A5056245702- Cancer Cells and Metastasis
- Cell Adhesion Molecules Research
- CAR-T cell therapy research
- interferon and immune responses
- Virus-based gene therapy research
- Cancer-related molecular mechanisms research
- Cancer Genomics and Diagnostics
- Hippo pathway signaling and YAP/TAZ
- Immune Cell Function and Interaction
- Fibroblast Growth Factor Research
- Radiopharmaceutical Chemistry and Applications
- Cardiac Fibrosis and Remodeling
- Infectious Diseases and Mycology
- Telomeres, Telomerase, and Senescence
- TGF-β signaling in diseases
- Peptidase Inhibition and Analysis
- Advanced Breast Cancer Therapies
- T-cell and B-cell Immunology
- Genetic Neurodegenerative Diseases
- Muscle Physiology and Disorders
- Kruppel-like factors research
- Proteoglycans and glycosaminoglycans research
- HER2/EGFR in Cancer Research
- Cancer-related Molecular Pathways
- Cellular Mechanics and Interactions
University of Ottawa
2017-2025
Ottawa Hospital Research Institute
2017-2025
Ottawa Hospital
2017-2025
High-grade serous ovarian cancer (HGSOC) is the deadliest and most common subtype of cancer. Unfortunately, patients develop recurrence and, ultimately, resistance to standard platinum chemotherapy. Large tumor suppressors LATS1 LATS2, core Hippo signaling kinases, have been implicated in various types, including The mechanism by which LATS1/2 suppresses progression currently elusive, but expression frequently reduced or lost these cancers. In this study, we demonstrate that inactivation...
Breast cancer is a highly heterogeneous disease with multiple drivers and complex regulatory networks. Periostin (Postn) matricellular protein involved in plethora of types other diseases. Postn has been shown to be various processes tumor development, such as angiogenesis, invasion, cell survival metastasis. The expression breast cells correlated more aggressive phenotype. Despite extensive research, it remains unclear how epithelial regulate expression.
SOX10 is a key regulator of melanoma progression and promotes melanocytic/differentiated state. Here we identified cell lines lacking expression which retain their in vivo growth capabilities. More importantly, find that can regulate T-cell infiltration while also decreasing common cancer stem (CSC) properties. We show regulates CEACAM1, surface protein with immunomodulatory directly binds to distal CEACAM1 promoter region approximately 3-4kbps from the transcriptional start site....
While conventional wisdom initially postulated that PD-L1 serves as the inert ligand for PD-1, an emerging body of literature suggests has cell-intrinsic functions in immune and cancer cells. In line with these studies, here we show engagement via cellular ligands or agonistic antibodies, including those used clinic, potently inhibits type I interferon pathway Hampered responses PD-L1–expressing cells resulted enhanced efficacy oncolytic viruses vitro vivo. Consistently, expression marked...
// Jillian Conway 1, 2 , Khalid N. Al-Zahrani Benjamin R. Pryce John Abou-Hamad 1,2 and Luc A. Sabourin 1 University of Ottawa, Department Cellular Molecular Medicine, Ontario, K1H8M5, Canada Ottawa Hospital Research Institute, Cancer Therapeutics, K1H8L6, Correspondence to: Sabourin, email: lsabourin@ohri.ca Keywords: SLK; Stk2; EMT; TGFβ; invasion Received: June 06, 2017 Accepted: August 26, Published: October 19, ABSTRACT Invasion can be stimulated in vitro using the soluble ligand...
Abstract Background Approximately 5–10% of HER2-positive breast cancers can be defined by low expression the Ste20-like kinase, SLK , and high SOX10. Our lab has observed that genetic deletion results in induction Sox10 significantly accelerates tumor initiation a HER2-induced mammary model. However, mechanism responsible for SOX10 gene this context remains unknown. Methods Using tumor-derived cell lines from MMTV-Neu mice lacking biochemical approaches, we have characterized signaling...
Abstract Natural Killer (NK) cells are critical for immunosurveillance yet become dysfunctional in contexts such as chronic stimulation by viral infections or cancer. This phenomenon is similar to T cell exhaustion but less well characterized, which limits therapeutic interventions. As shown cells, NK often display an increased expression of immune checkpoint proteins (ICP) following stimulation, and ICP blockade therapies currently being explored several cancer types, have remarkable...
Targeted therapy resistance frequently develops in melanoma due to intratumor heterogeneity and epigenetic reprogramming. This also typically induces cross-resistance immunotherapies. Whether this includes additional modes of has not been fully assessed. We show that co-treatments MAPKi with VSV-based oncolytics do function a synergistic fashion; rather, the MAPKis block infection. Melanoma vemurafenib further perturbs cells’ ability be infected by oncolytic viruses. Resistance can induced...
ABSTRACT Targeting the PD-1/PD-L1 axis has transformed field of immune-oncology. While conventional wisdom initially postulated that PD-L1 serves as inert ligand for PD-1, an emerging body literature suggests cell-intrinsic functions in immune and cancer cells. In line with these studies, here we show engagement via cellular ligands or agonistic antibodies, including those used clinic, potently inhibits type I interferon pathway Hampered responses PD-L1-expressing cells resulted enhanced...
Abstract Background: Approximately 5-10% of HER2-positive breast cancers can be defined by low expression the Ste20-like kinase, SLK, and high SOX10. Our lab has observed that genetic deletion SLK results in induction Sox10 significantly accelerates tumor initiation a HER2-induced mammary model. However, mechanism responsible for SOX10 gene this context remains unknown. Methods: Using derived cell lines from MMTV-Neu mice lacking biochemical approaches, we have characterized signaling...
Abstract Over the past two decades, mammalian Ste20-like kinase (SLK) has been characterized for its role in regulating cellular migration, proliferation and apoptosis fibroblasts myoblasts. In mammary epithelial cells, SLK shown to be required efficient epithelial-to-mesenchymal transition activated downstream of HER2/Neu-oncogene control chemotactic migration. Here, we assessed HER2/Neu-induced tumorigenesis vivo. As is HER2/Neu, hypothesized that loss would significantly delay tumor...