Literaturverzeichnis

↓113

[1] Bennett, J H (1845): Case of hypertrophy of the spleen and liver in which death took place from suppration of the blood, Edinburgh Medical and Surgical Journal, (vol. 64), pp. 413-423.

[2] Craigie, D (1845): Case of disease of the spleen in which death took place from suppuration of the blood, Edinburgh Medical and Surgical Journal, (vol. 64), pp. 400-12.

[3] Virchow, R (1845): Weisses Blut, Frorieps Notizen, (vol. 36), pp. 151-6.

[4] Brincker, H (1982): Population-based age- and sex-specific incidence rates in the main types of leukemia, Scand J Haematol, (vol. 29), No. 3, pp. 241-9.

[5] Fialkow, O J; Jacobson, R J and Papayannopoulou, T (1977): Chronic myelocytic leukemia: clonal origin in a stem cell common to the granulocyte, erythrocyte, platelet and monocyte/ macrophage, Am J Med, (vol. 63), pp. 125-30.

[6] Bernstein, R (1988): Cytogenetics of chronic myelogenous leukemia, Semin Hematol, (vol. 25), No. 1, pp. 20-34.

[7] Kantarjian, H; Dixon, D; Keating, M J; Talpaz, M; Walters, R S; McCreadie, K B and Freireich, E J (1988): Characteristics of accelerated disease in chronic myelogenous leukemia, Cancer, (vol. 61), No. 7, pp. 1441-6.

[8] Karanas, A and Silver, R T (1968): Characteristics of the terminal phase of chronic granulocytic leukemia, Blood, (vol. 32), pp. 445-59.

[9] Nowell, P C and Hungerford, D A (1960): A minute chromosome in human chronic granulocytic leukemia, Science, (vol. 132), p. 1497.

[10] Rowley, J D (1973): A new consistent chromsomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining, Nature, (vol. 243), pp. 290-293.

[11] Kurzrock, R; Kantarjian, H; Shtalrid, M; Gutterman, J U and Talpaz, M (1990): Philadelphia chromosome-negative chronic myelogenous leukemia without breakpoint cluster region rearrangenment: a chronic myeloid leukemia with a distinct clinical course, Blood, (vol. 75), No. 2, pp. 445-52.

[12] Melo, J V (1996): The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype, Blood, (vol. 88), No. 7, pp. 2375-84.

[13] Chissoe, S L; Bodenteich, A; Wang, Y F; Wang, Y P; Burian, D; Clifton, S W; Crabtree, J; Freeman, A; Iyer, K; Jian, L and al. (1995): Sequence and analysis of the human ABL gene, the BCR gene, and regions involved in the Philadelphia chromosomal translocation, Genomics, (vol. 27), No. 1, pp. 67-82.

[14] Pane, F; Frigeri, F; Sindona, M; Luciano, L and Ferrara, F (1996): Neutrophilic-chronic myeloid leukemia: a distinct disease with a specific molecular marker (BCR/ABL with C3/A2 junction), Blood, (vol. 88), No. 7, pp. 2410-4.

[15] Shtivelman, E; Lifshitz, B; Gale, R P and Canaani, E (1985): Fused transcript of abl and bcr genes in chronic myelogenous leukemia, Nature, (vol. 315), No. 6020, pp. 550-4.

[16] Lugo, T G; Pendergast, A M ; Muller, A J and Witte, O N (1990): Tyrosine kinase activity and transformation potency of bcr-abl oncogene products, Science, (vol. 247), No. 4946, pp. 1079-82.

[17] Groffen, J; Stephenson, J R; Heisterkamp, N; Bartram, C R; de Klein, A and Grosveld, G (1984): The human c-abl oncogene in the Philadelphia translocation, J Cell Physiol Suppl, (vol. 3), pp. 179-91.

[18] ten Hoeve, J; Kaartinen, V; Fioretos, T; Haataja, L; Voncken, J W; Heisterkamp, N and Groffen, J (1994): Cellular interactions of CRKL, and SH2-SH3 adapter protein, Cancer Res, (vol. 54), No. 10, pp. 2563-7.

[19] Oda, T; Heaney, C; Hagopian, J R; Okuda, K; Griffin, J D and Druker, B J (1994): Crkl is the major tyrosine-phosphorylated protein in neutrophils from patients with chronic myelogenous leukemia, J Biol Chem, (vol. 269), No. 37, pp. 22925-8.

[20] Nichols, G L; Raines, M A; Vera, J C ; Lacomis, L; Tempst, P and Golde, D W (1994): Identificatin of CRKL as the constitutively phosphorylated 39-kD tyrosine phosphoprotein in chronic myelogenous leukemia cells, Blood, (vol. 84), No. 9, pp. 2912-8.

[21] Puil, L; Liu, J; Gish, G; Mbamalu, G; Bowtell, D; Pelicci, P G; Arlinghaus, R and Pawson, T (1994): Bcr-Abl oncoproteins bind directly to activators of the Ras signalling pathway, EMBO, (vol. 13), No. 4, pp. 764-73.

[22] Carlesso, N; Frank, D A and Griffin, J D (1996): Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl, J Exp Med, (vol. 183), No. 3, pp. 811-20.

[23] Sawyers, C; McLaughlin, J and Witte, O N (1995): Genetic requirement for Ras in the transformation of fibroblasts and hematopoietic cells by the Bcr-Abl oncogene, J Exp Med, (vol. 181), No. 1, pp. 307-13.

[24] Skorski, T; Bellacosa, A; Nieborowska-Skorska, M; Majewski, M; Martinez, R; Choi, J K; Trotta, R; Wlodarski, P; Perrotti, D; Chan, T O; Wasik, M A; Tschichlis, P N and Calabretta, B (1997): Transformation of hematopoietic cells by BCR/ABL requires activation of a PI3k/Akt-dependent pathway, EMBO, (vol. 16), No. 20, pp. 6151-61.

[25] Skorski, T; Nieborowska-Skorska, M; Szczylik, C; Kanakaraj, P; Perrotti, D; Zon, G; Gewirtz, A; Perussia, B and Calabretta, B (1995): C-RAF-1 serine/threonine kinase is required in BCR/ABL-dependent and normal hematopoiesis, Cancer Res, (vol. 55), No. 11, pp. 2275-8.

[26] Warmuth, M; Danhauser-Riedl, S and Hallek, M (1999): Molecular pathogenesis of chronic myeloid leukemia: implications for new therapeutic strategies, Ann Hematol, (vol. 78), No. 2, pp. 49-57.

[27] Salgia, R; Li, J L; Ewaniuk, D S; Pear, W; Pisick, E; Burky, S A; Ernst, T; Sattler, M; Chen, L B and Griffin, J D (1997): BCR/ABL induces multiple abnormalities of cytoskeletal function, J Clin Invest, (vol. 100), No. 1, pp. 46-57.

[28] Deininger, M W; Vieira, S; Mendiola, R; Schultheis, B; Goldman, J M and Melo, J V (2000): BCR-ABL tyrosine kinase activity regulates the expression of multiple genes implicated in the pathogenesis of chronic myeloid leukemia, Cancer Res, (vol. 60), No. 7, pp. 2049-55.

[29] Senn, N (1903): Case of splenomedullary leukemia successfully treated by the use of Roentgen rays, Medical Records of New York, (vol. 64), pp. 281-2.

[30] Hehlmann, R; Heimpel, H; Kolb, H J; Heinze, B; Hochhaus, A; Griesshammer, M; Pralle, H; Queisser, W P; Esser, U; Falge, C and al. (1993): The German CML study, comparison of busulfan vs. hydroxyurea vs. interferon alpha and establishment of prognostic score 1, Leuk Lymphoma, (vol. 11), No. Suppl 1, pp. 159-68.

[31] Talpaz, M; Kantarjian, H; McCredie, K; Keating, M J; Trujillo, JM and Gutterman, J (1987): Clinical Investigation of human alpha interferon in chronic myelogenous leukemia, Blood, (vol. 69), No. 1280.

[32] Hehlmann, R; Heimpel, H and Hasford, J (1994): Randomized comparison of interferon-alpha with busulfan and hydroxyurea in chronic myelogenous leukemia, Blood, (vol. 84), pp. 4064-77.

[33] Gale, R P; Butturini, A and Reizenstein, P (1991): Autotransplants in leukemia: current state, future progress, Leuk Res, (vol. 15), No. 9, pp. 781-4.

[34] Silver, R T; Woolf, S H; Hehlmann, R; Appelbaum, F R; Anderson, J; Bennett, C; Goldman, J M; Guilhot, F; Kantarjian, H M; Lichtin, A E; Talpaz, M and Tura, S (1999): An evidence-based analysis of the effect of busulfan, hydroxyurea, interferon, and allogeneic bone marrow transplantation in treating the chronic phase of chronic myeloid leukemia: developed for the American Society of Hematology, Blood, (vol. 94), No. 5, pp. 1517-36.

[35] Gratwohl, A; Hermans, J; Goldman, J M; Arcese, W; Carreras, E; Devergie, A; Frassoni, F; Gahrton, G; Kolb, H J; Niederwieser, D; Ruutu, T; Vernant, J P; de Witte, T and Apperley, J (1998): Risk assessment for patients with chronic myeloid leukaemia before allogeneic blood or marrow transplantation, Lancet, (vol. 352), pp. 1987-92.

[36] Hasford, J; Pfirrmann, M; Hehlmann, R; Allan, N C; Baccarani, M; Kluin-Nelemans, J C; Alimena, G; Steegmann, J L and Ansari, H (1998): A new prognostic score for survival of patients with chronic myeloid leukemia treated with interferon alfa. Writing Committee for the Collaborative CML Prognostic Factors Project Group., J Natl Cancer Inst, (vol. 90), No. 11, pp. 850-8.

[37] (1998): The Italian Cooperative Study Group on chronic myeloid leukemia. Long-term follow-up of the italian trial of Interferon-alpha versus conventional chemotherapy in chronic myeloid leukemia, Blood, (vol. 92), No. 5, pp. 1541-1548.

[38] Lee, L G; Connell, C R and Bloch, W (1993): Allelic discrimination by nick-translation PCR with fluorogenic probes, Nucleic Acids Res, (vol. 21), pp. 3761-6.

[39] Wittwer, C T; Ririe, K M; Andrew, R V; David, D A; Gundry, R A and Balis, U J (1997): The Lightcycler: a microvolume multisample fluorimeter with rapid temperature control, Biotechniques, (vol. 22), No. 1, pp. 176-81.

[40] Wittwer, C T; Herrmann, M G; Moss, A A and Rasmussen, R P (1997): Continous fluorescences monitoring of rapid cycle DNA amplification, Biotechniques, (vol. 22), No. 1, pp. 134-8.

[41] Bernard, P S; Lay, M J and Wittwer, C T (1998): Integrated amplification and detection of the C677T point mutation in the methylenetetrahydrofolate reductase gene by fluorescence resonance energy transfer and probe melting curves, Anal Biochem, (vol. 255), No. 1, pp. 101-7.

[42] Lay, M J and Wittwer, C T (1997): Real-time fluorescence genotyping of factor V Leiden during rapid-cycle PCR, Clin Chem, (vol. 43), No. 12, pp. 2262-7.

[43] Santa-Lucia, J Jr; Allawi, H T and Seneviratne, P A (1996): Improved nearest-neighbor parameters for predicting DNA duplex stability, Biochemistry, (vol. 35), No. 11, pp. 3555-62.

[44] Kyger, E M; Krevolin, M D and Powell, M J (1998): Detection of the hereditary hemochromatosis gene mutation by real-time fluorescence polymerase chain reacion and peptide nucleic acid clamping, Anal Biochem, (vol. 260), No. 2, pp. 142-8.

[45] Thorpe, P H and Porteous, D J (1999): Rapid quantification of gene therapy specific CFTR expression using the amplification refractory mutation system, Biotechniques, (vol. 27), No. 1, pp. 122-6.

[46] Nielsen, P E; Egholm, M and Buchardt, O (1994): Peptide nucleic acid (PNA). A DNA mimic with a peptide backbone, Bioconjug Chem, (vol. 5), No. 1, pp. 3-7.

[47] Buchardt, O; Egholm, M; Berg, R H and Nielsen, P E (1993): Peptide nucleic acids and their potenial applictions in biotechnology, Trends Biotechnol, (vol. 11), No. 9, pp. 384-6.

[48] Nielsen, P E (1995): DNA analogues with nonphosphodiester backbones, Annu Rev Biomol Struct, (vol. 24), pp. 167-83.

[49] Orum, H; Nielsen, P E; Egholm, M; Berg, R H; Buchardt, O and Stanley, C (1993): Single base pair mutation analysis by PNA directed PCR clamping, Nucleic Acids Res, (vol. 21), pp. 5332-6.

[50] Behn, M; Thiede, C; Neubauer, A; Pankow, W and Schuermann, M (2000): Facilitated detection of oncogene mutations from exfolated tissue material by a PNA-mediated ´enriched PCR´ protocol, J Pathol, (vol. 190), No. 1, pp. 69-75.

[51] Thiede, C; Bayerdörffer, E; Blasczyk, R; Wittig, B and Neubauer, A (1996): Simple and sensitive detecion of mutations in the ras proto-oncogenes using PNA-mediated PCR clamping, Nucleic Acids Res, (vol. 24), No. 5, pp. 983-4.

[52] Druker, B J; Tamura, S; Buchdunger, E; Ohno, S; Segal, G M; Fanning, S; Zimmermann, J and Lydon, N B (1996): Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells, Nature Med, (vol. 2), No. 5, pp. 561-6.

[53] Druker, B J and Lyson, N B (2000): Lessons learned from the development of an Abl tyrosine kinase inhibitor for chronic myelogenous leukemia, J Clin Invest, (vol. 105), No. 1, pp. 3-7.

[54] Buchdunger, E; Zimmermann, J; Mett, H; Meyer, T; Muller, M; Regenass, U and Lydon, N B (1998): Selective inhibition of the platelet-derived growth factor signal transduction pathway by a protein-tyrosine kinase inhibitor of the 2-phenylaminopyrimidine class, Proc Am Assoc, (vol. 95), No. 20, p. >12069.

[55] Buchdunger, E; Zimmermann, J; Mett, H; Meyer, T; Müller, M; Druker, B J and Lydon, N B (1996): Inhibition of the Abl protein kinase in vitro and in vivo by a 2-Phenylaminopyrimidine Derivate, Cancer Res, (vol. 56), pp. 100-4.

[56] Gambacorti-Passerini, C; le Coutre, P and Mologni, L (1997): Inhibition of the ABL kinase activity selectively blocks the proliferation of BCR/ABL+ leukemic cells and induces apoptosis, Blood Cells Mol Dis, (vol. 23), pp. 380-94.

[57] le Coutre, P; Mologni, L; Marchesi, E; Buchdunger, E; Giardini, R; Formelli, F and Gambacorti-Passerini, C (1999): In vivo eradication of human BCR/ABL-positive leukemia cells with an Abl kinase inhibitor, J Natl Cancer Inst, (vol. 91), No. 2, pp. 163-8.

[58] Druker, B J; Talpaz, M; Resta, D J; Peng, B; Buchdunger, E; Ford, J M; Lydon, N B; Kantarjian, H; Capdeville, R; Ohno-Jones, S and Sawyers, C L (2001): Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia, N Engl J Med, (vol. 344), No. 14, pp. 1031-7.

[59] Druker, B J; Sawyers, C; Kantarjian, H; Resta, D J; Reese, S F; Ford, J M; Capdeville, R and Talpaz, M (2001): Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the philadelphia chromosome, N Engl J Med, (vol. 344), No. 14, pp. 1038-42.

[60] Kantarjian, H; Sawyers, C ; Hochhaus, A; Guilhot, F; Schiffer, C; Gambacorti-Passerini, C; Niederwieser, D; Resta, D J; Capdeville, R; Zoellner, U; Talpaz, M; Druker, B J; Goldman, J; O´Brien, S G; Russell, N; Fischer, T; Ottmann, O ; Cony-Makhoul, P; Facon, T; Stone, R; Miller, C ; Tallman, M; Brown, R; Schuster, M; Loughran, T; Gratwohl, A; Mandelli, F; Saglio, G; Lazzarino, M; Russo, D; Baccarani, M; Morra, E and Group, International STI571 CML Study (2002): Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia, N Engl J Med, (vol. 9), No. 28, pp. 645-52.

[61] Talpaz, M; Silver, R T; Druker, B J; Goldman, J M; Gambacorti-Passerini, C; Guilhot, F; Schiffer, C A; Fischer, T; Deininger, M W; Lennard, A L; Hochhaus, A; Ottmann, O G; Gratwohl, A; Baccarani, M; Stone, R; Tura, S; Mahon, F X; Fernandes-Reese, S; Gathmann, I; Capdeville, R; Kantarjian, H and Sawyers, C (2002): Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study, Blood, (vol. 99), No. 6, pp. 1928-37.

[62] Sawyers, C; Hochhaus, A; Feldman, E; Goldman, J M and Miller, C B (2002): Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study, Blood, (vol. 99), No. 10, pp. 3530-9.

[63] O´Brien, S G; Guilhot, F; Larson, R A; Gathmann, I; Baccarani, M; Cervantes, F; Cornelissen, J J; Fischer, T; Hochhaus, A; Hughes, T ; Lechner, C; Nielsen, J L; Rousselot, P; Reiffers, J; Saglio, G; Shepherd, J; Simonsson, B; Gratwohl, A; Goldman, J; Kantarjian, H; Taylor, K; Verhoef, G; Bolton, A E; Capdeville, R; Druker, B J and IRIS, Investigation (2003): Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia, N Engl J Med, (vol. 348), No. 11, pp. 994-1004.

[64] le Coutre, P; Tassi, E; Varella-Garcia, M; Barni, R; Mologni, L; Cabrita, G; Marchesi, E; Supino, R and Gambacorti-Passerini, C (2000): Induction of resistance to the Abelson inhibitor STI571 in human leukemic cells through gene amplification, Blood, (vol. 95), No. 5, pp. 1758-66.

[65] Mahon, F X; W, Deininger M; Schultheis, B; Chabrol, J; Reiffers, J; Goldman, J M and Melo, J V (2000): Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance, Blood, (vol. 96), No. 3, pp. 1070-9.

[66] Weisberg, E and Griffin, J D (2000): Mechanism of resistance to the ABL tyrosine kinase inhibitor STI 571 in BCR/ABL-transformed hematopoietic cell lines, Blood, (vol. 95), No. 11, pp. 3498-505.

[67] Gorre, M E; Mohammed, M; Ellwood, K; Hsu, N; R, Paquette; Rao, P N and Sawyers, C (2001): Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification, Science, (vol. 293), No. 5531, pp. 876-80.

[68] Hochhaus, A; Kreil, S; Corbin, A; La Rosee, P; Lahaye, T; Berger, U; Cross, N C; Linkesch, W; Druker, B J; Hehlmann, R; Gambacorti-Passerini, C; Corneo, G and D´Incalci, M (2001): Roots of clinical resistance to STI 571 cancer therapy, Science, (vol. 293), No. 5538, p. 2163.

[69] Ambudjar, S V; Lelong, I H; Zhang, L and Cardarelli, C (1998): Purification and reconstitution of human P-glycoprotein, Methods Enzymol, (vol. 292), pp. 492-504.

[70] Ashida, H; Oonishi, T and Uyesaka, N (1998): Kinetic analysis of the mechanism of action of the multidrug transporter, J Theor Biol, (vol. 195), No. 2, pp. 219-32.

[71] Cordon-Cardo, C; O´Brien, J P; Boccia, J; Casals, D; Bertino, J R and Melamed, M R (1990): Expression of the multidrug resistance gene product (P-glycoprotein) in human normal and tumor tissues, J Histochem Cytochem, (vol. 38), No. 9, pp. 1277-87.

[72] Scarborough, G A (1995): Drug-stimulated ATPase activity of the human P-glycoprotein, J Bioenerg Biomembr, (vol. 27), No. 1, pp. 37-41.

[73] Gros, P; Ben Neriah, Y B; Croop, J M and Housman, D E (1986): Isolation and expression of a complementary DNA that confers multidrug resistance, Nature, (vol. 323), No. 6090, pp.728-31.

[74] Pastan, I; Gottesman, M M; Ueda, K; Lovelace, E; Rutherford, A V and Willingham, M C (1988): A retrovirus carrying an MDR1 cDNA confers multidrug resistance and polarized expression of P-glycoprotein in MDCK cells, Proc Natl Acad Sci USA, (vol. 85), No. 12, pp. 4486-90.

[75] Germann, U A; Willingham, M C; Pastan, I and Gottesman, M M (1990): Expression of the human multidrug transporter in insect cells by a recombinant baculovirus, Biochemistry, (vol. 29), No. 9, pp. 2295-303.

[76] Castillo, G; Vera, J C; Yang, C P; Horwitz, S B and Rosen, O M (1990): Functional expression of murine multidrug resistance in Xenopus laevis oocytes, Proc Natl Acad Sci USA, (vol. 87), No. 12, pp. 4737-41.

[77] Dalton, W S (1997): Detection of multidrug resistance gene ecpression in multiple myeloma, Leukemia, (vol. 11), No. 7, pp. 1166-9.

[78] Leith, C P; Kopecky, K J; Chen, I M; Eijdems, L; Slovak, M L; McConnell, T S; Head, D R; Weick, J; Grever, M R; Appelbaum, F R and Willman, C L (1999): Frequency and clinical significance of the expression of the multidrug resistance proteins MDR1/P-glycoptotein, MRP1, and LRP in acute myeloid leukemia: a Southwest Oncology Group Study, Blood, (vol. 94), No. 3, pp. 1086-99.

[79] List, A F (1996): Role of multidrug resistance and its pharmacological modulation in acute myeloid leukemia, Leukemia, (vol. 10), No. 6, pp. 937-42.

[80] Marie, J P; Helou, C; Thevenin, D; Delmer, A and Zittoun, R (1992): In vitro effect of P-glycoprotein (P-gp) modulators on drug sensitivity of leukemic progenitors (CFU-L) in acute myelogenous leukemia (AML), Exp Hematol, (vol. 20), No. 5, pp. 565-8.

[81] Willman, C L (1996): Immunophenotyping and cytogenetics in older adults with acute myeloid leukemia: significance of expression of the multidrug resistance gene-1 (MDR1), Leukemia, (vol. 10), No. Suppl 1, pp. 33-5.

[82] Del Poeta, G; Venditti, A; Aronica, G; Stasi, R; Cox, M C; Buccisano, F; Bruno, A; Tamburini, A; Suppo, G; Simone, M D; Epiceno, A M; Del Moro, B; Masi, M; Papa, G and Amadori, S (1997): P-glycoprotein expression in de novo acute myeloid leukemia, Leuk Lymphoma, (vol. 27), No. 3-4, pp. 257-74.

[83] Turkina, A G; Baryshnikov, A Y ; Sedyakhina, N P; Folomeshkina, S V; Sokolova, M A; Choroshco, N D and Stavrovosaya, A A (1996): Studies of P-glycoprotein in chronic myelogenous leukaemia patients: expression, activity and correlation with CD34 antigen, Br J Haematol., (vol. 92), No. 1, pp. 88-96.

[84] Maia, R C; Carrico, M K; Klumb, C E; Noronha, H; Coelho, A M; Vasconcelos, F C and Ruimanek, V M (1997): Clinical approach to circumvention of multidrug resistance in refractory leukemic patients: association of cyclosporin A with etoposide, J Exp Clin Cancer Res, (vol. 16), No. 4, pp. 419-24.

[85] Kuwazuru, Y; Yoshimura, A; Hanada, S; Ichikawa, M; Saito, T; Uozumi, K; Utsunomiya, A; Arima, T and Akiyama, S (1990): Expression of the multidrug transporter, P-glycoprotein, in chronic myelogenous leukaemia cells in blast crisis, Br J Haematol., (vol. 74), No. 1, pp. 24-9.

[86] Michelutti, A; Michieli, M; Damiani, D; Melli, C; Geromin, A; Russo, D; Fanin, R and Baccarani, M (1994): Overexpression of MDR-related p170 glycoprotein in chronic myeloid leukemia, Haematologica, (vol. 79), No. 3, pp. 200-4.

[87] Shah, N P; Nicoll, J M; Nagar, B; Gorre, M E; Paquette, R L; Kuriyan, J and Sawyers, C (2002): Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia, Cancer Cell, (vol. 2), No. 2, pp. 117-25.

[88] Branford, S; Rudzki, Z; Walsh, S; Grigg, A; Arthur, C; Taylor, K; Herrmann, R; Lynch, K P and Hughes, T P (2002): High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance, Blood, (vol. 99), No. 9, pp. 3472-5.

[89] von Bubnoff, N; Schneller, F; Peschel, C and Duyster, J (2002): BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukemia to STI571: a prospective study, Lancet, (vol. 359), pp. 487-91.

[90] Roumiantsev, S; Shah, N P; Gorre, M E; Nicoll, J; Brasher, B B; Sawyers, C and Van Etten, R A (2002): Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Thr-253 in the Abl kinase domain P-loop, Proc Natl Acad Sci USA, (vol. 99), No. 16, pp. 10700-5.

[91] Barthe, C; Cony-Makhoul, P; Melo, J V and Mahon, J R (2001): Roots of clinical resistance to STI-571 cancer therapy, Science, (vol. 293), No. 5538, p. 2163.

[92] Gambacorti-Passerini, C B; Gunby, R H; Piazza, R; Galietta, A; Rostagno, R and Scapozza, L (2003): Molecular mechanisms of resistance to imatinib in Philadelphia-chromosome-positive leukaemias, Lancet Oncol, (vol. 4), No. 2, pp. 75-85.

[93] Roche-Lestienne, C; Soenen-Cornu, V; Grardel-Duflos, N; Lai, J L; Philippe, N; Facon, T; Fenaux, P and Preudhomme, C (2002): Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI 571, and they can pre-exist to the onset of treatment, Blood, (vol. 100), No. 3, pp. 1014-8.

[94] Shah, N P; Nicoll, J M; Gorre, M E; Paquette, R L and Ford, J M (2001): Resistance to Gleevec: Sequence Analysis reveals a spectrum of BCR/ABL kinase domain mutations in both acquired- and de novo- resistant cases of chronic myelogenous leukemia (CML) in myeloid blast crisis, Blood, (vol. 98), p. abs. #3205.

[95] Launeuville, P; Sun, G; Timm, M and Vekemans, M (1992): Clonal evolution in a myeloid cell line transformed to interleukin-3 independent growth by retroviral transduction and expression of p210bcr/abl, Blood, (vol. 80), pp. 1788-1797.

[96] Gambacorti-Passerini, C; Barni, R; le Coutre, P; Zucchetti, M; Cabrita, G; Cleris, L; Rossi, F; Gianazza, E; Brueggen, J; Cozens, R; Pioltelli, P; Pogliani, E; Corneo, G; Formelli, F and D´Incalci, M (2000): Role of alpha 1 acid glycoprotein in the in vivo resistance of human BCR-ABL(+) leukemic cells to the abl inhibitor STI 571, J Natl Cancer Inst, (vol. 92), No. 20, pp. 1641-50.

[97] Kremer, J M; Wilting, J and Janssen, L H (1988): Drug binding to human alpha-1-acid gycoprotein to monitor therapy of cancer patients, Pharmacol Rev, (vol. 40), No. 1, pp. 1-47.

[98] Ganz, P A; Shell, W E and Tokes, Z A (1983): Evaluation of a radioimmunoassay for alpha 1-acid glycoprotein to monitor therapy of cancer patients, J Natl Cancer Inst, (vol. 71), No. 1, pp. 25-30.

[99] Kreuzer, K-A; Lass, U; Nagel, S; Ellerbrok, H; Pauli, G; Pawlaczyk-Peter, B; Siegert, W; Huhn, D and Schmidt, C A (2000): Applicability of an absolute quantitative procedure to monitor intra-individual bcr/abl transcript kinetics in clinical samples from chronic myelogenous leukemia patients, Int J Cancer, (vol. 86), No. 5, pp.741-6.

[100] Kreuzer, K-A; Lass, U; Landt, O; Nitsche, A; Laser, J; Ellerbrok, H; Pauli, G; Huhn, D and Schmidt, C A (1999): Highly sensitive and specific fluorescence reverse transcription-PCR assay for the pseudogene-free detection of beta-actin transcripts as quantitative reference, Clin Chem, (vol. 45), No. 2, pp. 297-300.

[101] King-Underwood, L and Pritchard-Jones, K (1998): Wilms´ tumor (WT1) gene mutations occur mainly in acute myeloid leukemia and may vonfer drug resistance, Blood, (vol. 91), No. 8, pp. 2961-8.

[102] Scharnhorst, V; Dekker, P; van der Eb, A J and Jochemsen, A G (1999): Internal translation initiation generates novel WT1 protein isoforms with distinct biological properties, J Biol Chem, (vol. 274), No. 33, pp. 23456-62.

[103] Madden, S L; Cook, D M; Morris, J F; Gashler, A; Sukhatme, V P and Rauscher, F J 3rd (1991): Transcriptional repression mediated by the WT1 Wilms tumor gene product, Science, (vol. 253), No. 5027, pp. 1550-3.

[104] Wang, W L; Healy, M E; Sattler, M; Verma, S; Lin, J; Maulik, G; Stiles, C D; Griffin, J D; Johnson, B E and Salgia, R (2000): Growth inhibition and modulation of kinase pathways of small cell lung cancer cell lines by the novel tyrosine kinase inhibitor STI 571., Oncogene, (vol. 19), No. 31, pp. 3521-8.

[105] Goodyer, P; Dehbi, M; Torban, E; Bruening, W and Pelletier, J (1995): Repression of the retinoic acid receptor-alpha gene by the Wilms´ tumor suppressor gene product, wt1, Oncogene, (vol. 10), No. 6, pp. 1125-9.

[106] Hewitt, S M; Hamada, S; McDonnell, T J; Rauscher, F J 3rd and Saunders, G F (1995): Regulation of the proto-oncogenes bcl-2 and c-myc by the Wilms´ tumor suppressor gene WT1, Cancer Res, (vol. 55), No. 22, pp. 5386-9.

[107] Maheswaran, S; Park, S; Bernard, A; Morris, J F; Rauscher, F J 3rd; Hill, D E and Haber, D A (1993): Physical and functional interaction between WT1 and p53 proteins, Proc Natl Acad Sci USA, (vol. 90), No. 11, pp. 5100-4.

[108] Baird, P N and Simmons, P J (1997): Expression of the Wilms´ tumor gene (WT1) in normal hemapoiesis, Exp Hematol, (vol. 25), No. 4, pp. 312-20.

[109] Inoue, K; Ogawa, H; Sonoda, Y; Kimura, T; Sakabe, H; Oka, Y; Miyake, S; Tamaki, H; Oji, Y; Yamagami, T; Tatekawa, T; Soma, T; Kishimoto, T and Sugiyama, H (1997): Aberrant overexpression of the Wilms tumor gene (WT1) in human leukemia, Blood, (vol. 89), No. 4, pp. 1405-12.

[110] Inoue, K; Sugiyama, H; Ogawa, H; Nakagawa, M and Yamagami, T (1994): WT1 as a new prognostic factor and a new marker for the detection of minimal residual disease in acute leukemia, Blood, (vol. 84), No. 9, pp. 3071-9.

[111] Kreuzer, K-A; Saborowski, A; Lupberger, J; Appelt, C; Na, I-K; le Coutre, P and Schmidt, C A (2001): Fluorescent 5´-exonuclease assay for the absolute quantification of Wilms´ tumor gene (WT1) mRNA: implications of monitoring human leukaemias, Br J Haematol., (vol. 114), No. 2, pp. 313-8.

[112] le Coutre, P; Kreuzer, K-A; Na, I-K; Lupberger, J; Holdhoff, M; Appelt, C; Schwarz, M; Muller, C; Gambacorti-Passerini, C; Platzbecker, U; Bonnet, R; Ehninger, G and Schmidt, C A (2002): Determination of a-1 acid Glycoprotein in patients with Ph+ chronic myeloid leukemia during the first 13 weeks of therapy with STI571, Blood Cells Mol Dis, (vol. 28), No. 1, pp. 75-85.

[113] Brunner, E; Domhof, S and Langer, F (2003): Nonparametrical analysis of longitudinal data in factorial experiments, Wiley, New York.

[114] Cancer Therapy Evaluation Program. Common Toxicity Criteria 2.0. CDTD, NCI, NIH, DHSS. March 1998. [http://ctep.info.nih.gov/ctc3.htm].

[115] Schwarz, M; Kreuzer, K-A; Baskaynak, G; Dörken, B and le Coutre, P (2002): Imatinib-induced acute generalized exanthematous pustulosis (AGEP) in two patients with chronic myeloid leukemia, Eur J Haematol, (vol. 69), pp. 254-56.

[116] Parsons, B L and Heflich, R H (1997): Genotypic selection methods for the direct analysis of point mutations, Mutat Res, (vol. 387), No. 2, pp. 97-121.

[117] Pourzand, C and Cerutti, P (1993): Genotypic mutation analysis by RFLP/PCR, Mutat Res, (vol. 288), No. 1, pp. 113-21.

[118] van Houten, V M (2000): Molecular assays for the diagnosis of minimal residual head-and neck-cancer: methods, reliability, pitfalls, and solutions, Clin Cancer Res, (vol. 6), No. 10, pp. 3803-16.

[119] Sotlar, K; Escribano, L; Landt, O; Möhrle, S; Herrero, S; Torrelo, A; Lass, U; Horny, H P and Bultmann, B (2003): One-Step Detection of c-kit Point Mutations Using Peptide Nucleic Acid-Mediated Polymerase Chain Reaction Clamping and Hybridization Probes, Am J Pathol, (vol. 162), pp. 737-746.

[120] Kharbanda, S; Pandey, P; Yamauchi, T; Kumar, S; Kaneki, M; Kumar, V; Bharti, A; Yuan, Z M; Ghanem, L; Rana, A; Weichselbaum, R; Johnson, G and Kufe, D (2000): Activation of MEDK Kinase 1 by the c-Abl Protein Tyrosine Kinase in Response to DNA Damage, Molecular and Cellular Biology, (vol. 20), No. 14, pp. 4979-89.

[121] Buchdunger, E; Cioffi, C L; Law, N; Stover, D; Ohno-Jones, S; Druker, B J and Lydon, N B (2000): Abl protein-tyrosin inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors, J Pharmacol Exp Ther, (vol. 295), No. 1, pp. 139-45.

[122] Larghero, J; Mahon, F X and Madeleine-Chambrin, I (2001): Elevated levels of the plasma protein alpha 1 acid glycoprotein in chronic myelogenous leukemia in blast crisis mediate pharmacological resistance to Gleevec (STI571, imatinib) in vitro and are associated with primary resistance in vivo., Presented at the 43rd annual meeting of the American Society of Hematology, Orlando, FL, (vol. Dec 10).

[123] le Coutre, P; Kreuzer, K A ; Na, I K ; Schwarz, M; Lupberger, J; Holdhoff, M; Baskaynak, G; Gschaidmeier, H; Platzbecker, U; Ehninger, G; Prejzner, W; Huhn, D and Schmidt, C A (2003): Imatinib in Philadelphia chromosome-positive chronic phase CML patients: Molecular and cytogenetic response rates and prediction of clinical outcome, Am J Hematol, (vol. 73), pp. 249-255.

[124] Gahmberg, C G and Andersson, L C (1978): Leucocyte surface origin of human alpha1-acid glycoprotein (orosomucoid), J Exp Med, (vol. 148), No. 2, pp. 507-21.

[125] Kreuzer, K-A; Lass, U; Bohn, A; Landt, O and Schmidt, C A (1999): Lightcycler technology for the quantitation of bcr/abl fusion transcripts, Cancer Res, (vol. 59), pp. 3171-4.

[126] Sugiyama, H (1998): Wilms tumor gene (WT1) as a new marker for the detection of minimal residual disease in leukemia, Leuk Lymphoma, (vol. 30), No. 1-2, pp. 55-61.

[127] Wang, Z Y; Madden, S L; Deuel, T F and Rascher, F J (1995): The Wilms´tumor gene product, represses transcription of the platelet-derived growth factor A-chain gene, J Biol Chem, (vol. 267), pp. 21999-22002.

[128] Giles, F J; Kantarjian, H M; Cortes, J; Thomas, D A; Talpaz, M and Manshouri, T (1999): Multidrug resistance protein expression in chronic myeloid leukemia: associations and significance, Cancer, (vol. 86), pp. 805-13.

[129] Illmer, T; Schaich, M; Platzbecker, U; Freiberg-Richter, J; Oelschlägel, U; von Bonin, M; Pursche, S; Bergemann, T; Ehninger, G and Schleyer, E (2004): P-glycoprotein-mediated drug efflux is a resistance mechanism of chronic myelogenous leukemia cells to treatment with imatinib mesylate, Leukemia, (vol. 18), pp. 401-8.

[130] Mahon, F X; Belloc, F; Lagarde, V; Chollet, C; Moreau-Gaudry, F; Reiffers, J; Goldman, J M and Melo, J V (2003): MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models, Blood, (vol. 101), No. 6, pp. 2368-73.

[131] Dai, H; Marbach, P and Lemaire, M (2003): Distribution of STI-571 to the brain is limited by P-glycoprotein-mediated efflux, J Pharmacol Exp Ther, (vol. 304), pp. 1085-92.

[132] Müller, M C; Lahaye, T and Hochhaus, A (2002): Resistenz auf tumorspezifische Therapie mit Imatinib durch klonale Selektion mutierter Zellen, Dtsch Med Wochenschr, (vol. 127), pp. 2205-7.

[133] Tipping, A J; Mahon, F X; Lagarde, V; Goldman, J M and Melo, J V (2001): Restoration of sensitivity to STI571 in STI571-resistant chronic myeloid leukemia cells, Blood, (vol. 98), pp. 3864-67.

[134] Topaly, J; Zeller, W J and Fruehauf, S (2002): Combination therapy with imatinib mesylate (STI571): Synopsis of in vitro studies, Br J Haematol, (vol. 119), pp. 3-14.

[135] Kano, Y; Akutsu, M; Tsunoda, S; Mano, H; Sato, Y; Honma, Y and Furukawa, Y (2001): In vitro cytotoxic effects of a tyrosine kinase inhibitor STI571 in combination with commonly used antileukemicagents, Blood, (vol. 97), No. 7, pp. 1999-2007.

[136] Thiesing, J T; Ohno-Jones, S; Kolibaba, K S and Druker, B J (2000): Efficacy of STI571, an Abl tyrosine inhibitor, in conjunction with other antileukemic agents against Bcr-abl-positive cells, Blood, (vol. 96), No. 9, pp. 3195-9.

[137] Topaly, J; Schad, M; Zeller, W J; Ho, A D and Fruehauf, S (2001b): Strong synergism of different signal transduction inhibitors in chronic myelogenous leukemia, Blood, (vol. 98), p. 617a.

[138] Kantarjian, H; Talpaz, M; O´Brien, S; Giles, F; Garcia-Manero, G; Faderl, S; Thomas, D; Shan, J; Rios, M B and Cortes, J (2003): Dose escalation of imatinib mesylate can overcome resistance to standard-dose therapy in patients with chronic myelogenous leukemia, Blood, (vol. 101), No. 2, pp. 473-75.

[139] Pinilla-Ibarz, J; Cathcart, K; Korontsvit, T; Soignet, S; Boccia, J; Caggiano, J; Lai, L; Jimenez, J; Kolitz, J and Scheinberg, D A (2000): Vaccination of patients with chronic myelognous leukemia with bcr-abl oncogene breakpont fusion peptides generates specific immune responses, Blood, (vol. 95), pp. 1781-7.

[140] Westermann, J; Schlimper, C; Richter, G; Mohm, J; Dörken, B and Pezzuto, A (2004): T-cell recognition of bcr/abl in healthy donors and in patients with chronic myeloid leukemia, Br J Haematol, (vol. 125), pp. 213-6.

[141] Kantarjian, H; Smith, T L; O´Brien, S; Beran, M; Pierce, S and Talpaz, M (1995): Prolonged survival in chronic myelogenous leukemia after cytogenetic response to interferon-alpha therapy, Ann Intern Med, (vol. 122), No. 254.

[142] Talpaz, M; Kantarjian, H; McCredie, K; Trujillo, JM; Keating, JM and Gutterman, J U (1986): Hematologic remission and cytogenetic improvement induced by recombinant human interferlon alpha in chronic myelogenous leukemia, N Engl J Med, (vol. 314), No. 1065.

[143] Kantarjian, H; Keating, MJ; Estey, EH; O´Brien, S; Pierce, S; Beran, M; Koller, C; Feldman, E and Talpaz, M (1992): Treatment of advanced stages of Philadelphia chromosome-positive chronic myelogenous leukemia with interferon-alpha and low-dose cytarabine, J Clin Oncol, (vol. 10), No. 5, pp. 772-8.

[144] Kantarjian, H; Talpaz, M; Kontayiannis, D; Gutterman, J; Keating, M J; Estey, E H; O´Brien, S; Rios, M B; Beran, M and Deisseroth, A (1992): Treatment of chronic myelogenous leukemia in accelerated and blastic phase with daunorubicin, high-dose cytarabine and granulocyte macrophage colony stimulating factor, J Clin Oncol, (vol. 10), pp. 398-405.

[145] Tipping, A J; Deininger, M W; Goldman, J M and Melo, J V (2003): Comparative gene expression profile of chronic myeloid leukemia cells innately resistant to imatinib mesylate, Exp Hematol, (vol. 31), pp. 1073-80.


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