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1. Porter DL, Alyea EP, Antin JH, DeLima M, Estey E, Falkenburg JH, Hardy N, Kroeger N, Leis J, Levine J, Maloney DG, Peggs K, Rowe JM, Wayne AS, Giralt S, Bishop MR, van Besien K: NCI First International Workshop on the Biology, Prevention, and Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation: Report from the Committee on Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation. Biol Blood Marrow Transplant; 2010 Nov;16(11):1467-503
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NCI First International Workshop on the Biology, Prevention, and Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation: Report from the Committee on Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation.
  • Relapse is a major cause of treatment failure after allogeneic hematopoietic stem cell transplantation (alloHSCT).
  • Treatment options for relapse have been inadequate, and the majority of patients ultimately die of their disease.
  • There is no standard approach to treating relapse after alloHSCT.
  • Withdrawal of immune suppression and donor lymphocyte infusions are commonly used for all diseases; although these interventions are remarkably effective for relapsed chronic myelogenous leukemia, they have limited efficacy in other hematologic malignancies.
  • Conventional and novel chemotherapy, monoclonal antibody therapy, targeted therapies, and second transplants have been utilized in a variety of relapsed diseases, but reports on these therapies are generally anecdotal and retrospective.
  • As such, there is an immediate need for well-designed, disease-specific trials for treatment of relapse after alloHSCT.
  • This report summarizes current treatment options under investigation for relapse after alloHSCT in a disease-specific manner.
  • In addition, recommendations are provided for specific areas of research necessary in the treatment of relapse after alloHSCT.
  • [MeSH-major] Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Hodgkin Disease / therapy. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / therapy. Lymphocyte Transfusion. Lymphoma, Non-Hodgkin. Multiple Myeloma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Recurrence. Transplantation, Homologous. Treatment Failure

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  • (PMID = 20699125.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24 CA117879
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS241037; NLM/ PMC2955517
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2. Kim YJ, Kim DW, Lee S, Chung NG, Hwang JY, Kim YL, Min CK, Kim CC: Preemptive treatment of minimal residual disease post transplant in CML using real-time quantitative RT-PCR: a prospective, randomized trial. Bone Marrow Transplant; 2004 Mar;33(5):535-42
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  • [Title] Preemptive treatment of minimal residual disease post transplant in CML using real-time quantitative RT-PCR: a prospective, randomized trial.
  • Immunotherapy in the form of donor lymphocyte infusions in early-phase relapse might be advantageous as it induces a higher response, but this may be offset by increased toxicity, especially during the early period after transplantation.
  • Among 45 consecutive patients receiving an allograft for CML, 13 patients were diagnosed to have molecular relapse (MRel), as defined by real-time quantitative reverse transcriptase-polymerase chain reaction, and another four patients were diagnosed to have cytogenetic relapse (CRel) within 6 months.
  • Patients with MRel were randomly assigned to either a 'no therapy' group (group A, n=6), in which immunotherapy was reserved until CRel, or an 'immunotherapy' group (group B, n=7).
  • In patients relapsing directly into CRel (n=4), immunotherapy induced MR in two patients (50%).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Neoplasm, Residual / diagnosis. Neoplasm, Residual / therapy. Reverse Transcriptase Polymerase Chain Reaction
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Benzamides. Combined Modality Therapy. Disease Progression. Female. Graft vs Host Disease / drug therapy. Humans. Imatinib Mesylate. Immunosuppressive Agents / administration & dosage. Male. Middle Aged. Piperazines / administration & dosage. Polymerase Chain Reaction. Prospective Studies. Pyrimidines / administration & dosage. Recurrence. Remission Induction. Survival Analysis. Transplantation, Homologous

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  • (PMID = 14716340.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Immunosuppressive Agents; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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3. Rea D, Legros L, Raffoux E, Thomas X, Turlure P, Maury S, Dupriez B, Pigneux A, Choufi B, Reman O, Stéphane D, Royer B, Vigier M, Ojeda-Uribe M, Recher C, Dombret H, Huguet F, Rousselot P, Intergroupe Français des Leucémies Myéloïdes Chronique, Group for Research in Adult Acute Lymphoblastic Leukemia: High-dose imatinib mesylate combined with vincristine and dexamethasone (DIV regimen) as induction therapy in patients with resistant Philadelphia-positive acute lymphoblastic leukemia and lymphoid blast crisis of chronic myeloid leukemia. Leukemia; 2006 Mar;20(3):400-3
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  • [Title] High-dose imatinib mesylate combined with vincristine and dexamethasone (DIV regimen) as induction therapy in patients with resistant Philadelphia-positive acute lymphoblastic leukemia and lymphoid blast crisis of chronic myeloid leukemia.
  • Imatinib combined with high-dose chemotherapy is now becoming the gold standard for treatment of Philadelphia chromosome-positive acute leukemias.
  • Thirty-one patients (18 relapsing or refractory Ph+ acute lymphoblastic leukemias and 13 lymphoid blast crisis chronic myelogenous leukemias) were enrolled.
  • The median bcr-abl/abl ratio after the induction course was 0.1%.
  • Median time to neutrophil recovery was 21 days.
  • Nine out of 19 patients under 55 years received allogenic stem cell transplantation after a median time of 78 days post-CR.
  • Patients older than 55 years experienced a 90% CR rate without additional toxicities, suggesting the DIV regimen may also be proposed as a front line therapy in older patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Benzamides. Dexamethasone / administration & dosage. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Pilot Projects. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Vincristine / administration & dosage


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4. Hasselbalch HC, Birgens H, Dufva IH, Dalseg AM, Brown Pde N, Jensen MK, Vangsted A: [Novel medical treatment modalities in hematology]. Ugeskr Laeger; 2008 Jun 9;170(24):2115-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Novel medical treatment modalities in hematology].
  • Today several monoclonal antibodies, including the anti-CD20 antibody (rituximab), the anti-CD52 antibody (alemtuzumab) and the anti-CD33 antibody (gemtuzumab ozogamacin) are all integrated in the therapeutic armamentarium of patients with malignant lymphoma, chronic lymphocytic leukaemia and acute myelogenous leukaemia, respectively.
  • Rituximab has also been shown to be highly effective in the treatment of refractory autoimmune haemolytic anemias, idiopathic thrombocytopenia, and relapsing thrombotic thrombocytopenic purpura.
  • New signal transduction inhibitors, dasatinib and nilotinib, are being used in patients with chronic myelogeneous leukaemia who develop resistance to imatinib.
  • Thalidomide, lenalidomide and bortezomib have all been shown to be highly effective in multiple myeloma, and JAK2-inhibitors have entered phase II studies of patients with JAK2-positive primary myelofibrosis and related diseases.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Hematologic Diseases / drug therapy. Immunologic Factors / therapeutic use. Leukemia / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Aminoglycosides / therapeutic use. Anemia, Hemolytic / drug therapy. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Benzamides. Benzoates / therapeutic use. Boronic Acids / therapeutic use. Bortezomib. Carbazoles / therapeutic use. Carrier Proteins / therapeutic use. Cyclophosphamide / therapeutic use. Dasatinib. Humans. Hydrazines / therapeutic use. Imatinib Mesylate. Indoles / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Multiple Myeloma / drug therapy. Myelodysplastic Syndromes / drug therapy. Piperazines / therapeutic use. Purpura, Thrombocytopenic / drug therapy. Pyrazines / therapeutic use. Pyrazoles / therapeutic use. Pyrimidines / therapeutic use. Receptors, Fc / therapeutic use. Recombinant Fusion Proteins. Rituximab. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use. Thiazoles / therapeutic use. Thrombopoietin. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

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  • (PMID = 18565291.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzoates; 0 / Boronic Acids; 0 / Carbazoles; 0 / Carrier Proteins; 0 / Hydrazines; 0 / Immunologic Factors; 0 / Indoles; 0 / Piperazines; 0 / Pyrazines; 0 / Pyrazoles; 0 / Pyrimidines; 0 / Receptors, Fc; 0 / Recombinant Fusion Proteins; 0 / Thiazoles; 0 / eltrombopag; 0 / gemtuzumab; 0 / romiplostim; 4F4X42SYQ6 / Rituximab; 4Z8R6ORS6L / Thalidomide; 639089-54-6 / VX680; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; 8N3DW7272P / Cyclophosphamide; 9014-42-0 / Thrombopoietin; A3ULP0F556 / eculizumab; DO989GC5D1 / lestaurtinib; F0P408N6V4 / lenalidomide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; RBZ1571X5H / Dasatinib
  • [Number-of-references] 40
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5. 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, D'Incalci M: Role of alpha1 acid glycoprotein in the in vivo resistance of human BCR-ABL(+) leukemic cells to the abl inhibitor STI571. J Natl Cancer Inst; 2000 Oct 18;92(20):1641-50
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  • [Title] Role of alpha1 acid glycoprotein in the in vivo resistance of human BCR-ABL(+) leukemic cells to the abl inhibitor STI571.
  • BACKGROUND: Chronic myeloid leukemia is caused by a chromosomal translocation that results in an oncogenic fusion protein, Bcr-Abl.
  • Bcr-Abl is a tyrosine kinase whose activity is inhibited by the antineoplastic drug STI571.
  • This drug can cure mice given an injection of human leukemic cells, but treatment ultimately fails in animals that have large tumors when treatment is initiated.
  • METHODS Nude mice were injected with KU812 Bcr-Abl(+) human leukemic cells.
  • Cells recovered from relapsing animals were used for in vitro experiments.
  • RESULTS: Tumors regressed initially in all STI571-treated mice, but all mice treated 15 days after injection of tumor cells eventually relapsed.
  • Relapsed animals did not respond to further STI571 treatment, and their Bcr-Abl kinase activity in vivo was not inhibited by STI571, despite high plasma concentrations of the drug.
  • However, tumor cells from resistant animals were sensitive to STI571 in vitro, suggesting that a molecule in the plasma of relapsed animals may inactivate the drug.
  • The plasma protein alpha1 acid glycoprotein (AGP) bound STI571 at physiologic concentrations in vitro and blocked the ability of STI571 to inhibit Bcr-Abl kinase activity in a dose-dependent manner.
  • When animals bearing large tumors were treated with STI571 alone or with a combination of STI571 and erythromycin, greater tumor reductions and better long-term tumor-free survival (10 of 12 versus one of 13 at day 180; P:<.001) were observed after the combination treatment.
  • CONCLUSION: AGP in the plasma of relapsed animals binds to STI571, preventing this compound from inhibiting the Bcr/Abl tyrosine kinase.
  • Molecules such as erythromycin that compete with STI571 for binding to AGP may enhance the therapeutic potential of this drug.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Fusion Proteins, bcr-abl / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Orosomucoid / drug effects. Orosomucoid / metabolism. Piperazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Benzamides. Blotting, Western. Drug Resistance, Neoplasm. Drug Synergism. Drug Therapy, Combination. Enzyme Inhibitors / pharmacology. Erythromycin / pharmacology. Female. Humans. Imatinib Mesylate. Mice. Mice, Nude. Phosphorylation / drug effects. Time Factors. Tumor Cells, Cultured

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  • [CommentIn] J Natl Cancer Inst. 2000 Oct 18;92(20):1626-7 [11036101.001]
  • (PMID = 11036109.001).
  • [ISSN] 0027-8874
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Orosomucoid; 0 / Piperazines; 0 / Pyrimidines; 63937KV33D / Erythromycin; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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6. Larghero J, Leguay T, Mourah S, Madelaine-Chambrin I, Taksin AL, Raffoux E, Bastie JN, Degos L, Berthaud P, Marolleau JP, Calvo F, Chomienne C, Mahon FX, Rousselot P: Relationship between elevated levels of the alpha 1 acid glycoprotein in chronic myelogenous leukemia in blast crisis and pharmacological resistance to imatinib (Gleevec) in vitro and in vivo. Biochem Pharmacol; 2003 Nov 15;66(10):1907-13
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  • [Title] Relationship between elevated levels of the alpha 1 acid glycoprotein in chronic myelogenous leukemia in blast crisis and pharmacological resistance to imatinib (Gleevec) in vitro and in vivo.
  • The Abl tyrosine kinase inhibitor imatinb is becoming a standard for the treatment of chronic myelogenous leukemia (CML).
  • However, Bcr-Abl gene mutations have been reported mainly in relapsing or resistant patients.
  • We aimed to investigate if alpha 1 acid glycoprotein (AGP), an acute phase drug binding protein, could be a biological marker for pharmacological resistance to imatinib in nine patients in acute phase CML.
  • No mutation in the adenosine triphosphate domain of Abl were detected before the initiation of imatinib therapy.
  • By using in vitro tests combining various imatinib concentrations (1-10 microM) with purified human AGP (1 and 3 mg/mL), we demonstrate that imatinib-induced apoptosis of K562 or fresh leukemic CML cells is abrogated or reduced.
  • In patients with CML in blastic phase, AGP levels could reflect pharmacological resistance to imatinib, suggesting that increased dosage of imatinib or the use of a competitor to drug binding should be recommended to optimize the therapeutic effect of the drug.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Blast Crisis / pathology. Drug Resistance, Neoplasm / physiology. Orosomucoid / metabolism. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Apoptosis. Benzamides. Humans. Imatinib Mesylate. K562 Cells. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Tumor Cells, Cultured

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  • (PMID = 14599548.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Orosomucoid; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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7. Levine JE, Barrett AJ, Zhang MJ, Arora M, Pulsipher MA, Bunin N, Fort J, Loberiza F, Porter D, Giralt S, Drobyski W, Wang D, Pavletic S, Ringden O, Horowitz MM, Collins R Jr: Donor leukocyte infusions to treat hematologic malignancy relapse following allo-SCT in a pediatric population. Bone Marrow Transplant; 2008 Aug;42(3):201-5
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  • [Title] Donor leukocyte infusions to treat hematologic malignancy relapse following allo-SCT in a pediatric population.
  • Donor leukocyte infusions (DLI) can reverse relapse of hematologic malignancy following allogeneic hematopoietic stem cell transplant (HSCT) in some cases.
  • Little is known regarding the effectiveness of DLI in children who relapse after HSCT.
  • We report outcomes of 49 children who received DLI for relapse after allogeneic transplant.
  • Prognosis was particularly poor (0/14 responses) for patients relapsing within 6 months from transplant.
  • DLI rarely induced remission when given as sole therapy for marrow relapse.
  • One-year disease-free survival was 30% (6/20) in patients who received DLI as consolidation following chemotherapy.
  • The development of GVHD grades 1-2 was associated with superior 3-year survival than patients who developed GVHD grades 3-4 (P<0.002).
  • To determine the benefit of DLI, 45 children who received DLI for relapse (four children without matches were excluded) were compared to 1229 children with similar characteristics whose relapse was not treated with DLI.
  • There was no difference in survival (P=0.30) once adjustments were made to account for the time from relapse to DLI.
  • Although a few children achieved durable remissions when DLI was used as part of a post-relapse treatment strategy, DLI was unsuccessful in the majority of cases.
  • Strategies may be better directed at preempting post transplant relapse.
  • [MeSH-major] Hematologic Neoplasms / surgery. Hematologic Neoplasms / therapy. Leukocyte Transfusion. Stem Cell Transplantation / methods
  • [MeSH-minor] Acute Disease. Child. Combined Modality Therapy. Disease-Free Survival. Female. Graft vs Host Disease / epidemiology. Graft vs Tumor Effect. Humans. Leukemia / surgery. Leukemia / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Male. Recurrence. Tissue Donors. Transplantation, Homologous

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  • (PMID = 18490913.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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9. Kobbe G, Schneider P, Rohr U, Fenk R, Neumann F, Aivado M, Dietze L, Kronenwett R, Hünerlitürkoglu A, Haas R: Treatment of severe steroid refractory acute graft-versus-host disease with infliximab, a chimeric human/mouse antiTNFalpha antibody. Bone Marrow Transplant; 2001 Jul;28(1):47-9
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  • [Title] Treatment of severe steroid refractory acute graft-versus-host disease with infliximab, a chimeric human/mouse antiTNFalpha antibody.
  • Patients with severe aGVHD not responding to treatment with steroids have a poor prognosis.
  • Patients (CML 2, MM 1, AML 1) developed grade III-IV GVHD at a median of 34 days (range 15-76) after myeloablative PBSCT (two), donor lymphocyte infusion for relapsed CML (one) or non-myeloablative PBSCT (one), respectively.
  • All patients had severe intestinal involvement in addition to skin and/or liver disease and had received treatment with high-dose steroids (four) for a median of 11 days (range 5-17) in addition to CsA (four) and MMF (three).
  • At present two patients are alive >200 days after therapy, one with limited cGVHD.
  • Infliximab is apparently an active drug for the treatment of aGVHD.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Graft vs Host Disease / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Animals. Anti-Inflammatory Agents / administration & dosage. Female. Hematologic Neoplasms / complications. Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Infliximab. Male. Mice. Middle Aged. Recombinant Fusion Proteins / administration & dosage. Salvage Therapy. Steroids / therapeutic use. Transplantation, Homologous / adverse effects. Treatment Outcome. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 11498743.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Recombinant Fusion Proteins; 0 / Steroids; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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10. Leventakos K, Lewis RE, Kontoyiannis DP: Fungal infections in leukemia patients: how do we prevent and treat them? Clin Infect Dis; 2010 Feb 1;50(3):405-15
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  • [Title] Fungal infections in leukemia patients: how do we prevent and treat them?
  • Invasive fungal infections (IFIs) remain an important cause of morbidity and mortality in patients with acute or chronic leukemia.
  • Advances in the pharmacotherapy of fungal infections and a shift in the epidemiological characteristics of fungal pathogens toward fluconazole-resistant Candida species and saprophytic molds have placed a greater emphasis on selection of broader-spectrum agents for empirical therapy of IFIs in this high-risk population.
  • Newer diagnostic modalities, such as the Aspergillus galactomannan test, the 1,3-beta-d-glucan test, and polymerase chain reaction detection of fungal DNA, may facilitate the earlier diagnosis of IFIs, but their role in detecting breakthrough infection and their usefulness as a marker to withhold antifungal therapy in high-risk leukemia patients with IFI are less obvious, especially in patients who are receiving antifungal prophylaxis.
  • Only 2 strategies have been shown in prospective studies to improve survival from mold infection in patients with acute myelogenous leukemia or myelodysplastic syndrome:.
  • (1) preemptive initiation of antifungal therapy at first sign of invasive aspergillosis on computed tomography (CT) scan and (2) antifungal prophylaxis with posaconazole.
  • CT-guided treatment decisions are more complex in patients with advanced leukemia, however, because of concomitant infection or relapsing malignancy.
  • Similarly, posaconazole is often not a viable prophylaxis or treatment option in patients with poor oral intake, gastrointestinal dysfunction, or possible drug interaction (eg, proton pump inhibitor prophylaxis in patients on high-dose glucocorticosteroids).
  • As a result, the management of IFI in patients with leukemia demands an individualized treatment plan.
  • [MeSH-major] Antifungal Agents / therapeutic use. Chemoprevention / methods. Leukemia / complications. Mycoses / epidemiology. Mycoses / prevention & control

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  • (PMID = 20047485.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents
  • [Number-of-references] 104
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11. Wassmann B, Klein SA, Scheuring U, Pfeifer H, Martin H, Gschaidmeier H, Hoelzer D, Ottmann OG: Hematologic and cytogenetic remission by STI571 (Glivec) in a patient relapsing with accelerated phase CML after second allogeneic stem cell transplantation. Bone Marrow Transplant; 2001 Oct;28(7):721-4
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  • [Title] Hematologic and cytogenetic remission by STI571 (Glivec) in a patient relapsing with accelerated phase CML after second allogeneic stem cell transplantation.
  • We describe the clinical activity of the ABL kinase inhibitor STI571 in a patient with accelerated phase of chronic myeloid leukemia (CML) relapsing after a second allogeneic BMT and with minimal levels of donor chimerism.
  • STI571 induced sustained hematological and cytogenetic remission combined with controllable GvHD, therapeutic goals not achieved by two preceding allogeneic transplants and repeated donor lymphocyte transfusions (DLT).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow Transplantation. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Accelerated Phase / drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Salvage Therapy
  • [MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Benzamides. Colitis / chemically induced. Combined Modality Therapy. Enzyme Inhibitors / adverse effects. Enzyme Inhibitors / therapeutic use. Female. Graft Survival. Graft vs Host Disease / etiology. Graft vs Leukemia Effect. Humans. Hydroxyurea / therapeutic use. Imatinib Mesylate. Immunosuppression. Interferon-alpha / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / therapy. Lymphocyte Transfusion. Middle Aged. Neoplasm, Residual. Neutropenia / chemically induced. Remission Induction. Transplantation Conditioning. Transplantation, Homologous

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  • (PMID = 11704799.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; X6Q56QN5QC / Hydroxyurea
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12. Usuki K, Kanda Y, Iijima K, Iki S, Hirai H, Urabe A: [Chronic myelogenous leukemia in cessation of therapy after sustained CCR with interferon]. Rinsho Ketsueki; 2003 Dec;44(12):1161-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chronic myelogenous leukemia in cessation of therapy after sustained CCR with interferon].
  • In Ph(+) CML patients who achieved complete cytogenetic response (CCR) with interferon-alpha (IFN) treatment, how long the treatment should be continued has not well been investigated.
  • We report here 2 CML cases who stopped the treatment after CCR had been sustained with IFN for 2-3 years.
  • A 49-year-old male (case 1) achieved CCR 6 months after the initiation of IFN treatment.
  • CCR had been maintained for 3 years, and then the treatment was ceased.
  • CCR has been sustained without any therapy for 4 years.
  • In case 2, a 50-year-old male, CCR was achieved after 8 years of IFN treatment, and maintained for 2 years.
  • One month after cessation of the treatment, CML relapsed cytogenetically.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Interferon-alpha / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Cytogenetic Analysis. Drug Administration Schedule. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Treatment Outcome

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  • (PMID = 14978932.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha
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13. Gopcsa L, Barta A, Bányai A, Dolgos J, Halm G, Pálóczi K: Salvage chemotherapy with donor lymphocyte infusion and STI 571 in a patient relapsing with B-lymphoblastic phase chronic myeloid leukemia after allogeneic bone marrow transplantation. Pathol Oncol Res; 2003;9(2):131-3
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  • [Title] Salvage chemotherapy with donor lymphocyte infusion and STI 571 in a patient relapsing with B-lymphoblastic phase chronic myeloid leukemia after allogeneic bone marrow transplantation.
  • Relapse is the main cause of treatment failure following hematopoietic stem cell transplantation for blastic phase chronic myeloid leukemia.
  • Treatment options including donor lymphocyte infusion, second transplantation, interferon- and re-induction chemotherapy are often unsuccessful.
  • We report a patient with blastic phase chronic myeloid leukemia relapsing after allogeneic stem cell transplantation.
  • The post-transplant leukemia was characterized with B-lymphoid markers and multiple genetic abnormalities including double Ph-chromosomes.
  • The disease was treated with three courses of salvage chemotherapy combined with donor lymphocyte infusion and bcr-abl tyrosine kinase inhibitor.
  • The leukemia proved to be non-responsive both to immune therapy and STI 571.
  • The presented case demonstrates the need for combination approaches in post-transplant relapsed leukemia and discusses the possible contributing mechanisms of STI-571 resistance.
  • [MeSH-major] Blast Crisis / therapy. Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukocyte Transfusion. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. B-Lymphocytes / pathology. Benzamides. Drug Resistance, Neoplasm. Enzyme Inhibitors / therapeutic use. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction. Salvage Therapy. Tissue Donors. Transplantation, Homologous. Treatment Outcome


14. Riera L, Koziner B: [Donor lymphocyte infusions as adoptive immunotherapy in patients with relapsed hematologic neoplasms post-allogenic transplant of hematopoietic progenitor cells]. Medicina (B Aires); 2000;60(2):259-69
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  • [Title] [Donor lymphocyte infusions as adoptive immunotherapy in patients with relapsed hematologic neoplasms post-allogenic transplant of hematopoietic progenitor cells].
  • An increasing body of literature has documented the usefulness of donor lymphocyte infusions in inducing remissions in patients relapsing post allogeneic hematopoietic progenitor cell transplantation.
  • Efficacy was shown to depend on the disease entity; the best results have been reported in chronic myeloid leukemia in chronic phase, where the remission rate varied between 60 and 80%.
  • In acute myeloid leukemia and myelodysplastic syndromes the remission rate ranged between 20 and 40% and in multiple myeloma the response rate was approximately 40%.
  • In contrast, results have been poor in acute lymphoid leukemia with only 10-20% and even lower reported responses.
  • Considering the efficacy of donor lymphocyte infusions in inducing responses in several hematologic neoplasias post allogeneic transplantation, as will be described in detail in this review, it is justified to anticipate an increasing role for this modality of treatment in relapsed non transplanted patients and as maintenance of the responses achieved with chemotherapy at conventional or high doses.
  • [MeSH-major] Hematologic Neoplasms / etiology. Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation. Immunotherapy, Adoptive / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion / methods
  • [MeSH-minor] Humans. Killer Cells, Natural / immunology. Multiple Myeloma / therapy. Recurrence. T-Lymphocytes / immunology. Tumor Lysis Syndrome / immunology

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  • (PMID = 10962823.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] ARGENTINA
  • [Number-of-references] 87
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15. Fassas AB, Rapoport AP, Cottler-Fox M, Chen T, Tricot G: Encouraging preliminary results in 12 patients with high-risk haematological malignancies by omitting graft-versus-host disease prophylaxis after allogeneic transplantation. Br J Haematol; 2000 Nov;111(2):662-7
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  • Immunosuppressive therapy, routinely given after allogeneic transplantation to modulate graft-versus-host disease (GVHD) may have an adverse effect on the graft-versus-tumour (GVT) effect.
  • Prompt haematological recovery [absolute neutrophil count (ANC) > 1.0 x 109/l] was observed (median time 9 d).
  • All patients developed grade III-IV GVHD (median onset 9 d), involving the skin (11), intestine (five) and liver (three).
  • Of nine evaluable patients, seven developed chronic GVHD [extensive (six), limited (one)].
  • Three patients died from treatment-related complications, two from acute GVHD and one from relapsing disease.
  • [MeSH-major] Bone Marrow Transplantation. Graft vs Tumor Effect. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukemia, Myeloid / surgery. Lymphoma, B-Cell / surgery
  • [MeSH-minor] Acute Disease. Adult. Female. Follow-Up Studies. Glucocorticoids / therapeutic use. Graft vs Host Disease / drug therapy. Humans. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / surgery. Lymphoma, Mantle-Cell / immunology. Lymphoma, Mantle-Cell / surgery. Male. Middle Aged. Multiple Myeloma / immunology. Multiple Myeloma / surgery. Pilot Projects. Prednisone / therapeutic use. Transplantation, Homologous


16. Kim YJ, Kim DW, Lee S, Kim YL, Hwang JY, Park YH, Kim HJ, Lee JW, Min WS, Kim CC: Cytogenetic clonal evolution alone in CML relapse post-transplantation does not adversely affect response to imatinib mesylate treatment. Bone Marrow Transplant; 2004 Jan;33(2):237-42
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  • [Title] Cytogenetic clonal evolution alone in CML relapse post-transplantation does not adversely affect response to imatinib mesylate treatment.
  • Good prognosis after imatinib mesylate treatment has been reported if cytogenetic clonal evolution (CE) is the only criterion of accelerated phase (AP) chronic myelogenous leukemia (CML).
  • To evaluate the impact of CE upon imatinib treatment in post-transplant settings, responses and toxicities in the relapsed AP-CE were analyzed in comparison with those in the relapsed chronic phase (CP).
  • Nonhematological adverse events were mild and tolerable in both groups and only one (7%) of the 13 patients experienced recurrent graft-versus-host disease after imatinib treatment.
  • Although this is a relatively small group of patients, we suggest that imatinib mesylate should be considered as a front-line treatment for relapsed CML as it showed the high response rate and low toxicity.
  • We also suggest that CE alone is not an important factor in the induction of cytogenetic and molecular remissions in post-transplant relapse.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Benzamides. Clone Cells. Combined Modality Therapy. Female. Graft vs Host Disease / drug therapy. Humans. Imatinib Mesylate. Male. Middle Aged. Neoplasm, Residual / drug therapy. Neoplasm, Residual / pathology. Recurrence. Remission Induction

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  • (PMID = 14628081.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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17. Blau IW, Basara N, Bischoff M, Günzelmann S, Römer E, Kirsten D, Schmetzer B, Kiehl MG, Fauser AA: Second allogeneic hematopoietic stem cell transplantation as treatment for leukemia relapsing following a first transplant. Bone Marrow Transplant; 2000 Jan;25(1):41-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Second allogeneic hematopoietic stem cell transplantation as treatment for leukemia relapsing following a first transplant.
  • We report 27 patients with relapsed acute or chronic leukemia who underwent a second hematopoietic stem cell transplant (HSCT) from a related or unrelated donor.
  • Seventeen patients were diagnosed with acute myelogenous leukemia (AML), six with acute lymphocytic leukemia (ALL) and four with chronic myeloid leukemia (CML).
  • Relapse was diagnosed between 1 and 45 months after the first HSCT.
  • Sixteen patients who relapsed had received an autologous transplant initially and 11 an allogeneic transplant.
  • Ten patients relapsed within 6 months and 17 patients later than 6 months.
  • Chemotherapy was used as reinduction for relapse after HSCT in 16 patients who had received an autologous transplant and in three who had received an allogeneic transplant, since the latter did not respond to reduction of immunosuppression to induce a graft-versus-leukemia (GVL) reaction.
  • Five of these 19 patients (26%) achieved complete remission (CR), seven patients did not respond to chemotherapy and seven achieved a partial remission (PR).
  • One patient is alive and disease-free after two allogeneic transplants (day +1538), eight patients, who relapsed after an autologous transplant followed by an allogeneic transplant (days +248 to +1140), acute myeloid leukaemia (n = 6) and chronic myeloid leukemia (n = 2) are alive and disease-free.
  • It is suggested that a second HSCT is possible for patients with leukemia relapse following the first autologous transplant.
  • A second transplant might also be offered to patients relapsing after the first allogeneic HSCT.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia / pathology. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Adult. Chronic Disease. Female. Humans. Male. Middle Aged. Recurrence. Survival Analysis. Transplantation, Homologous

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  • (PMID = 10654013.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
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18. Introna M, Borleri G, Conti E, Franceschetti M, Barbui AM, Broady R, Dander E, Gaipa G, D'Amico G, Biagi E, Parma M, Pogliani EM, Spinelli O, Baronciani D, Grassi A, Golay J, Barbui T, Biondi A, Rambaldi A: Repeated infusions of donor-derived cytokine-induced killer cells in patients relapsing after allogeneic stem cell transplantation: a phase I study. Haematologica; 2007 Jul;92(7):952-9
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  • [Title] Repeated infusions of donor-derived cytokine-induced killer cells in patients relapsing after allogeneic stem cell transplantation: a phase I study.
  • We performed a phase I study of allogeneic (donor's) CIK cells in patients relapsing after allogeneic haematopoietic stem cell transplantation (HSCT).
  • DESIGN AND METHODS: Eleven patients with acute myelogenous leukemia (n=4), Hodgkin's disease (n=3), chronic myelomonocytic leukemia, (n=1), pre-B acute lymphoblastic leukemia (n=1) and myelodysplasia (n=2), all of whom had relapsed after sibling (n=6) or matched unrelated donor (n=5) HSCT, entered this study.
  • RESULTS: Before CIK administration, six patients had received other salvage treatments including chemotherapy (n=5), radiotherapy (n=1) and unmanipulated donor lymphocytes (n=6) without any significant tumor response.
  • Acute GVHD (grade I and II) was observed in four patients, 30 days after the last CIK infusion, and progressed into extensive chronic GVHD in two cases.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / transplantation. Lymphocyte Transfusion / methods. Salvage Therapy / methods
  • [MeSH-minor] Adult. Cytokines / pharmacology. Female. Hematologic Neoplasms / therapy. Humans. Male. Middle Aged. Recurrence. Transplantation, Homologous

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  • (PMID = 17606446.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cytokines
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19. Au WY, Lie AK, Ma SK, Wan TS, Liang R, Chan EC, Kwong YL: Tyrosine kinase inhibitor STI571 in the treatment of Philadelphia chromosome-positive leukaemia failing myeloablative stem cell transplantation. Bone Marrow Transplant; 2002 Oct;30(7):453-7
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  • [Title] Tyrosine kinase inhibitor STI571 in the treatment of Philadelphia chromosome-positive leukaemia failing myeloablative stem cell transplantation.
  • Eight patients with Philadelphia chromosome-positive (Ph(+)) leukaemia relapsing from stem cell transplantation (SCT) (one syngeneic and seven allogeneic) were treated with the tyrosine kinase inhibitor STI571.
  • Five patients relapsing as chronic myeloid leukaemia (CML) in chronic phase achieved a complete haematological response, with complete and major cytogenetic responses occurring in four and one cases, respectively.
  • One patient became negative for BCR/ABL in the bone marrow.
  • Three patients relapsed as acute leukaemia (two CML in myeloblastic crisis and one Ph(+) acute lymphoblastic leukaemia), all of whom achieved haematological and cytogenetic responses.
  • One patient also became BCR/ABL negative.
  • However, pancytopenia and graft-versus-host disease led to cessation of treatment in the remaining two cases, which was followed by disease recurrence refractory to further STI treatment.
  • Our results showed that Ph(+) leukaemic relapses after SCT might respond well to STI571 therapy.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Salvage Therapy / methods
  • [MeSH-minor] Adolescent. Adult. Benzamides. Drug Evaluation. Female. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloablative Agonists. RNA, Neoplasm / analysis. Recurrence. Remission Induction. Transplantation Conditioning / methods. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 12368958.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Myeloablative Agonists; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Neoplasm; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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20. Porter DL, Levine BL, Bunin N, Stadtmauer EA, Luger SM, Goldstein S, Loren A, Phillips J, Nasta S, Perl A, Schuster S, Tsai D, Sohal A, Veloso E, Emerson S, June CH: A phase 1 trial of donor lymphocyte infusions expanded and activated ex vivo via CD3/CD28 costimulation. Blood; 2006 Feb 15;107(4):1325-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Donor lymphocyte infusions (DLIs) induce potent graft versus tumor (GVT) effects for relapsed chronic myelogenous leukemia (CML) after allogeneic stem cell transplantation (SCT) but are disappointing for other diseases.
  • We performed a phase 1 trial of ex vivo-activated DLI (aDLI) for 18 patients with relapse after SCT.
  • Patients with aggressive malignancies received induction chemotherapy, and all patients received conventional DLI (median, 1.5 x 10(8) mononuclear cells/kg) followed 12 days later by aDLI.
  • Seven patients developed acute graft versus host disease (GVHD) (5 grade I-II, 2 grade III), and 4 developed chronic GVHD.
  • Eight patients achieved complete remission, including 4 of 7 with acute lymphocytic leukemia (ALL), 2 of 4 with acute myelogenous leukemia (AML), 1 with chronic lymphocytic leukemia (CLL), and 1 of 2 with non-Hodgkin lymphoma (NHL).
  • Four complete responders relapsed while 4 remain alive in remission a median 23 months after aDLI.
  • [MeSH-major] Antigens, CD28 / blood. Antigens, CD8 / blood. Leukemia / therapy. Lymphocyte Transfusion / adverse effects. Lymphoma / therapy. Stem Cell Transplantation / adverse effects

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  • (PMID = 16269610.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD28; 0 / Antigens, CD8
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