SEARCH

SEARCH BY CITATION

References

  • 1
    Schiller JH,Harrington D,Belani CP,Langer C,Sandler A,Krook J,Zhu J,Johnson DH, for theEastern Cooperative Oncology Group. Comparison of four chemotherapy regimens for advanced non-small-cell lung cancer. N Engl J Med 2002; 346: 928.
  • 2
    Shepherd FA,Pereira JR,Ciuleanu T,Tan EH,Hirsh V,Thongprasert S,Campos D,Maoleekoonpiroj S,Smylie M,Martins R,van Kooten M,Dediu M, et al. Erlotinib in previously treated non-small-cell lung cancer. N Engl J Med 2005; 353: 12332.
  • 3
    Johnstone RW,Ruefli AA,Lowe SW. Apoptosis: a link between cancer genetics and chemotherapy. Cell 2002; 108: 15364.
  • 4
    Kastan MB,Bartek J. Cell-cycle checkpoints and cancer. Nature 2004; 432: 31623.
  • 5
    Green DR. Apoptotic pathways: ten minutes to dead. Cell 2005; 121: 6714.
  • 6
    Cory S,Adams JM. The Bcl2 family: regulators of the cellular life-or-death switch. Nat Rev Cancer 2002; 2: 64756.
  • 7
    Willis SN,Fletcher JI,Kaufmann T,van Delft MF,Chen L,Czabotar PE,Ierino H,Lee EF,Fairlie WD,Bouillet P,Strasser A,Kluck RM, et al. Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not bax or bak. Science 2007; 315: 8569.
  • 8
    Li P,Nijhawan D,Budihardjo I,Srinivasula SM,Ahmad M,Alnemri ES,Wang X. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell 1997; 91: 47989.
  • 9
    Kim H-E,Du F,Fang M,Wang X. Formation of apoptosome is initiated by cytochrome c-induced dATP hydrolysis and subsequent nucleotide exchange on Apaf-1. Proc Natl Acad Sci USA 2005; 102: 1754550.
  • 10
    Strasser A,Harris AW,Jacks T,Cory S. DNA damage can induce apoptosis in proliferating lymphoid cells via p53-independent mechanisms inhibitable by bcl-2. Cell 1994; 79: 32939.
  • 11
    Schmitt CA,Rosenthal CT,Lowe SW. Genetic analysis of chemoresistance in primary murine lymphomas. Nat Med 2000; 6: 102935.
  • 12
    Kaufmann SH,Vaux DL. Alterations in the apoptotic machinery and their potential role in anticancer drug resistance. Oncogene 2003; 22: 741430.
  • 13
    Meiler J,Schuler M. Therapeutic targeting of apoptotic pathways in cancer. Curr Drug Targets 2006; 7: 13619.
  • 14
    Urlinger S,Baron U,Thellmann M,Hasan MT,Bujard H,Hillen W. Exploring the sequence space for tetracycline-dependent transcriptional activators: novel mutations yield expanded range and sensitivity. Proc Natl Acad Sci USA 2000; 97: 79638.
  • 15
    Schuler M,Bossy-Wetzel E,Goldstein JC,Fitzgerald P,Green DR. p53 induces apoptosis by caspase activation through mitochondrial cytochrome c release. J Biol Chem 2000; 275: 733742.
  • 16
    Schuler M,Maurer U,Goldstein JC,Breitenbücher F,Hoffarth S,Waterhouse NJ,Green DR. p53 triggers apoptosis in oncogene-expressing fibroblasts by the induction of Noxa and mitochondrial Bax translocation. Cell Death Differ 2003; 10: 45160.
  • 17
    Remmele W,Stegner HE. [Recommendation for uniform definition of an immunoreactive score (IRS) for immunohistochemical estrogen receptor detection (ER-ICA) in breast cancer tissue]. Pathologe 1987; 8: 13840.
  • 18
    Lindsten T,Ross AJ,King A,Zong W-X,Rathmell JC,Shiels HA,Ulrich E,Waymire KG,Mahar P,Frauwirth K,Chen Y,Wei M, et al. The combined functions of proapoptotic Bcl-2 family members Bak and Bax are essential for normal development of multiple tissues. Mol Cell 2000; 6: 138999.
  • 19
    Wei MC,Zong W-X,Cheng EHY,Lindsten T,Panoutsakopoulou V,Ross AJ,Roth KA,MacGregor GR,Thompson CB,Korsmeyer SJ. Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death. Science 2001; 292: 72730.
  • 20
    Oltersdorf T,Elmore SW,Shoemaker AR,Armstrong RC,Augeri DJ,Belli BA,Bruncko M,Deckwerth TL,Dinges J,Hajduk PJ,Joseph MK,Kitada S, et al. An inhibitor of Bcl-2 family proteins induces regression of solid tumours. Nature 2005; 435: 67781.
  • 21
    Chen L,Willis SN,Wei A,Smith BJ,Fletcher JI,Hinds MG,Colman PM,Day CL,Adams JM,Huang DCS. Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. Mol Cell 2005; 17: 393403.
  • 22
    Kuwana T,Bouchier-Hayes L,Chipuk JE,Bonzon C,Sullivan BA,Green DR,Newmeyer DD. BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly. Mol Cell 2005; 17: 52535.
  • 23
    Willis SN,Chen L,Dewson G,Wei A,Naik E,Fletcher JI,Adams JM,Huang DCS. Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins. Genes Dev 2005; 19: 1294305.
  • 24
    Haraguchi M,Torii S,Matsuzawa S,Xie Z,Kitada S,Krajewski S,Yoshida H,Mak TW,Reed JC. Apoptotic protease activating factor 1 (Apaf-1)-independent cell death suppression by Bcl-2. J Exp Med 2000; 191: 170920.
  • 25
    Scott CL,Schuler M,Marsden VS,Egle A,Pellegrini M,Nesic D,Gerondakis S,Nutt SL,Green DR,Strasser A. Apaf-1 and Caspase-9 do not act as tumor suppressors in myc-induced lymphomagenesis or mouse embryo fibroblast transformation. J Cell Biol 2004; 164: 8996.
  • 26
    Huang DCS,Strasser A. BH3-Only Proteins—essential initiators of apoptotic cell death. Cell 2001; 103: 83942.
  • 27
    Degterev A,Lugovskoy A,Cardone M,Mulley B,Wagner G,Mitchison T,Yuan J. Identification of small-molecule inhibitors of interaction between the BH3 domain and Bcl-xL. Nat Cell Biol 2001; 3: 17382.
  • 28
    Letai A,Bassik MC,Walensky LD,Sorcinelli MD,Weiler S,Korsmeyer SJ. Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. Cancer Cell 2002; 2: 18392.
  • 29
    Walensky LD,Kung AL,Escher I,Malia TJ,Barbuto S,Wright RD,Wagner G,Verdine GL,Korsmeyer SJ. Activation of apoptosis in vivo by a hydrocarbon-stapled BH3 helix. Science 2004; 305: 146670.
  • 30
    Shoemaker AR,Oleksijew A,Bauch J,Belli BA,Borre T,Bruncko M,Deckwirth T,Frost DJ,Jarvis K,Joseph MK,Marsh K,McClellan W, et al. A small-molecule inhibitor of Bcl-XL potentiates the activity of cytotoxic drugs in vitro and in vivo. Cancer Res 2006; 66: 87319.
  • 31
    Saito M,Korsmeyer SJ,Schlesinger PH. BAX-dependent transport of cytochrome c reconstituted in pure liposomes. Nat Cell Biol 2000; 2: 5535.
  • 32
    Green DR,Kroemer G. The pathophysiology of mitochondrial cell death. Science 2004; 305: 6269.
  • 33
    Radetzki S,Köhne CH,von Haefen C,Gillisen B,Sturm I,Dörken B,Daniel PT. The apoptosis promoting Bcl-2 homologues Bak and Nbk/Bik overcome drug resistance in Mdr-1-negative and Mdr-1-overexpressing breast cancer cell lines. Oncogene 2002; 21: 22738.
  • 34
    van Delft MF,Wei AH,Mason KD,Vandenberg CJ,Chen L,Czabotar PE,Willis SN,Scott CL,Day CL,Cory S,Adams JM,Roberts AW, et al. The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized. Cancer Cell 2006; 10: 38999.
  • 35
    Konopleva M,Contractor R,Tsao T,Samudio I,Ruvolo PP,Kitada S,Deng X,Zhai D,Shi Y-X,Sneed T,Verhaegen M,Soengas M, et al. Mechanisms of apoptosis sensitivity and resistance to the BH3 mimetic ABT-737 in acute myeloid leukemia. Cancer Cell 2006; 10: 37588.
  • 36
    Chen S,Dai Y,Harada H,Dent P,Grant S. Mcl-1 down-regulation potentiates ABT-737 lethality by cooperatively inducing Bak activation and Bax translocation. Cancer Res 2007; 67: 78291.
  • 37
    Tahir SK,Yang X,Anderson MG,Morgan-Lappe SE,Sarthy AV,Chen J,Warner RB,Ng SC,Fesik SW,Elmore SW,Rosenberg SH,Tse C. Influence of Bcl-2 family members on the cellular response of small-cell lung cancer cell lines to ABT-737. Cancer Res 2007; 67: 117683.