Rabbit cytochrome P450 4B1: A novel prodrug activating gene for pharmacogene therapy of hepatocellular carcinoma
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[1] R. Warnick,et al. In vitro evidence that metabolic cooperation is responsible for the bystander effect observed with HSV tk retroviral gene therapy. , 1993, Human gene therapy.
[2] R. Arceci,et al. Clinical relevance of transmembrane drug efflux as a mechanism of multidrug resistance. , 1998, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[3] I. Pastan,et al. P-glycoprotein and multidrug resistance. , 1996, Current opinion in genetics & development.
[4] M. Boyd,et al. In vivo studies on the relationship between target organ alkylation and the pulmonary toxicity of a chemically reactive metabolite of 4-ipomeanol. , 1978, The Journal of pharmacology and experimental therapeutics.
[5] K. Dobberstein,et al. A chimeric fusion protein of cytochrome CYP4B1 and green fluorescent protein for detection of pro-drug activating gene delivery and for gene therapy in malignant glioma. , 1998, Advances in experimental medicine and biology.
[6] P. Galle,et al. Drug-induced apoptosis in hepatoma cells is mediated by the CD95 (APO-1/Fas) receptor/ligand system and involves activation of wild-type p53. , 1997, The Journal of clinical investigation.
[7] B. O’Malley,et al. Combination gene therapy for oral cancer in a murine model. , 1996, Cancer research.
[8] J. Trinchet,et al. Treatment of hepatocellular carcinoma in patients with cirrhosis. , 1997, Journal of hepatology.
[9] H. Blum,et al. Primary hepatocellular carcinoma. , 1991, The New England journal of medicine.
[10] J. Prieto,et al. Gene Therapy of Liver Tumors: Principles and Applications , 1998, Digestion.
[11] J. Roh,et al. Combined use of tamoxifen, cyclosporin A, and verapamil for modulating multidrug resistance in human hepatocellular carcinoma cell lines. , 1993, Yonsei medical journal.
[12] S. Hirohashi,et al. p53 gene mutation spectrum in hepatocellular carcinoma. , 1992, Cancer research.
[13] D. Dinsdale,et al. CYP4B1 activates 4-ipomeanol in rat lung. , 1993, Toxicology and applied pharmacology.
[14] V. Mazzaferro,et al. Liver transplantation for the treatment of small hepatocellular carcinomas in patients with cirrhosis. , 1996, The New England journal of medicine.
[15] D. Israeli,et al. p53 Activates the CD95 (APO-1/Fas) Gene in Response to DNA Damage by Anticancer Drugs , 1998, The Journal of experimental medicine.
[16] S. Kuriyama,et al. Bystander effect caused by suicide gene expression indicates the feasibility of gene therapy for hepatocellular carcinoma , 1995, Hepatology.
[17] M. Christian,et al. Phase I study of a five-day dose schedule of 4-Ipomeanol in patients with non-small cell lung cancer. , 1998, Clinical cancer research : an official journal of the American Association for Cancer Research.
[18] X. Breakefield,et al. Synergistic anticancer effects of ganciclovir/thymidine kinase and 5-fluorocytosine/cytosine deaminase gene therapies. , 1998, Journal of the National Cancer Institute.
[19] J. Wands,et al. p53 mutation in hepatocellular carcinoma after aflatoxin exposure , 1991, The Lancet.
[20] C. Contant,et al. Combination suicide and cytokine gene therapy for hepatic metastases of colon carcinoma: sustained antitumor immunity prolongs animal survival. , 1996, Cancer research.
[21] M. Boyd,et al. The in vitro formation of glutathione conjugates with the microsomally activated pulmonary bronchiolar aklylating agent and cytotoxin, 4-ipomeanol. , 1980, The Journal of pharmacology and experimental therapeutics.
[22] J. Gebert,et al. Double suicide gene (cytosine deaminase and herpes simplex virus thymidine kinase) but not single gene transfer allows reliable elimination of tumor cells in vivo. , 1998, Human gene therapy.
[23] J. Wands,et al. The increasing incidence of hepatocellular carcinoma. , 1999, The New England journal of medicine.
[24] C. Wolf,et al. Cytochrome p-450: localization in rabbit lung. , 1980, Science.
[25] Bert Vogelstein,et al. p53 function and dysfunction , 1992, Cell.
[26] C. Qian,et al. Induction of sensitivity to ganciclovir in human hepatocellular carcinoma cells by adenovirus‐mediated gene transfer of herpes simplex virus thymidine kinase , 1995, Hepatology.
[27] F. Ponchel,et al. Hepatocarcinoma-specific mutant p53-249ser induces mitotic activity but has no effect on transforming growth factor beta 1-mediated apoptosis. , 1994, Cancer research.
[28] K. Dobberstein,et al. New prodrug activation gene therapy for cancer using cytochrome P450 4B1 and 2-aminoanthracene/4-ipomeanol. , 1998, Human gene therapy.
[29] H. Wakimoto,et al. In vivo gene therapy for alpha-fetoprotein-producing hepatocellular carcinoma by adenovirus-mediated transfer of cytosine deaminase gene. , 1997, Cancer research.
[30] J. Wands,et al. Selective G to T mutations of p53 gene in hepatocellular carcinoma from southern Africa , 1991, Nature.
[31] E K Fishman,et al. Phase I and pharmacological study of the pulmonary cytotoxin 4-ipomeanol on a single dose schedule in lung cancer patients: hepatotoxicity is dose limiting in humans. , 1993, Cancer research.
[32] M. Boyd. Role of metabolic activation in the pathogenesis of chemically induced pulmonary disease: mechanism of action of the lung-toxic furan, 4-ipomeanol. , 1976, Environmental health perspectives.
[33] H. El‐Serag,et al. Rising incidence of hepatocellular carcinoma in the United States. , 1999, The New England journal of medicine.
[34] M. Boyd,et al. Species and strain differences in target organ alkylation and toxicity by 4-ipomeanol. Predictive value of covalent binding in studies of target organ toxicities by reactive metabolites. , 1979, Biochemical pharmacology.
[35] J. Bruix,et al. Treatment of hepatocellular carcinoma. , 2006, Critical reviews in oncology/hematology.
[36] K. Korzekwa,et al. Metabolic activation of 4-ipomeanol by complementary DNA-expressed human cytochromes P-450: evidence for species-specific metabolism. , 1991, Cancer research.
[37] J. Gu,et al. Overexpression of the MDR1 gene and P-glycoprotein in human hepatocellular carcinoma. , 1992, Journal of the National Cancer Institute.
[38] S. Freeman,et al. The "bystander effect": tumor regression when a fraction of the tumor mass is genetically modified. , 1993, Cancer research.