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216 results on '"Addison, Christina L."'

10. VEGF-Mediated Induction of PRD1-BF1/Blimp1 Expression Sensitizes Tumor Vasculature to Oncolytic Virus Infection

Author

Arulanandam, Rozanne, Batenchuk, Cory, Angarita, Fernando A., Ottolino-Perry, Kathryn, Cousineau, Sophie, Mottashed, Amelia, Burgess, Emma, Falls, Theresa J., De Silva, Naomi, Tsang, Jovian, Howe, Grant A., Bourgeois-Daigneault, Marie-Claude, Conrad, David P., Daneshmand, Manijeh, Breitbach, Caroline J., Kirn, David H., Raptis, Leda, Sad, Subash, Atkins, Harold, Huh, Michael S., Diallo, Jean-Simon, Lichty, Brian D., Ilkow, Carolina S., Le Boeuf, Fabrice, Addison, Christina L., McCart, J. Andrea, and Bell, John C.

Published
2015
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18. Reciprocal cellular cross-talk within the tumor microenvironment promotes oncolytic virus activity

Author

Ilkow, Carolina S., Marguerie, Monique, Batenchuk, Cory, Mayer, Justin, Neriah, Daniela Ben, Cousineau, Sophie, Falls, Theresa, Jennings, Victoria A., Boileau, Meaghan, Bellamy, David, Bastin, Donald, de Souza, Christiano Tanese, Alkayyal, Almohanad, Zhang, Jiqing, Boeuf, Fabrice Le, Arulanandam, Rozanne, Stubbert, Lawton, Sampath, Padma, Thorne, Steve H., Paramanthan, Piriya, Chatterjee, Avijit, Strieter, Robert M., Burdick, Marie, Addison, Christina L., Stojdl, David F., Atkins, Harold L., Auer, Rebecca C., Diallo, Jean-Simon, Lichty, Brian D., and Bell, John C.

Subjects
Tumors -- Physiological aspects, Fibroblasts -- Health aspects, Cancer cells -- Health aspects, Cellular control mechanisms -- Health aspects, Biological sciences, Health
Abstract

Tumors are complex ecosystems composed of networks of interacting 'normal' and malignant cells. It is well recognized that cytokine-mediated cross-talk between normal stromal cells, including cancer-associated fibroblasts (CAFs), vascular endothelial cells, immune cells, and cancer cells, influences all aspects of tumor biology (1). Here we demonstrate that the cross-talk between CAFs and cancer cells leads to enhanced growth of oncolytic virus (OV)-based therapeutics. Transforming growth factor-β (TGF-β) produced by tumor cells reprogrammed CAFs, dampened their steady-state level of antiviral transcripts and rendered them sensitive to virus infection. In turn, CAFs produced high levels of fibroblast growth factor 2 (FGF2), initiating a signaling cascade in cancer cells that reduced retinoic acid-inducible gene I (RIG-I) expression and impeded the ability of malignant cells to detect and respond to virus. In xenografts derived from individuals with pancreatic cancer, the expression of FGF2 correlated with the susceptibility of the cancer cells to OV infection, and local application of FGF2 to resistant tumor samples sensitized them to virotherapy both in vitro and in vivo. An OV engineered to express FGF2 was safe in tumor-bearing mice, showed improved therapeutic efficacy compared to parental virus and merits consideration for clinical testing., Metabolic coupling and paracrine communication between cancer cells and CAFs can determine the response of tumors to a variety of cancer therapeutics (2-8). A number of virus based anticancer therapeutics [...]

Published
2015

38. Mapping vitamin B6 metabolism by hydrazoCEST magnetic resonance imaging.

Author

Brun, Emilie Marie Sophie Patit-Tha, Calvert, Nicholas David, Suchý, Mojmír, Kirby, Alexia, Melkus, Gerd, Garipov, Ruslan, Addison, Christina L., and Shuhendler, Adam J.

Subjects
MAGNETIC resonance imaging, CONTRAST media, VITAMINS, METABOLISM, AROMATIC aldehydes, BIOTRANSFORMATION (Metabolism)
Abstract

A new CEST-MRI contrast agent, 2-HYNIC, capable of sensing aromatic aldehydes is reported. Pyridoxal 5′-phosphate, a key Vitamin B6 metabolite necessary for >140 biotransformations was mapped by CEST-MRI in vitro and in vivo in lung cancer. 2-HYNIC provided access to this key biomarker associated with a variety of human diseases. [ABSTRACT FROM AUTHOR]

Published
2021
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44. The response of VEGF-stimulated endothelial cells to angiostatic molecules is substrate-dependent

Author

Polverini Peter J, Linn Stephanie A, Zhao Huijun, Nör Jacques E, Addison Christina L, and Delaney Christie E

Subjects
Cytology, QH573-671
Abstract

Abstract Background The microenvironment surrounding cells can exert multiple effects on their biological responses. In particular the extracellular matrix surrounding cells can profoundly influence their behavior. It has been shown that the extracellular matrix composition in tumors is vastly different than that found in normal tissue with increased amounts of certain matrices such as collagen I. It has been previously demonstrated that VEGF stimulation of endothelial cells growing on type I collagen results in the induction of bcl-2 expression and enhanced endothelial cell survival. We sought to investigate whether this increased endothelial cell survival resulted in the failure of angiostatic molecules to inhibit angiogenesis. Results We now demonstrate that VEGF-induced survival on collagen I impairs the ability of three known angiostatic molecules, TSP-1, IP-10 and endostatin to inhibit endothelial cell proliferation. Apoptosis of endothelial cells, growing on collagen I, induced by TSP-1 and IP-10 was also inhibited following VEGF stimulation. In contrast, endostatin induced apoptosis in these same cells. Further analysis determined that endostatin did not decrease the expression of bcl-2 nor did it increase activation of caspase-3 in the presence of VEGF. Alternatively, it appeared that in the presence of VEGF, endostatin induced the activation of caspase-8 in endothelial cells grown on collagen I. Furthermore, only endostatin had the ability to inhibit VEGF-induced sprout formation in collagen I gels. Conclusion These data suggest that TSP-1, IP-10 and endostatin inhibit endothelial cells via different mechanisms and that only endostatin is effective in inhibiting angiogenic activities in the presence of collagen I. Our results suggest that the efficacy of angiostatic treatments may be impaired depending on the context of the extracellular matrix within the tumor environment and thus could impede the efficacy of angiostatic therapies.

Published
2005
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45. Overexpression of the duffy antigen receptor for chemokines (DARC) by NSCLC tumor cells results in increased tumor necrosis

Author

Burdick Marie D, Belperio John A, Addison Christina L, and Strieter Robert M

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background The Duffy antigen receptor for chemokines (DARC) is known to be a promiscuous chemokine receptor that binds a variety of CXC and CC chemokines in the absence of any detectable signal transduction events. Within the CXC group of chemokines, DARC binds the angiogenic CXC chemokines including IL-8 (CXCL8), GROα (CXCL1) and ENA-78 (CXCL5), all of which have previously been shown to be important in non-small cell lung carcinoma (NSCLC) tumor growth. We hypothesized that overexpression of DARC by a NSCLC tumor cell line would result in the binding of the angiogenic ELR+ CXC chemokines by the tumor cells themselves, and thus interfere with the stimulation of endothelial cells and induction of angiogenesis by the tumor cell-derived angiogenic chemokines. Results NSCLC tumor cells that constitutively expressed DARC were generated and their growth characteristics were compared to control transfected cells in vitro and in vivo in SCID animals. We found that tumors derived from DARC-expressing cells were significantly larger in size than tumors derived from control-transfected cells. However, upon histological examination we found that DARC-expressing tumors had significantly more necrosis and decreased tumor cellularity, as compared to control tumors. Expression of DARC by NSCLC cells was also associated with a decrease in tumor-associated vasculature and a reduction in metastatic potential. Conclusions The expression of DARC in the context of NSCLC tumors may act as a chemokine decoy receptor and interferes with normal tumor growth and chemokine-induced tumor neovascularization.

Published
2004
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49. Focal Adhesion Kinase Inhibitors in Combination with Erlotinib Demonstrate Enhanced Anti-Tumor Activity in Non-Small Cell Lung Cancer

Author

Howe, Grant A., primary, Xiao, Bin, additional, Zhao, Huijun, additional, Al-Zahrani, Khalid N., additional, Hasim, Mohamed S., additional, Villeneuve, James, additional, Sekhon, Harmanjatinder S., additional, Goss, Glenwood D., additional, Sabourin, Luc A., additional, Dimitroulakos, Jim, additional, and Addison, Christina L., additional

Published
2016
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