Mechanism of cell death induced by the novel enzyme-prodrug combination, nitroreductase/CB1954, and identification of synergism with 5-fluorouracil
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L. Young | A. Milner | D. H. Palmer | D. Kerr
[1] M. Fukushima,et al. Metabolic basis of the synergistic antitumor activities of 5-fluorouracil and cisplatin in rodent tumor models in vivo , 2004, Cancer Chemotherapy and Pharmacology.
[2] D. Kerr,et al. Immune enhancement of nitroreductase‐induced cytotoxicity: Studies using a bicistronic adenovirus vector , 2003, International journal of cancer.
[3] D. Kerr,et al. Induction of apoptosis by chemotherapeutic drugs: the role of FADD in activation of caspase-8 and synergy with death receptor ligands in ovarian carcinoma cells , 2002, Cell Death and Differentiation.
[4] D. Kerr,et al. Virus-directed, enzyme prodrug therapy with nitroimidazole reductase: a phase I and pharmacokinetic study of its prodrug, CB1954. , 2001, Clinical cancer research : an official journal of the American Association for Cancer Research.
[5] Cun-Yu Wang,et al. Nuclear Factor-κB-inducible Death Effector Domain-containing Protein Suppresses Tumor Necrosis Factor-mediated Apoptosis by Inhibiting Caspase-8 Activity* , 2001, The Journal of Biological Chemistry.
[6] Y. Lazebnik,et al. Deficiency in caspase-9 or caspase-3 induces compensatory caspase activation , 2000, Nature Medicine.
[7] I. Tannock,et al. A controlled trial of intratumoral ONYX-015, a selectively-replicating adenovirus, in combination with cisplatin and 5-fluorouracil in patients with recurrent head and neck cancer , 2000, Nature Medicine.
[8] D. Kerr,et al. Sensitisation of human carcinoma cells to the prodrug CB1954 by adenovirus vector‐mediated expression of E. coli nitroreductase , 2000, International journal of cancer.
[9] D. Kerr,et al. Expression of Escherichia coli B nitroreductase in established human tumor xenografts in mice results in potent antitumoral and bystander effects upon systemic administration of the prodrug CB1954 , 2000, Cancer Gene Therapy.
[10] R. Steinman,et al. The Induction of Tolerance by Dendritic Cells That Have Captured Apoptotic Cells , 2000, The Journal of experimental medicine.
[11] S. Fulda,et al. Functional CD95 ligand and CD95 death-inducing signaling complex in activation-induced cell death and doxorubicin-induced apoptosis in leukemic T cells. , 2000, Blood.
[12] A. Melcher,et al. Apoptosis or necrosis for tumor immunotherapy: what's in a name? , 1999, Journal of Molecular Medicine.
[13] A. López-Rivas,et al. p53-mediated up-regulation of CD95 is not involved in genotoxic drug-induced apoptosis of human breast tumor cells , 1999, Cell Death and Differentiation.
[14] M MacFarlane,et al. Distinct Caspase Cascades Are Initiated in Receptor-mediated and Chemical-induced Apoptosis* , 1999, The Journal of Biological Chemistry.
[15] M. Peter,et al. Activation of the CD95 (APO-1/Fas) pathway in drug- and γ-irradiation-induced apoptosis of brain tumor cells , 1998, Cell Death and Differentiation.
[16] C. Y. Wang,et al. NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation. , 1998, Science.
[17] N. D’alessandro,et al. The CD95/CD95 ligand system is not the major effector in anticancer drug-mediated apoptosis , 1998, Cell Death and Differentiation.
[18] I. McNeish,et al. Virus directed enzyme prodrug therapy for ovarian and pancreatic cancer using retrovirally delivered E. coli nitroreductase and CB1954 , 1998, Gene Therapy.
[19] S. Fulda,et al. Chemosensitivity of solid tumor cells in vitro is related to activation of the CD95 system , 1998, International journal of cancer.
[20] M. Martínez-Lorenzo,et al. Doxorubicin‐induced apoptosis in human T‐cell leukemia is mediated by caspase‐3 activation in a Fas‐independent way , 1997, FEBS letters.
[21] G. Schuurhuis,et al. The Pgp specific combination Syto-R16/PSC833 detects early apoptosis in CD34 positive progenitor cells , 1997 .
[22] I. Herr,et al. The CD95 (APO-1/Fas) system mediates drug-induced apoptosis in neuroblastoma cells. , 1997, Cancer research.
[23] R. Greil,et al. Drug-induced apoptosis is associated with enhanced Fas (Apo-1/CD95) ligand expression but occurs independently of Fas (Apo-1/CD95) signaling in human T-acute lymphatic leukemia cells. , 1997, Cancer research.
[24] W. Earnshaw,et al. Comparison of apoptosis in wild-type and Fas-resistant cells: chemotherapy-induced apoptosis is not dependent on Fas/Fas ligand interactions. , 1997, Blood.
[25] E. Solary,et al. Sensitization of cancer cells treated with cytotoxic drugs to fas-mediated cytotoxicity. , 1997, Journal of the National Cancer Institute.
[26] C. Link,et al. Gene therapy for colon cancer with the herpes simplex thymidine kinase gene , 1997, Journal of surgical oncology.
[27] I. Herr,et al. Involvement of the CD95 (APO–1/Fas) receptor/ligand system in drug–induced apoptosis in leukemia cells , 1996, Nature Medicine.
[28] C. Springer,et al. Expression of the bacterial nitroreductase enzyme in mammalian cells renders them selectively sensitive to killing by the prodrug CB1954. , 1995, European journal of cancer.
[29] B. Kramer,et al. Combination cytotoxic effects of cis-diamminedichloroplatinum(II) and 5-fluorouracil with and without leucovorin against human non-small cell lung cancer cell lines. , 1993, Cancer research.
[30] G. Wilkinson,et al. Constitutive and enhanced expression from the CMV major IE promoter in a defective adenovirus vector. , 1992, Nucleic acids research.
[31] T. Chou,et al. Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors. , 1984, Advances in enzyme regulation.