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  • Identification of new lymphoma sub-group by Terry Fox Research Institute-funded cancer researchers opens door for potential new treatments for hard-to-treat cancer

    by Peter Mothe | Dec 03, 2018

    Scott_DavidVANCOUVER, BC – The discovery by BC researchers of a group of bad actors ‘hidden’ within a cohort of good ones may translate into new hope for cancer patients diagnosed with a type of lymphoma that doesn’t respond well to treatment.

    Patients with double- and triple-hit lymphoma currently represent a small percentage of the most common form of non-Hodgkin lymphoma, diffuse large B-cell lymphoma (DLBCL), but their survival is poor. Their cancer has re-arrangements of two or three genes (MYC, BCL2 and or BCL6) while most other forms of lymphoma have only one or none of these genes re-arranged. As a result, it is aggressive and hard to treat.

    The Terry Fox Research Institute-funded team’s identification of a gene expression signature for this cancer in what was otherwise known as a good prognosis lymphoma called germinal center B-cell like diffuse large B-cell lymphoma (GCB-DLBCL), is published today in the Journal of Clinical Oncology (JCO). The identified hidden group consisted of double hit lymphomas and an equally large group of lymphomas that shared the same gene expression signature, biology and poor outcome. The team also identified a large group (GCB-DLBCL negative) that have excellent outcomes.

    “This is a big step forward in improving outcomes for lymphoma patients. The findings identify a new sub-group within DLBCL that has a distinct biology that is potentially targetable. It may be possible to build clinical trials around this new lymphoma sub-group going forward,” explains co-senior author of the publication Dr. David Scott, a clinician-scientist at the BC Cancer Centre for Lymphoid Cancer in Vancouver and associate professor at the University of British Columbia. 

    The team has since created a clinical assay that can be used to test patient biosamples for potential targeted treatments in clinical trials.

    Dr. Scott is in San Diego, California this week presenting the BC group’s findings at the 60th annual American Society of Hematology conference, the largest gathering of this group of experts.  For their study, the team, including co-senior author Dr. Ryan Morin, (BC Cancer and Simon Fraser University, Vancouver) analyzed RNA sequencing data from a cohort of 157 patients with GCB-DLBCL to better understand the biology of both high-grade B cell lymphoma (HGBL) and DLBCL.

    Appearing alongside the BC’s group’s published paper is a second study from a research team in the United Kingdom that reached an identical conclusion while using a different approach. Dr. Scott is pleased the UK study further validates their results and he predicts it is possible that the identification of the new sub-group will lead to a reclassification of lymphoma by the World Health Organization.

    The study is also supported by a number of other funders.

    About The Terry Fox Research Institute (TFRI)

    Launched in October 2007, The Terry Fox Research Institute is the brainchild of The Terry Fox Foundation and today functions as its research arm. TFRI seeks to improve significantly the outcomes of cancer research for the patient through a highly collaborative, team-oriented, milestone-based approach to research that will enable discoveries to translate quickly into practical solutions for cancer patients worldwide. TFRI collaborates with more than 80 cancer hospitals and research organizations across Canada. TFRI headquarters are in Vancouver, B.C. For more information please visit www.tfri.ca and follow us on Twitter @tfri_research.

    Information for media:

    Dr. Scott is reachable in San Diego Dec. 3-4 for interview. To speak with him, please contact:

    Kelly Curwin
    Chief Communications Officer
    Terry Fox Research Institute
    675 West 10th Avenue
    Vancouver BC Canada V5Z1L3
    kcurwin@tfri.ca
    Office: 604-675-8223; cell: 778-237-8158

    LINK TO JCO
    http://ascopubs.org/journal/jco
    JCO.18.01583R1
    PHOTO CAPTION: Dr. David Scott

  • TFRI BC Node researchers present their work during 2018 BC Cancer Summit

    by Peter Mothe | Nov 14, 2018
    BCNode


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

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

    The TFRI would like to thank all of researchers who participated in the event, and congratulate the following scientists for winning the rapid fire and poster competitions. 

    Rapid fire talks competition winners:

    • ​Daiana Becker-Santos, "NFIB is a target of oncofetal miRNAs and is linked to tumour aggressiveness in lung adenocarcinoma"
    • Samantha Pollard, "Facilitating communication of genetic test results for hereditary cancer syndromes: What are the barriers?"
    • Christopher Rushton, "Advanced Methods for Cancer Detection by Vaginal Screening (ADVISE): feasibility and assessment of deep sequencing based self-sampling methods."

    Poster prize winners:

    • ​Adam Sage, "Expression of long non-coding RNAs from immune cells in the lung tumour microenvironment"
    • Kristen Allen, "Integration of a Web-Based Follow-Up Platform into BC Cancer for Improving Quality of Life Care and Research"
    • Zamzam Al-Hashami, "The impact of socioeconomic status and geographic location on palliative chemotherapy uptake in patients with metastatic non-small cell lung cancer treated in British Columbia"
    • Sonja Murchison, "Breast cancer patients’ perceptions of adjuvant radiotherapy: an assessment of pre-treatment knowledge and informational needs"
    • Luka Culibrk, "Ploidetect: interpretable detection of tumor content and aneuploidy from whole genome sequence data"
    • Linda Wang, "BAF complex mutations dysregulate enhancer landscapes in malignant rhabdoid tumor and ovarian clear cell carcinoma" 

     

    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, titled Host determinants of cancer immune response: New pathways for new therapies, will be hosted by Drs. Marianne Koritzinsky, Trevor Shepherd, Carolina Ilkow, Peter Greer, Kristin Hope, Meredith Irwin, and Robert Rottapel.

    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

    • Abstract book
    • Registration (free)
    • Agenda
    • 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
      • Poster Guidelines
      • 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

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