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4. Weisser M, Tischer J, Schnittger S, Schoch C, Ledderose G, Kolb HJ: A comparison of donor lymphocyte infusions or imatinib mesylate for patients with chronic myelogenous leukemia who have relapsed after allogeneic stem cell transplantation. Haematologica; 2006 May;91(5):663-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparison of donor lymphocyte infusions or imatinib mesylate for patients with chronic myelogenous leukemia who have relapsed after allogeneic stem cell transplantation.
  • Imatinib mesylate is highly effective in relapsed chronic myelogenous leukemia (CML) after allogeneic hematopoetic stem cell transplantation (HSCT).
  • The outcome of CML patients transplanted at our center who had received only imatinib for relapse after HSCT was compared with that of patients treated with donor lymphocyte infusions (DLI).
  • Imatinib therapy resulted in a higher incidence of relapse and inferior leukemia-free survival (p=0.006 and p=0.016, respectively).
  • These data suggest that imatinib alone probably does not cure relapse after HSCT.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Salvage Therapy
  • [MeSH-minor] Adult. Benzamides. Biomarkers, Tumor / biosynthesis. Disease-Free Survival. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / biosynthesis. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / surgery. Leukemia, Myeloid, Chronic-Phase / surgery. Living Donors. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 16627251.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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5. Leda M, Ladon D, Pieczonka A, Boruczkowski D, Jólkowska J, Witt M, Wachowiak J: Donor lymphocyte infusion followed by interferon-alpha plus low dose cyclosporine A for modulation of donor CD3 cells activity with monitoring of minimal residual disease and cellular chimerism in a patient with first hematologic relapse of chronic myelogenous leukemia after allogeneic bone marrow transplantation. Leuk Res; 2001 Apr;25(4):353-7
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  • [Title] Donor lymphocyte infusion followed by interferon-alpha plus low dose cyclosporine A for modulation of donor CD3 cells activity with monitoring of minimal residual disease and cellular chimerism in a patient with first hematologic relapse of chronic myelogenous leukemia after allogeneic bone marrow transplantation.
  • A 15-year-old girl with Ph-positive chronic myelogenous leukemia in first chronic phase received bone marrow from her human leukocyte antigen matched brother.
  • Twenty three months after bone marrow transplantation hematological relapse occured which was treated with two infusions of donor lymphocytes (DLI) (0.5x10(8) CD3/kg b.w./infusion).
  • To enforce the graft-versus-leukemia effect (GvL), the first DLI was followed by administration of interferon-alpha (INF-alpha) 6x10(6) U/day for 30 days, whereas, after the second infusion INF-alpha was given at the same dose until hematological remission was achieved (80 doses).
  • Minimal residual disease (MRD) was detected by conventional cytogenetics (Ph chromosome), fluorescence in situ hybridization (FISH) cytogenetics (BCR/ABL translocation) and reverse transcriptase-polymerase chain reaction (RT-PCR) Ecotropic virus integration site-1 (EVI-1 gene expression), whereas cellular chimerism was monitored by assessment of microsatellite markers PCR and Y-chromosomal DNA content FISH.
  • Graft-versus-host disease was not observed at any stage of the treatment.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion / methods
  • [MeSH-minor] Adolescent. Antigens, CD3 / blood. Antigens, CD3 / drug effects. Bone Marrow Transplantation / methods. Cyclosporine / administration & dosage. Female. Graft vs Leukemia Effect / drug effects. Humans. Interferon-alpha / administration & dosage. Neoplasm, Residual. Recurrence. Transplantation Chimera. Transplantation, Homologous / methods

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  • (PMID = 11248334.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Interferon-alpha; 83HN0GTJ6D / Cyclosporine
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6. Sao H, Kato C, Kitaori K, Adachi T, Yano K, Kobayashi M, Kojima H, Tanimoto M, Hirabayashi N, Minami S, Yamada H, Morishita GY, Morishima Y, Kodera Y: Effective and safe interferon treatment for Japanese patients with chronic myelogenous leukemia relapse after bone marrow transplantation. The Nagoya Blood and Marrow Transplantation Group. Int J Hematol; 2000 Aug;72(2):237-42
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  • [Title] Effective and safe interferon treatment for Japanese patients with chronic myelogenous leukemia relapse after bone marrow transplantation. The Nagoya Blood and Marrow Transplantation Group.
  • The purpose of this study was to assess the efficacy and safety of interferon (IFN) treatment in patients with a relapse of chronic myelogenous leukemia (CML) after bone marrow transplantation in Japan.
  • One of 3 patients with hematologic relapse and all 5 patients with cytogenetic relapse achieved complete cytogenetic response (CCR).
  • The median time to achieve CCR was 8 months (range, 3-16 months).
  • One patient relapsed 9 months after starting IFN and died of blast crisis.
  • At the time of this report, 2 patients who did not attain CCR have survived for 81 months and 142 months after starting IFN, respectively.
  • During IFN treatment, 1 patient showed a transient deterioration of chronic graft-versus-host disease, and no treatment-related deaths were observed.
  • These results suggest that treatment with IFN for CML patients who relapse after bone marrow transplantation is effective and safe.
  • A prospective study to compare IFN with donor lymphocyte infusion is necessary to establish the optimal strategy for the treatment of CML patients who relapse after bone marrow transplantation.
  • [MeSH-major] Bone Marrow Transplantation. Interferons / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Adult. Cytogenetic Analysis. Disease-Free Survival. Drug Evaluation. Female. Follow-Up Studies. Graft vs Host Disease. Humans. Male. Recurrence. Retrospective Studies. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 11039675.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 9008-11-1 / Interferons
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7. Savani BN, Montero A, Kurlander R, Childs R, Hensel N, Barrett AJ: Imatinib synergizes with donor lymphocyte infusions to achieve rapid molecular remission of CML relapsing after allogeneic stem cell transplantation. Bone Marrow Transplant; 2005 Dec;36(11):1009-15
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  • [Title] Imatinib synergizes with donor lymphocyte infusions to achieve rapid molecular remission of CML relapsing after allogeneic stem cell transplantation.
  • Donor lymphocyte infusions (DLI) have been the mainstay of treatment for chronic myeloid leukemia (CML) relapsing after allogeneic stem cell transplantation (allo-SCT).
  • However, advanced phase relapse (APRel) responds poorly with either treatment.
  • To test the possibility that combinations of DLI and IM might be more effective, 37 patients with CML relapsing after allo-SCT between August 1994 and May 2004 were studied.
  • Ten had molecular relapse (MRel), 14 hematological relapse (HRel) and 13 APRel.
  • Thirty (81%) patients responded (actuarial survival and current leukemia-free survival of 80.6 +/- 6.7% and 69.1 +/- 7.7%).
  • Of 30 patients, 26 are in molecular remission (MR), median follow-up of 1,226 days (range 249-3257) since relapse.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Drug Synergism. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Recurrence. Remission Induction / methods. Retrospective Studies. Survival Analysis. Transplantation, Homologous

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  • (PMID = 16205732.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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8. 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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  • [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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  • [Copyright] Copyright © 2010 American Society for Blood and Marrow Transplantation. All rights reserved.
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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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9. 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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10. Phan CL, Megat Baharuddin PJ, Chin LP, Zakaria Z, Yegappan S, Sathar J, Tan SM, Purushothaman V, Chang KM: Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2008 Jan 1;180(1):60-4
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  • [Title] Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia.
  • The Philadelphia (Ph) chromosome, or t(9;22), is the hallmark of chronic myelogenous leukemia (CML).
  • It results in juxtaposition of the 5' part of the BCR gene on chromosome 22 to the 3' part of the ABL1 gene (previously ABL) on chromosome 9.
  • CML is clinically characterized by three distinct phases: chronic, accelerated, and blast phase.
  • We report a case of myeloid blast crisis of CML resistant to imatinib mesylate and chemotherapy.
  • By use of cytogenetic, fluorescence in situ hybridization, and comparative genomic hybridization methods, we identified a cluster of BCR-ABL amplification on inverted duplication of the Ph chromosome with t(3;21)(q26;q22) and increased genomic levels of the RUNX1 gene (previously AML1).
  • The t(3;21)(q26;q22) is a recurrent chromosomal abnormality in some cases of CML blast phase and in treatment-related myelodysplastic syndrome and acute myeloid leukemia.
  • Amplification or copy number increase of RUNX1 has been reported in childhood acute lymphoblastic leukemia.
  • Our study indicated that the progenitor of CML was BCR-ABL dependent through the amplification of Ph chromosome as a mechanism of resistance to imatinib therapy.
  • The coexistence of BCR-ABL and t(3;21)(q26;q22) with RUNX1 rearrangement might play a pivotal role in the CML blast transformation.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 3. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic

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  • (PMID = 18068536.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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11. 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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  • 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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12. Koldehoff M, Elmaagacli AH: Therapeutic targeting of gene expression by siRNAs directed against BCR-ABL transcripts in a patient with imatinib-resistant chronic myeloid leukemia. Methods Mol Biol; 2009;487:451-66
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  • [Title] Therapeutic targeting of gene expression by siRNAs directed against BCR-ABL transcripts in a patient with imatinib-resistant chronic myeloid leukemia.
  • Now, one major focus is to further explore its potential in vivo, including the development of novel therapeutic strategies.
  • Thus, the efficient delivery of target gene-specific siRNAs is one major challenge in the establishment of therapeutic RNAi.
  • Here we show that in vivo application of targeted nonvirally delivered synthetic bcr-abl siRNA in a female patient with recurrent Philadelphia chromosome positive chronic myeloid leukemia (CML) resistant to imatinib (Y253F mutation) and chemotherapy after allogeneic hematopoietic stem cell transplantation can silence the expression of bcr-abl gene.
  • We found a remarkable inhibition of the overexpressed bcr-abl oncogene resulting in increased apoptosis of CML cells.
  • Our findings imply that the clinical application of synthetic siRNA is feasible, safe and has real potential for genetic-based therapies using synthetic nonviral carriers.
  • [MeSH-major] Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / genetics. Gene Expression Regulation, Leukemic / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. RNA, Small Interfering / therapeutic use
  • [MeSH-minor] Benzamides. Female. Genetic Therapy / methods. Humans. Imatinib Mesylate. Middle Aged. Philadelphia Chromosome. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 19301661.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / RNA, Small Interfering; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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13. Oshikawa G, Kurosu T, Arai A, Murakami N, Miura O: Clonal evolution with double Ph followed by tetraploidy in imatinib-treated chronic myeloid leukemia with e19a2 transcript in transformation. Cancer Genet Cytogenet; 2010 May;199(1):56-61
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  • [Title] Clonal evolution with double Ph followed by tetraploidy in imatinib-treated chronic myeloid leukemia with e19a2 transcript in transformation.
  • Chronic myeloid leukemia (CML) with the e19a2 transcript coding for p230 is typically associated with a benign clinical course unless accompanied at presentation with additional chromosomal abnormalities.
  • We report here a case of CML with e19a2 who did not show additional chromosomal abnormalities at diagnosis, but progressed to the fatal advanced stage in approximately 2 years.
  • The patient was initially treated with imatinib, which, however, could be administered only intermittently at reduced doses because of recurrent thrombocytopenia and fluid retention.
  • Nine months after starting imatinib, fluorescence in situ hybridization (FISH) with the BCR/ABL-ES fusion probe revealed 96% and 3% of bone marrow cells with one and two BCR/ABL1 fusion signals, respectively.
  • Two years after starting therapy, leukocytosis recurred and the bone marrow contained 8.2% large and bizarre myeloblasts.
  • FISH analysis confirmed the presence of cells with two to five BCR/ABL1 fusion signals.
  • No point mutation was detected in the region coding for the BCR/ABL tyrosine kinase domain by sequence analysis.
  • It is speculated that the amplification of the BCR/ABL1 fusion gene by duplication of Ph and tetraploidy led to the progression of CML with the e19a2 transcript.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Philadelphia Chromosome. Piperazines / therapeutic use. Polyploidy. Pyrimidines / therapeutic use. RNA, Neoplasm / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Benzamides. Bone Marrow / pathology. Clone Cells. DNA Mutational Analysis. Female. Gene Expression Regulation, Leukemic. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Molecular Sequence Data. RNA, Messenger / genetics. RNA, Messenger / metabolism. Time Factors

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20417871.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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14. Yamada M, Miyamura K, Fujiwara T, Yokoyama H, Tomiya Y, Ishizawa K, Harigae H, Kameoka J, Sasaki T: Imatinib mesylate in conjunction with allogeneic hematopoietic stem cell transplantation in patients with Philadelphia chromosome positive leukemias: report of 4 cases. Tohoku J Exp Med; 2004 Sep;204(1):79-84
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  • [Title] Imatinib mesylate in conjunction with allogeneic hematopoietic stem cell transplantation in patients with Philadelphia chromosome positive leukemias: report of 4 cases.
  • We described here four patients diagnosed with Philadelphia chromosome positive (Ph+) leukemia, consisting of chronic myeloid leukemia (CML) (n=2) and Ph+ acute lymphoblastic leukemia (ALL) (n=2).
  • All patients were treated with imatinib mesylate (300-400 mg/day) for the treatment of relapsed CML after allogeneic hematopoietic stem cell transplantation (SCT) (n=2), relapsed Ph+ ALL after SCT (n=1), and Ph+ ALL preceding SCT (n=1).
  • Notably, serum cyclosporine A concentration increased after the initiation of imatinib treatment, probably through competitive inhibition of P450 3A4 isoenzyme.
  • Our data suggest that imatinib in conjunction with SCT for the Ph+ leukemia may be a promising treatment strategy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Transplantation, Homologous
  • [MeSH-minor] Adult. Benzamides. Cyclosporine / therapeutic use. Enzyme Inhibitors / therapeutic use. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome

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  • (PMID = 15329466.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 83HN0GTJ6D / Cyclosporine; 8A1O1M485B / Imatinib Mesylate
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15. Medeiros BC, Chun K, Kamel-Reid S, Lipton J: Inv (11)(p15q21) in donor-derived Ph-negative cells in a patient with chronic myeloid leukemia in relapse successfully treated with imatinib mesylate post allogeneic stem cell transplantation. Am J Hematol; 2007 Aug;82(8):758-60
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  • [Title] Inv (11)(p15q21) in donor-derived Ph-negative cells in a patient with chronic myeloid leukemia in relapse successfully treated with imatinib mesylate post allogeneic stem cell transplantation.
  • Imatinib mesylate (IM) is the standard first-line treatment for patients with chronic myeloid leukemia (CML).
  • Following hematopoietic stem cell transplantation (HSCT), IM induces complete molecular responses (CMR) in approximately 70% patients with relapsed CML, and no IM-related cytogenetic abnormalities in Ph-negative donor-derived cells have been described after HSCT.
  • We report a 56-year-old female who presented with a relapse from CML in September 2002.
  • She had received a matched related HSCT for CML in chronic phase.
  • Donor lymphocyte infusion was given 3 years post-HSCT for a relapse.
  • This observation reinforces the possibility that IM therapy may be casually linked to the phenomenon of secondary cytogenetic changes in diploid cells.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Stem Cell Transplantation
  • [MeSH-minor] Adult. Benzamides. Female. Humans. Imatinib Mesylate. Karyotyping. Male. Middle Aged. Philadelphia Chromosome. Recurrence. Tissue Donors. Transplantation, Homologous


16. Yamamoto K, Nagata K, Morita Y, Inagaki K, Hamaguchi H: Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10). Leuk Res; 2007 May;31(5):713-8
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  • [Title] Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10).
  • We describe here the first case of acute lymphoblastic leukemia (ALL) with an isodicentric Philadelphia [idic(Ph)] chromosome.
  • A 35-year-old man was diagnosed as ALL because of the infiltration of CD10(+)CD19(+)CD33(+)CD34(+) lymphoblasts in the bone marrow and the expression of p190-type BCR/ABL fusion transcript.
  • The idic(Ph) chromosome was spindle-shaped and supposed to be formed by two Ph chromosomes joined at their q terminals, whereas idic(Ph) chromosomes in chronic myelogenous leukemia (CML) have been shown to be fused at the satellite regions of p arms.
  • The results indicate that the structure of idic(Ph) chromosomes appears to be different between ALL and CML.
  • The patient did not respond to any chemotherapy and could not achieve remission.
  • This chromosome aberration in ALL may suggest poor prognosis as observed in some cases of CML.
  • Furthermore, considering other three reported cases, der(7;12)(q10;q10) may be one of the recurrent translocations in ALL.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

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  • (PMID = 16979235.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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17. Cortes J, Giles F, O'Brien S, Thomas D, Albitar M, Rios MB, Talpaz M, Garcia-Manero G, Faderl S, Letvak L, Salvado A, Kantarjian H: Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders. Cancer; 2003 Jun 1;97(11):2760-6
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  • [Title] Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders.
  • BACKGROUND: Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R).
  • c-kit is expressed in most patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) and PDGF has been implicated in the pathogenesis of myeloproliferative disorders (MPD).
  • Forty-eight patients with AML (n = 10), MDS (n = 8), myelofibrosis (n = 18), atypical chronic myeloid leukemia (CML; n = 7), chronic myelomonocytic leukemia (CMML; n = 3), or polycythemia vera (n = 2) were treated with imatinib 400 mg daily.
  • One patient with atypical CML had erythroid hematologic improvement.
  • Both patients with polycythemia vera needed fewer phlebotomies (from 2-3 per year to none during the 8 months of therapy and from 3-6 per year to 1 during 9 months of therapy).
  • Treatment was well tolerated.
  • The side effects were similar to those observed in patients with CML.
  • CONCLUSIONS: Within these small subgroups of disease types, single-agent imatinib did not achieve a significant clinical response among patients with AML, MDS, atypical CML, or CMML without PDGF-R fusion genes.
  • Therefore, a combination treatment regimen including imatinib may be more effective.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Myeloproliferative Disorders / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Middle Aged. Polycythemia Vera / drug therapy. Primary Myelofibrosis / drug therapy. Recurrence


18. Pan J, Xue Y, Qiu H, Chen S, Zhang J, Wu Y, Shen J, Wang Y: A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia. Cancer Genet Cytogenet; 2010 Dec;203(2):333-40
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  • [Title] A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia.
  • A pericentric inv(9)(p22q34) of the derivative chromosome 9 that resulted from a standard t(9;22)(q34;q11.2) was identified by R-banding karyotypic analysis and fluorescence in situ hybridization (FISH) assays in 4 (0.18%) of 2,200 Philadelphia chromosome (Ph)-positive leukemia patients, including 3 with chronic myeloid leukemia (CML) in chronic phase and 1 with acute myeloid leukemia (AML) in our hospital since 2004.
  • All four patients had two malignant clones: one with only t(9;22)(q34;q11.2) and another with der(9)t(9;22)(q34;q11.2)inv(9)(p22q34) that resulted in the separation of the ABL1/BCR fusion gene.
  • FISH also found a deletion of partial sequence of BCR on der(9)t(9;22)(q34;q11.2)inv(9)(p22q34) in 67.5% of bone marrow cells in the AML patient, but did not detect the deletion of the sequence of ASS/9q34 in these four patients.
  • Reverse transcriptase-polymerase chain reaction revealed a b3a2 type of BCR/ABL1 fusion transcript in all of them, proving their disease to be Ph-positive leukemia.
  • On reviewing the literature, only two solitary Ph-positive leukemia patients have been noticed to have the inv(9)(p22q34) anomaly.
  • These two patients, together with our four documented patients, indicate that inv(9)(p22q34) is a novel, rare, but recurrent secondary chromosomal abnormality for Ph-positive leukemia.
  • Despite receiving hydroxyurea therapy (n = 3 patients), combined chemotherapy (n = 2), even imatinib treatment (n = 1), three patients, including one with AML and two with CML (one of whom progressed into the lymphoblastic blast phase), died with survival times of 28 days, 13 months, and 34 months, respectively.
  • Only one patient with CML remained alive for 5.5 months.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21156255.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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19. Koldehoff M, Steckel NK, Beelen DW, Elmaagacli AH: Therapeutic application of small interfering RNA directed against bcr-abl transcripts to a patient with imatinib-resistant chronic myeloid leukaemia. Clin Exp Med; 2007 Jun;7(2):47-55
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  • [Title] Therapeutic application of small interfering RNA directed against bcr-abl transcripts to a patient with imatinib-resistant chronic myeloid leukaemia.
  • We herein present a first report on the in vivo application of targeted non-virally delivered synthetic bcr-abl siRNA in a female patient with recurrent Philadelphia chromosome-positive chronic myeloid leukaemia (CML) resistant to imatinib (Y253F mutation) and chemotherapy after allogeneic haematopoietic stem cell transplantation.
  • We found a remarkable inhibition of the overexpressed bcr-abl oncogene resulting in increased apoptosis of CML cells.
  • Our findings imply that the clinical application of synthetic siRNA is feasible, safe and has real potential for genetic-based therapies using synthetic non-viral carriers.
  • [MeSH-major] Drug Resistance, Neoplasm / drug effects. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. RNA, Small Interfering / genetics. Transcription, Genetic / genetics
  • [MeSH-minor] Benzamides. Blood Cell Count. Blood Platelets / cytology. Cell Line. Cell Proliferation. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Genetic Therapy. Humans. Imatinib Mesylate. Middle Aged. Philadelphia Chromosome. Transfection

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  • (PMID = 17609876.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Small Interfering; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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20. Agis H, Mannhalter C, Sperr WR, Keil F, Kalhs P, Pirc-Danoewinata H, Krauth MT, Haas OA, Geissler K, Lechner K, Valent P: Detection of trisomy 8 in donor-derived Ph- cells in a patient with Ph+ chronic myeloid leukemia successfully treated with Imatinib (STI571) in relapse after allogeneic transplantation. Leuk Lymphoma; 2004 Jul;45(7):1453-8
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  • [Title] Detection of trisomy 8 in donor-derived Ph- cells in a patient with Ph+ chronic myeloid leukemia successfully treated with Imatinib (STI571) in relapse after allogeneic transplantation.
  • Recent data suggest that STI571 (Imatinib) induces complete cytogenetic responses in patients with chronic myeloid leukemia (CML) who relapse after allogeneic stem cell transplantation (SCT).
  • However, little is known about molecular responses to STI571 and the duration of leukemia-free survival in these patients.
  • We report on a 43 year old female patient who presented with a relapse from Ph+ CML in December 2000.
  • At the time of relapse, she presented with marked leukocytosis (89,000 microl) and 10% blasts.
  • In December 2000, therapy with Imatinib was started.
  • Moreover, in response to Imatinib, BCR/ABL transcripts decreased and were no longer detectable after 6 months.
  • After a total observation period of 36 months, the patient is still in complete cytogenetic and molecular remission without signs of occurrence of a donor-type hematopoietic neoplasm or CML relapse.
  • These data suggest that Imatinib is a useful agent for long term treatment of relapsed CML after allogeneic SCT.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Neoplastic Stem Cells / drug effects. Peripheral Blood Stem Cell Transplantation. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Salvage Therapy. Trisomy
  • [MeSH-minor] Adult. Benzamides. Female. Fusion Proteins, bcr-abl / analysis. Humans. Imatinib Mesylate. Karyotyping. Male. Philadelphia Chromosome. Recurrence. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction. Transplantation Chimera. Transplantation, Homologous


21. Mielcarek M, Storer BE, Flowers ME, Storb R, Sandmaier BM, Martin PJ: Outcomes among patients with recurrent high-risk hematologic malignancies after allogeneic hematopoietic cell transplantation. Biol Blood Marrow Transplant; 2007 Oct;13(10):1160-8
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  • [Title] Outcomes among patients with recurrent high-risk hematologic malignancies after allogeneic hematopoietic cell transplantation.
  • We retrospectively analyzed outcomes among 307 consecutive patients who had recurrent or persistent acute leukemia (n = 244), chronic myelogenous leukemia in blast phase (CML; n = 28), or advanced myelodysplastic syndromes (MDS; n = 35) after allogeneic hematopoietic cell transplantation and who received at least 1 relapse-directed intervention: withdrawal of immunosuppression, chemotherapy, or donor lymphocyte infusion (DLI).
  • Transplants were performed at a single institution between 1995 and 2004, and outcomes were analyzed according to time intervals from transplantation to detection of malignancy: "early," <100 days (n = 111); "intermediate," 100-200 days (n = 73); and "late," >200 days (n = 123).
  • Individual types or combinations of these nonrandomly assigned relapse-directed interventions were not associated with higher or lower probabilities of remission or survival.
  • More effective intervention strategies are needed for treatment of recurrent high-risk hematologic malignancies after hematopoietic cell transplantation.

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  • (PMID = 17889352.001).
  • [ISSN] 1083-8791
  • [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 / CA18029; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / CA78902; United States / NIDDK NIH HHS / DK / DK064715; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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22. Yalman N, Sarper N, Devecioğlu O, Anak S, Eryilmaz E, Can M, Yenilmez H, Ağaoğlu L, Gedikoğlu G: Fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) for the treatment of relapsed or poor risk childhood acute leukemia. Turk J Pediatr; 2000 Jul-Sep;42(3):198-204
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  • [Title] Fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) for the treatment of relapsed or poor risk childhood acute leukemia.
  • The prognosis of relapsed acute leukemia or chronic leukemia in acute blast crisis is poor and new chemotherapeutic regimens could be useful for these patients.
  • Six relapsed acute lymphoblastic leukemia (ALL), nine relapsed acute myeloblastic leukemia (AML), one chronic myelomonocytic leukemia (CMML) and one chronic myeloid leukemia (CML) in acute blast crisis between three to 18 years (median 10 years) received fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) chemotherapy (CT).
  • Five of the AML relapses were after bone marrow transplantation (BMT) and four were recurrent relapses.
  • The regimen was ineffective in B-cell ALL as in acute blastic crisis of CMML and CML.
  • FLAG-IDA appears to be a myelotoxic therapy for relapsed or poor risk leukemia in a developing country.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy / methods. Vidarabine / analogs & derivatives

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  • (PMID = 11105617.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] TURKEY
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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23. Serrano J, Prieto E, Mazarbeitia F, Román A, Llamas P, Tomás JF: Atypical chronic graft-versus-host disease following interferon therapy for chronic myeloid leukaemia relapsing after allogeneic BMT. Bone Marrow Transplant; 2001 Jan;27(1):85-7
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  • [Title] Atypical chronic graft-versus-host disease following interferon therapy for chronic myeloid leukaemia relapsing after allogeneic BMT.
  • We report a 54-year-old woman who received interferon alpha for haematological relapse of Ph-positive CML, 7 years after allogeneic BMT from an HLA-identical brother.
  • Eighteen months after relapse, cytogenetic and molecular remission was achieved.
  • She received interferon therapy for 25 months and it was discontinued when she developed skin lesions on her face and trunk, dysphagia and fever with respiratory failure and bilateral patchy airspace consolidation of the lung without microbiologic findings.
  • Histologic features showed discoid lupus erythematosis, oesophagitis with pseudomembranes and a mixed pattern of lymphocytic bronchiolitis involving the alveoli and interstitial spaces all compatible with chronic GVHD.
  • The patient was commenced on immunosuppressive therapy with complete clinical and radiological resolution.
  • The available evidence supports an atypical presentation of chronic GVHD and suggests a role for interferon alpha in the pathogenesis of GVHD.
  • To the best of our knowledge, this is the first case reported of severe chronic GVHD occurring during the course of interferon therapy for relapsed CML.
  • [MeSH-major] Graft vs Host Disease / chemically induced. Interferon-alpha / toxicity. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / toxicity. Bone Marrow Transplantation. Chronic Disease. Female. Humans. Middle Aged. Recurrence. Transplantation, Homologous

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  • (PMID = 11244442.001).
  • [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 / Interferon-alpha
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26. Nelson RP Jr, Cornetta K, Ward KE, Ramanuja S, Fausel C, Cripe LD: Desensitization to imatinib in patients with leukemia. Ann Allergy Asthma Immunol; 2006 Aug;97(2):216-22
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  • [Title] Desensitization to imatinib in patients with leukemia.
  • BACKGROUND: Imatinib mesylate is a tyrosine kinase inhibitor used for the treatment of chronic myeloid leukemia and hypereosinophilic syndrome.
  • OBJECTIVE: To evaluate the safety and efficacy of oral desensitization by administering incremental dosages of imatinib mesylate to patients with leukemia who have had rashes associated with prior exposure.
  • METHODS: Ten patients with leukemia and imatinib-associated recurrent rash underwent a 4-hour outpatient oral desensitization procedure.
  • Four patients (all with urticaria) had no recurrence of rash after desensitization, and 4 had recurrent rash that resolved after temporary glucocorticosteroid and antihistamine administration.
  • Two patients developed a recurrent rash 5 hours and several days after the procedure and were unable to resume therapy.
  • CONCLUSION: This oral desensitization protocol appears to help some leukemic patients with recurrent rash tolerate imatinib mesylate, thus permitting continuation of this life-prolonging therapy.
  • These findings suggest that some adverse cutaneous reactions to imatinib may be due to a hypersensitivity mechanism rather than a pharmacologic effect.
  • [MeSH-major] Antineoplastic Agents / immunology. Desensitization, Immunologic. Drug Hypersensitivity / prevention & control. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / immunology. Pyrimidines / immunology

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  • (PMID = 16937754.001).
  • [ISSN] 1081-1206
  • [Journal-full-title] Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
  • [ISO-abbreviation] Ann. Allergy Asthma Immunol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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27. Milojkovic D, Nicholson E, Apperley JF, Holyoake TL, Shepherd P, Drummond MW, Szydlo R, Bua M, Foroni L, Reid A, Khorashad JS, de Lavallade H, Rezvani K, Paliompeis C, Goldman JM, Marin D: Early prediction of success or failure of treatment with second-generation tyrosine kinase inhibitors in patients with chronic myeloid leukemia. Haematologica; 2010 Feb;95(2):224-31
Hazardous Substances Data Bank. IMATINIB MESYLATE .

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  • [Title] Early prediction of success or failure of treatment with second-generation tyrosine kinase inhibitors in patients with chronic myeloid leukemia.
  • BACKGROUND: Second-generation tyrosine kinase inhibitors induce cytogenetic responses in approximately 50% of patients with chronic myeloid leukemia in chronic phase in whom imatinib treatment has failed.
  • However, it has not yet been established which of the patients in whom imatinib treatment fails are likely to benefit from therapy with second-generation tyrosine kinase inhibitors.
  • DESIGN AND METHODS: We analyzed a cohort of 80 patients with chronic myeloid leukemia who were resistant to imatinib and who were treated with dasatinib or nilotinib while still in first chronic phase.
  • RESULTS: The system was based on three factors: cytogenetic response to imatinib, Sokal score and recurrent neutropenia during imatinib treatment.
  • Moreover, patients who had less than 95% Philadelphia chromosome-positive metaphases at 3 months, those with 35% or less Philadelphia chromosome-positive metaphases at 6 months and patients in complete cytogenetic response at 12 months all had significantly better outcomes than patients with lesser degrees of cytogenetic response.
  • CONCLUSIONS: Factors measurable before starting treatment can accurately predict response to second-generation tyrosine kinase inhibitors.
  • Cytogenetic responses at 3, 6 and 12 months may influence the decision to continue treatment with second-generation tyrosine kinase inhibitors.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adult. Benzamides. Cohort Studies. Cytogenetic Analysis. Dasatinib. Drug Resistance. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / pharmacology. Prognosis

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  • (PMID = 19833633.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [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 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC2817024
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28. Wen PY, Yung WK, Lamborn KR, Norden AD, Cloughesy TF, Abrey LE, Fine HA, Chang SM, Robins HI, Fink K, Deangelis LM, Mehta M, Di Tomaso E, Drappatz J, Kesari S, Ligon KL, Aldape K, Jain RK, Stiles CD, Egorin MJ, Prados MD: Phase II study of imatinib mesylate for recurrent meningiomas (North American Brain Tumor Consortium study 01-08). Neuro Oncol; 2009 Dec;11(6):853-60
Hazardous Substances Data Bank. IMATINIB MESYLATE .

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  • [Title] Phase II study of imatinib mesylate for recurrent meningiomas (North American Brain Tumor Consortium study 01-08).
  • The North American Brain Tumor Consortium conducted a phase II study to evaluate the therapeutic potential of imatinib mesylate (Gleevec), a PDGFR inhibitor, in patients with recurrent meningiomas.
  • Patients requiring enzyme-inducing antiepileptic drugs were ineligible.
  • Tissue was available only from a minority of patients, but in these specimens there was uniform distribution of PDGFR, the drug target.
  • Single-agent imatinib was well tolerated but had no significant activity in recurrent meningiomas.
  • Trough plasma concentrations of imatinib exceeded those associated with imatinib activity in chronic myelogenous leukemia.

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  • (PMID = 19293394.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062407; United States / NCRR NIH HHS / RR / M01 RR000079; United States / NCRR NIH HHS / RR / M01 RR003186; United States / NCRR NIH HHS / RR / M01 RR000056; United States / NCRR NIH HHS / RR / M01 RR000865; United States / NCI NIH HHS / CA / U01 CA062399; United States / NCRR NIH HHS / RR / M01 RR000633; United States / NCI NIH HHS / CA / U01 CA062412; United States / NCI NIH HHS / CA / CA 62399; United States / NCI NIH HHS / CA / CA062421-07; United States / NCI NIH HHS / CA / U01 CA062421-07; United States / NCI NIH HHS / CA / U01 CA062421; United States / NCI NIH HHS / CA / U01 CA105663
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; 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; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC2802405
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29. Kim R, Toge T: Changes in therapy for solid tumors: potential for overcoming drug resistance in vivo with molecular targeting agents. Surg Today; 2004;34(4):293-303
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  • [Title] Changes in therapy for solid tumors: potential for overcoming drug resistance in vivo with molecular targeting agents.
  • The current success of molecular targeting therapy is shown by: imatinib mesylate (STI571, Gleevec), targeted to the Bcr/Abl fusion protein derived from a translocation between chromosomes 9 and 22 in chronic myelogenous leukemia; rituximab (Rituxan), a monoclonal antibody to CD20 used in non-Hodgkin's lymphoma; trastuzumab (Herceptin), a chimeric monoclonal antibody to HER-2 used in breast cancer; and gefinitib (ZD1839, Irresa), a tyrosine kinase inhibitor of the epidermal growth factor receptor used in non-small cell lung cancer.
  • The superior therapeutic efficacy of these molecular targeting agents over traditional chemotherapy has been shown by the survival benefit achieved for patients with advanced or recurrent cancers.
  • Although the precise molecular mechanisms by which these agents produce or enhance an antitumor effect, alone or in combination with anticancer drugs, are not known, the specific inhibition of target genes critically involved in tumor progression and metastasis by the agent is clear.
  • However, further studies to determine which patient groups and anticancer drugs are appropriate for combination therapy with these molecular targeting agents are needed.
  • Herein, we discuss the current status and potential for overcoming drug resistance in solid tumors and focus on the differential features of the tumor microenvironment in solid and hematologic malignancies.
  • [MeSH-major] Drug Resistance, Neoplasm. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Disease Progression. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Molecular Biology. Paracrine Communication / drug effects. Paracrine Communication / radiation effects. Piperazines / pharmacology. Piperazines / therapeutic use. Platelet-Derived Growth Factor / physiology. Protein-Tyrosine Kinases. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. Quinazolines / pharmacology. Quinazolines / therapeutic use. Receptor, ErbB-2 / metabolism. Signal Transduction / drug effects. Signal Transduction / physiology. Trastuzumab

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  • (PMID = 15052442.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Platelet-Derived Growth Factor; 0 / Pyrimidines; 0 / Quinazolines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.2 / Fusion Proteins, bcr-abl; P188ANX8CK / Trastuzumab; S65743JHBS / gefitinib
  • [Number-of-references] 81
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30. Bilgi N, Bell K, Ananthakrishnan AN, Atallah E: Imatinib and Panax ginseng: a potential interaction resulting in liver toxicity. Ann Pharmacother; 2010 May;44(5):926-8
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  • OBJECTIVE: To report a case of imatinib-induced hepatotoxicity after concurrent ginseng ingestion in a patient with chronic myelogenous leukemia (CML).
  • CASE SUMMARY: A 26-year-old man with CML who had taken imatinib 400 mg daily for 7 years with no complications presented with right upper quadrant pain.
  • Liver biopsy showed acute lobular hepatitis favoring a drug-induced etiology, and a diagnosis of imatinib-induced hepatotoxicity was made.
  • The patient's only lifestyle modification prior to the diagnosis of hepatotoxicity was daily ingestion of Panax ginseng via energy drinks for the past 3 months.
  • Imatinib was later restarted at the same dose with no recurrent elevations in his liver enzyme levels.
  • DISCUSSION: Imatinib-associated hepatotoxicity usually presents within 1-2 years of therapy initiation, with the median time to hepatotoxicity being 100 days.
  • Based on the Naranjo probability scale, it is probable that imatinib caused this patient's hepatotoxicity, and the Horn drug interaction probability scale also indicates a probable interaction between imatinib and ginseng.
  • CONCLUSIONS: This case emphasizes the importance of continuous monitoring of liver function tests even after several years of imatinib therapy and the importance of advising patients to avoid ginseng and any other over-the-counter herbal supplements that may interact with imatinib.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Drug-Induced Liver Injury / etiology. Herb-Drug Interactions. Panax / adverse effects. Piperazines / adverse effects. Pyrimidines / adverse effects
  • [MeSH-minor] Adult. Benzamides. Cytochrome P-450 CYP3A / metabolism. Dietary Supplements / adverse effects. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Liver Function Tests. Male

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  • (PMID = 20332334.001).
  • [ISSN] 1542-6270
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A
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31. Carpenter PA, Snyder DS, Flowers ME, Sanders JE, Gooley TA, Martin PJ, Appelbaum FR, Radich JP: Prophylactic administration of imatinib after hematopoietic cell transplantation for high-risk Philadelphia chromosome-positive leukemia. Blood; 2007 Apr 1;109(7):2791-3
Hazardous Substances Data Bank. IMATINIB MESYLATE .

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  • [Title] Prophylactic administration of imatinib after hematopoietic cell transplantation for high-risk Philadelphia chromosome-positive leukemia.
  • Relapse occurs frequently after allogeneic hematopoietic cell transplantation (HCT) for treatment of high-risk Philadelphia chromosome-positive (Ph+) leukemia.
  • Administration of imatinib early after HCT might provide an effective approach for preventing recurrent Ph+ leukemia, but the feasibility of this approach has not been systematically tested.
  • Twenty-two patients, 15 with Ph+ acute lymphoblastic leukemia and 7 with high-risk chronic myelogenous leukemia, were enrolled in a prospective study and given imatinib from the time of engraftment until 365 days after HCT.
  • We conclude that imatinib can be safely administered early after myeloablative allogeneic HCT at a dose intensity comparable to that used in primary therapy.

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  • (PMID = 17119111.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / CA18029
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1852215
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32. Wen PY, Yung WK, Lamborn KR, Dahia PL, Wang Y, Peng B, Abrey LE, Raizer J, Cloughesy TF, Fink K, Gilbert M, Chang S, Junck L, Schiff D, Lieberman F, Fine HA, Mehta M, Robins HI, DeAngelis LM, Groves MD, Puduvalli VK, Levin V, Conrad C, Maher EA, Aldape K, Hayes M, Letvak L, Egorin MJ, Capdeville R, Kaplan R, Murgo AJ, Stiles C, Prados MD: Phase I/II study of imatinib mesylate for recurrent malignant gliomas: North American Brain Tumor Consortium Study 99-08. Clin Cancer Res; 2006 Aug 15;12(16):4899-907
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of imatinib mesylate for recurrent malignant gliomas: North American Brain Tumor Consortium Study 99-08.
  • PURPOSE: Phase I: To determine the maximum tolerated doses, toxicities, and pharmacokinetics of imatinib mesylate (Gleevec) in patients with malignant gliomas taking enzyme-inducing antiepileptic drugs (EIAED) or not taking EIAED.
  • Phase II: To determine the therapeutic efficacy of imatinib.
  • Five phase II patients developed intratumoral hemorrhages.
  • CYP3A4 inducers, such as EIAEDs, substantially decreased plasma exposure of imatinib and should be avoided in patients receiving imatinib for chronic myelogenous leukemia and gastrointestinal stromal tumors.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Glioma / drug therapy. Piperazines / adverse effects. Piperazines / therapeutic use. Pyrimidines / adverse effects. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Anticonvulsants / therapeutic use. Benzamides. Drug Interactions. Female. Genotype. Humans. Imatinib Mesylate. Male. Middle Aged

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  • (PMID = 16914578.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R03CA102974-02
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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33. 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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34. Kaufmann SH, Karp JE, Letendre L, Kottke TJ, Safgren S, Greer J, Gojo I, Atherton P, Svingen PA, Loegering DA, Litzow MR, Sloan JA, Reid JM, Ames MM, Adjei AA, Erlichman C: Phase I and pharmacologic study of infusional topotecan and Carboplatin in relapsed and refractory acute leukemia. Clin Cancer Res; 2005 Sep 15;11(18):6641-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I and pharmacologic study of infusional topotecan and Carboplatin in relapsed and refractory acute leukemia.
  • PURPOSE: To assess the maximum tolerated dose, toxicities, pharmacokinetics, and antileukemic activity of topotecan and carboplatin in adults with recurrent or refractory acute leukemias.
  • RESULTS: Fifty-one patients received a total of 69 courses of therapy.
  • Dose-limiting toxicity consisted of grade 4/5 typhlitis and grade 3/4 mucositis after one course of therapy or grade 4 neutropenia and thrombocytopenia lasting >50 days when a second course was administered on day 21.
  • Among 45 evaluable patients, there were 7 complete remissions, 2 partial remissions, 1 incomplete complete remission, and 1 reversion to chronic-phase chronic myelogenous leukemia.
  • No accumulation of topotecan or ultrafilterable platinum occurred between days 1 and 5 of therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Carboplatin / administration & dosage. Carboplatin / adverse effects. Carboplatin / pharmacokinetics. Cell Cycle Proteins / metabolism. Combined Modality Therapy. DNA Topoisomerases, Type I / metabolism. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. HL-60 Cells. Hematopoietic Stem Cell Transplantation. Humans. Immunoblotting. Infusions, Intravenous. Male. Middle Aged. Neoplasm Recurrence, Local. Proliferating Cell Nuclear Antigen / metabolism. Topotecan / administration & dosage. Topotecan / adverse effects. Topotecan / pharmacokinetics. Treatment Outcome

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  • (PMID = 16166443.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA73709; United States / NCI NIH HHS / CA / U01 CA69854; United States / NCI NIH HHS / CA / U01 CA69912
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Proliferating Cell Nuclear Antigen; 7M7YKX2N15 / Topotecan; BG3F62OND5 / Carboplatin; EC 5.99.1.2 / DNA Topoisomerases, Type I
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35. 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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36. Olavarria E, Ottmann OG, Deininger M, Clark RE, Bandini G, Byrne J, Lipton J, Vitek A, Michallet M, Siegert W, Ullmann A, Wassmann B, Niederwieser D, Fischer T, Chronic Leukaemia Working Party of the European Group of Bone and Marrow Transplantation (EBMT): Response to imatinib in patients who relapse after allogeneic stem cell transplantation for chronic myeloid leukemia. Leukemia; 2003 Sep;17(9):1707-12
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  • [Title] Response to imatinib in patients who relapse after allogeneic stem cell transplantation for chronic myeloid leukemia.
  • We studied 128 patients with chronic myeloid leukemia (CML) relapsing after allogeneic stem cell transplantation (SCT).
  • Disease at the time of treatment with Imatinib was in chronic phase (CP) in 51 patients, accelerated phase (AP) in 31 and blastic crisis (BC) in 46.
  • The median interval between relapse and Imatinib therapy was 5 months (0-65).
  • A total of 50 patients had failed treatment with donor lymphocyte infusions prior to Imatinib.
  • The overall hemato-logical response rate was 84% (98% for patients relapsing in CP).
  • We conclude that Imatinib has significant activity against CML in relapse after allogeneic SCT.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Female. Graft vs Leukemia Effect. Humans. Imatinib Mesylate. Male. Middle Aged. Retrospective Studies. Salvage Therapy. Survival Rate. Transplantation, Homologous. Treatment Outcome


37. Roche-Lestienne C, Deluche L, Corm S, Tigaud I, Joha S, Philippe N, Geffroy S, Laï JL, Nicolini FE, Preudhomme C, Fi-LMC group: RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance. Blood; 2008 Apr 1;111(7):3735-41
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  • [Title] RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance.
  • Acquired molecular abnormalities (mutations or chromosomal translocations) of the RUNX1 transcription factor gene are frequent in acute myeloblastic leukemias (AMLs) and in therapy-related myelodysplastic syndromes, but rarely in acute lymphoblastic leukemias (ALLs) and chronic myelogenous leukemias (CMLs).
  • Among 18 BCR-ABL+ leukemias presenting acquired trisomy of chromosome 21, we report a high frequency (33%) of recurrent point mutations (4 in myeloid blast crisis [BC] CML and one in chronic phase CML) within the DNA-binding region of RUNX1.
  • We did not found any mutation in de novo BCR-ABL+ ALLs or lymphoid BC CML.
  • Emergence of the RUNX1 mutations was detected at diagnosis or before the acquisition of trisomy 21 during disease progression.
  • In addition, we also report a high frequency of cryptic chromosomal RUNX1 translocation to a novel recently described gene partner, PRDM16 on chromosome 1p36, for 3 (21.4%) of 14 investigated patients: 2 myeloid BC CMLs and, for the first time, 1 therapy-related BCR-ABL+ ALL.
  • These events are associated with a short survival and support the concept of a cooperative effect of BCR-ABL with molecular RUNX1 abnormalities on the differentiation arrest phenotype observed during progression of CML and in BCR-ABL+ ALL.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / genetics. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia / genetics. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Transcription Factors / genetics. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Benzamides. Chromosomes, Human. Chronic Disease. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / mortality. Phenotype. Point Mutation. Retrospective Studies. Survival Rate. Translocation, Genetic / drug effects. Translocation, Genetic / genetics

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  • (PMID = 18202228.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / PRDM16 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RUNX1 protein, human; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [General-notes] NLM/ Investigator list not found.
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38. Kotone-Miyahara Y, Takaori-Kondo A, Fukunaga K, Goto M, Hayashino Y, Miki M, Takayama H, Sasada M, Uchiyama T: E148Q/M694I mutation in 3 Japanese patients with familial Mediterranean fever. Int J Hematol; 2004 Apr;79(3):235-7
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  • The first patient is a 38-year-old man who also has chronic myelogenous leukemia (CML).
  • Interferon alpha therapy was effective against not only the CML but also the FMF.
  • The second patient is a 42-year-old man with consanguineous parents and a 14-year history of recurrent lower abdominal and back pain associated with fever.
  • He successfully responded to colchicine treatment.
  • The third patient is a 23-year-old woman who has a family history of FMF and since the age of 11 years has had recurrent chest and abdominal pain with fever.
  • [MeSH-minor] Adult. Colchicine / therapeutic use. DNA Mutational Analysis. Family Health. Female. Heterozygote. Humans. Interferon-alpha / therapeutic use. Japan. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Male

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  • (PMID = 15168590.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Interferon-alpha; SML2Y3J35T / Colchicine
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39. Aschoff P, Häntschel M, Oksüz M, Werner MK, Lichy M, Vogel W, Pfannenberg C: Integrated FDG-PET/CT for detection, therapy monitoring and follow-up of granulocytic sarcoma. Initial results. Nuklearmedizin; 2009;48(5):185-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrated FDG-PET/CT for detection, therapy monitoring and follow-up of granulocytic sarcoma. Initial results.
  • AIM: Granulocytic sarcomas (GS) are rare extramedullary manifestations of myeloid or lymphoblastic leukaemia.
  • Laboratory examinations are of limited use for diagnosis of extramedullary disease.
  • The FDG uptake of GS was analyzed and the sensitivity of lesion detection was compared to PET and CT alone.
  • The changes in FDG uptake after therapy were compared to morphological changes detected by CT and follow-up / clinical outcome.
  • RESULTS: 52 untreated or recurrent GS lesions were detected by FDG-PET/CT and all showed an increased FDG uptake with a mean SUVmax and SUVavg of 5.1 and 3.4, respectively.
  • Combined PET/CT avoided 5 false positive findings compared to PET alone and 13 false negative findings and 1 false positive compared to CT alone.
  • Changes in FDG uptake after therapy correlated with clinical outcome and were more reliable than CT assessment alone.
  • PET/CT identified recurrent GS in 3 patients.
  • Using this metabolic information and morphologic CT criteria, combined FDG-PET/CT was more accurate in lesion detection than FDG-PET or CT alone.
  • Changes in FDG uptake after therapy might be a useful additional parameter for therapy monitoring.
  • [MeSH-minor] Adult. Female. Fluorodeoxyglucose F18. Follow-Up Studies. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / radiography. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / radionuclide imaging. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / radiography. Leukemia, Myeloid, Acute / radionuclide imaging. Male. Middle Aged. Neoplasm Staging. Positron-Emission Tomography. Retrospective Studies. Tomography, X-Ray Computed. Young Adult

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  • (PMID = 19710955.001).
  • [ISSN] 0029-5566
  • [Journal-full-title] Nuklearmedizin. Nuclear medicine
  • [ISO-abbreviation] Nuklearmedizin
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
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40. Saglio G, Cilloni D, Rancati F, Boano L: Glivec and CML: a lucky date. J Biol Regul Homeost Agents; 2004 Apr-Jun;18(2):246-51
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  • [Title] Glivec and CML: a lucky date.
  • Chronic Myeloid Leukemia (CML) has always been an ideal model to understand the molecular pathogenesis of human leukaemias and the way to cure them.
  • This can be ascribed to the fact that CML was the first human cancer demonstrated to be strongly associated to the presence of a recurrent chromosomal translocation (the t(9;22)(q34;q11) that creates the Philadelphia (Ph)-chromosome) and to a specific molecular defect, the formation of a hybrid BCR-ABL gene that generates new fusion proteins endowed with a constitutive tyrosine-kinase (TK) activity, strongly implicated in the pathogenesis of the disease.
  • The introduction into clinical practice of imatinib, (Glivec, Gleevec, Novartis), a potent tyrosine kinase inhibitor of the Bcr-Abl protein as well as of a restricted number of other TKs, has not only produced a substantial improvement in the treatment of CML, but represents a major break-through in the perspective of opening a new era, that of molecularly targeted therapy, in the management of other types of leukemia, lymphoma and cancer in general.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Benzamides. Bone Marrow Transplantation. Clinical Trials as Topic. Drug Monitoring. Drug Resistance, Neoplasm / physiology. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Leukemia / drug therapy. Leukemia / genetics. Leukemia / therapy. Philadelphia Chromosome. Protein Kinase Inhibitors / administration & dosage. Protein Kinase Inhibitors / pharmacokinetics. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
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  • (PMID = 15739279.001).
  • [ISSN] 0393-974X
  • [Journal-full-title] Journal of biological regulators and homeostatic agents
  • [ISO-abbreviation] J. Biol. Regul. Homeost. Agents
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 48
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41. Bernheim A: Cytogenomics of cancers: from chromosome to sequence. Mol Oncol; 2010 Aug;4(4):309-22
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  • Imatinib, an inhibitor of the tyrosine kinase ABL, the prototype of these targeting drugs, is yielding complete remissions in most CML patients.
  • Knowledge of chromosomal abnormalities is becoming an essential contribution to the diagnosis and prognosis of cancers but also for monitoring minimal residual disease or relapse.
  • The concept of the "cytogenetic uniqueness" of each cancer has resulted in personalized treatment.
  • This investigation will expound upon, besides the recurrent genomic alterations, the numerous products of perverted Darwinian selection at the cellular level.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzamides. Chromosome Aberrations. Cytogenetics / methods. Disease Progression. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

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  • [Copyright] (c) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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  • (PMID = 20599448.001).
  • [ISSN] 1878-0261
  • [Journal-full-title] Molecular oncology
  • [ISO-abbreviation] Mol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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42. Slomovitz BM, Broaddus RR, Schmandt R, Wu W, Oh JC, Ramondetta LM, Burke TW, Gershenson DM, Lu KH: Expression of imatinib mesylate-targeted kinases in endometrial carcinoma. Gynecol Oncol; 2004 Oct;95(1):32-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has been shown to be an effective treatment for patients with chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST).
  • To determine whether imatinib mesylate could be a potentially useful agent in the treatment of endometrial cancer, we assessed the expressions of Abl, c-Kit, and PDGFR in both primary and recurrent endometrial carcinoma.
  • EXPERIMENTAL DESIGN: We performed immunohistochemical analysis on formalin-fixed, paraffin-embedded sections from 63 patients: 33 with endometrioid endometrial carcinoma (EEC), 11 with uterine papillary serous carcinoma (UPSC), 12 with recurrent EEC, and seven with recurrent UPSC.
  • RESULTS: Among the primary EEC, 28/33 (85%) stained positively for Abl and 30/33 (91%) were positive for PDGFR.
  • Of the primary UPSC, 8/11 (73%) were positive for Abl.
  • In addition, 8/11 (73%) of the primary UPSC tumors were positive for PDGFR.
  • Of the recurrent EEC tumors, 11/12 (92%) were positive for Abl expression, 12/12 (100%) were positive for PDGFR, and 2/8 (25%) were positive for c-Kit.
  • Of the recurrent UPSC, 6/7 (86%) were positive for Abl, 7/7 (100%) were positive for PDGFR, and 2/4 (50%) for c-Kit.
  • In addition, the majority of primary and recurrent tumors were positive for phosphorylated Abl (primary EEC, 91%; primary UPSC, 64%; recurrent EEC, 83%; recurrent UPSC, 86%), and phosphorylated PDGFR (primary EEC, 46%; primary UPSC, 40%; recurrent EEC, 58%; recurrent UPSC, 100%).
  • CONCLUSIONS: The majority of primary and recurrent EEC, as well as primary and recurrent UPSC express Abl and PDGFR.
  • This preclinical data suggest that imatinib mesylate may be useful in the treatment of patients with endometrial carcinoma.
  • [MeSH-major] Carcinoma, Endometrioid / drug therapy. Carcinoma, Endometrioid / enzymology. Endometrial Neoplasms / drug therapy. Endometrial Neoplasms / enzymology. Enzyme Inhibitors / pharmacology. Piperazines / pharmacology. Protein-Tyrosine Kinases / biosynthesis. Pyrimidines / pharmacology

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  • (PMID = 15385107.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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43. Dölken G: Detection of minimal residual disease. Adv Cancer Res; 2001;82:133-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of minimal residual disease.
  • A high percentage of patients with leukemia, lymphoma, and solid tumors achieve a complete clinical remission after initial treatment, but the majority of these patients will finally relapse from residual tumor cells detectable in clinical remission only by the most sensitive methods.
  • Depending on the underlying malignant disease and therapeutic treatment, the presence of residual tumor cells in an individual patient may herald relapse, but a long-term stable situation or slowly vanishing tumor cells are also possible.
  • Molecular monitoring of residual leukemia and lymphoma cells by quantitative PCR techniques has provided important information about the effectiveness of treatment and the risk of recurrent disease as shown by minimal residual disease (MRD) analysis in patients with various malignant diseases.
  • Such diseases include childhood acute lymphoblastic leukemia, after induction therapy; acute promyelocytic leukemia, during and after chemotherapy; and chronic myelogenous leukemia, during treatment with alpha-interferon and after allogeneic bone marrow transplantation.
  • Evaluation of the predictive value of the detection of MRD has to take into account its evolution and course, the pathogenesis, biology, and natural course of the underlying malignant disease, the molecular genetic lesion, and finally, the type of treatment.
  • Quantification of minimal residual cells by the recently developed real-time quantitative PCR technique will surely have a major impact on our therapeutic strategies for patients with leukemia, lymphomas, and solid tumors.
  • Based on quantitative PCR data, the terms molecular remission and molecular relapse have to be exactly defined and validated in prospective clinical trials to assess the biological and clinical significance of MRD in various types of malignancies.
  • [MeSH-major] Neoplasm, Residual / diagnosis

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  • (PMID = 11447762.001).
  • [ISSN] 0065-230X
  • [Journal-full-title] Advances in cancer research
  • [ISO-abbreviation] Adv. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 326
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