Centenary Institute of Cancer Medicine and Cell Biology

Newtown, Australia

Centenary Institute of Cancer Medicine and Cell Biology

Newtown, Australia
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Patent
University of Sydney and Centenary Institute Of Cancer Medicine And Cell Biology | Date: 2017-02-28

The invention relates to the identification of antigens, including Mycobacterium sulphate assimilation pathway components such as CysD, for preventing and treating Mycobacterium infection, especially but not exclusively Mycobacterium tuberculosis infection; to expression systems including live Mycobacterium for expression of said antigens for prevention and treatment of said infection; and to use of said antigens and expression systems for prevention and treatment of said infection.


Shklovskaya E.,Centenary Institute of Cancer Medicine and Cell Biology | O'Sullivan B.J.,University of Queensland | Ng L.G.,Centenary Institute of Cancer Medicine and Cell Biology | Ng L.G.,University of Sydney | And 7 more authors.
Proceedings of the National Academy of Sciences of the United States of America | Year: 2011

Antigen-dependent interactions between T lymphocytes and dendritic cells (DCs) can produce two distinct outcomes: tolerance and immunity. It is generally considered that all DC subsets are capable of supporting both tolerogenic and immunogenic responses, depending on their exposure to activating signals. Here, we tested whether epidermal Langerhans cells (LCs) can support immunogenic responses in vivo in the absence of antigen presentation by other DC subsets. CD4 T cells responding to antigen presentation by activated LCs initially proliferated but then failed to differentiate into effector/memory cells or to survive long term. The tolerogenic function of LCs was maintained after exposure to potent adjuvants and occurred despite up-regulation of the costimulatory molecules CD80, CD86, and IL-12, but was consistent with their failure to translocate the NF-κB family member RelB from the cytoplasm to the nucleus. Commitment of LCs to tolerogenic function may explain why commensal microorganisms expressing Toll-like receptor (TLR) ligands but confined to the skin epithelium are tolerated, whereas invading pathogens that breach the epithelial basement membrane and activate dermal DCs stimulate a strong immune response.


Patent
Centenary Institute Of Cancer Medicine And Cell Biology, Wenkart Foundation, Medvet Science Pty Ltd. and University of Sydney | Date: 2010-06-04

The present invention relates to methods for modulating angiogenesis, comprising administering to a subject, or cells or tissue derived therefrom: (i) one or more miRNA, or precursors or variants thereof, wherein at least one of said miRNA comprises a seed region comprising the sequence UCACAGU (SEQ ID NO:37) to inhibit angiogenesis; or (ii) one or more antagonists of a miRNA, wherein said miRNA comprises a seed region comprising the sequence UCACAGU (SEQ ID NO:37) to promote or induce angiogenesis. Also provided are methods of diagnosis of conditions associated with abnormal angiogenesis, or determining predisposition thereto. Suitable pharmaceutical compositions are also provided.


Kota B.P.,University of Sydney | Allen J.D.,Centenary Institute of Cancer Medicine and Cell Biology | Roufogalis B.D.,University of Sydney
Basic and Clinical Pharmacology and Toxicology | Year: 2011

The vitamin D3 metabolite 1,25-dihydroxycholecalciferol (DHC) and analogues derived from it are being investigated as potential agents for the treatment of cancer. Combining ketoconazole (KTZ) with DHC has been recommended to enhance the anticancer activity of DHC. DHC exerts its biological activities through the vitamin D receptor (VDR). VDR is recognized to be a regulator of P-glycoprotein (P-gp), a member of the ABC transporter family well known for its role in multidrug resistance in cancer chemotherapy. We have investigated the effect of DHC and adding KTZ together with DHC on P-gp and VDR expression and the functional consequences of P-gp induction in intestinal human colonic adenocarcinoma cells LS174T cells. DHC increased P-gp expression by two times, and the addition of KTZ further increased the expression to four times. The combination of DHC+KTZ also significantly increased VDR expression, consistent with the enhanced increase in P-gp expression by this combination. The increase in P-gp expression was accompanied by increased P-gp function, as measured by decreased Rh123 accumulation in the LS174T cells. In addition, DHC significantly decreased colchicine cytotoxicity in a dose-sensitive manner, and the addition of KTZ further decreased the colchicine cytotoxicity, indicating the chemo-protective effect of DHC is enhanced by KTZ, consistent with the enhanced expression of P-gp. The results of this study raise the possibility that DHC and the addition of KTZ to DHC treatment may decrease the effectiveness of cancer chemotherapy by promoting P-gp-mediated drug resistance. © 2011 The Authors. Basic & Clinical Pharmacology & Toxicology © 2011 Nordic Pharmacological Society.


Munoz M.A.,Centenary Institute of Cancer Medicine and Cell Biology | Biro M.,Centenary Institute of Cancer Medicine and Cell Biology | Biro M.,University of Sydney | Weninger W.,Centenary Institute of Cancer Medicine and Cell Biology | And 2 more authors.
Current Opinion in Cell Biology | Year: 2014

In the lymph node, T cells migrate rapidly and with striking versatility in a continuous scan for antigen presenting dendritic cells. The scanning process is greatly facilitated by the lymph node structure and composition. In vivo imaging has been instrumental in deciphering the spatiotemporal dynamics of intranodal T cell migration in both health and disease. Here we review recent developments in uncovering the migration modes employed by T cells in the lymph node, the underlying molecular mechanisms, and the scanning strategies utilised by T cells to ensure a timely response to antigenic stimuli. © 2014 The Authors.


Biro M.,Centenary Institute of Cancer Medicine and Cell Biology | Biro M.,University of Sydney | Munoz M.A.,Centenary Institute of Cancer Medicine and Cell Biology | Weninger W.,Centenary Institute of Cancer Medicine and Cell Biology | And 2 more authors.
British Journal of Pharmacology | Year: 2014

Leukocytes are unmatched migrators capable of traversing barriers and tissues of remarkably varied structural composition. An effective immune response relies on the ability of its constituent cells to infiltrate target sites. Yet, unwarranted mobilization of immune cells can lead to inflammatory diseases and tissue damage ranging in severity from mild to life-threatening. The efficacy and plasticity of leukocyte migration is driven by the precise spatiotemporal regulation of the actin cytoskeleton. The small GTPases of the Rho family (Rho-GTPases), and their immediate downstream effector kinases, are key regulators of cellular actomyosin dynamics and are therefore considered prime pharmacological targets for stemming leukocyte motility in inflammatory disorders. This review describes advances in the development of small-molecule inhibitors aimed at modulating the Rho-GTPase-centric regulatory pathways governing motility, many of which stem from studies of cancer invasiveness. These inhibitors promise the advent of novel treatment options with high selectivity and potency against immune-mediated pathologies. © 2014 The Authors. British Journal of Pharmacology published by John Wiley &. Sons Ltd on behalf of The British Pharmacological Society.


Roediger B.,Centenary Institute of Cancer Medicine and Cell Biology | Roediger B.,University of Sydney | Weninger W.,Centenary Institute of Cancer Medicine and Cell Biology | Weninger W.,University of Sydney | Weninger W.,Royal Prince Alfred Hospital
Advances in Immunology | Year: 2015

Type 2 cytokine-driven immune responses are important against parasite infections but also underlie the development of inflammatory allergic diseases. Type 2 CD4+ T (Th2) cells have long been believed to act as central regulators of allergic conditions via the production of the signature cytokines IL-4, IL-5, and IL-13. However, the more recent identification of group 2 innate lymphoid cells ILC (ILC2) cells, which also produce the same cytokines, necessitates a reevaluation of the relative roles these two populations play during type 2 inflammation. ILC2 cells preferentially localize to the interface between the host and the environment (lung, intestine, skin) and respond to epithelium-derived cytokines associated with barrier disruption, such as IL-25, IL-33, and thymic stromal lymphopoietin. ILC2 cells are a major source of IL-5 and IL-13 in vivo but may also produce IL-4 and IL-9 under more defined conditions. ILC2 cells regulate local inflammatory responses to environmental challenges, and this in turn enables them to influence downstream adaptive immune responses. Here, we discuss our current understanding of ILC2 cell phenotype, development and function, and detail the expanding array of cell surface receptor and signaling pathways that enable ILC2 cells to perform a variety of biological functions in vivo. We give special attention to the most recently described and poorly understood member of the ILC2 cell family, the dermal ILC2 cells, and discuss their role in regulating skin inflammation. © 2015 Elsevier Inc.


Patent
Centenary Institute Of Cancer Medicine And Cell Biology, Mirrx Therapeutics A S and University of Sydney | Date: 2013-10-02

The present invention provides oligonucleotides that inhibit the binding of miR-27a to VE-cadherin mRNA, particularly in the form of blockmirs. The invention also provides compositions comprising such oligonucleotides and methods of use of such oligonucleotides to modulate the activity of VE-cadherin, inhibit or reduce vascular permeability, treat or prevent a vascular permeability-associated disease or condition, inhibit tumour growth, treat ischaemic injury, enhance recovery from ischaemic injury, treat surgical wounds and/or promotes post-operative recovery, and promote or induce angiogenesis.


Patent
Centenary Institute Of Cancer Medicine And Cell Biology, University of Sydney and Wenkart Foundation | Date: 2016-03-22

The present invention relates to methods for modulating angiogenesis, comprising administering to a subject, or cells or tissue derived therefrom: (i) one or more miRNA, or precursors or variants thereof, wherein at least one of said miRNA comprises a seed region comprising the sequence UCACAGU (SEQ ID NO:37) to inhibit angiogenesis; or (ii) one or more antagonists of a miRNA, wherein said miRNA comprises a seed region comprising the sequence UCACAGU (SEQ ID NO:37) to promote or induce angiogenesis. Also provided are methods of diagnosis of conditions associated with abnormal angiogenesis, or determining predisposition thereto. Suitable pharmaceutical compositions are also provided.


Patent
Centenary Institute Of Cancer Medicine And Cell Biology | Date: 2011-04-15

The present invention relates to methods and kits for identifying, quantifying and isolating regulatory T cells, to methods and kits for diagnosing or monitoring autoimmune diseases, immunoinflammatory diseases, allergic diseases, predispositions thereto, infectious diseases, cancer, cancer treatment and/or organ transplantation based on regulatory T cell quantity, to methods and kits for predicting responses to therapy for autoimmune diseases, immunoinflammatory diseases, allergic diseases, predispositions thereto, infectious diseases, cancer and/or organ transplantation based on regulatory T cell quantity, and to methods and kits for therapy using isolated regulatory T cells.

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