Another mechanism causing the bystander effect besides the gap junction's role during the glioma gene therapy with HSV-TK/GCV system

Advances in Experimental Medicine and Biology

Volumn 451, Issue , 1998, Pages 133-138

  Du, Liping ^a   Bai, Shaochun ^a   Whittle, Ian R ^b   He, Lin ^a  

^a INSTITUTE OF GEOLOGY AND GEOPHYSICS   (China)

^b Western Hospital   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

GANCICLOVIR; THYMIDINE KINASE;

ANIMAL CELL; APOPTOSIS; ARTICLE; CELL GROWTH; CELL STRUCTURE; COCULTURE; CONTROLLED STUDY; GAP JUNCTION; GENE THERAPY; GLIOMA; GLIOMA CELL; GROWTH INHIBITION; HERPES SIMPLEX VIRUS; NONHUMAN; PRIORITY JOURNAL; RAT;

EID: 0031724007     PISSN: 00652598     EISSN: None     Source Type: Book Series    
DOI: 10.1007/978-1-4615-5357-1_21     Document Type: Article

References (8)

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3. Izquierdo M et al. Human malignant brain tumor response to herpes simplex thymidine kinase(HSV tk)ganciclovir gene therapy.Gene Ther 1996; 3: 491-495.
4. Freeman S M et al. The 'bystander effect': tumor regression when a fraction of tumor mass is genetically modifided.Cancer Res 1993; 53: 5274-5283.
5. Mesnil M, et al. Bystander killing of cancer cells by herpes simplex virus thymidine kinase gene is mediated by connexins. Proc Natl Acad Sci USA 1996; 93: 1831-1835
6. Akio Ido, Keisuke nakata, Yuji kato et al. Gene Therapy for Hepatoma Cells Using a Retrovirus Vector Carring Herpes Simplex Virus Thymidine Kinase Gene under the Control of Human α-Fetoprotein Gene Promoter. Cancer Res 1995; 55: 3105-3109.
7. Dilber MS et al. Gap junctions promote the bystander effect of herpes simplex virus thymidine kinase in vivo. Cancer Res 1997; 57: 1523-1528.
8. Julian K, Wu, M. D., William G. Cano, M. D., et al. Bystander atumoricial effect in the Treatment of Experimental Brain tumors. Neurosurgery 1994; 33(6): 1094-1102.