Document Detail


Thymidine kinase activation of ganciclovir in recurrent malignant gliomas: a gene-marking and neuropathological study.
MedLine Citation:
PMID:  10794295     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECT: The gene therapy paradigm of intratumoral activation of ganciclovir (GCV) following transduction of tumor cells by retroviral vectors bearing the thymidine kinase (tk) gene has produced dramatic remissions of malignant gliomas in animal models. In human trials, although the technique has been deemed safe, little antitumor effect has been demonstrated. To evaluate the basis of this inefficacy in human gliomas, the authors conducted a gene-marking trial involving neuropathological and biochemical studies of treated tumor specimens. METHODS: Five patients with malignant recurrent gliomas underwent stereotactic biopsy sampling and intratumoral implantation procedures with three aliquots of 10(6) vector-producing cells (VPCs) in columns. After 5 days, the tumor was resected and the tumor bed reimplanted with VPCs, and a course of GCV was given. Patients received clinical and radiological follow up for 6 months. Tumor specimens were analyzed neuropathologically and for tk gene expression by anti-TK immunohistochemistry and TK enzymatic activity. Four patients tolerated the treatment well but experienced tumor progression. The other developed an abscess after the second operation and died. Increased TK enzymatic activity was demonstrated in the one tumor specimen analyzed. Immunohistochemical evidence of tk gene expression was limited to VPCs. Transduction of tumor cells was not seen. Viable tumor cells were seen near VPCs containing TK. The lymphocytic immune response was mild. CONCLUSIONS: Except for the risk of infection inherent in reoperation, this tk-GCV paradigm was both feasible and safe. Pathological studies indicated that limited dissemination of VPCs and vector from the infusion site and failure to transduce tumor cells with the tk gene are major barriers to efficacy.
Authors:
G R Harsh; T S Deisboeck; D N Louis; J Hilton; M Colvin; J S Silver; N H Qureshi; J Kracher; D Finkelstein; E A Chiocca; F H Hochberg
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of neurosurgery     Volume:  92     ISSN:  0022-3085     ISO Abbreviation:  J. Neurosurg.     Publication Date:  2000 May 
Date Detail:
Created Date:  2000-05-17     Completed Date:  2000-05-17     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0253357     Medline TA:  J Neurosurg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  804-11     Citation Subset:  AIM; IM    
Affiliation:
Department of Neurology, Massachusetts General Hospital Brain Tumor Center, USA. gharsh@stanford.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Animals
Antineoplastic Agents / therapeutic use*
Antiviral Agents / therapeutic use*
Brain Abscess / etiology
Brain Neoplasms / pathology,  surgery,  therapy*
Disease Models, Animal
Disease Progression
Feasibility Studies
Female
Follow-Up Studies
Ganciclovir / therapeutic use*
Genetic Vectors
Glioma / pathology,  surgery,  therapy*
Humans
Immunohistochemistry
Injections, Intralesional
Lymphocytes / immunology
Male
Middle Aged
Neoplasm Recurrence, Local / pathology,  surgery,  therapy*
Remission Induction
Retroviridae / genetics
Stereotaxic Techniques
Thymidine Kinase / genetics*
Transduction, Genetic
Grant Support
ID/Acronym/Agency:
5PO1CA69246/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Antiviral Agents; 82410-32-0/Ganciclovir; EC 2.7.1.21/Thymidine Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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