Anti-interleukin-6 monoclonal antibody induces regression of human prostate cancer xenografts in nude mice
dc.contributor.author | Smith, Peter C. | en_US |
dc.contributor.author | Keller, Evan T. | en_US |
dc.date.accessioned | 2006-04-19T13:49:08Z | |
dc.date.available | 2006-04-19T13:49:08Z | |
dc.date.issued | 2001-06-15 | en_US |
dc.identifier.citation | Smith, Peter C.; Keller, Evan T. (2001)."Anti-interleukin-6 monoclonal antibody induces regression of human prostate cancer xenografts in nude mice." The Prostate 48(1): 47-53. <http://hdl.handle.net/2027.42/34760> | en_US |
dc.identifier.issn | 0270-4137 | en_US |
dc.identifier.issn | 1097-0045 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/34760 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=11391686&dopt=citation | en_US |
dc.description.abstract | BACKGROUND Despite clinical associations and in vitro data suggesting that autocrine interleukin-6 (IL-6) production contributes to prostate cancer progression or chemotherapy resistance, there have been no reports that explore the role of IL-6 on prostate tumors in vivo. In the present study, we investigated the effect of IL-6 inhibition on the growth of human prostate cancer xenografts in nude mice. METHODS To determine if autocrine IL-6 production contributes to prostate cancer growth and chemotherapy resistance in vivo, xenografts of a human prostate cancer cell line that produces IL-6 (PC-3) were established in nude mice. The mice were randomly divided into four treatment groups: (1) saline (vehicle control) + murine IgG (isotype control); (2) etoposide + murine IgG; (3) saline + anti-IL-6 monoclonal antibody; and (4) etoposide + anti-IL-6 monoclonal antibody. Tumors were measured twice weekly during a 4-week treatment period. At the conclusion of the study, all mice were sacrificed, and in addition to final volume, tumors were evaluated for the degree of apoptosis by TUNEL analysis. RESULTS Anti-IL-6 Ab (with saline or etoposide) induced tumor apoptosis and regression (∼60% compared to initial tumor size). Etoposide alone did not induce tumor regression or apoptosis in this animal model, and there was no synergy between anti-IL-6 Ab and etoposide. CONCLUSIONS These studies suggest that IL-6 contributes to prostate cancer growth in vivo, and that targeting IL-6 may contribute to prostate cancer therapy. Prostate 48:47–53, 2001. © 2001 Wiley-Liss, Inc. | en_US |
dc.format.extent | 186463 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | John Wiley & Sons, Inc. | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Cancer Research, Oncology and Pathology | en_US |
dc.title | Anti-interleukin-6 monoclonal antibody induces regression of human prostate cancer xenografts in nude mice | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Unit for Laboratory Animal Medicine, University of Michigan, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Unit for Laboratory Animal Medicine, University of Michigan, Ann Arbor, Michigan ; Department of Pathology, University of Michigan, Ann Arbor, Michigan ; Connective Tissue Oncology, University of Michigan, Ann Arbor, Michigan ; Institute of Gerontology, University of Michigan, Ann Arbor, Michigan ; Unit for Laboratory Animal Medicine, and Department of Pathology, University of Michigan School of Medicine, 1500 E. Medical Ctr. Dr., Ann Arbor, MI 48109-0940. | en_US |
dc.identifier.pmid | 11391686 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/34760/1/1080_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/pros.1080 | en_US |
dc.identifier.source | The Prostate | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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