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8 results on '"Aird, R. E."'

4. MDR1 deficiency impairs mitochondrial homeostasis and promotes intestinal inflammation

Author

Ho, G-T, primary, Aird, R E, additional, Liu, B, additional, Boyapati, R K, additional, Kennedy, N A, additional, Dorward, D A, additional, Noble, C L, additional, Shimizu, T, additional, Carter, R N, additional, Chew, E T S, additional, Morton, N M, additional, Rossi, A G, additional, Sartor, R B, additional, Iredale, J P, additional, and Satsangi, J, additional

Published
2018
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7. Inhibition of Cancer Cell Growth by Ruthenium(II) Arene Complexes

Author

Morris, R. E., Aird, R. E., Murdoch, P. del Socorro, Chen, H., Cummings, J., Hughes, N. D., Parsons, S., Parkin, A., Boyd, G., Jodrell, D. I., and Sadler, P. J.

Abstract

Inhibition of the growth of the human ovarian cancer cell line A2780 by organometallic ruthenium(II) complexes of the type [(η6-arene)Ru(X)(Y)(Z)], where arene is benzene or substituted benzene, X, Y, and Z are halide, acetonitrile, or isonicotinamide, or X,Y is ethylenediamine (en) or N-ethylethylenediamine, has been investigated. The X-ray crystal structures of the complexes [(η6-p-cymene)Ru(en)Cl]PF6 (5), [(η6-p-cymene)RuCl2(isonicotinamide)] (7), and [(η6-biphenyl)Ru(en)Cl]PF6 (9) are reported. They have “piano stool” geometries with η6 coordination of the arene ligand. Complexes with X,Y as a chelated en ligand and Z as a monofunctional leaving group had the highest activity. Complexes 5, 6 (the iodo analogue of 5), 9, and 10 (ethylethylenediamine analogue of 9) were as active as carboplatin. Hydrolysis of the reactive Ru−Cl bond in complex 5 was detected by HPLC but was suppressed by the addition of chloride ions. Complex 5 binds strongly and selectively to G bases on DNA oligonucleotides to form monofunctional adducts. No inhibition of topoisomerase I or II by complexes 5, 6, or 9 was detected. These chelated Ru(II) arene complexes have potential as novel metal-based anticancer agents with a mechanism of action different from that of the Ru(III) complex currently on clinical trial.

Published
2001

8. A clinical study assessing the tolerability and biological effects of infliximab, a TNF-alpha inhibitor, in patients with advanced cancer.

Author

Brown ER, Charles KA, Hoare SA, Rye RL, Jodrell DI, Aird RE, Vora R, Prabhakar U, Nakada M, Corringham RE, DeWitte M, Sturgeon C, Propper D, Balkwill FR, and Smyth JF

Subjects
Adult, Aged, Antibodies, Monoclonal administration & dosage, Antibodies, Monoclonal adverse effects, C-Reactive Protein analysis, Chemokine CCL2 blood, Dose-Response Relationship, Drug, Drug Administration Schedule, Female, Humans, Infliximab, Infusions, Intravenous, Interleukin-6 blood, Linear Models, Male, Middle Aged, Neoplasms blood, Neoplasms pathology, Sensitivity and Specificity, Stomatitis chemically induced, Treatment Outcome, Tumor Necrosis Factor-alpha blood, Antibodies, Monoclonal therapeutic use, Drug Hypersensitivity, Hypersensitivity, Delayed chemically induced, Neoplasms drug therapy, Tumor Necrosis Factor-alpha antagonists & inhibitors
Abstract

Background: Tumour necrosis factor-alpha (TNF-alpha) is an important regulator of the chronic inflammation contributing to tumour progression. Infliximab, an anti-TNF-alpha monoclonal antibody was investigated in this trial of patients with advanced cancer. The primary objectives were to determine the safety profile and biological response of infliximab in a cancer population. Clinical response was a secondary objective., Patients and Methods: Forty-one patients received infliximab at 5 mg/kg (n = 21) or 10 mg/kg (n = 20) i.v. at 0 and 2 weeks and then every 4 weeks. Post-treatment samples were measured for changes in plasma and serum TNF-alpha, CCL2, IL-6 and C-reactive protein (CRP)., Results: Infliximab was well tolerated with no dose-limiting toxic effects. At both doses of infliximab, neutralisation of serum TNF-alpha was observed after 1 h while plasma CCL2, IL-6 and serum CRP were decreased 24 and 48 h following infliximab administration. Seven patients experienced disease stablisation (range 10-50+ weeks). There was no evidence of disease acceleration in any patient., Conclusions: Infliximab treatment was safe and well tolerated in patients with advanced cancer. There was evidence of biological activity with baseline TNF-alpha and CCL2 being correlated with infliximab response.

Published
2008
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