Abstract | BACKGROUND: METHODS: We measured the level of EMAP-II in a TNF-resistant soft tissue sarcoma. We subsequently stabile-transfected this cell line with a retroviral construct containing the EMAP gene. In an extremity perfusion model in tumor-bearing rats, we measured response rates to TNF therapy. RESULTS: Functional EMAP-II production was increased after this transfection. Immunostaining of paraffin-embedded tumor tissue sections in rats showed an overexpression of human EMAP-II. Results of the TNF perfusions in rats suggest that this tumor is more sensitive to TNF therapy. CONCLUSIONS:
EMAP-II is produced in various levels. One can increase the sensitivity of tumor for TNF therapy in vivo by upregulating the EMAP-II production. This result leaves an opportunity for enhanced TNF response of tumors in future settings.
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Authors | T E Lans, T L M ten Hagen, R van Horssen, P C Wu, S T van Tiel, S K Libutti, H R Alexander, A M M Eggermont |
Journal | Annals of surgical oncology
(Ann Surg Oncol)
Vol. 9
Issue 8
Pg. 812-9
(Oct 2002)
ISSN: 1068-9265 [Print] United States |
PMID | 12374666
(Publication Type: Journal Article)
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Chemical References |
- Antineoplastic Agents
- Cytokines
- Neoplasm Proteins
- RNA-Binding Proteins
- Tumor Necrosis Factor-alpha
- small inducible cytokine subfamily E, member 1
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Topics |
- Animals
- Antineoplastic Agents
(administration & dosage)
- Chemotherapy, Cancer, Regional Perfusion
(methods)
- Cytokines
(genetics, metabolism)
- Disease Models, Animal
- Extremities
- Male
- Neoplasm Proteins
(genetics, metabolism)
- RNA-Binding Proteins
(genetics, metabolism)
- Rats
- Rats, Inbred BN
- Sarcoma
(therapy)
- Soft Tissue Neoplasms
(therapy)
- Transfection
(methods)
- Tumor Necrosis Factor-alpha
(administration & dosage)
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