI-related talks will take place in the Junior Ballroom B. As a platinum sponsor of the event, the TFRI will also have a booth in the reception area, where its research investment in the province. 

    BC Node Day 2018 Schedule

    10:15am – 10:45am Next Generation Pathology – Where Does the Glass Slide Fit In The Era of Genome-Based Precision Medicine? – Dr. Stephen Yip
    10:45am – 11:15am Profiling specific sensitivities of patient breast tumours by in vivo xenograft CRISPR screening – Dr. Peter Eirew
    11:15am – 11:45am Inducing synthetic lethality through oncogenic stimulation: a novel paradigm for lung cancer treatment – Dr. William Lockwood
    1:30pm – 2:00pm Precision Medicine for Prostate Cancer – Dr. Kim N. Chi
    2:00pm – 2:30pm Replication-transcription conflict as a source of cancer genome instability – Dr. Peter C. Stirling
    2:30pm – 3:00pm Terry Fox PROFYLE: A Pan-Canadian Marathon of Hope for Children with Cancer – Dr. Rod Rassekh
    3:15pm – 3:45pm 3:15pm – 3:45pm Universal Access to Health Research in a Universal Health Care System: How are we doing? – Dr. Nadine Caron
    3:45pm – 5:00pm Trainee rapid-fire presentation session





  • Agenda posted for TFRI's Atlantic Node 2018 Cancer Research Conference

    by Peter Mothe | Oct 16, 2018
    BHCRI_TFRI

    The Terry Fox Research Institute's Atlantic Node and Beatrice Hunter Cancer Research Institute will be hosting their annual Cancer Research Conference on November 5th and 6th, 2018. 

    This year's conference will be held in the Lord Nelson Hotel in Halifax, and will have both Trainee and Scientific sessions. The main themes will be Precision and Personalized Medicine for Cancer Care. 

    More information on the event can be found, here. A link to the event's tentative agenda can be found here.


  • 2018 Terry Fox Run Challenge: TFRI teams show immense support, raise over $90k for research

    by Peter Mothe | Oct 01, 2018

    Headquarters Team
    ​A group of purple-clad researchers pose with members of the TFRI headquarters team at the start line of the Terry Fox Run in Stanley Park (Vancouver). 

    TFRI-funded researchers showed up in full force for the 38th annual Terry Fox Run, adding a splash of purple to run sites across the country and raising a whopping $90,399.45 for cancer research. 

    This number, which is still an early estimate and does not include the money raised from the sale of researcher-designated purple shirts, marks a 63 per cent increase in donations from last year.

    “It was great to see so many members of our research community come together to raise money for cancer research,” said Dr. Victor Ling, TFRI President and Scientific Director.

    In total, a record-breaking 24 TFRI teams participated, with the Vancouver Prostate Centre team bringing in over $28,500 and taking home the coveted Terry Fox Run Challenge 2018 title. Second place went to the TFRI Headquarters team ($12,888), and third went to the Canadian Oncolytic Virus Consortium (COVCo) team, which raised $10,707.50.

    Notable individual fundraisers this year included Dr. Peter Black (Vancouver Prostate Centre), who raised an incredible $19,029, Dr. Rebecca Auer (COVCo) who raised $7,105, and Dr. Ling who raised $5,765.

    Dr. Ling, who gave an emotional speech to kick off the run at Stanley Park in Vancouver, was thrilled by the strong turnout and expressed his thanks to everyone who helped to make this year's team challenge and fundraising efforts so successful.  

    The final numbers raised this year through the annual national run are not yet known. These numbers will be released by The Terry Fox Foundation at a later date.

    Below is a summary list of the TFRI teams that participated in the run and team challenge (according to online records):

    NOTE: Please send us team pictures or let us know if we missed your team by emailing us at info@tfri.ca.

    Quebec 
    GCRC Foxtrotters
    TFRI CRCHUM

    Ontario
    iTNT: ImmunoTherapy Network
    TFRI The MAGICians
    Stemness
    COVCo Team
    TFRI Team Hippo
    TFRI – The Gang-sters
    TFRI Hypoxia Program
    The Hydra Killers
    TFRI Team Rottapel for Terry
    TFRI-TNBC
    TFRI GBM
    LFS Central
    Calvin's Blood Cell Crew
    Lymphomaniacs

    British Columbia
    Bloodrunners
    Vancouver Prostate Centre
    TFRI Headquarters
    Pancreas Centre BC
    TFRI – Sarcoma Research
    Lung Team

    Nova Scotia
    TFRI Cancer Research Training Program

    New Brunswick
    Reiman Research Lab

    Photos

    TFRI GBM Researchers from the Glioblastoma PPG Team led by Dr. Sheila Singh (McMaster) pose at the Oakville run in Ontario.

    Lymphomaniacs
    The Lymphomaniacs led by TFRI New Investigator Dr. Robert Kridel pose before the run in Ontario. 

    TFRI Pancreas Centre BC
    The TFRI Pancreas Centre BC team at the Stanley Park Run (Vancouver)

    GRC Foxtrotters 2
    Researchers from the GCRC Foxtrotters team run in Montreal.

    MCC Team
    Researchers from the Montreal Cancer Consortium sub-project led by Dr. Ian Watson pose after the run in Montreal.

  • TFRI Ontario Node Day to be held on December 10, 2018

    by Peter Mothe | Sep 25, 2018

    The Terry Fox Research Institute's Ontario Node will be holding its annual Research Symposium on December 10, 2018 at the MaRS Auditorium (conference facility/lower level).

    The event, which will be hosted by Drs. Marianne Koritzinsky, Trevor Shepherd, Carolina Ilkow, Peter Greer, Kristin Hope, Meredith Irwin, and Robert Rottapel, will focus on the Microbiome and Cancer.

    This year's keynote speakers will be Drs. Thomas Gajewski (University of Chicago) and Christian Jobin (University of Florida). Other speakers include: Drs. Michele Ardolino (Ottawa Hospital Research Institute); Carolina Ilkow (Ottawa Hospital Research Institute) Madhuri Koti (Queen’s Cancer Research Institute); Jonathan Bramson (McMaster University), Anthony Mutsaers, (University of Guelph), and Geoffrey Wood (University of Guelph).

    Important information and links

    • Registration (free)
    • Agenda (Latest draft)
    • Abstract Submission
      • OPENS: Thursday, September 26th
      • CLOSES: Monday, November 19th at 5:00 PM.
      • Abstract Criteria
    • Rapid Fire Talks
      • The top 10 postdoc abstracts submitted will be given a unique opportunity to showcase their work!
    • Poster Session & Reception
      • Monday, December 10th (5:00pm-6:30PM) The Heritage Atrium, located on the 1st level of the MaRS Bldg.)

    Questions?

    For additional information on the TFRI Symposium, please contact Donna De Francesco (donna.defrancesco@uhnresearch.ca).

     




  • Discovery of CD33 in human cord blood cells may affect design of targeted AML therapies

    by Peter Mothe | Sep 10, 2018

    Leukemia


    A BC-based team of TFRI-funded researchers has discovered that CD33, a protein from the sialic acid-binding receptor family that was previously believed to be unique to normal maturing white blood cell precursors and acute myeloid leukemias (AML), is also present on human cord blood stem cells with the highest regenerative ability.

    The findings, published in Nature Cell Biology (June 2018), could significantly affect the design of targeted AML therapies, according to Dr. David Knapp (BC Cancer/UBC) and Colin Hammond (PhD candidate, UBC), the study’s two co-first authors.

    “This finding suggests a potentially serious complication with some current anti-AML treatments that aim to kill all cells expressing CD33,” said Dr. Connie Eaves (BC Cancer/UBC) who led the team study funded by a  Terry Fox New Frontiers Program Project Grant.

    This new discovery provides a possible explanation of why some trials that have used CD33 as a potential target for AML therapies have shown specific toxicities expected from a loss of normal stem cells, according to the Eaves’ group.

    Their investigation also revealed previously unknown functional and molecular differences between individual human blood stem cells. The study also sets the ground work for identifying shared features that could be critical to the high regenerative ability unique to these rare cells.

    “This paper presents the first description of associated molecular and biological properties of individual human blood stem cells and has made the detailed results available in a permanently accessible form for other investigators to consult and use,” Hammond said. “These findings could thus be a major aid to the development of better protocols for expanding human blood stem cells in the laboratory, and therefore contribute to an improved availability of donor cells useful for clinical transplants.”

    Study

    Single-cell analysis identifies a CD33+ subset of human cord blood cells with high regenerative potential

    Authors

    David J. H. F. Knapp, Colin A. Hammond, Tony Hui, Marijn T. J. van Loenhout, Fangwu Wang, Nima Aghaeepour, Paul H. Miller, Michelle Moksa, Gabrielle M. Rabu, Philip A. Beer, Davide Pellacani, R. Keith Humphries, Carl Hansen, Martin Hirst and Connie J. Eaves.

    Funding

    This work was supported by a TFRI New Frontiers Program Project Grant in Exploiting Pathogenic Mechanisms in Acute Leukemia for Clinical Translation.

  • New discovery answers long-held question about myelodysplastic syndromes

    by Peter Mothe | Sep 10, 2018

    Karsan_Photo


    A new discovery by a group of TFRI-funded researchers is helping to answer a question long-held by scientists studying a group of rare blood and bone marrow cancers known as myelodysplastic syndromes (MDS): how the same disease could lead to the development of two seemingly opposite conditions.

    In a study published in Nature Communications (June 2018), the team led by Dr. Aly Karsan (BC Cancer) suggests that the key to understanding how both bone marrow failure and acute leukemia can be caused by MDS lays in the loss of two microRNAs (143 and 145), which are both present in the long arm of chromosome 5, a chromosome commonly deleted in patients with MDS.

    “While we have known for a while that the deletion of chromosome 5q is the most common chromosomal aberration in MDS, what we discovered in this study is that the loss of miR-143/145 actually activates a signalling pathway in marrow blood cells called TGFβ, which suppresses the creation of blood stem cells while expanding the number of slightly more mature progenitor cells being created in the bone marrow,” said Dr. Karsan.

    This explains why MDS can lead to bone marrow failure caused by low levels of healthy blood cells, while also causing acute leukemias associated with the proliferation of malignant cells derived from progenitor cells that flood the bone marrow.

    This discovery opens the door for the development of potential therapies that could improve outcomes for patients with MDS by identifying a new therapeutic target.

    “These findings suggest that clinical trials with inhibitors of the TGFβ pathway may be warranted in MDS patients with deletion of chromosome 5,” said Dr. Karsan.

    Study

    miR-143/145 differentially regulate hematopoietic stem and progenitor activity through suppression of canonical TGFβ signaling

    Authors

    Jeffrey Lam, Marion van den Bosch, Joanna Wegrzyn, Jeremy Parker, Rawa Ibrahim, Kate Slowski, Linda Chang, Sergio Martinez-Høyer, Gianluigi Condorelli, Mark Boldin, Yu Deng, Patricia Umlandt, Megan Fuller and Aly Karsan.

    Funding

    This study was partially funded by a Terry Fox New Frontiers Program Project Grant in Exploiting Pathogenic Mechanisms in Acute Leukemia for Clinical Translation

  • Co-targeting EphA2/A3 reduces rGBM tumour growth in mice models

    by Peter Mothe | Sep 10, 2018

    Qazi_Maleeha
    Maleeha Qazi is a PhD candidate at McMaster University and the lead author of the paper published in Cancer Research (July 2018). 


    Co-targeting two specific proteins in cancer stem cells could significantly reduce tumour growth in patients with recurrent glioblastoma (rGBM), a McMaster University-based TFRI team has learned.

    According to Maleeha Qazi, a PhD candidate and lead author of a recent paper published in Cancer Research (July 2018), the team arrived at this conclusion after realizing that high levels of both EphA2 and EphA3, two members of the Ephrin receptor family involved in important signalling in brain development, marked the tumorigenic, therapy-resistant glioblastoma stem cell (GSC) population.

    “We used cell lines derived from GBM patients that had already received chemotherapy and radiation therapy and profiled the expression of all 14 Ephrin receptors. We found that together, these two proteins – EphA2 and EphA3 – marked a very potent GSC population within treatment-refractory rGBM,” said Qazi, who is part of Dr. Sheila Singh’s Terry Fox New Frontiers Program Project Grant (PPG). With a partner group at the U of T led by Dr. Jason Moffat, PPG co-investigator and an expert in gene editing technology, Dr. Singh’s team mined large glioma datasets and conducted validation studies that underscored their finding that both EphA2 and EphA3 were potent targets. “Learning that was great because it provided us with two GSC-specific targets against which we could then develop new therapeutics for patients with rGBM.”

    To develop these new therapies, Qazi work with Dr. Sachdev Sidhu (UofT), a protein engineer and co-investigator in Dr. Singh’s PPG team. Together the researchers were able to create a bi-specific antibody (BsAb) that simultaneously targeted these two markers and began testing it in mice.

    It was during these preclinical trials that Qazi and her team saw the most promising results, including a decrease in the frequency of GSCs and a 30 per cent reduction in tumour volume when the antibody was delivered intracranially.

    “Recurrent GBM is the deadliest human brain cancer and has no effective therapies, so for us to block even 30 per cent of tumour growth is quite significant, especially because these tumours have already evaded standard-of-care chemotherapy and radiation,” said Qazi, adding that these results could be even more positive in humans, since BsAbs could be delivered more effectively in humans than in mice.

    The team is now excited to transition the antibodies into clinical trials, bringing much-needed hope to patients with rGBM.

    “The best thing about these antibodies is that they are already humanized and are perfectly poised for further development for human clinical trials. Patients suffering from recurrent GBM really do not have any other options, so for us to offer a poly-targeting therapy that shows preclinical efficacy in proof-of- concept models makes it much easier to present it as a treatment option for patients with recurrent GBM,” Qazi said. “That's the kind of thing that we hope to do moving forward with this antibody and other targeted therapies under development within the framework of our TFRI PPG grant.” 

    Study

    Co-targeting ephrin receptor tyrosine kinases A2 and A3 in cancer stem cells reduces growth of recurrent glioblastoma

    Authors

    Maleeha A. Qazi, Parvez Vora, Chitra Venugopal, Jarrett Adams, Mohini Singh, Amy Hu, Maryna Gorelik, Minomi K. Subapanditha, Neil Savage, Jiahe Yang, Chirayu Chokshi, Max London, Alexander Gont, David Bobrowski, Natalie Grinshtein, Kevin R. Brown, Naresh K. Murty, Johan Nilvebrant, David Kaplan, Jason Moffat, Sachdev Sidhu, Sheila K. Singh

    Funding

    This study was funded by a Terry Fox New Frontiers Program Project Grant awarded to Drs. Jason Moffat, Sachdev Sidhu and Sheila K. Singh.

  • How do doctors really feel about active surveillance?

    by Peter Mothe | Sep 10, 2018

    Doctors


    Over the past decade, active surveillance (AS) has emerged as a safe, primary management strategy that reduces the risk of overtreatment for men with low-risk prostate cancer. But despite significant evidence proving the benefits of AS, many men still opt against it, choosing instead to undergo invasive therapies that can lead to damaging side-effects.

    So, what are some of the barriers that prevent more men from embracing AS, and how can health care professionals encourage them to accept this evidence-based approach to prostate cancer management?

    These are just two of the questions tackled by members of the TFRI-funded Canadian Prostate Cancer Biomarker Network in Describing perspectives of health care professionals on active surveillance for the management of prostate cancer, a new study that looks at AS from the perspective of health care professionals.

    “It is critically important to understand the perspectives of the professionals who treat patients with prostate cancer with regards to active surveillance to better understand why some physicians and patients are reluctant or open to the concept of active surveillance,” said the paper’s lead author Dr. Fred Saad (Centre de recherche du Centre hospitalier de l'Université de Montréal (CRCHUM)).

    To gain these insights, researchers met with 48 health care professionals (HCPs), including general practitioners, urologists and radiation oncologists from six Canadian academic institutions in four different provinces. During these discussions it became apparent that several factors converged to make it harder for physicians to “sell” the idea of AS to their patients.

    “The AS approach conflicts with the usual message promoted to the public of undergoing curative treatment promptly following a cancer diagnosis and is often perceived as “doing nothing” during a time of heightened emotional distress for men and their families, which can make new learning and decision-making difficult,” reads the study.

    Because AS is initially perceived as counterintuitive, things like age, mood and personality play an important role in a patient’s decision to embrace it, according to the health care professionals interviewed in the study, who also highlighted that anxiety and depression made men more likely to select radical treatment over AS.

    The study also reveals that HCPs often struggle to “sell” AS to their patients because some of them are still reticent about the approach themselves. This occurs partly because of a lack of clear biomarkers that indicate exactly when it is the best option for patients, placing a large responsibility on physicians to help their patient’s make the right choice.

    “Most participants agreed that the development of a standardized approach for AS would be beneficial, given the current variations in terms of protocol, level of patient education materials, methods, and medical community philosophy on AS,” wrote the study authors.

    Given this information, Dr. Saad believes that the insights derived from this study will fuel the team’s pursuit to develop biomarkers that can clearly show when AS is most appropriate, helping to make it easier for both HCPs and patients to embrace this effective approach to prostate cancer.

    “These findings will allow us to attempt to create tools that more accurately address the issues faced by clinicians,” he said. “Physicians that are better equipped to predict outcomes of AS will feel more confident in helping patients make decisions regarding therapeutic choices in dealing with a diagnosis of prostate cancer.”

    Study

    Describing perspectives of health care professionals on active surveillance for the management of prostate cancer

    Authors

    Kittie Pang, Margaret Fitch, Veronique Ouellet, Simone Chevalier, Darrel E. Drachenberg, Antonio Finelli, Jean-Baptiste Lattouf, Alan So, Simon Sutcliffe, Simon Tanguay, Fred Saad and Anne-Marie Mes-Masson

    Funding

    This research was funded by the Terry Fox Research Institute as part of a pan-Canadian initiative named the Canadian Prostate Cancer Biomarker Network.

  • Team identifies CDC25 as a common therapeutic target for triple-negative breast cancer

    by Peter Mothe | Sep 10, 2018

    Zacksenhaus_2
    The diagram on the left shows how RB1-positive TNBC cells are sensitive to both CDK4/6 inhibitors and CDC25 inhibitors, while the diagram on the right shows how RB1-deficient TNBC cells are resistant to CDK4/6 inhibitors but remain sensitive to CDC25 inhibition.


    A Toronto-based group of TFRI-funded scientists has discovered a new therapeutic target that could bring hope to patients with triple-negative breast cancer (TNBC), an aggressive breast cancer with no effective treatments.

    Led by Dr. Eldad Zacksenhaus (Toronto General Research Institute, UofT), the research team used mouse models and human cell lines to help identify CDC25, a phosphate enzyme that promotes cell proliferation, as a common therapeutic target for diverse TNBCs, including tumours with mutations in RB1, PTEN and p53, three tumour-suppression genes frequently inactivated in TNBC.

    The team found that inhibiting CDC25 pharmacologically or genetically promoted cancer cell death in tumours that were RB1-deficient. This breakthrough, which was published in Cell Reports (April 2018), marks a big leap forward in this area of cancer research. Until now, researchers have struggled to find ways to treat RB1-deficient tumours, as they are unresponsive to CDK4/6 inhibitors, which are commonly used against cancer cells expressing the RB1 gene.

    Researchers are hoping that this discovery will inspire others in the scientific community to develop new CDC25 inhibitors that work alone or in combination with other drugs to bring much needed hope to people living with TNBC.

    “Although many such inhibitors are available; no anti-CDC25 drug has been approved for use in the clinic yet,” said Dr. Zacksenhaus. “Hopefully these findings will renew interest in the development of safe and effective CDC25 inhibitors that can be used in clinics.”

    Study

    Identification of CDC25 as a Common Therapeutic Target for Triple-Negative Breast Cancer

    Authors

    Jeff C. Liu, Letizia Granieri, Mariusz Shrestha, Dong-Yu Wang, Ioulia Vorobieva, Elizabeth A. Rubie, Rob Jones, YoungJun Ju, Giovanna Pellecchia, Zhe Jiang, Carlo A. Palmerini, Yaacov Ben-David, Sean E. Egan, James R. Woodgett, Gary D. Bader, Alessandro Datti, and Eldad Zacksenhaus

    Funding

    This study was partially funded by a Terry Fox New Frontiers Program Project Grant for Killing the Hydra: Genetic dissection of actionable targets required for maintenance of metastatic disease

  • Deep-sea bacteria inspire researchers to develop new ways to see, treat tumours

    by Peter Mothe | Sep 10, 2018

    Zheng_2
    The green sulphur bacteria has the most efficient known light-to-energy conversion ratio in the natural world, which is exactly why Dr. Zheng's team decided to copy its molecular structure to see if it could be used as a contrast agent.


    A hundred metres below the surface of the Black Sea, life is tough. At that depth, oxygen levels are low and sunlight is practically invisible to the human eye. But despite these adverse conditions, one organism still manages to thrive in this hostile environment. Its secret? An incredible ability to convert small amounts of light into energy.

    Scientists are fascinated by the way green sulphur bacteria use hyper-sensitive, antenna-like structures called chlorosomes to efficiently convert the tiny particles of light that reach this part of the sea into chemical energy. And recently a group of Toronto-based researchers has found a way to harness the power of these light-harvesting organelles for an unexpected purpose: to improve our ability to see and treat cancerous tumours hidden deep inside our bodies.  

    In a study published in Angewandte Chemie (June 2018; first author Dr. Kara Harmatys), a TFRI-funded New Frontiers Program Project Grant team led by Dr. Gang Zheng (Princess Margaret Cancer Centre) explains how they set out to replicate the unique properties of these incredibly efficient light-harvesting organisms in their lab, hoping that they could serve as a contrast agent that would allow doctors to better understand the shape and size of hard-to-reach tumours.

    After successfully creating a biomimetic system that copied the molecular structure of the chlorosome organelles that live in the bacteria, the team was faced with a second challenge: making it safe and useful in humans. To do this, they drew inspiration from a high-density lipoprotein nanoparticle that transports fat molecules in human blood, which they managed to replicate in their lab and combine with their newly created biomimetic chlorosome.

    This dual-biomimetic system is the first of its kind and has several promising applications: in addition to being a contrast agent that will help researchers see tumours more clearly, it will also play a role in photodynamic therapy (PDT), a promising treatment against cancer that uses light-activated drugs, called photosensitizing agents, to kill cancer cells.

    “We envision this agent will improve current surgical procedures by helping surgeons view tumours they are operating on in real-time, while also providing minimally invasive and curable PDT for surgically inaccessible tumours or tumours that are close to anatomical structures,” said Dr. Zheng. “So far we’ve had promising preliminary results and are excited to continue exploring the imaging and phototherapeutic applications of this agent.”

    Study

    Multipronged Biomimetic Approach to Create Optically Tunable Nanoparticles

    Authors

    Kara M. Harmatys, Juan Chen, Danielle M. Charron, Christina M. MacLaughlin, and Gang Zheng

    Funding

    This study is partly funded by a Terry Fox New Frontiers Program Project Grant in Nanoparticle-Enhanced Photoacoustic Imaging for Cancer Localization and Therapeutic Guidance

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