CoChat
Sign Up
Cited by 62

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Chronic Myelogenous Leukemia

Druker, Brian J., O’Brien, Stephen G., Cortes, Jorge, Radich, Jerald·2002·Hematology
DOI 10.1182/asheducation-2002.1.111
Open this paper in CoChat — free account

Abstract

The treatment options for chronic myelogenous leukemia (CML) continue to evolve rapidly. Imatinib mesylate (Gleevec, Glivec, formerly STI571) has continued to show remarkable clinical benefits and the updated results with this agent are reviewed. As relapses using single agent imatinib have occurred, particularly in advanced phase patients, the issue of whether combinations of other antileukemic agents with imatinib may yield improved results is addressed. In addition, data on new agents that have potential in the treatment of CML are reviewed. These agents are presented in the context of their molecular mechanism of action. The most recent data for stem cell transplantation, along with advances in nonmyeloablative transplants, are also reviewed. In Section I, Drs. Stephen O’Brien and Brian Druker update the current status of clinical trials with imatinib and review ongoing investigations into mechanisms of resistance and combinations of imatinib with other agents. They also present their views on integration of imatinib with other therapies. In Section II, Dr. Jorge Cortes describes the most recent data on novel therapies for CML, including farnesyl transferase inhibitors, arsenic trioxide, decitabine, and troxatyl, among others. These agents are discussed in the context of their molecular mechanism of action and rationale for use. In Section III, Dr. Jerald Radich updates the results of stem cell transplants for CML, including emerging data on nonmyeloablative transplants. He also presents data on using microarrays to stratify patients into molecularly defined risk groups.

Overview

Integrity signals

Registry

Crossref · 10.1182/asheducation-2002.1.111

Cites

3 of 3 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Research works printed but not linked: 168

  1. Buchdunger E, Matter A, Druker BJ. Bcr-Abl inhibition as a modality of CML therapeutics. Biochim Biophys Acta. 2001;1551:M11–18. · DOI
  2. Nowell PC, Hungerford DA. A minute chromosome in human chronic granulocytic leukaemia. Science. 1960;132:1497.
  3. Bartram CR, de Klein A, Hagemeijer A, et al. Translocation of c-ab1 oncogene correlates with the presence of a Philadelphia chromosome in chronic myelocytic leukaemia. Nature. 1983;306:277–280. · DOI
  4. Heisterkamp N, Stephenson JR, Groffen J, et al. Localization of the c-ab1 oncogene adjacent to a translocation break point in chronic myelocytic leukaemia. Nature. 1983;306:239–242. · DOI
  5. Groffen J, Stephenson JR, Heisterkamp N, de Klein A, Bartram CR, Grosveld G. Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22. Cell. 1984;36:93–99. · DOI
  6. Shtivelman E, Lifshitz B, Gale RP, Canaani E. Fused transcript of abl and bcr genes in chronic myelogenous leukaemia. Nature. 1985;315:550–554. · DOI
  7. Lugo TG, Pendergast AM, Muller AJ, Witte ON. Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. Science. 1990;247:1079–1082. · DOI
  8. Daley GQ, Van Etten RA, Baltimore D. Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. Science. 1990;247:824–830. · DOI · Paper page
  9. Heisterkamp N, Jenster G, ten Hoeve J, Zovich D, Pattengale PK, Groffen J. Acute leukaemia in bcr/abl transgenic mice. Nature. 1990;344:251–253. · DOI
  10. Kelliher MA, McLaughlin J, Witte ON, Rosenberg N. Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL [published correction appears in Proc Natl Acad Sci U S A 1990; 6687:9072]. Proc Natl Acad Sci U S A. 1990;87:6649–6653. · DOI
  11. Elefanty AG, Hariharan IK, Cory S. bcr-abl, the hallmark of chronic myeloid leukaemia in man, induces multiple haemopoietic neoplasms in mice. Embo J. 1990;9:1069–1078. · DOI
  12. Buchdunger E, Zimmermann J, Mett H, et al. Inhibition of the Abl protein-tyrosine kinase in vitro and in vivo by a 2-phenylaminopyrimidine derivative. Cancer Res. 1996;56:100–104.
  13. Druker BJ, Tamura S, Buchdunger E, et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med. 1996;2:561–566. · DOI · Paper page
  14. Buchdunger E, Cioffi CL, Law N, Stover D, Ohno-Jones S, Druker BJ, Lydon NB. Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors. J Pharmacol Exp Ther. 2000;295:139–145.
  15. Heinrich MC, Griffith DJ, Druker BJ, Wait CL, Ott KA, Zigler AJ. Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. Blood. 2000;96:925–932. · DOI
  16. Apperley JF, Gardembas M, Melo JV, et al. Chronic myeloproliferative diseases involving rearrangements of the platelet derived growth factor receptor beta showing rapid responses to the tyrosine kinase inhibitor imatinib mesylate. N Engl J Med. In press.
  17. Okuda K, Weisberg E, Gilliland DG, Griffin JD. ARG tyrosine kinase activity is inhibited by STI571. Blood. 2001;97:2440–2448. · DOI
  18. Schindler T, Bornmann W, Pellicena P, Miller WT, Clarkson B, Kuriyan J. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Science. 2000;289:1938–1942. · DOI
  19. Druker BJ, Talpaz M, Resta D, et al. Efficacy and safety of a specific inhibitor of the Bcr-Abl tyrosine kinase in chronic myeloid leukemia. N Engl J Med. 2001;344:1031–1037. · DOI
  20. Druker BJ, Sawyers CL, Kantarjian H, et al. 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. 2001;344:1038–1042. · DOI · Paper page
  21. Kantarjian H, Sawyers C, Hochhaus A, et al. Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia. New Engl J Med. 2002;346:645–652. · DOI
  22. Talpaz M, Silver RT, Druker BJ, et al. Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study. Blood. 2002;99:1928–1937. · DOI
  23. Sawyers CL, Hochhaus A, Feldman E, et al. Imatinib induces hematologic and cytogenetic responses in patients with chronic myeloid leukemia in myeloid blast crisis: results of a phase II study. Blood. 2002;99:3530–3539. · DOI
  24. Ottmann OG, Druker BJ, Sawyers CL, et al. A phase II study of imatinib mesylate (Glivec) in patients with relapsed or refractory Philadelphia chromosome positive acute lymphoid leukemias. Blood. In press.
  25. Druker BJ, for the IRIS (International Randomized IFN vs. STI571) Study Group. STI571 (Gleevec/Glivec, imatinib) versus interferon (IFN) + cytarabine as initial therapy for patients with CML: results of a randomized study. c2" align="center"Proc Am Soc Clin Onc. 2002;21:1a.
  26. Druker BJ, Sawyers CL, Capdeville R, Ford JM, Baccarani M, Goldman JM. Chronic myelogenous leukemia. Hematology (Am Soc Hematol Educ Program). 2001:87–112. · DOI
  27. O’Dwyer ME, Mauro MJ, Kurilik G, et al. The impact of clonal evolution on response to imatinib mesylate (STI571) in accelerated phase CML. Blood. 2002;100:1628–1633. · DOI
  28. Kantarjian H, Jorge C, O’Brien S, et al. High rates of early major and complete cytogenetic responses with imatinib mesylate therapy given at 400 mg or 800 mg orally daily in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase. Proc Am Soc Clin Onc. 2002;21:261a.
  29. van Oosterom AT, Judson I, Verweij J, et al. Safety and efficacy of imatinib (STI571) in metastatic gastrointestinal stromal tumours: a phase I study. Lancet. 2001;358:1421–1423. · DOI
  30. Thiesing JT, Ohno-Jones S, Kolibaba KS, Druker BJ. Efficacy of an Abl tyrosine kinase inhibitor in conjunction with other anti-leukemic agents against Bcr-Abl positive cells. Blood. 2000;96:3195–3199. · DOI
  31. Marley SB, Davidson RJ, Goldman JM, Gordon MY. Effects of combinations of therapeutic agents on the proliferation of progenitor cells in chronic myeloid leukaemia. Br J Haematol. 2002;116:162–165. · DOI
  32. Kano Y, Akutsu M, Tsunoda S, et al. In vitro cytotoxic effects of a tyrosine kinase inhibitor STI571 in combination with commonly used antileukemic agents. Blood. 2001;97:1999–2007. · DOI
  33. O’Dwyer ME, Mauro MJ, Kuyl J, Paquette R, Sawyers CL, Druker BJ. Preliminary evaluation of the combination of imatinib mesylate (gleevec) in combination with low dose interferon-alpha for the treatment of chronic phase CML [abstract]. Blood. 2001;98:846a.
  34. O’Brien SG, Vallance SE, Craddock C, Holyoake TL, Goldman JM, the UK PISCES Group. PEGIntron and STI571 combination evaluation study (PISCES) in chronic phase chronic myeloid leukaemia [abstract]. Blood. 2001;98:846a.
  35. Fang G, Kim CN, Perkins CL, et al. CGP57148B (STI-571) induces differentiation and apoptosis and sensitizes Bcr-Abl-positive human leukemia cells to apoptosis due to antileukemic drugs. Blood. 2000;96:2246–2253. · DOI
  36. Topaly J, Zeller WJ, Fruehauf S. Synergistic activity of the new ABL-specific tyrosine kinase inhibitor STI571 and chemotherapeutic drugs on BCR-ABL-positive chronic myelogenous leukemia cells. Leukemia. 2001;15:342–347. · DOI
  37. Druker B, Kantarjian H, Talpaz M, et al. A phase I study of the combination of gleevec (imatinib mesylate) with low dose Ara-C [abstract]. Blood. 2001;98:845a.
  38. La Rosée P, Johnson K, Moseson EM, O’Dwyer ME, Druker BJ. Preclinical evaluation of the efficacy of STI571 in combination with a variety of novel anticancer agents [abstract]. Blood. 2001;98:839a.
  39. La Rosee P, O’Dwyer ME, Druker BJ. Insights from pre-clinical studies for new combination treatment regimens with the Bcr-Abl kinase inhibitor imatinib mesylate (Gleevec/Glivec) in chronic myelogenous leukemia: a translational perspective. Leukemia. 2002;16:1213–1219. · DOI
  40. Hochhaus A, Kreil S, Corbin AS, et al. Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy. Leukemia. In press.
  41. Shah NP, Nicoll JM, Nagar B, et al. 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. 2002;2:117–125. · DOI
  42. Branford S, Rudzki Z, Walsh S, et al. 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. 2002;99:3472–3475. · DOI
  43. von Bubnoff N, Schneller F, Peschel C, Duyster J. BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study. Lancet. 2002;359:487–491. · DOI
  44. Roche-Lestienne C, Soenen-Cornu V, Grardel-Duflos N, et al. Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment. Blood. 2002;100:1014–1018. · DOI
  45. Hofmann WK, Jones LC, Lemp NA, et al. Ph(+) acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation. Blood. 2001;99:1860–1862. · DOI
  46. Graham SM, Jorgensen HG, Allan E, et al. Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood. 2002;99:319–325. · DOI
  47. Holtz MS, Slovak ML, Zhang F, Sawyers CL, Forman SJ, Bhatia R. Imatinib mesylate (STI571) inhibits growth of primitive malignant progenitors in chronic myelogenous leukemia through reversal of abnormally increased proliferation. Blood. 2002;99:3792–3800. · DOI
  48. Mow BM, Chandra J, Svingen PA, et al. Effects of the Bcr/abl kinase inhibitors STI571 and adaphostin (NSC 680410) on chronic myelogenous leukemia cells in vitro. Blood. 2002;99:664–671. · DOI
  49. Sun X, Layton JE, Elefanty A, Lieschke GJ. Comparison of effects of the tyrosine kinase inhibitors AG957, AG490, and STI571 on BCR-ABL—expressing cells, demonstrating synergy between AG490 and STI571. Blood. 2001;97:2008–2015. · DOI
  50. Dorsey JF, Jove R, Kraker AJ, Wu J. The pyrido[2,3-d]pyrimidine derivative PD180970 inhibits p210Bcr-Abl tyrosine kinase and induces apoptosis of K562 leukemic cells. Cancer Res. 2000;60:3127–3131.
  51. Topaly J, Schad M, Zeller WJ, Ho AD, Fruehauf S. Strong synergism of different signal transduction inhibitors in chronic myelogenous leukemia. [abstract] Blood. 2001;98:617a.
  52. Hoover RR, Mahon FX, Melo JV, Daley GQ. Overcoming STI571 resistance with the farnesyl transferase inhibitor SCH66336. Blood. 2002;100:1068–1071. · DOI
  53. La Rosee P, Johnson K, O’Dwyer ME, Druker BJ. In vitro studies of the combination of imatinib mesylate (Gleevec) and arsenic trioxide (Trisenox) in chronic myelogenous leukemia. Exp Hematol. 2002;30:729–737. · DOI
  54. Porosnicu M, Nimmanapalli R, Nguyen D, Worthington E, Perkins C, Bhalla KN. Co-treatment with As2O3 enhances selective cytotoxic effects of STI-571 against Bcr-Abl-positive acute leukemia cells. Leukemia. 2001;15:772–778. · DOI
  55. Sawyers CL. Chronic myeloid leukemia. N Engl J of Med. 1999;340:1330–1340. · DOI
  56. Silver RT, Woolf SH, Hehlmann R, et al. 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. 1999;94:1517–1536.
  57. Goldman JM, Druker BJ. Chronic myeloid leukemia: current treatment options. Blood. 2001;98:2039–2042. · DOI
  58. Bonifazi F, de Vivo A, Rosti G, et al. Chronic myeloid leukemia and interferon-alpha: a study of complete cytogenetic responders. Blood. 2001;98:3074–3081. · DOI
  59. Gratwohl A, Baldomero H, Urbano-Ispizua A. Transplantation in chronic myeloid leukaemia. Lancet. 2002;359:712. · DOI
  60. Marin D, Bua M, Marktel S, et al. The combination of cytogenetic response after 6 months treatment with STI571 and the presence of cytopenias in patients with CML in chronic phase resistant to or intolerant of interferon-alfa defines four different prognostic groups. [abstract] Blood. 2001;98:846a.
  61. O’Dwyer ME, Mauro MJ, Blasdel C, et al. Lack of cytogenetic response is an adverse prognostic factor for relapse of chronic phase CML patients treated with imatinib mesylate (STI571) [abstract]. Blood. 2001;98:137a
  62. Sawafuji K, Miyakawa Y, Weisberg E, Griffin JD, Ikeda Y, Kizaki M. Effects of aminopeptidase inhibitors on STI571 resistant cell lines. [abstract] Blood. 2001;98:309a
  63. Vigneri P, Wang JY. Induction of apoptosis in chronic myelogenous leukemia cells through nuclear entrapment of BCR-ABL tyrosine kinase. Nat Med. 2001;7:228–234. · DOI
  64. Yu C, Krystal G, Varticovksi L, et al. Pharmacologic mitogen-activated protein/extracellular signal-regulated kinase kinase/mitogen-activated protein kinase inhibitors interact synergistically with STI571 to induce apoptosis in Bcr/Abl-expressing human leukemia cells. Cancer Res. 2002;62:188–199.
  65. Klejman A, Rushen L, Morrione A, Slupianek A, Skorski T. Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571. Oncogene. 2002;21:5868–5876. · DOI
  66. Gatto SR, Scappini B, Verstovsek S, et al. In vitro effects of PS-341 alone and in combination with STI571 in Bcr-Abl positive cell lines both sensitive and resistant to STI571. [abstract] Blood. 2001;98:101a.
  67. Nimmanapalli R, Porosnicu M, Nguyen D, et al. Cotreatment with STI-571 enhances tumor necrosis factor alpha-related apoptosis-inducing ligand (TRAIL or apo-2L)-induced apoptosis of Bcr-Abl-positive human acute leukemia cells. Clin Cancer Res. 2001;7:350–357.
  68. Grove KL, Guo X, Liu SH, et al. Anticancer activity of beta-L-dioxolane-cytidine, a novel nucleoside analogue with the unnatural L configuration. Cancer Res. 1995;55:3008–3011.
  69. Giles FJ, Cortes JE, Baker SD, et al. Troxacitabine, a novel dioxolane nucleoside analog, has activity in patients with advanced leukemia. J Clin Oncol. 2001;19:762–771. · DOI
  70. Giles FJ, Garcia-Manero G, Cortes JE, et al. Phase II study of troxacitabine, a novel dioxolane nucleoside analog, in patients with refractory leukemia. J Clin Oncol. 2002;20:656–664. · DOI
  71. O’Brien S, Kantarjian H, Keating M, et al. Homoharringtonine therapy induces responses in patients with chronic myelogenous leukemia in late chronic phase. Blood. 1995;86:3322–3326. · DOI
  72. Kantarjian HM, Talpaz M, Smith TL, et al. Homoharringtonine and low-dose cytarabine in the management of late chronic-phase chronic myelogenous leukemia. J Clin Oncol. 2000;18:3513–3521. · DOI
  73. Visani G, Russo D, Ottaviani E, et al. Effects of homoharringtonine alone and in combination with alpha interferon and cytosine arabinoside on ‘in vitro’ growth and induction of apoptosis in chronic myeloid leukemia and normal hematopoietic progenitors. Leukemia. 1997;11:624–628. · DOI
  74. O’Brien S, Kantarjian H, Koller C, et al. Sequential homoharringtonine and interferon-alpha in the treatment of early chronic phase chronic myelogenous leukemia. Blood. 1999;93:4149–4153. · DOI
  75. Scappini B, Onida F, Kantarjian H, et al. In vitro effects of STI571-containing drug combinations on growth of Ph-positive myelogenous leukemia-derived cells [abstract]. Blood. 2000;96:99a.
  76. Santini V, Kantarjian HM, Issa JP. Changes in DNA methylation in neoplasia: pathophysiology and therapeutic implications. Ann Intern Med. 2001;134:573–586. · DOI
  77. Issa JP, Kantarjian H, Mohan A, et al. Methylation of the ABL1 promoter in chronic myelogenous leukemia: lack of prognostic significance. Blood. 1999;93:2075–2080. · DOI
  78. Zion M, Ben-Yehuda D, Avraham A, et al. Progressive de novo DNA methylation at the bcr-abl locus in the course of chronic myelogenous leukemia. Proc Natl Acad Sci U S A. 1994;91:10722–10726. · DOI
  79. Ben-Yehuda D, Krichevsky S, Rachmilewitz EA, et al. Molecular follow-up of disease progression and interferon therapy in chronic myelocytic leukemia. Blood. 1997;90:4918–4923. · DOI
  80. Sacchi S, Kantarjian HM, O’Brien S, et al. Chronic myelogenous leukemia in nonlymphoid blastic phase: analysis of the results of first salvage therapy with three different treatment approaches for 162 patients. Cancer. 1999;86:2632–2641. · DOI
  81. Kantarjian HM, O’Brien SM, Keating M, et al. Results of decitabine therapy in the accelerated and blastic phases of chronic myelogenous leukemia. Leukemia. 1997;11:1617–1620 · DOI
  82. Issa JP, Garcia-Manero G, Mannari R, et al. Minimal effective dose of the hypomethylating agent decitabine in hematopoietic malignancies [abstract]. Blood. 2001;98:594a.
  83. Beaupre DM, Kurzrock R. RAS and leukemia: from basic mechanisms to gene-directed therapy. J Clin Oncol. 1999;17:1071–1079. · DOI
  84. Karp JE, Lancet JE, Kaufmann SH, et al. Clinical and biologic activity of the farnesyltransferase inhibitor R115777 in adults with refractory and relapsed acute leukemias: a phase 1 clinical-laboratory correlative trial. Blood. 2001;97:3361–3369. · DOI
  85. Kurzrock R, Sebti SM, Kantarjian HM, et al. Phase I study of a farnesyl transferase inhibitor, R115777, in patients with myelodysplastic syndrome [abstract]. Blood. 2001;98:623a.
  86. Kurzrock R, Cortes JE, Ryback ME, et al. Phase II study of R115777, a farnesyltransferase inhibitor, in myelodysplastic syndrome [abstract]. Blood. 2001;98:848a.
  87. Peters DG, Hoover RR, Gerlach MJ, et al. Activity of the farnesyl protein transferase inhibitor SCH66336 against BCR/ABL-induced murine leukemia and primary cells from patients with chronic myeloid leukemia. Blood. 2001;97:1404–1412. · DOI
  88. Reichert A, Heisterkamp N, Daley GQ, Groffen J. Treatment of Bcr/Abl-positive acute lymphoblastic leukemia in P190 transgenic mice with the farnesyl transferase inhibitor SCH66336. Blood. 2001;97:1399–1403. · DOI
  89. Hoover RR, Mahon F-X, Melo JV, Daley GQ. Overcoming STI571 resistance with the farnesyltransferase inhibitor SCH66336 [abstract]. Blood. 2001;98:617a. · DOI
  90. Thomas D, Cortes J, O’Brien S, et al. R115777, a Farnesyl Transferase Inhibitor (FTI), has significant anti-leukemia activity in patients with chronic myeloid leukemia [abstract]. Blood. 2001;98:727a.
  91. Rousselot P, Labaume S, Marolleau JP, et al. Arsenic trioxide and melarsoprol induce apoptosis in plasma cell lines and in plasma cells from myeloma patients. Cancer Res. 1999;59:1041–1048
  92. Wang ZG, Rivi R, Delva L, et al. Arsenic trioxide and melarsoprol induce programmed cell death in myeloid leukemia cell lines and function in a PML and PML-RARalpha independent manner. Blood. 1998;92:1497–1504. · DOI
  93. Perkins C, Kim CN, Fang G, Bhalla KN. Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-x(L). Blood. 2000;95:1014–1022. · DOI
  94. Puccetti E, Guller S, Orleth A, et al. BCR-ABL mediates arsenic trioxide-induced apoptosis independently of its aberrant kinase activity. Cancer Res. 2000;60:3409–3413.
  95. La Rosee P, Johnson K, Moseson EM, O’Dwyer M, Druker BJ. Preclinical evaluation of the efficacy of STI571 in combination with a variety of novel anticancer agents [abstract]. Blood. 2001;98:839a.
  96. Porosnicu M, Nimmanapalli R, Nguyen D, Worthington E, Perkins C, Bhalla KN. Co-treatment with As2O3 enhances selective cytotoxic effects of STI-571 against Brc-Abl-positive acute leukemia cells. Leukemia. 2001;15:772–778. · DOI
  97. Adams J, Palombella VJ, Sausville EA, et al. Proteasome inhibitors: a novel class of potent and effective antitumor agents. Cancer Res. 1999;59:2615–2622.
  98. Rothwarf DM, Karin M. The NF-kappa B activation pathway: a paradigm in information transfer from membrane to nucleus. Science’s STKE [Electronic Resource]: Signal Transduction Knowledge Environment. 1999;1999:RE1. · DOI
  99. Hamdane M, David-Cordonnier MH, D’Halluin JC. Activation of p65 NF-kappaB protein by p210BCR-ABL in a myeloid cell line (P210BCR-ABL activates p65 NF-kappaB). Oncogene. 1997;15:2267–2275. · DOI
  100. Reuther JY, Reuther GW, Cortez D, Pendergast AM, Baldwin AS, Jr. A requirement for NF-kappaB activation in Bcr-Abl-mediated transformation. Genes Devel. 1998;12:968–981. · DOI
  101. Dou QP, McGuire TF, Peng Y, An B. Proteasome inhibition leads to significant reduction of Bcr-Abl expression and subsequent induction of apoptosis in K562 human chronic myelogenous leukemia cells. J Pharmacol Exper Therapeut. 1999;289:781–790.
  102. Gatto SR, Scappini B, Verstovsek S, et al. In vitro effects of PS-341 alone and in combination with STI571 in BCR-ABL positive cell lines both sensitive and resistant to STI571 [abstract]. Blood. 2001;98:101a.
  103. Aguayo A, Kantarjian H, Manshouri T, et al. Angiogenesis in acute and chronic leukemias and myelodysplastic syndromes. Blood. 2000;96:2240–2245. · DOI
  104. Gabrilovich DI, Chen HL, Girgis KR, et al. Production of vascular endothelial growth factor by human tumors inhibits the functional maturation of dendritic cells. Nature Med. 1996;2:1096–1103. · DOI · Paper page
  105. Gabrilovich DI, Ishida T, Nadaf S, Ohm JE, Carbone DP. Antibodies to vascular endothelial growth factor enhance the efficacy of cancer immunotherapy by improving endogenous dendritic cell function. Clin Cancer Res. 1999;5:2963–2970.
  106. Verstovsek S, Kantarjian H, Manshouri T, et al. Prognostic significance of cellular vascular endothelial growth factor expression in chronic phase chronic myeloid leukemia. Blood. 2002;99:2265–2267. · DOI
  107. Chen W, Peace DJ, Rovira DK, You SG, Cheever MA. T-cell immunity to the joining region of p210BCR-ABL protein. Proc Natl Acad Sci U S A. 1992;89:1468–1472. · DOI
  108. Yotnda P, Firat H, Garcia-Pons F, et al. Cytotoxic T cell response against the chimeric p210 BCR-ABL protein in patients with chronic myelogenous leukemia. J Clin Invest. 1998;101:2290–2296. · DOI
  109. Pinilla-Ibarz J, Cathcart K, Korontsvit T, et al. Vaccination of patients with chronic myelogenous leukemia with bcr-abl oncogene breakpoint fusion peptides generates specific immune responses. Blood. 2000;95:1781–1787. · DOI
  110. Cathcart K, Pinilla-Ibarz J, Korontsvit T, et al. All CML patients vaccinated with a multivalent bcr-abl peptide vaccine show specific immune responses in a phase II trial [abstract]. Blood. 2001;98:728a.
  111. Molldrem J, Dermime S, Parker K, et al. Targeted T-cell therapy for human leukemia: cytotoxic T lymphocytes specific for a peptide derived from proteinase 3 preferentially lyse human myeloid leukemia cells. Blood. 1996;88:2450–2457. · DOI
  112. Molldrem JJ, Clave E, Jiang YZ, et al. Cytotoxic T lymphocytes specific for a nonpolymorphic proteinase 3 peptide preferentially inhibit chronic myeloid leukemia colony-forming units. Blood. 1997;90:2529–2534. · DOI
  113. Molldrem JJ, Lee PP, Wang C, et al. Evidence that specific T lymphocytes may participate in the elimination of chronic myelogenous leukemia. Nature Med. 2000;6:1018–1023. · DOI
  114. Wieder ED, Kant S, Lu S, et al. Effective specific immunity induced after PR1 peptide vaccination correlates with cytogenetic remission [abstract]. Blood. 2001;98:407a.
  115. Svingen PA, Tefferi A, Kottke TJ, et al. Effects of the bcr/abl kinase inhibitors AG957 and NSC 680410 on chronic myelogenous leukemia cells in vitro. Clin Cancer Res. 2000;6:237–249.
  116. Sun X, Layton JE, Elefanty A, Lieschke GJ. Comparison of effects of the tyrosine kinase inhibitors AG957, AG490, and STI571 on BCR-ABL—expressing cells, demonstrating synergy between AG490 and STI571. Blood. 2001;97:2008–2015. · DOI
  117. Mow BM, Chandra J, Svingen PA, et al. Effects of the Bcr/abl kinase inhibitors STI571 and adaphostin (NSC 680410) on chronic myelogenous leukemia cells in vitro. Blood. 2002;99:664–671. · DOI
  118. Clift RA, Radich J, Appelbaum FR, et al. Long-term follow-up of a randomized study comparing cyclophosphamide and total body irradiation with busulfan and cyclophosphamide for patients receiving allogeneic marrow transplants during chronic phase of chronic myeloid leukemia. Blood. 1999;94(11):3960–3962. · DOI
  119. Gratwohl A, Hermans J, Goldman JM, et al. Risk assessment for patients with chronic myeloid leukaemia before allogeneic blood or marrow transplantation. Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation. Lancet. 1998;352(9134):1087–1092. · DOI
  120. Gale RP, Hehlmann R, Zhang MJ, et al. Survival with bone marrow transplantation versus hydroxyurea or interferon for chronic myelogenous leukemia. The German CML Study Group. Blood. 1998;91(5):1810–1819.
  121. van Rhee F, Szydlo RM, Hermans J, et al. Long-term results after allogeneic bone marrow transplantation for chronic myelogenous leukemia in chronic phase: a report from the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation. Bone Marrow Transplant. 1997;20(7):553–560. · DOI
  122. Craddock C, Szydlo RM, Klein JP, et al. Estimating leukemia-free survival after allografting for chronic myeloid leukemia: a new method that takes into account patients who relapse and are restored to complete remission. Blood. 2000;96(1):86–90. · DOI
  123. Clift RA, Buckner CD, Thomas ED, et al. Marrow transplantation for chronic myeloid leukemia: a randomized study comparing cyclophosphamide and total body irradiation with busulfan and cyclophosphamide. Blood. 1994;84(6):2036–2043. · DOI
  124. Slattery JT, Clift RA, Buckner CD, et al. Marrow transplantation for chronic myeloid leukemia: the influence of plasma busulfan levels on the outcome of transplantation. Blood. 1997;89(8):3055–3060. · DOI
  125. Goldman JM, Szydlo R, Horowitz MM, et al. Choice of pretransplant treatment and timing of transplants for chronic myelogenous leukemia in chronic phase. Blood. 1993;82(7):2235–2238. · DOI
  126. Lee SJ, Klein JP, Anasetti C, et al. The effect of pretransplant interferon therapy on the outcome of unrelated donor hematopoietic stem cell transplantation for patients with chronic myelogenous leukemia in first chronic phase. Blood. 2001;98(12):3205–3211. · DOI
  127. Giralt S, Szydlo R, Goldman JM, et al. Effect of short-term interferon therapy on the outcome of subsequent HLA-identical sibling bone marrow transplantation for chronic myelogenous leukemia: an analysis from the international bone marrow transplant registry. Blood. 2000;95(2):410–415.
  128. Morton AJ, Gooley T, Hansen JA, et al. Association between pretransplant interferon-alpha and outcome after unrelated donor marrow transplantation for chronic myelogenous leukemia in chronic phase. Blood. 1998;92(2):394–401. · DOI
  129. Hehlmann R, Hochhaus A, Kolb HJ, et al. Interferon-alpha before allogeneic bone marrow transplantation in chronic myelogenous leukemia does not affect outcome adversely, provided it is discontinued at least 90 days before the procedure. Blood. 1999;94(11):3668–3677. · DOI
  130. Beelen DW, Graeven U, Elmaagacli AH, et al. Prolonged administration of interferon-alpha in patients with chronic-phase Philadelphia chromosome-positive chronic myelogenous leukemia before allogeneic bone marrow transplantation may adversely affect transplant outcome. Blood. 1995;85(10):2981–2990. · DOI
  131. Davies SM, DeFor TE, McGlave PB, et al. Equivalent outcomes in patients with chronic myelogenous leukemia after early transplantation of phenotypically matched bone marrow from related or unrelated donors. Am J Med. 2001;110(5):339–346. · DOI
  132. Hansen JA, Gooley TA, Martin PJ, et al. Bone marrow transplants from unrelated donors for patients with chronic myeloid leukemia. N Engl J Med. 1998;338(14):962–968. · DOI
  133. Weisdorf DJ, Anasetti C, Antin JH, et al. Allogeneic bone marrow transplantation for chronic myelogenous leukemia: comparative analysis of unrelated versus matched sibling donor transplantation. Blood. 2002;99(6):1971–1977. · DOI
  134. McGlave PB, Shu XO, Wen W, et al. Unrelated donor marrow transplantation for chronic myelogenous leukemia: 9 years’ experience of the national marrow donor program. Blood. 2000;95(7):2219–2225. · DOI
  135. Bensinger WI, Martin PJ, Storer B, et al. Transplantation of bone marrow as compared with peripheral-blood cells from HLA-identical relatives in patients with hematologic cancers. N Engl J Med. 2001;344(3):175–181. · DOI
  136. Elmaagacli AH, Beelen DW, Opalka B, Seeber S, Schaefer UW. The risk of residual molecular and cytogenetic disease in patients with Philadelphia-chromosome positive first chronic phase chronic myelogenous leukemia is reduced after transplantation of allogeneic peripheral blood stem cells compared with bone marrow. Blood. 1999;94(2):384–389. · DOI
  137. Elmaagacli AH, Basoglu S, Peceny R, et al. Improved disease-free-survival after transplantation of peripheral blood stem cells as compared with bone marrow from HLA-identical unrelated donors in patients with first chronic phase chronic myeloid leukemia. Blood. 2002;99(4):1130–1135. · DOI
  138. Remberger M, Ringden O, Blau IW, et al. No difference in graft-versus-host disease, relapse, and survival comparing peripheral stem cells to bone marrow using unrelated donors. Blood. 2001;98(6):1739–1745. · DOI
  139. Childs R, Chernoff A, Contentin N, et al. Regression of metastatic renal-cell carcinoma after nonmyeloablative allogeneic peripheral-blood stem-cell transplantation. N Engl J Med. 2000;343(11):750–758. · DOI
  140. Giralt S, Thall PF, Khouri I, et al. Melphalan and purine analog-containing preparative regimens: reduced-intensity conditioning for patients with hematologic malignancies undergoing allogeneic progenitor cell transplantation. Blood. 2001;97(3):631–637. · DOI
  141. McSweeney PA, Niederwieser D, Shizuru JA, et al. Hematopoietic cell transplantation in older patients with hematologic malignancies: replacing high-dose cytotoxic therapy with graft-versus-tumor effects. Blood. 2001;97(11):3390–3400. · DOI
  142. McGlave PB, De Fabritiis P, Deisseroth A, et al. Autologous transplants for chronic myelogenous leukaemia: results from eight transplant groups. Lancet. 1994;343(8911):1486–1488. · DOI
  143. Olavarria E, Kanfer E, Szydlo R, et al. High-dose busulphan alone as cytoreduction before allogeneic or autologous stem cell transplantation for chronic myeloid leukaemia: a single-centre experience. Br J Haematol. 2000;108(4):769–777. · DOI
  144. Carella AM, Lerma E, Corsetti MT, et al. Autografting with Philadelphia chromosome-negative mobilized hematopoietic progenitor cells in chronic myelogenous leukemia. Blood. 1999;93(5):1534–1539. · DOI
  145. Meloni G, Capria S, Vignetti M, et al. Ten-year follow-up of a single center prospective trial of unmanipulated peripheral blood stem cell autograft and interferon-alpha in early phase chronic myeloyd leukemia. Haematologica. 2001;86(6):596–601.
  146. Gaiger A, Lion T, Kalhs P, et al. Frequent detection of BCR-ABL specific mRNA in patients with chronic myeloid leukemia (CML) following allogeneic and syngeneic bone marrow transplantation (BMT). Leukemia. 1993;7(11):1766–1772.
  147. Hughes TP, Morgan GJ, Martiat P, Goldman JM. Detection of residual leukemia after bone marrow transplant for chronic myeloid leukemia: role of polymerase chain reaction in predicting relapse. Blood. 1991;77(4):874–878. · DOI
  148. Lin F, van Rhee F, Goldman JM, Cross NC. Kinetics of increasing BCR-ABL transcript numbers in chronic myeloid leukemia patients who relapse after bone marrow transplantation. Blood. 1996;87(10):4473–4478. · DOI
  149. Lion T, Henn T, Gaiger A, Kalhs P, Gadner H. Early detection of relapse after bone marrow transplantation in patients with chronic myelogenous leukaemia. Lancet. 1993;341(8840):275–276. · DOI
  150. Mensink E, van de Locht A, Schattenberg A, et al. Quantitation of minimal residual disease in Philadelphia chromosome positive chronic myeloid leukaemia patients using real-time quantitative RT-PCR. Br J Haematol. 1998;102(3):768–774. · DOI
  151. Miyamura K, Tahara T, Tanimoto M, et al. Long persistent bcr-abl positive transcript detected by polymerase chain reaction after marrow transplant for chronic myelogenous leukemia without clinical relapse: a study of 64 patients. Blood. 1993;81(4):1089–1093. · DOI
  152. Olavarria E, Kanfer E, Szydlo R, et al. Early detection of BCR-ABL transcripts by quantitative reverse transcriptase-polymerase chain reaction predicts outcome after allogeneic stem cell transplantation for chronic myeloid leukemia. Blood. 2001;97(6):1560–1565. · DOI
  153. Pichert G, Roy DC, Gonin R, et al. Distinct patterns of minimal residual disease associated with graft-versus-host disease after allogeneic bone marrow transplantation for chronic myelogenous leukemia. J Clin Oncol. 1995;13(7):1704–1713. · DOI
  154. Radich JP, Gehly G, Gooley T, et al. Polymerase chain reaction detection of the BCR-ABL fusion transcript after allogeneic marrow transplantation for chronic myeloid leukemia: results and implications in 346 patients. Blood. 1995;85(9):2632–2638. · DOI
  155. Radich JP, Gooley T, Bryant E, et al. The significance of bcr-abl molecular detection in chronic myeloid leukemia patients “late,” 18 months or more after transplantation. Blood. 2001;98(6):1701–1707. · DOI
  156. Roth MS, Antin JH, Ash R, et al. Prognostic significance of Philadelphia chromosome-positive cells detected by the polymerase chain reaction after allogeneic bone marrow transplant for chronic myelogenous leukemia. Blood. 1992;79(1):276–282. · DOI
  157. Sawyers CL, Timson L, Kawasaki ES, Clark SS, Witte ON, Champlin R. Molecular relapse in chronic myelogenous leukemia patients after bone marrow transplantation detected by polymerase chain reaction. Proc Natl Acad Sci U S A. 1990;87(2):563–567. · DOI
  158. Branford S, Hughes TP, Rudzki Z. Monitoring chronic myeloid leukaemia therapy by real-time quantitative PCR in blood is a reliable alternative to bone marrow cytogenetics. Br J Haematol. 1999;107(3):587–599. · DOI
  159. Mughal TI, Yong A, Szydlo RM, et al. Molecular studies in patients with chronic myeloid leukaemia in remission 5 years after allogeneic stem cell transplant define the risk of subsequent relapse. Br J Haematol. 2001;115(3):569–574. · DOI
  160. Higano CS, Chielens D, Raskind W, et al. Use of alpha-2a-interferon to treat cytogenetic relapse of chronic myeloid leukemia after marrow transplantation. Blood. 1997;90(7):2549–2554. · DOI
  161. van Rhee F, Lin F, Cross NC, et al. Detection of residual leukaemia more than 10 years after allogeneic bone marrow transplantation for chronic myelogenous leukaemia. Bone Marrow Transplant. 1994;14(4):609–612.
  162. Dazzi F, Szydlo RM, Cross NC, et al. Durability of responses following donor lymphocyte infusions for patients who relapse after allogeneic stem cell transplantation for chronic myeloid leukemia. Blood. 2000;96(8):2712–2716. · DOI
  163. Formankova R, Honzatkova L, Moravcova J, et al. Prediction and reversion of post-transplant relapse in patients with chronic myeloid leukemia using mixed chimerism and residual disease detection and adoptive immunotherapy. Leuk Res. 2000;24(4):339–347. · DOI
  164. Hasford J, Pfirrmann M, Hehlmann R, et al. 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. 1998;90(11):850–858. · DOI
  165. Sokal JE, Cox EB, Baccarani M, et al. Prognostic discrimination in “good-risk” chronic granulocytic leukemia. Blood. 1984;63(4):789–799. · DOI
  166. Golub TR, Slonim DK, Tamayo P, et al. Molecular classification of cancer: class discovery and class prediction by gene expression monitoring. Science. 1999;286(5439):531–537. · DOI · Paper page
  167. Alizadeh AA, Eisen MB, Davis RE, et al. Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling. Nature. 2000;403(6769):503–511. · DOI · Paper page
  168. Hofmann WK, de Vos S, Elashoff D, et al. Relation between resistance of Philadelphia-chromosome-positive acute lymphoblastic leukaemia to the tyrosine kinase inhibitor STI571 and gene-expression profiles: a gene-expression study. Lancet. 2002;359(9305):481–486. · DOI

Cited by

See all 62

Metadata

Authors
Druker, B. J., O’Brien, S. G., Cortes, J., & Radich, J.
Venue
Hematology
Publisher
American Society of Hematology
Published
2002-01-01
Volume
2002
Issue
1
Pages
111-135
ISSN
  • 1520-4391
  • 1520-4383
DOI
10.1182/asheducation-2002.1.111
Cited by
62
References
3
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review