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BIBLIOGRAPHY

BIBLIOGRAPHY

1) Alonso K., Pontiggia P., Sabato A. et al: Systemic hyperthermia in the treatment of HIV related disseminated Kaposi's Sanrcoma. Long term follow-up of patients treated wityh low flow extracorporeal perfusional hyperthermia. Am. J. Clin. Oncol ., 17: 353, 1994

2) Di Filippo F., Carlini S., Cavaliere F., Giannarelli D., Cavallero L. et al: The role of hyperthermic perfusion in the treatment of tumors of the extremities. In: “Consensus on hyperthermia for the 1990's”. Adv. Exp. Med . And Biol . Vol 267, Plenum Press 1990

3) Leveen H., Wapnicks G., Piccone V.A., Falk G. and Ahmed N.: Tumor eradication by radiofrequency thermotherapy. Jama , 235, 2198, 1976

4) Streffer C.: Metabolic changes during and after hyperthermia. Int. Journal of hyperthermia , 1: 305, 1985

5) Pontiggia P., Mc Laren J., Baronzio G., Freitas I.: The biological response to heat. In: “Consensus on hyperthermia for the 1990's”, Adv. Exp. Med. And Biol . Vol. 267, Plenum Press, 1990.

6) Dahl O.: Mechanisms of thermal enhancement of chemotherapeutic cytotoxicity in hyperthermia and oncology. Urano and Douple Eds. VPS Utrecht, 1994

7) Pontiggia P. Mathè G.: A new mode of cancer cell death induced by hyperthermia and non specific (macrophagic) cancer immunotherapy: lysosomal exocytosis. Biomed . Pharmacother.: 48, 331, 1994

8) Pontiggia P., Barni S. Mathè G., Bertone V. Pontiggia E.: Lysosomal exocytosis induced by hyperthermia: a new model of cancer death II- Effect on peritoneal macrophages. Biomed. Pharmacother . 49, 1995

9) Los G., Van Vugt MJH, Pinedo HM: Response of peritoneal solid tumors after intraperitoneal chemohyperthermia treatment with Cisplatin or Carboplatin. Br. J. Cancer 1994; 69. 235-41

10) Rau B., Wust P., Hohenberger P., Loffel H.M., Below C. et al: Preoperative hyperthermia combined with radiochemotherapy in locally advanced rectal cancer. Annals of Surgery 227, 3, 380-389; 1998

11) Reitbroek R., Schglthuis M, bakker P., Van Dijk J, Postma A. et al: Phase II trial of weekly locoregional hyperthermia and Cispltin in patients with previously irradiated recurrent carcinoma of uterine cervix. Cancer 1997; 79: 935-43

12) Lucchetti F., Burattini S., Ferri P., Papa S., Falcieri E.: Actin involvement in apoptotic chromatin changes of hemopoietic cells undergoing hyperthermia. Apoptosis 2002 ; 7(2): 143-52

13) Wachsberger P., Burd R. Wahl M, Leeper D.B.: Betulinici acid sensitization of low pH adapted human melanoma cells to hyperthermia. Int. J. Hyperthermia 2002; 18 (2): 153-64

14) Hildebrandt B., Wust P., Ahlers O., Dieing A.,Kerner T. et al: The cellular and molecular basis of hyperthermia. Crit. Rev. Oncol. Hematol 2002; 43 (1): 33-56

15) YuguchiT., Saito M., Yokoyama Y, Nagata T. Sakamoto T. Tsukada K.: Combined use of hyperthermia and irradiation cause antiporoliferative activity and cell death to humal esophageal carcinoma cells: mainly cycle examination. Hum. Cell 2002; 15 (1) 33-42

16) Wust P. Hildebrandt B., Sreenivasa G., Rau B. Gellermann J. At al: Hyperthermia in combined treatment of cancer. Lancet Oncol 2002; 3 (8); 487-97

17) Li G.C., Mivechi N. and Weitzel G.: Heat shock proteins, thermotolerance and therir relevance for clinical hyperthermia. Int. J. Hyperthermia 1995; 11, 459-488

18) Field SB, Franconi C, editors. Physics and Technology of Hyperthermia . Boston: Nijhoff, 1987

19) RA Read and JS Bedford. Thermal tolerance Br J Radiol 1980. 53: 920-921

20) Hahn GM, Adwankar MK, Basrur VS, Anderson RL. Survival of cells exposed to anticancer drugs after stress. In: Pardue ML, Feramisco JR, Lindquist S. Stress-Induced Proteins . New York, NY: Liss; 1989. p. 223 233

21) Hiraoka and GM Hahn. Changes in pH and blood flow induced by glucose and their effects on hyperthermia with or without BCNU in RIF-1 tumours Int J Hypertherm 1990. 6: 97-103

22) Morimoto RI, Tissieres A, Georgopoulos C. Stress Proteins in Biology and Medicine. Cold Spring Harbor, New York. 1990.

23) HI Robins, A Hugander, and JD Cohen. Whole body hyperthermia in the treatment of neoplastic disease Radiol Clin North Am 1989. 27: 603-610.

24) TV Samulski, ST Clegg, S Das, J MacFall, and DM Prescott. Application of new technology in clinical hyperthermia Int J Hypertherm 1994. 10: 389-394.

25) JR Oleson, TV Samulski, KA Leopold, ST Clegg, MW Dewhirst, RK Dodge, and SL George. Sensitivity of hyperthermia trial outcomes to temperature and time: implications for thermal goals of treatment Int J Radiat Oncol . Biol Phys 1993. 25: 289-297.

26) DS Kapp and R Cox. Thermal treatment parameters are most predictive of outcome in patients with single tumor nodules per treatment field in recurrent adenocarcinoma of the breast Int J Radiat Oncol Biol Phys 1995. 33: 887-899.

27) J van der Zee, GC van Rhoon, JL Wike-Hooley, NS Faithfull, and HS Reinhold. Whole-body hyperthermia in cancer therapy: a report of a phase I-II study Eur J Cancer Clin Oncol 1983. 19: 1189-1200.

28) M Serin, HS Erkal, and A Cakmak. Radiation therapy, cisplatin and hyperthermia in combination in management of patients with recurrent carcinomas of the head and neck with metastatic cervical lymph nodes Int J Hyperthermia 1999. 15: 371-381.

29) CC Vernon. International Collaborative Hyperthermia Group. Radio therapy with or without hyperthermia in the treatment of superficial localized breast cancer: results from five randomized controlled trials Int J Radiol Oncol Biol Phys 1996. 35: 731-744.

30) J Overgaard, D Gonzalez Gonzalez, MCCM Hulshof, G Arcangeli, O Dahl, O Molls, and SM Bentzen. Randomized trial of hyperthermia as adjuvant to radiotherapy for recurrent or metastatic malignant melanoma Lancet 1995. 345: 540-543.

31) R Valdagni and M Amichetti. Report of long-term follow-up in a randomized trial comparing radiation therapy and radiation therapy plus hyperthermia to metastatic lymph-nodes in Stage IV head and neck patients Int J Radiat Oncol Biol Phys 1994. 28: 163-169.

32) IA Petersen and DS Kapp. Local hyperthermia and radiation therapy in the retreatment of superficially located recurrences in Hodgkin's disease Int J Radiat Oncol Biol Phys 1990. 18: 603-611

33) T Sakamoto, H Katoh, T Shimizu, I Yamashita, S Takemori, K Tazawa, and M Fujimaki. Clinical results of treatment of advanced esophageal carcinoma with hyperthermia in combination with chemoradiotherapy Chest 1997. 112: 1487-1493.

34) LH Hartwell and TA Weinert. Checkpoints: controls that ensure the order of cell cycle events Science 1989. 246: 629-634.

35) DO Morgan. Cyclin-dependent kinases: engines, clocks, and microprocessors Ann Rev Cell Dev Biol 1997. 13: 261-291.

36) G Zugmaier and ME Lippman. Effects of TGF beta on normal and malignant mammary epithelium Ann N Y Acad Sci 1990. 593: 272-275.

37) BJ Druker, HJ Mamon, and TM Roberts. Oncogenes, growth factors, and signal transduction N Engl J Med 1989. 321: 1383-1391.

38) AB Pardee. G1 events and regulation of cell proliferation Science 1989. 246: 603-608.

39) DW Goodrich, NP Wang, YW Qian, EY Lee, and WH Lee. The retinoblastoma gene product regulates progression through the G1 phase of the cell cycle Cell 1991. 67: 293-302.

40)S Barni, P Pontiggia, V Bertone, R Vaccarone, MG Siulvotti, E Pontiggia, G Mathè. Hyperthermia-induced cell death by apoptosis in myeloma cells. Biomed Pharmacother 2001; 55: 170-3

41) V Bertone, S Barni, MG Silvotti, I Freitas, G Mathè et al. Hyperthermic effect on the human metastatic liver: a TEM study. Anticancer Res. 1997; 17: 4713-6

42) A Amundson, TG Myers, AJ Fornace, and Jr. Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress Oncogene 1998. 17: 3287-3299

43) JI Fabrikant and J Cherry. The kinetics of cellular proliferation in normal and malignant tissues. V. Analysis of labeling indices and potential tissue doubling times in human tumor cell populations J Surg Oncol 1969. 1: 23-47.

44) K Fukuda, T Iwasaka, and T Hachisuga et al . Immunocytochemical detection of S-phase cells in normal and neoplastic cervical epithelium by anti-BrdU monoclonal antibody Anal Quant Cytol Histol 1990. 12: 135-138.

45) L Teodori, ML Trinca, and W Goehde et al . Cytokinetic investigation of lung tumors using the anti-bromodeoxyuridine (BUdR) monoclonal antibody method: comparison with DNA flow cytometric data Int J Cancer 1990. 45: 995-1001.

46) G Weber. Biochemical strategy of cancer cells and the design of chemotherapy: G. H. A. Clowes Memorial Lecture Cancer Res 1983. 43: 3466-3492.

47) R Juliano. Cooperation between soluble factors and integrin-mediated cell anchorage in the control of cell growth and differentiation Bioessays 1996. 18: 911-917.

48) M Hall and G Peters. Genetic alterations of cyclins, cyclin-dependent kinases, and Cdk inhibitors in human cancer Adv Cancer Res 1996. 68: 67-108.

49) CJ Sherr. Cancer cell cycles Science 1996. 274: 1672-1677.

50) A Kamb. Cyclin-dependent kinase inhibitors and human cancer Curr Top Microbiol Immunol 1998. 227: 139-148

51) DW Goodrich and WH Lee. The molecular genetics of retinoblastoma Cancer Surveys 1990. 9: 529-554

52) C Prives and PA Hall. The p53 pathway J Pathol 1999. 187: 112-126.

53) M Akashi and HP Koeffler. Li-Fraumeni syndrome and the role of the p53 tumor suppressor gene in cancer susceptibility Clin Obstet Gynecol 1998. 41: 172-199

54) N Weidner, PR Carroll, J Flax, W Blumenfeld, and J Folkman. Tumor angiogenesis correlates with metastasis in invasive prostate carcinoma Am J Pathol 1993. 143: 401-409.

55) N Weidner, JP Semple, WR Welch, and J Folkman. Tumor angiogenesis and metastasis correlation in invasive breast carcinoma N Engl J Med 1991. 324: 1-8.

56) LR Bernstein and LA Liotta. Molecular mediators of interactions with extracellular matrix components in metastasis and angiogenesis Curr Opin Oncol 1994. 6: 106-113.

57) B Mintz and RA Fleischman. Teratocarcinomas and other neoplasms as developmental defects in gene expression Adv Cancer Res 1981. 34: 211-278.

58) MF Pittenger, AM Mackay, and SC Beck et al . Multilineage potential of adult human mesenchymal stem cells Science 1999. 284: 143-147.

59) JJ WilleJr , PB Maercklein, and RE Scott. Neoplastic transformation and defective control of cell proliferation and differentiation Cancer Res 1982. 42: 5139-5146.

60) DB Rifkin and D Moscatelli. Recent developments in the cell biology of basic fibroblast growth factor J Cell Biol 1989. 109: 1-6.

61) E Rozengurt. Early signals in the mitogenic response Science 1986. 234: 161-166

62) HL Moses, EY Yang, and JA Pietenpol. TGF-beta stimulation and inhibition of cell proliferation: new mechanistic insights Cell 1990. 63: 245-247.

63) M Peter and I Herskowitz. Joining the complex: cyclin-dependent kinase inhibitory proteins and the cell cycle [comment] Cell 1994. 79: 181-184.

64) CJ Sherr. G1 phase progression: cycling on cue [see comments] Cell 1994. 79: 551-555.

65) JL Bennington. Cellular kinetics of invasive squamous carcinoma of the human cervix Cancer Res 1969. 29: 1082-1088.

66) V Castronovo, M Kusaka, A Chariot, J Gielen, and M Sobel. Homeobox genes: potential candidates for the transcriptional control of the transformed and invasive phenotype Biochem Pharmacol 1994. 47: 137-143

67) A McCormick and J Campisi. Cellular aging and senescence Curr Opin Cell Biol 1991. 3: 230-234.

68) R Singal and GD Ginder. DNA methylation Blood 1999. 93: 4059-4070.

69) AP Feinberg and B Vogelstein. Hypomethylation distinguishes genes of some human cancers from their normal counterparts Nature 1983. 301: 89-92.

70) SE Goelz, B Vogelstein, SR Hamilton, and AP Feinberg. Hypomethylation of DNA from benign and malignant human colon neoplasms Science 1985. 228: 187-190.

71) M Carlsson, TH Totterman, P Matsson, and K Nilsson. Cell cycle progression of B-chronic lymphocytic leukemia cells induced to differentiate by TPA Blood 1988. 71: 415-421

72) Gorstein F, Thor A. Tumor markers in diagnostic pathology. In Clinics in Laboratory Medicine. Edited by F Gorstein, A Thor. Philadelphia: WB Saunders, 1990.

73) M Reiss, C Gamba-Vitalo, and AC Sartorelli. Induction of tumor cell differentiation as a therapeutic approach: preclinical models for hematopoietic and solid neoplasms Cancer Treat Rep 1986. 70: 201-218

74) Waxman S, Rossi GB, Takaku F. The Status of Differentiation Therapy of Cancer. New York: Raven, 1988.

75) M Andreeff, R Stone, and J Michaeli et al . Hexamethylene bisacetamide in myelodyplastic syndrome and acute myelogenous leukemia: A Phase II clinical trial with a differentiation-inducing agent Blood 1992. 80: 2604-2609.

76) TR Breitman, SJ Collins, and BR Keene. Terminal differentiation of human promyelocytic leukemic cells in primary culture in response to retinoic acid Blood 1981. 57: 1000-1004.

77) BA Chabner. Biological basis for cancer treatment [comment] Ann Intern Med 1993. 118: 633-637.

78) BD Cheson, DM Jasperse, HG Chun, and MA Friedman. Differentiating agents in the treatment of human malignancies Cancer Treat Rev 1986. 13: 129-145.

79) M Andreeff, S Jiang, and X Zhang et al . Expression of bcl-2-related genes in normal and AML progenitors: changes induced by chemotherapy and retionic acid Leukemia 1999. 13: 1881-1892.

80) WK Hong, SM Lippman, and LM Itri et al . Prevention of second primary tumors with isotretinoin in squamous-cell carcinoma of the head and neck [see comments] N Engl J Med 1990. 323: 795-801.

81) FL MeyskensJr . Coming of age the chemoprevention of cancer [editorial; comment] [see comments] N Engl J Med 1990. 323: 825-827.

82) JD Rowley, JC Aster, and J Sklar. The clinical applications of new DNA diagnostic technology on the management of cancer patients JAMA 1993. 270: 2331-2337.

83) JC Reed. Dysregulation of apoptosis in cancer J Clin Oncol 1999. 17: 2941-2953.

84) MO Hengartner and HR Horvitz. Programmed cell death in Caenorhabditis elegans Curr Opin Genet Dev 1994. 4: 581-586.

85) K Hofmann, P Bucher, and J Tschopp. The CARD domain: a new apoptotic signalling motif Trends Biochem Sci 1997. 22: 155-156.

86) P Li, D Nijhawan, and I Budihardjo et al . Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade Cell 1997. 91: 479-489

87) JJ Chou, H Matsuo, H Duan, and G Wagner. Solution structure of the RAIDD CARD and model for CARD/CARD interaction in caspase-2 and caspase-9 recruitment Cell 1998. 94: 171-180.

88) K Kuida, TF Haydar, and CY Kuan et al . Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking Caspase 9 Cell 1998. 94: 325-337.

89) DW Nicholson and NA Thornberry. Caspases: killer proteases Trends Biochem Sci 1997. 22: 299-306.

90) RV Talanian, C Quinlan, and S Trautz et al . Substrate specificities of caspase family proteases J Biol Chem 1997. 272: 9677-9682.

91) NA Thornberry, TA Rano, and EP Peterson et al . A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis J Biol Chem 1997. 272: 17907-17911.

92) MP Boldin, TM Goncharov, YV Goltsev, and D Wallach. Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death Cell 1996. 85: 803-815.

93) M Muzio, AM Chinnaiyan, and FC Kischkel et al . FLICE, a novel FADDl-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death-inducing signaling complex Cell 1996. 85: 817-827.

94) L Faleiro, R Kobayashi, H Fearnhead, and Y Lazebnik. Multiple species of CPP32 and Mch2 are the major active caspases present in apoptotic cells EMBO J 1997. 16: 2271-2281.

95) M MacFarlane, K Cain, XM Sun, ES Alnemri, and GM Cohen. Processing/activation of at least four interleukin-1 beta converting enzyme-like proteases occurs during the execution phase of apoptosis in human monocytic tumor cells J Cell Biol 1997. 37: 469-479.

96) SM Srinivasula, T Fernandes-Alnemri, and J Zangrilli et al . The CED-3/interleukin-1 beta converting enzyme-like homolog Mch6 and the lamin-cleaving enzyme Mch2 alpha are substrates for the apoptotic mediator CPP32 J Biol Chem 1996. 271: 27099-27106.

97) X Liu, CN Kim, J Yang, R Jemmerson, and X Wang. Induction of apoptotic programin cell-free extracts: requirement for dATP and cytochrome c Cell 1996. 86: 147-157.

98) J Yang, X Liu, and K Bhalla et al . Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked [see comments] Science 1997. 275: 1129-1132.

99) DR Green and JC Reed. Mitochondria and apoptosis Science 1998. 281: 1309-1312.

100) DR Green. Apoptotic pathways: the roads to ruin Cell 1998. 94: 695-698.

101) H Sakahira, M Enari, and S Nagata. Cleavage of CAD inhibitor in CAD activation and DNA degradation during apoptosis [see comments] Nature 1998. 391: 96-99.

102) N Fujita, A Nagahashi, K Nagashima, S Rokudai, and T Tsuruo. Acceleration of apoptotic cell death after the cleavage of Bcl-XL protein by caspase-3-like proteases Oncogene 1998. 17: 1295-1304.

103) EH Cheng, DG Kirsch, and RJ Clem et al . Conversion of bcl-2 to a Bax-like death effector by caspases Science 1997. 278: 1966-1968.

104) RA MacCorkle, KW Freeman, and DM Spencer. Synthetic activation of caspases: artificial death switches Proc Natl Acad Sci U S A 1998. 95: 3655-3660.

105) RJ Clem and LK Miller. Control of programmed cell death by the baculovirus genes p35 and iap Mol Cell Biol 1994. 14: 5212-5222.

106) N Roy, MS Mahadevan, and M McLean et al . The gene for neuronal apoptosis inhibitory protein is partially deleted in individuals with spinal muscular atrophy Cell 1995. 80: 167-178.

107) AG Uren, M Pakusch, CJ Hawkins, KL Puls, and DL Vaux. Cloning and expression of apoptosis inhibitory protein homologs that function to inhibit apoptosis and/or bind tumor necrosis factor receptor-associated factors PNAS 1996. 93: 4974-4978.

108) HR Stennicke, QL Deveraux, and EW Humke et al . Caspase-9 can be activated without proteolytic processing J Biol Chem 1999. 274: 8359-8362.

109) QL Deveraux, N Roy, and HR Stennicke et al . IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases EMBO J 1998. 17: 2215-2223

110) J Dierlamm, M Baens, and I Wlodarska et al . The apoptosis inhibitor gene API2 and a novel 18q gene, MLT, are recurrently rearranged in the t(11;18)(q21;q21)p6ssociated with mucosa-associated lymphoid tissue lymphomas Blood 1999. 93: 3601-3609.

111) A Greiner, H Seeberger, C Knorr, P Starostik, and HK Muller-Hermelinck. MALT-type B-cell lymphomas escape the sensoring FAS-mediated apoptosis Blood 1998. 92: 484a.

112) G Ambrosini, C Adida, and DC Altieri. A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma Nat Med 1997. 3: 917-921.

113) F Li, G Ambrosini, and EY Chu et al . Control of apoptosis and mitotic spindle checkpoint by survivin Nature 1998. 396: 580-584.

114) I Tamm, Y Wang, E Sausville, DA Scudiero, N Vigna, T Oltersdorf, and JC Reed. IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax, caspases, and anticancer drugs Cancer Res 1998. 58: 5315-5320.

115) CD Lu, DC Altieri, and N Tanigawa. Expression of a novel antiapoptosis gene, survivin, correlated with tumor cell apoptosis and p53 accumulation in gastric carcinomas Cancer Res 1998. 58: 1808-1812.

116) H Kawasaki, DC Altieri, and CD Lu et al . Inhibition of apoptosis by survivin predicts shorter survival rates in colorectal cancer Cancer Res 1998. 58: 5071-5074.

117) G Ambrosini, C Adida, G Sirugo, and DC Altieri. Induction of apoptosis and inhibition of cell proliferation by survivin gene targeting J Biol Chem 1998. 273: 11177-11182.

118) C Adida, PL Crotty, and J McGrath et al . Developmentally regulated expression of the novel cancer anti-apoptosis gene survivin in human and mouse differentiation Am J Pathol 1998. 152: 43-49.

119) CA Smith, T Farrah, and RG Goodwin. The TNF receptor superfamily of cellular and viral proteins: activation, costimulation, and death Cell 1994. 76: 959-962.

120) S Nagata. Apoptosis by death factor Cell 1997. 88: 355-365.

121) M Hahne, D Rimoldi, and M Schroter et al . Melanoma cell expression of Fas(Apo-1/CD95) ligand: implications for tumor immune escape Science 1996. 274: 1363-1366.

122) S Nagata and P Golstein. The Fas death factor Science 1997. 267: 1449-1456.

123) AM Chinnaiyan, K O'Rourke, M Tewari, and VM Dixit. FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis Cell 1995. 81: 505-512.

124) AM Chinnaiyan, CG Tepper, and MF Seldin et al . FADD/MORT1 is a common mediator of CD95 (Fas/APO1) and tumor necrosis factor recreptor-induced apoptosis J Biol Chem 1996. 271: 4961-4965.

125) M Muller, S Wilder, and D Bannasch et al . p53 activates the CD95 (APO-1/Fas) gene in response to DNA damage by anticancer drugs J Exp Med 1998. 188: 2033-2045.

126) LB Owen-Schaub, W Zhang, and JC Cusack et al . Wild-type human p53 and a temperature-sensitive mutant induce Fas/APO-1 expression Mol Cell Biol 1995. 15: 3032-3040.

127) J Ogasawara, R Watanabe-Fukunaga, and M Adachi et al . Lethal effect of the anti-fas antibody in mice Nature 1993. 364: 806-809.

128) P Schneider, N Holler, and JL Bodmer et al . Conversion of membrane-bound Fas(CD95) ligand to its soluble form is associated with downregulation of its proapoptotic activity and loss of liver toxicity J Exp Med 1998. 187: 1205-1213.

129) J Kitson, T Raven, and YP Jiang et al . A death-domain-containing receptor that mediates apoptosis Nature 1996. 384: 372-375.

130) AM Chinnaiyan, K O'Rourke, and GL Yu et al . Signal transduction by DR3, a death domain-containing receptor related to TNFR-1 and CD95 Science 1996. 274: 990-992.

131) Y Hitoshi, J Lorens, and SI Kitada et al . Toso, a cell surface, specific regulator of Fas-induced apoptosis in T cells Immunity 1998. 8: 461-471.

132) RW Johnstone, E Cretney, and MJ Smyth. P-glycoprotein protects leukemia cells against caspase-dependent, but not caspase-independent, cell death Blood 1999. 93: 1075-1085.

133) WD Thomas and P Hersey. TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in Fas ligand-resistant melanoma cells and mediates CD4 T cell killing of target cells J Immunol 1998. 161: 2195-2200.

134) V Snell, K Clodi, and S Zhao et al . Activity of TNF-related apoptosis-inducing ligand (TRAIL) in haematological malignancies Br J Cancer 1997. 99: 624.

135) M Andreeff, G Wong, B Koziner, E Espiritu, and B Clarkson. Non B-Non T acute lymphoblastic leukemia (ALL): evidence for complete b cell differentiation of a quiescent subpopulation and their response to induction therapy Proc Am Assoc Cancer Res 1985. 26: 28.

136) MM Keane, SA Ettenberg, MM Nau, EK Russell, and S Lipkowitz. Chemotherapy augments TRAIL-induced apoptosis in breast cell lines Cancer Res 1999. 59: 734-741.

137) P Golstein. Cell death: trail and its receptors Curr Biol 1997. 7: R750-R753.

138) H Walczak, RE Miller, and K Ariail et al . Tumoricidal activity of tumor necrosis factor-related apoptosis- inducing ligand in vivo [see comments] Nat Med 1999. 5: 157-163.

139) L Gibson, SP Holmgreen, and DC Huang et al . Bcl-w, a novel member of the bcl-2 family, promotes cell survival Oncogene 1996. 13: 665-675.

140) E Yang, J Zha, and J Jockel et al . Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death Cell 1995. 80: 285-291.

141)M JJ Hunter, BL Bond, and TG Parslow. Functional dissection of the human Bcl2 protein: sequence requirements for inhibition of apoptosis Mol Cell Biol 1996. 16: 877-883.

142) C Borner, I Martinou, and C Mattmann et al . The protein bcl-2 alpha does not require membrane attachment, but two conserved domains to suppress apoptosis J Cell Biol 1994. 126: 1059-1068.

143) T Ito, X Deng, B Carr, and WS May. Bcl-2 phosphorylation required for anti-apoptosis function J Biol Chem 1997. 272: 11671-11673.

144) MV Blagosklonny, T Schulte, P Nguyen, J Trepel, and LM Neckers. Taxol-induced apoptosis and phosphorylation of Bcl-2 protein involves c-Raf-1 and represents a novel c-Raf-1 signal transduction pathway Cancer Res 1996. 56: 1851-1854.

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Persistent Cookies

As the name suggests, this type of cookie is saved on your computer so that when you close it down and start it up again, it can still be there.

Persistent cookies are created by giving them an expiry date. If that expiry date is reached, it will be destroyed by the computer. If the expiry date is not set then it is automatically a session cookie.

The expiry date will normally be saved as the time the cookie was first created plus a number of seconds, determined by the programmer who wrote the code for the cookie. However, there is no real limit on the expiry date - so it could be set to be 20 years in the future. In addition, if you revisit the website that served up the cookie, it may automatically place an updated version on your computer - with a revised future expiry date.

If you login into a website, then shut down your computer, start it up again, and go back to the website to find you are still logged in - then it is using a persistent cookie to remember you.

Persistent cookies are also used to track visitor behaviour as you move around a site, and this data is used to try and understand what people do and don't like about a site so it can be improved. This practice is known as Web Analytics. Since Google started providing its own analytics technology free of charge to website owners, almost all websites use some form of it - although there are also paid-for services available to rival Google's.

Analytics cookies are probably the most common form of persistent cookies in use today.

However, persistent cookies can also, oddly, have a shorter life span than some session cookies, as they can be coded to be destroyed within a second or two of being set, whereas a session cookie will always last until you close down your browser.

Secure Cookies

Secure cookies are only transmitted via HTTPS - which you will typically find in the checkout pages of online shopping sites.

This ensures that any data in the cookie will be encrypted as it passes between the website and the browser. As you might imagine – cookies that are used by e-commerce sites to remember credit card details, or manage the transaction process in some way, would normally be secure, but any other cookie might also be made secure.

HTTPOnly Cookies

When a cookie has an HTTPOnly attribute set, the browser will prevent any client script in the page (like JavaScript) from accessing the contents of the cookie.

This protects it from so-called cross-site-scripting (XSS) attacks, where a malicious script tries to send the content of a cookie to a third party website.

How to Manage Cookies

Almost all modern browsers provide ways for you to control how your computer handles cookies. This includes the ability to block all or different types of cookies – and preventing them from being placed on your machine in the first place. They also enable you to delete the cookies that you already have. However each browser is different – and some offer more fine-grained control than others, or at least control that is easier to find. Anyone wishing to take better control over their online privacy would be well advised to spend some time familiarising themselves with the controls in their browser. However, below we provide a bit of an overview for the most common browsers.

Browsers are of course found on smartphone and tablets as well as traditional computers. Generally speaking smartphone browsers do not provide anywhere near the level of functionality in respect of cookie controls that ones on your PC or laptop do. However this is changing quickly so it is worthwhile trying to find out what controls you can make use of.

Google Chrome

Google Chrome provides quite a good level of control over cookies. These can be found under the ‘Settings’ menu, which you can get to by clicking on the spanner icon in the top right hand corner.

Under ‘Advanced Settings’ you can find a section dedicated to Privacy, which includes being able to clear your browsing history – which has several settings options, including deleting all your cookies.

You can also use Chrome to send a ‘Do Not track’ signal to the websites you visit.

However, the ‘Content Settings’ button also gives access to further controls including the ability to list all cookies and delete them individually. This list also includes HTML5 local storage and databases that modern sites sometimes use instead of cookies.

FireFox

With Firefox you get to the cookie settings by clicking in the menu box in the top left hand corner and selecting ‘Options’. On the pop-up, then select the ‘Privacy’ icon.

With Firefox you can tick a box that tells every website you visit that you do not want to be tracked. This functionality is known as Do Not Track (DNT), however there is no guarantee at the moment that a website will respect that request – and there are no legal requirements for them to do that.

You can also set your preferences for what Firefox will record of your browsing history, including the way it treats cookies. For example, you can choose to accept third party cookies, but have them deleted when you close the browser. Like with Chrome you can also see a list of all the cookies saved and either delete them all or delete just the ones you don’t like.

More recently, the Mozilla foundation have announced that newer releases of Firefox, most likely from June 2013 onwards, will block third party cookies by default.

Internet Explorer

In most recent versions of Internet Explorer you select the cog icon in the top right corner, choose ‘Internet Options’ from the drop down menu, then select the ‘Privacy’ tab in the pop-up that appears.

IE uses a slider control which you can use to select different levels of privacy, although you can also select the ‘Advanced’ button for a more custom setting for allowing or blocking first and third party cookies.

It also enables you to create lists of sites where you always want to allow or block cookies. However it does not give you the ability to list the cookies you have, or selectively delete them, through this menu.

To do that – you have to use the ‘Developer Tools’, which you can get to either from the cog icon, or by hitting the F12 button on your keyboard. Then select the ‘cache’ menu and view or clear cookies options in the drop down. The problem with this is that have to be on the site in question to do this, and it is not particularly user friendly – most people would be put off by the idea of using the developer tools, because they are not developers!

Under the Internet Options>General tab you also have a tick box that you can set to delete your browsing history when you shut it down. Ticking this will mean all your cookies are deleted when you close your browser.

From Internet Explorer 10 onwards, Microsoft introduced Do Not Track functionality. This will usually have been switched on by default when the browser was first installed. To check your own settings, go to Internet Options>Advanced. Scroll down to the Security Settings, and there you will find a tick box labelled ‘Always send Do Not Track header’. If you tick or un-tick this box, you will need to re-start the browser for the change to take effect.