alexa Characterization of Treatment Response to Recombinant Interferon-a2b in Osteosarcoma Xenografts
ISSN: 1948-5956

Journal of Cancer Science & Therapy
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Research Article

Characterization of Treatment Response to Recombinant Interferon-a2b in Osteosarcoma Xenografts

Christoph R Müller1, Heidi M Namløs1, Johan Bjerner2, Ingrid HG Østensen3, Gunnar Sæter4, Sigbjørn Smeland4, Øyvind S Bruland4,5 and Ola Myklebost1,3*

1Institute for Cancer research, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway

2Department of Medical Biochemistry, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway

3Norwegian Microarray Consortium, Department of Molecular Biosciences, University of Oslo, Norway

4Department of Oncology, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway

5Faculty of Medicine, University of Oslo, Norway

*Corresponding Author:
Dr. Ola Myklebost, Myklebost
Institute for Cancer research, The Norwegian Radium Hospital
Oslo University Hospital,N-0310 Oslo, Norway
Tel: +47:22781779
Fax: +47:22781795
E-Mail: [email protected]

Received Date: October 12, 2009; Accepted Date: February 20, 2010; Published Date:February 20, 2010

Citation: Müller CR, Namløs HM, Bjerner J, Østensen IHG, Sæter G, et al. (2010) Characterization of Treatment Response to Recombinant Interferon- 2b in Osteosarcoma Xenografts. J Cancer Sci Ther 1: 016-025. doi: 10.4172/1948-5956.1000018

Copyright: © 2010 Müller CR, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Interferons (IFNs) may target cancer cells both through their regulation of the immune response, effect on angiogenesis and through direct effect on cancer cells. Treatment response has been demonstrated in osteosarcoma patients, but tumour resistance to IFN-a is common. Hence, understanding the molecular mechanisms involved in response and resistance is essential for improving therapeutic efficacy. Of five xenografts screened for specific growth delay in response to treatment with unconjugated and PEGylated IFN-a2b, one displayed growth inhibition and tumour shrinkage. Growth inhibition increased on a dosing schedule of PEGylated IFN every third day. Xenografts resistant to PEGylated IFN were similarly resistant to unconjugated IFN. Combination treatment with IFN-a2b and doxorubicin resulted in improved growth control rates. Transcriptional profiling analysis of the one sensitive and two resistant xenografts identified a common set of 79 genes significantly affected by IFN-a2b treatment independent of tumour growth inhibition. All but four of the 79 genes were up-regulated. The majority of these genes were well characterized IFN-stimulated genes and core members of the IFN-a signalling pathway. The expression of a set of 128 unique genes changed only in the sensitive xenograft; 52/128 genes were up-regulated. The specific geneexpression pattern seen in the responsive xenograft identified possible pathways important for the antitumor effect of IFN-a in osteosarcoma, including ssubsets of genes involved in cell adhesion and osteogenic tissue development. The observed improved control rates of combined treatment with IFN and doxorubicin are encouraging and should be further explored.

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