Document Detail


Frequent, moderate-dose cyclophosphamide administration improves the efficacy of cytochrome P-450/cytochrome P-450 reductase-based cancer gene therapy.
MedLine Citation:
PMID:  11389073     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Transduction of tumor cells with a cyclophosphamide (CPA)-activating cytochrome P-450 (P450) gene provides the capacity for localized prodrug activation and greatly sensitizes solid tumors to CPA treatment in vivo. The therapeutic impact of this P450-based cancer gene therapy strategy can be substantially enhanced by cotransduction of P450 reductase, a rate-limiting component of P450-dependent intratumoral CPA activation. The present study examined the possibility of further improving P450/P450 reductase-based gene therapy by using a novel schedule of CPA administration, involving repeated CPA injection every 6 days and previously shown to have an antiangiogenic component. 9L gliosarcoma cells transduced with the CPA-activating enzyme couple P450 2B6/P450 reductase and grown s.c. in immunodeficient severe combined immunodeficient (scid) mice were repeatedly challenged with 140 mg/kg CPA every 6 days. Full tumor regression leading to eradication of six of eight tumors was observed when the tumor size at the time of initial drug treatment was approximately 400 mm(3) (approximately 1.5% of body weight). Little or no overt toxicity of the repeated CPA treatment regimen was observed. The same CPA schedule was much less effective in inducing regression of 9L tumors that were not transduced with P450/P450 reductase. Repeated CPA treatment of mice bearing large, late-stage P450/P450 reductase-transduced tumors (approximately 9-16% of body weight) resulted in major (> or =95%) regression in 15 of 16 tumors, with tumor eradication observed in 2 cases. Although CPA resistance was found to emerge in the population of P450/P450 reductase-transduced tumors, this resistance primarily involved a loss of expression of the transduced P450 and/or P450 reductase gene, rather than development of intrinsic cellular resistance to the activated form of CPA. These findings demonstrate that repeated CPA treatment on a 6 day schedule can be highly effective when combined with P450/P450 reductase gene therapy and suggest that repeated transduction of tumors with prodrug-activation genes may be necessary to achieve tumor eradication and a sustained therapeutic response.
Authors:
Y Jounaidi; D J Waxman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cancer research     Volume:  61     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-06-04     Completed Date:  2001-06-21     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4437-44     Citation Subset:  IM    
Affiliation:
Division of Cell and Molecular Biology, Department of Biology, Boston University, Boston, MA 02215, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antineoplastic Agents, Alkylating / administration & dosage*,  pharmacokinetics
Biotransformation
Brain Neoplasms / drug therapy,  enzymology,  genetics,  therapy
Combined Modality Therapy
Cyclophosphamide / administration & dosage*,  pharmacokinetics
Cytochrome P-450 Enzyme System / genetics*,  metabolism
Dose-Response Relationship, Drug
Drug Administration Schedule
Gene Therapy / methods*
Gliosarcoma / drug therapy,  enzymology,  genetics,  therapy
Humans
Male
Mice
Mice, Inbred ICR
NADPH-Ferrihemoprotein Reductase / genetics*,  metabolism
Rats
Transduction, Genetic
Grant Support
ID/Acronym/Agency:
CA49248/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antineoplastic Agents, Alkylating; 50-18-0/Cyclophosphamide; 9035-51-2/Cytochrome P-450 Enzyme System; EC 1.6.2.4/NADPH-Ferrihemoprotein Reductase

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