Onkologie, Hämatologie - Daten und Informationen

Literatur zu Kapitel 8.2: Therapie der AML mit neuen Substanzen

Autor/en: U. Krug, H. Serve, C. Müller-Tidow, W.E. Berdel
Letzte Änderung: 01.07.2008
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    Phase II dosing study of cytarabine chemotherapy in combination with cenersen (EL625) and idarubicin in refractory and relapsed acute myelogenous leukemia (AML).
    J Clin Oncol 2007;25:374.

  • Arguello F et al.
    Flavopiridol induces apoptosis of normal lymphoid cells, causes immunosuppression, and has potent antitumor activity in vivo against human leukemia and lymphoma xenografts.
    Blood 1998;91:2482-2490.

  • Baer MR et al.
    Phase 3 study of the multidrug resistance modulator PSC-833 in previously untreated patients 60 years of age and older with acute myeloid leukemia: Cancer and Leukemia Group B Study 9720.
    Blood 2002;100:1224-1232.

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    Deguelin, A PI3K/AKT inhibitor, enhances chemosensitivity of leukaemia cells with an active PI3K/AKT pathway.
    Br J Haematol 2005;129:677-686.

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    Imatinib mesylate in the treatment of Core Binding Factor leukemias with KIT mutations. A report of three cases.
    Leuk Res 2005;29:397-400.

  • Cammenga J et al.
    Extracellular KIT receptor mutants, commonly found in core binding factor AML, are constitutively active and respond to imatinib mesylate.
    Blood 2005;106:3958-3961.

  • Campos L et al.
    High expression of bcl-2 protein in acute myeloid leukemia cells is associated with poor response to chemotherapy.
    Blood 1993;81:3091-3096.

  • Care RS et al.
    Incidence and prognosis of c-KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias.
    Br J Haematol 2003;121:775-777.

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    Targeting Survivin expression induces cell proliferation defect and subsequent cell death involving mitochondrial pathway in myeloid leukemic cells.
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    Small-molecule XIAP inhibitors derepress downstream effector caspases and induce apoptosis of acute myeloid leukemia cells.
    Blood 2005;105:4043-4050.

  • Claus R, Almstedt M, Lubbert M.
    Epigenetic treatment of hematopoietic malignancies: in vivo targets of demethylating agents.
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  • Cortes J et al.
    A randomized trial of liposomal daunorubicin and cytarabine versus liposomal daunorubicin and topotecan with or without thalidomide as initial therapy for patients with poor prognosis acute myelogenous leukemia or myelodysplastic syndrome.
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  • Cortes J et al.
    Phase I study of bortezomib in refractory or relapsed acute leukemias.
    Clin Cancer Res 2004;10:3371-3376.

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    Predictors of Clinical Response in Patients with High Risk Acute Myeloid Leukemia Receiving Treatment with the Histone Deacetylase Inhibitor Sodium Valproate.
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    A Randomized, Placebo-Controlled, Double Blind Trial of the MDR Modulator, Zosuquidar, during Conventional Induction and Post-Remission Therapy for Pts >60 Years of Age with Newly Diagnosed Acute Myeloid Leukemia (AML) or High-Risk Myelodysplastic Syndrome (HR-MDS): ECOG 3999.
    Blood 2006;108:164A.

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    Thalidomide is an inhibitor of angiogenesis.
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  • Dai Y et al.
    Farnesyltransferase inhibitors interact synergistically with the Chk1 inhibitor UCN-01 to induce apoptosis in human leukemia cells through interruption of both Akt and MEK/ERK pathways and activation of SEK1/JNK.
    Blood 2005;105:1706-1716.

  • Dias S et al.
    Autocrine stimulation of VEGFR-2 activates human leukemic cell growth and migration.
    J Clin Invest 2000;106:511-521.

  • Fabre C et al.
    Treatment of AML with Azacytidine (AZA): Current results of the French ATU Program.
    Blood 2007;110:1849a.

  • Farmer JA, Torre-Amione G.
    Comparative tolerability of the HMG-CoA reductase inhibitors.
    Drug Saf 2000;23:197-213.

  • Fiedler W et al.
    A phase 2 clinical study of SU5416 in patients with refractory acute myeloid leukemia.
    Blood 2003;102:2763-2767.

  • Fiedler W et al.
    A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease.
    Blood 2005;105:986-993.

  • Fiedler W et al.
    An open, phase 1 study of Cediranib in Patients with Acute Myeloid Leukemia (AML).
    Blood 2007;110:895a.

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    Clinical activity and safety of the histone deacetylase inhibitor MGCD0103: Results of a phase I study in patients with leukemia or myelodysplastic syndromes (MDS).
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  • Garcia-Manero G et al.
    Phase 1/2 study of the combination of 5-aza-2'-deoxycytidine with valproic acid in patients with leukemia.
    Blood 2006b;108:3271-3279.

  • Garcia-Manero G et al.
    Phase I/II study of a novel oral isotype-selective histone deacetylase (HDAC) inhibitor MGCD0103 in combination with azacytidine in patients (pts) with high-risk myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML).
    J Clin Oncol 2007;25:372.

  • Gore SD et al.
    Combined Methyltransferase/Histone Deacetylase Inhibition with 5-Azacytidine and MS-275 in Patients with MDS, CMMoL and AML: Clinical Response, Histone Acetylation and DNA Damage.
    Blood 2006;108:156a.

  • Gottlicher M et al.
    Valproic acid defines a novel class of HDAC inhibitors inducing differentiation of transformed cells.
    Embo J 2001;20:6969-6978.

  • Grandage VL et al.
    PI3-kinase/Akt is constitutively active in primary acute myeloid leukaemia cells and regulates survival and chemoresistance via NF-kappaB, Mapkinase and p53 pathways.
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  • Greenberg PL et al.
    Mitoxantrone, etoposide, and cytarabine with or without valspodar in patients with relapsed or refractory acute myeloid leukemia and high-risk myelodysplastic syndrome: a phase III trial (E2995).
    J Clin Oncol 2004;22:1078-1086.

  • Harousseau J-L et al.
    A randomised phase 3 study of Tipifarnib compared to best supportive care (including Hydroxyurea) in the treatment of newly diagnosed Acute Myeloid Leukemia (AML) in patients 70 years and older.
    Blood 2007;110:439a.

  • Hidalgo M, Rowinsky EK.
    The rapamycin-sensitive signal transduction pathway as a target for cancer therapy.
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  • Hu J et al.
    Arsenic in cancer therapy.
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  • Hubeek I et al.
    Potentiation of in vitro ara-C cytotoxicity by ribonucleotide reductase inhibitors, cyclin-dependent kinase modulators and the DNA repair inhibitor aphidicolin in paediatric acute myeloid leukaemia.
    Br J Haematol 2005;131:219-222.

  • Jentsch-Ullrich K et al.
    Complete molecular remission in a patient with Philadelphia-chromosome positive acute myeloid leukemia after conventional therapy and imatinib.
    Haematologica 2004;89:ECR15.

  • Kadia TM et al.
    A phase I study of the combination of a DNA topoisomerase inhibitor, idarubicin, with the histone deacetylase inhibitor vorinostat, in advanced acute leukemia.
    J Clin Oncol 2007;25:373.

  • Kaminskas E et al.
    FDA drug approval summary: azacytidine (5-azacytidine, Vidaza) for injectable suspension.
    Oncologist 2005;10:176-182.

  • Kantarjian H et al.
    Phase 2 clinical and pharmacologic study of clofarabine in patients with refractory or relapsed acute leukemia.
    Blood 2003;102:2379-2386.

  • Karp JE 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.

  • Kim R et al.
    Therapeutic potential of antisense Bcl-2 as a chemosensitizer for cancer therapy.
    Cancer 2004;101:2491-2502.

  • Kindler T et al.
    Sustained complete hematologic remission after administration of the tyrosine kinase inhibitor imatinib mesylate in a patient with refractory, secondary AML.
    Blood 2003;101:2960-2962.

  • Kindler T et al.
    Efficacy and safety of imatinib in adult patients with c-kit-positive acute myeloid leukemia.
    Blood 2004;103:3644-3654.

  • Kizaki M et al.
    Effects of novel retinoid X receptor-selective ligands on myeloid leukemia differentiation and proliferation in vitro.
    Blood 1996;87:1977-1984.

  • Lee EJ et al.
    Low dose 5-azacytidine is ineffective for remission induction in patients with acute myeloid leukemia.
    Leukemia 1990;4:835-838.

  • Levis M et al.
    A FLT3-targeted tyrosine kinase inhibitor is cytotoxic to leukemia cells in vitro and in vivo.
    Blood 2002;99:3885-3891.

  • Levis M et al.
    A Randomized, Open-Label Study of Lestaurtinib (CEP-701), an Oral FLT3 Inhibitor, Administered in Sequence with Chemotherapy in Patients with Relapsed AML Harboring FLT3 Activating Mutations: Clinical Response Correlates with Successful FLT3 Inhibition.
    Blood 2005;106:121a.

  • Lickliter JD et al.
    HA14-1 selectively induces apoptosis in Bcl-2-overexpressing leukemia/lymphoma cells, and enhances cytarabine-induced cell death.
    Leukemia 2003;17:2074-2080.

  • Liu XM et al.
    Induction of differentiation and down-regulation of c-myb gene expression in ML-1 human myeloblastic leukemia cells by the clinically effective anti-leukemia agent meisoindigo.
    Biochem Pharmacol 1996;51:1545-1551.

  • Lübbert M et al.
    Continued low-dose decitabine (DAC) is an active first-line treatment in ALL cytogenetic subgroups of older AML patients: Results of the FR00331 multicenter phase II study.
    Blood 2007;110:300a.

  • Marcucci G et al.
    A phase III randomized trial of intensive induction and consolidation chemotherapy +/- oblimersen, a pro-apoptotic Bcl-2 antisense oligonucleotide in untreated acute myeloid leukemia patients >60 years old.
    J Clin Oncol 2007;25:360.

  • Masuda Y et al.
    Beta-hydroxyisovalerylshikonin induces apoptosis in human leukemia cells by inhibiting the activity of a polo-like kinase 1 (PLK1).
    Oncogene 2003;22:1012-1023.

  • Mesa RA et al.
    Heat shock protein 90 inhibition sensitizes acute myelogenous leukemia cells to cytarabine.
    Blood 2005;106:318-327.

  • Mesters RM et al.
    Stable remission after administration of the receptor tyrosine kinase inhibitor SU5416 in a patient with refractory acute myeloid leukemia.
    Blood 2001;98:241-243.

  • Minucci S et al.
    Histone deacetylases: a common molecular target for differentiation treatment of acute myeloid leukemias?
    Oncogene 2001;20:3110-3115.

  • Mizuki M et al.
    Flt3 mutations from patients with acute myeloid leukemia induce transformation of 32D cells mediated by the Ras and STAT5 pathways.
    Blood 2000;96:3907-3914.

  • Morgan MA et al.
    Synergistic cytotoxic effects in myeloid leukemia cells upon cotreatment with farnesyltransferase and geranylgeranyl transferase-I inhibitors.
    Leukemia 2003;17:1508-1520.

  • Newman A et al.
    Selective inhibition of primary acute myeloid leukaemia cell growth by simvastatin.
    Leukemia 1994;8:2023-2029.

  • Niu C et al.
    Studies on treatment of acute promyelocytic leukemia with arsenic trioxide: remission induction, follow-up, and molecular monitoring in 11 newly diagnosed and 47 relapsed acute promyelocytic leukemia patients.
    Blood 1999;94:3315-3324.

  • O'Farrell AM et al.
    SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo.
    Blood 2003;101:3597-3605.

  • O'Reilly MS et al.
    Endostatin: an endogenous inhibitor of angiogenesis and tumor growth.
    Cell 1997;88:277-285.

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    Phase 1 trial of the proteasome inhibitor bortezomib and pegylated liposomal doxorubicin in patients with advanced hematologic malignancies.
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  • Padro T et al.
    Increased angiogenesis in the bone marrow of patients with acute myeloid leukemia.
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  • Padro T et al.
    Overexpression of vascular endothelial growth factor (VEGF) and its cellular receptor KDR (VEGFR-2) in the bone marrow of patients with acute myeloid leukemia.
    Leukemia 2002;16:1302-1310.

  • Pearce D et al.
    The Specific Aurora Kinase Inhibitor AZD1152 Significantly Affects the Growth of Human Leukaemic Cells in an In Vivo AML Model.
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    Pilot study of 5-aza-2'-deoxycytidine (Decitabine) in the treatment of poor prognosis acute myelogenous leukemia patients: preliminary results.
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    MDR1 gene expression and treatment outcome in acute myeloid leukemia.
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  • Prendergast GC.
    Farnesyltransferase inhibitors: antineoplastic mechanism and clinical prospects.
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  • Quintas-Cardama A et al.
    Phase I trial of intermittent administration of sorafenib (BAY 43-9006) for patients (pts) with refractory/relapsed acute myelogenous leukemia (AML).
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  • Recher C et al.
    Antileukemic activity of rapamycin in acute myeloid leukemia.
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  • Reiter A.
    Identification of molecular targets and treatments options in myeloproliferative disorders.
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    Targeting the Ras signaling pathway: a rational, mechanism-based treatment for hematologic malignancies?
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    DNA methylation and human disease.
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    Potentiation of the lethality of the histone deacetylase inhibitor LAQ824 by the cyclin-dependent kinase inhibitor roscovitine in human leukemia cells.
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    Functional blocks in caspase activation pathways are common in leukemia and predict patient response to induction chemotherapy.
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    Complete remission of third recurrence of acute myeloid leukemia after treatment with imatinib (STI-571).
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    Decitabine (5-Aza-2'-deoxycytidine; DAC) plus daunorubicin as a first line treatment in patients with acute myeloid leukemia: preliminary observations.
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    Randomized controlled trial of azacytidine in patients with the myelodysplastic syndrome: a study of the cancer and leukemia group B.
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    Single-agent CEP-701, a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia.
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    Constitutive activation of STAT3 and STAT5 is induced by leukemic fusion proteins with protein tyrosine kinase activity and is sufficient for transformation of hematopoietic precursor cells.
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    Blood 2005a;106:121a.

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    Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412.
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    Blocking the Raf/MEK/ERK pathway sensitizes acute myelogenous leukemia cells to lovastatin-induced apoptosis.
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    Blocking protein geranylgeranylation is essential for lovastatin-induced apoptosis of human acute myeloid leukemia cells.
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    Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies.
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