Tumor-cell resistance to death receptor–induced apoptosis through mutational inactivation of the proapoptotic Bcl-2 homolog Bax (original) (raw)

• Ashkenazi, A. & Dixit, V.M. Death receptors: signaling and modulation. Science 281, 1305–1308 (1998).
  Article CAS Google Scholar
• Green, D. Apoptotic pathways: paper wraps stone blunts scissors. Cell 102, 1–4 (2000).
  Article CAS Google Scholar
• Li, H., Zhu, H., Xu, C.-J. & Yuan, J. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway to apoptosis. Cell 94, 491–501 (1998).
  Article CAS Google Scholar
• Luo, X., Budihardjo, I., Zou, H., Slaughter, C. & Wang, X. Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors. Cell 94, 481–490 (1998).
  Article CAS Google Scholar
• Gross, A. et al. Caspase cleaved Bid targets mitochondria and is required for cytochrome c release, while Bcl-XL prevents this release but not tumor necrosis factor-R1/Fas death. J. Biol. Chem. 274, 1156–1163 (1999).
  Article CAS Google Scholar
• Roy, S. & Nicholson, D. Cross-talk in cell death signaling. J. Exp. Med. 192, F21–F25 (2000).
  Article CAS Google Scholar
• Eskes, R., Desagher, S., Antonsson, B. & Martinou, J. Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane. Mol. Cell. Biol. 20, 929–935 (2000).
  Article CAS Google Scholar
• Wei, M. et al. tBID, a membrane targeted death ligand, oligomerizes Bak to release cytochrome c. Genes Dev. 14, 2060–2071 (2000).
  CAS PubMed PubMed Central Google Scholar
• Yin, X.-M. et al. Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis. Nature 400, 886–891 (1999).
  Article CAS Google Scholar
• Lindsten, T. et al. The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues. Molec. Cell 6, 1389–1399 (2000).
  Article CAS Google Scholar
• Wei, M.C. et al. Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death. Science 292, 727–730 (2001).
  Article CAS Google Scholar
• Nicholson, D.W. From bench to clinic with apoptosis-based therapeutic agents. Nature 407, 810–816 (2000).
  Article CAS Google Scholar
• Lengauer, C., Kinzler, K. & Vogelstein, B. Genetic instabilities in human cancers. Nature 396, 643–649 (1998).
  Article CAS Google Scholar
• Rampino, N. et al. Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype. Science 275, 967–969 (1997).
  Article CAS Google Scholar
• Zhang, L., Yu, J., Park, B., Kinzler, K. & Vogelstein, B. Role of BAX in the apoptotic response to anticancer agents. Science 290, 989–992 (2000).
  Article CAS Google Scholar
• Ionov, Y., Yamamoto, H., Krajewski, S., Reed, J.C. & Perucho, M. Mutational inactivation of the proapoptotic gene Bax confers selective advantage during tumor clonal evolution. Proc. Natl. Acad. Sci. USA 97, 10872–10877 (2000).
  Article CAS Google Scholar
• Perucho, M. Cancer of the microsatellite mutator phenotype. Biol. Chem. 377, 675–684 (1996).
  CAS PubMed Google Scholar
• Kischkel, F.C. et al. Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signaling complex (DISC) with the receptor. EMBO J. 14, 5579–5588 (1995).
  Article CAS Google Scholar
• Kischkel, F.C. et al. Apo2L/TRAIL-dependent recruitment of endogenous FADD and caspase-8 to death receptors 4 and 5. Immunity 12, 611–620 (2000).
  Article CAS Google Scholar
• Sprick, M.R. et al. FADD/MORT1 and Caspase-8 are recruited to TRAIL receptors 1 and 2 and are essential for apoptosis mediated by TRAIL receptor 2. Immunity 12, 599–609 (2000).
  Article CAS Google Scholar
• Bodmer, J.L. et al. TRAIL receptor-2 signals apoptosis through FADD and caspase-8. Nature Cell Biol. 2, 241–243 (2000).
  Article CAS Google Scholar
• Boldin, M., Goncharov, T., Goltsev, Y. & Wallach, D. Involvement of MACH, a novel MORT1/FADD-interacting protease, in FAS/APO-1-and TNF receptor-induced cell death. Cell 85, 803–815 (1996).
  Article CAS Google Scholar
• Muzio, M. et al. FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recurited to the CD95 (Fas/APO1) death-inducing signaling complex. Cell 85, 817–827 (1996).
  Article CAS Google Scholar
• Evan, G. & Littlewood, T. A matter of life and cell death. Science 281, 1317–1322 (1998).
  Article CAS Google Scholar
• Wu, G.S. et al. KILLER/DR5 is a DNA damage-inducible p53-regulated death receptor gene. Nature Genet. 17, 141–143 (1997).
  Article CAS Google Scholar
• Scaffidi, C. et al. Differential modulation of apoptosis sensitivity in CD95 type I and type II cells. J. Biol. Chem. 274, 22532–22538 (1999).
  Article CAS Google Scholar
• Pitti, R. et al. Genomic amplification of a decoy receptor for Fas ligand in lung and colon cancer. Nature 396, 699–703 (1998).
  Article CAS Google Scholar
• Djerbi, M. et al. The inhibitor of death receptor signaling, FLICE-inhibitory protein defines a new class of tumor progression factors. J. Exp. Med. 190, 1025–1031 (1999).
  Article CAS Google Scholar
• Medema, J., de Jong, J., van Hall, T., Melief, C. & Offringa, R. Immune escape of tumors in vivo by expression of cellular FLICE-inhibitory protein. J. Exp. Med. 190, 1033–1038 (1999).
  Article CAS Google Scholar
• Ashkenazi, A. et al. Safety and anti-tumor activity of recombinant soluble Apo2 ligand. J. Clin. Invest. 104, 155–162 (1999).
  Article CAS Google Scholar
• Lawrence, D. et al. Differential hepatocyte toxicity of recombinant Apo2L/TRAIL versions. Nature Med. 7, 383–385 (2001).
  Article CAS Google Scholar
• Qin, J.Z., Chaturvedi, V., Bonish, B. & Nickoloff, B.J. Avoiding premature apoptosis of normal epidermal cells. Nature Med. 7, 385–386 (2001).
  Article CAS Google Scholar
• Ashkenazi, A. & Dixit, V.M. Apoptosis control by death and decoy receptors. Curr. Opin. Cell Biol. 11, 255–260 (1999).
  Article CAS Google Scholar
• Walczak, H. et al. Tumoricidal activity of tumor necrosis factor-related apoptosis-inducing ligand in vivo. Nature Med. 5, 157–163 (1999).
  Article CAS Google Scholar
• Chinnaiyan, A.M. et al. Combined effect of tumor necrosis factor-related apoptosis-inducing ligand and ionizing radiation in breast cancer therapy. Proc. Natl. Acad. Sci. USA 97, 1754–1759 (2000).
  Article CAS Google Scholar
• Roth, W. et al. Locoregional Apo2L/TRAIL eradicates intracranial human malignant glioma xenografts in athymic mice in the absence of neurotoxicity. Biochem. Biophys. Res. Commun. 265, 1999 479–483 (1999).
  Article CAS Google Scholar
• Pollack, I.F., Erff, M. & Ashkenazi, A. Direct Stimulation of apoptotic signaling by soluble Apo2L/tumor necrosis factor-related apoptosis-inducing ligand leads to selective killing of glioma cells. Clin. Cancer Res. 7, 1362–1369 (2001).
  CAS PubMed Google Scholar
• Chuntharapai, A. et al. Isotype-dependent inhibition of tumor growth in vivo by monoclonal antibodies to death receptor 4. J. Immunol. 166, 4891–4898 (2001).
  Article CAS Google Scholar
• Ichikawa, K. et al. Tumoricidal activity of a novel anti-human DR5 monoclonal antibody without hepatocyte cytotoxicity. Nature Med. 7, 954 (2001).
  Article CAS Google Scholar
• Nicoletti, I., Migliorati, G., Pagliacci, M.C., Grignani, F. & Riccardi, C. A rapid and simple method for measuring thymocyte apoptosis by propidium iodide staining and flow cytometry. J. Immunol. Meth. 139, 271–279 (1991).
  Article CAS Google Scholar
• Chinnaiyan, A.M., O'Rourke, K., Lane, B.R. & Dixit, V.M. Interaction of CED-4 with CED-3 and CED-9: A molecular framework for cell death. Science 275, 1122–1126 (1997).
  Article CAS Google Scholar