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1. 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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2. 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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  • [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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3. 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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4. 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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5. 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.
  • [Cites] Bone Marrow Transplant. 1997 May;19(10):977-82 [9169641.001]
  • [Cites] Leukemia. 1997 May;11(5):729-31 [9180299.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1664-72 [9269787.001]
  • [Cites] Rinsho Ketsueki. 1997 Aug;38(8):643-6 [9311269.001]
  • [Cites] Blood. 1997 Oct 1;90(7):2549-54 [9326220.001]
  • [Cites] Blood. 1997 Nov 15;90(10):4206-11 [9354693.001]
  • [Cites] J Immunol. 1997 Dec 15;159(12):5921-30 [9550389.001]
  • [Cites] Blood. 1998 May 15;91(10):3671-80 [9573003.001]
  • [Cites] Leuk Lymphoma. 1998 Apr;29(3-4):301-13 [9684928.001]
  • [Cites] Bone Marrow Transplant. 1998 Oct;22(7):639-43 [9818690.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1201-8 [10438707.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):208-15 [10458235.001]
  • [Cites] Biol Blood Marrow Transplant. 1999;5(4):253-61 [10465105.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3361-3 [15292062.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3797-803 [15280203.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3535-42 [15304387.001]
  • [Cites] Blood. 2004 Dec 15;104(13):3865-71 [15304395.001]
  • [Cites] J Exp Med. 2004 Dec 20;200(12):1623-33 [15611290.001]
  • [Cites] Bone Marrow Transplant. 2005 Jan;35(2):165-9 [15531895.001]
  • [Cites] Br J Haematol. 2005 Feb;128(4):496-502 [15686458.001]
  • [Cites] Haematologica. 2003 May;88(5):555-60 [12745275.001]
  • [Cites] Leukemia. 2003 May;17(5):841-8 [12750695.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1035-7 [12764364.001]
  • [Cites] Bone Marrow Transplant. 2003 Jun;31(11):973-9 [12774047.001]
  • [Cites] Blood. 2003 Jul 15;102(2):442-8 [12560224.001]
  • [Cites] Blood. 2003 Jul 15;102(2):571-6 [12576330.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2747-53 [12860954.001]
  • [Cites] Exp Hematol. 2003 Sep;31(9):743-51 [12962719.001]
  • [Cites] Ann Hematol. 2003 Sep;82(9):548-51 [14504811.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2379-86 [12791647.001]
  • [Cites] Bone Marrow Transplant. 2003 Oct;32(8):835-42 [14520431.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2892-900 [12829610.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:331-49 [14633789.001]
  • [Cites] Bone Marrow Transplant. 2003 Dec;32(12):1159-63 [14647270.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4407-12 [14645431.001]
  • [Cites] Leukemia. 2004 Jan;18(1):165-6 [14603333.001]
  • [Cites] Exp Hematol. 2004 Jan;32(1):28-35 [14725898.001]
  • [Cites] Blood. 2004 Feb 1;103(3):790-5 [14525766.001]
  • [Cites] Blood. 2004 Feb 1;103(3):784-9 [14551141.001]
  • [Cites] Hematol J. 2004;5(1):47-54 [14745430.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1548-56 [14576063.001]
  • [Cites] Transplantation. 2004 Feb 15;77(3):391-8 [14966413.001]
  • [Cites] Leukemia. 2004 Mar;18(3):659-62 [14671630.001]
  • [Cites] Biol Blood Marrow Transplant. 2004 Mar;10(3):204-12 [14993886.001]
  • [Cites] Rinsho Ketsueki. 2004 Feb;45(2):155-60 [15045825.001]
  • [Cites] J Clin Oncol. 2004 May 1;22(9):1696-705 [15117992.001]
  • [Cites] Blood. 2004 May 15;103(10):3982-5 [14764538.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4362-4 [14976044.001]
  • [Cites] Leuk Lymphoma. 2004 Apr;45(4):731-3 [15160947.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 25;101(21):8120-5 [15148407.001]
  • [Cites] Exp Hematol. 2004 Jun;32(6):556-62 [15183896.001]
  • [Cites] Cancer. 2004 Jun 15;100(12):2583-91 [15197800.001]
  • [Cites] Bone Marrow Transplant. 2004 Jul;34(2):123-8 [15133487.001]
  • [Cites] Semin Hematol. 2004 Jul;41(3):201-6 [15269880.001]
  • [Cites] Bone Marrow Transplant. 2004 Sep;34(5):391-7 [15273707.001]
  • [Cites] Biol Blood Marrow Transplant. 2004 Sep;10(9):579-90 [15319770.001]
  • [Cites] Leukemia. 2004 Sep;18(9):1557-8 [15229619.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1793-800 [15172969.001]
  • [Cites] Bone Marrow Transplant. 2004 Oct;34(8):721-7 [15322568.001]
  • [Cites] Blood. 2007 Jan 15;109(2):399-404 [17003373.001]
  • [Cites] Blood. 2007 Feb 1;109(3):1103-12 [17023585.001]
  • [Cites] Blood. 2007 Feb 1;109(3):944-50 [17032921.001]
  • [Cites] Transfusion. 2007 Mar;47(3):520-8 [17319835.001]
  • [Cites] Haematologica. 2007 Mar;92(3):414-7 [17339194.001]
  • [Cites] J Clin Oncol. 2007 Mar 20;25(9):1114-20 [17296974.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3588-94 [17158231.001]
  • [Cites] Mol Ther. 2007 May;15(5):981-8 [17375070.001]
  • [Cites] Clin Exp Immunol. 2007 Jun;148(3):520-8 [17493020.001]
  • [Cites] Cancer Res. 2007 Jun 1;67(11):5489-97 [17545631.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5136-42 [17344466.001]
  • [Cites] Br J Haematol. 2007 Oct;139(1):70-80 [17854309.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2620-30 [17507664.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2761-3 [17579184.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2744-8 [17595333.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Oct;13(10):1160-8 [17889352.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2838-45 [17609424.001]
  • [Cites] Leuk Lymphoma. 2007 Oct;48(10):1931-9 [17917961.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2316-23 [17597807.001]
  • [Cites] Vaccine. 2007 Nov 14;25(46):7955-61 [17933439.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2600-2 [15205268.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2:14639-45 [15381769.001]
  • [Cites] Leukemia. 2004 Nov;18(11):1789-97 [15385924.001]
  • [Cites] Nature. 1975 Aug 7;256(5517):495-7 [1172191.001]
  • [Cites] Lancet. 1978 Sep 9;2(8089):537-40 [79913.001]
  • [Cites] N Engl J Med. 1979 May 10;300(19):1068-73 [34792.001]
  • [Cites] Am J Pathol. 1987 Oct;129(1):86-91 [2821817.001]
  • [Cites] J Clin Oncol. 1989 Jan;7(1):50-7 [2642540.001]
  • [Cites] Br J Haematol. 1988 Nov;70(3):317-20 [3061443.001]
  • [Cites] Bone Marrow Transplant. 1988 Nov;3(6):619-24 [3063329.001]
  • [Cites] Blood. 1990 Feb 1;75(3):555-62 [2297567.001]
  • [Cites] Blood. 1990 Dec 15;76(12):2462-5 [2265242.001]
  • [Cites] Blood. 1991 Feb 1;77(3):649-53 [1991174.001]
  • [Cites] Blood. 1991 Apr 1;77(7):1423-8 [2009366.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4766-70 [1647016.001]
  • [Cites] Blood. 1991 Sep 1;78(5):1162-5 [1652308.001]
  • [Cites] Bone Marrow Transplant. 1992 Oct;10(4):391-5 [1422499.001]
  • [Cites] Bone Marrow Transplant. 1993 Feb;11(2):109-11 [8435660.001]
  • [Cites] J Clin Oncol. 1993 Dec;11(12):2342-50 [8246023.001]
  • [Cites] N Engl J Med. 1994 Jan 13;330(2):100-6 [8259165.001]
  • [Cites] N Engl J Med. 1994 Nov 10;331(19):1253-8 [7935682.001]
  • [Cites] Blood. 1994 Dec 1;84(11):3983 [7949156.001]
  • [Cites] Blood. 1994 Nov 1;84(9):3148-57 [7949187.001]
  • [Cites] Bone Marrow Transplant. 1994 Aug;14(2):331-2 [7994252.001]
  • [Cites] Blood. 1995 Feb 15;85(4):1122-31 [7849300.001]
  • [Cites] Blood. 1995 Mar 15;85(6):1580-9 [7888675.001]
  • [Cites] Lancet. 1995 Apr 22;345(8956):1016-20 [7723498.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1261-8 [7632930.001]
  • [Cites] Blood. 1995 Sep 1;86(5):2041-50 [7655033.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4337-43 [7492795.001]
  • [Cites] Exp Hematol. 1995 Dec;23(14):1553-62 [8542946.001]
  • [Cites] Blood. 1996 Feb 1;87(3):1196-8 [8562947.001]
  • [Cites] Lancet. 1996 Mar 23;347(9004):800-1 [8622337.001]
  • [Cites] J Clin Oncol. 1996 Feb;14(2):572-8 [8636773.001]
  • [Cites] J Immunol. 1996 Jun 15;156(12):4609-16 [8648103.001]
  • [Cites] Blood. 1996 Jul 1;88(1):41-8 [8704200.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2787-93 [8839877.001]
  • [Cites] Clin Lab Haematol. 1996 Mar;18(1):45-6 [9118604.001]
  • [Cites] Bone Marrow Transplant. 1996 Sep;18(3):669-72 [8879640.001]
  • [Cites] Leukemia. 1997 Feb;11(2):281-3 [9009093.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):433-44 [9053463.001]
  • [Cites] Bone Marrow Transplant. 1997 Mar;19(5):461-6 [9052912.001]
  • [Cites] Br J Haematol. 1997 Apr;97(1):165-8 [9136960.001]
  • [Cites] Bone Marrow Transplant. 1997 Apr;19(7):697-702 [9156247.001]
  • [Cites] J Clin Oncol. 2008 Nov 1;26(31):5094-100 [18711173.001]
  • [Cites] Haematologica. 2008 Nov;93(11):1702-11 [18728020.001]
  • [Cites] Clin Cancer Res. 2008 Nov 1;14(21):6907-15 [18980985.001]
  • [Cites] Br J Haematol. 2008 Nov;143(4):468-80 [18710379.001]
  • [Cites] J Clin Oncol. 2008 Nov 10;26(32):5151-3 [18824700.001]
  • [Cites] Bone Marrow Transplant. 2008 Nov;42(9):569-79 [18711351.001]
  • [Cites] Int J Hematol. 2008 Nov;88(4):463-4 [18836792.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4371-83 [19029455.001]
  • [Cites] Leuk Res. 2009 Jan;33(1):174-7 [18471874.001]
  • [Cites] Pediatr Blood Cancer. 2009 Feb;52(2):177-81 [18816698.001]
  • [Cites] Eur J Haematol. 2009 Jan;82(1):61-8 [18801058.001]
  • [Cites] Leukemia. 2008 Dec;22(12):2142-50 [18818707.001]
  • [Cites] Exp Hematol. 2009 Jan;37(1):135-42 [19100523.001]
  • [Cites] Blood. 2009 Jan 15;113(3):726-32 [18945962.001]
  • [Cites] J Clin Oncol. 2009 Jan 20;27(3):426-32 [19064981.001]
  • [Cites] Bone Marrow Transplant. 2009 Jan;43(2):107-13 [18776928.001]
  • [Cites] Haematologica. 2009 Feb;94(2):230-8 [19066328.001]
  • [Cites] Haematologica. 2009 Feb;94(2):296-8 [19109219.001]
  • [Cites] Br J Haematol. 2009 Mar;144(5):794-5 [19036096.001]
  • [Cites] Blood. 2009 Feb 12;113(7):1581-8 [18974373.001]
  • [Cites] Exp Hematol. 2005 Mar;33(3):286-94 [15730852.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2473-9 [15572591.001]
  • [Cites] Bone Marrow Transplant. 2005 Mar;35(6):549-56 [15756282.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1993-2003 [15774790.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2973-8 [15613541.001]
  • [Cites] Blood. 2005 May 15;105(10):3945-50 [15692072.001]
  • [Cites] Bone Marrow Transplant. 2005 May;35(10):943-51 [15806128.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3433-8 [15809449.001]
  • [Cites] Br J Haematol. 2005 Jun;129(5):631-43 [15916686.001]
  • [Cites] J Clin Oncol. 2005 Jun 1;23(16):3819-29 [15809448.001]
  • [Cites] Lancet. 2005 Jun 4-10;365(9475):1934-41 [15936420.001]
  • [Cites] Clin Cancer Res. 2005 Jun 15;11(12):4504-11 [15958636.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] Blood. 2005 Jul 15;106(2):458-63 [15817679.001]
  • [Cites] Br J Haematol. 2005 Aug;130(3):325-32 [16042682.001]
  • [Cites] Bone Marrow Transplant. 2005 Aug;36(4):315-23 [15968284.001]
  • [Cites] Bone Marrow Transplant. 2005 Sep;36(5):437-41 [15980879.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Nov;11(11):823-61 [16275588.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:292-8 [16304394.001]
  • [Cites] Klin Padiatr. 2005 Nov-Dec;217(6):351-6 [16307422.001]
  • [Cites] Cancer Immunol Immunother. 2006 Feb;55(2):197-209 [16025268.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4389-96 [16131571.001]
  • [Cites] Semin Hematol. 2005 Oct;42(4 Suppl 4):S3-8 [16344099.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Feb;12(2):172-83 [16443515.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1724-30 [16239425.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1325-31 [16269610.001]
  • [Cites] Leukemia. 2006 Mar;20(3):542-5 [16408097.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Apr;12(4):414-21 [16545725.001]
  • [Cites] Cancer. 2006 Apr 1;106(7):1569-80 [16502413.001]
  • [Cites] J Clin Oncol. 2006 Apr 1;24(10):1575-81 [16520464.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3415-6 [16597603.001]
  • [Cites] Blood. 2006 May 1;107(9):3804-7 [16384924.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4563-9 [16449533.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1040-6 [16525495.001]
  • [Cites] Exp Hematol. 2006 Jun;34(6):770-5 [16728282.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4961-7 [16493003.001]
  • [Cites] Bone Marrow Transplant. 2006 Jun;37(12):1135-41 [16757975.001]
  • [Cites] Haematologica. 2006 Jun;91(6 Suppl):ECR16 [16785122.001]
  • [Cites] Leuk Lymphoma. 2006 Jun;47(6):978-85 [16840186.001]
  • [Cites] Best Pract Res Clin Haematol. 2006;19(4):737-55 [16997180.001]
  • [Cites] Leuk Lymphoma. 2006 Sep;47(9):1754-67 [17064985.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Oct;12(10):1056-64 [17084369.001]
  • [Cites] J Clin Oncol. 2006 Dec 1;24(34):5343-9 [17088571.001]
  • [Cites] Haematologica. 2006 Dec;91(12):1653-61 [17145602.001]
  • [Cites] Leukemia. 1999 Dec;13(12):2079-86 [10602432.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1214-21 [10666193.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1572-9 [10688810.001]
  • [Cites] Br J Haematol. 2000 Feb;108(2):400-7 [10691873.001]
  • [Cites] Leuk Lymphoma. 2000 Jul;38(3-4):221-34 [10830730.001]
  • [Cites] J Clin Oncol. 2000 Jun;18(11):2273-81 [10829048.001]
  • [Cites] Biol Blood Marrow Transplant. 2000;6(3):272-9 [10871152.001]
  • [Cites] Biol Blood Marrow Transplant. 2000;6(3A):321-6 [10905769.001]
  • [Cites] Bone Marrow Transplant. 2000 Sep;26(5):511-6 [11019840.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2712-6 [11023502.001]
  • [Cites] Br J Haematol. 2000 Sep;110(4):1013-4 [11054097.001]
  • [Cites] Bone Marrow Transplant. 2000 Dec;26(11):1179-84 [11149728.001]
  • [Cites] Br J Haematol. 2001 Feb;112(2):421-3 [11167841.001]
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1414-20 [11230486.001]
  • [Cites] Blood. 2001 Jul 1;98(1):210-6 [11418482.001]
  • [Cites] Blood. 2001 Aug 15;98(4):934-9 [11493435.001]
  • [Cites] J Clin Oncol. 2001 Aug 15;19(16):3675-84 [11504749.001]
  • [Cites] J Clin Oncol. 2001 Dec 1;19(23):4314-21 [11731514.001]
  • [Cites] J Clin Oncol. 2002 Jan 15;20(2):405-12 [11786567.001]
  • [Cites] Science. 2002 Mar 15;295(5562):2097-100 [11896281.001]
  • [Cites] J Clin Oncol. 2007 Nov 1;25(31):4938-45 [17909197.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):824-31 [18021093.001]
  • [Cites] Haematologica. 2007 Nov;92(11):1533-48 [18024402.001]
  • [Cites] Leukemia. 2007 Dec;21(12):2569-74 [17611558.001]
  • [Cites] Leukemia. 2007 Dec;21(12):2540-4 [17611563.001]
  • [Cites] Leukemia. 2007 Dec;21(12):2452-5 [17728782.001]
  • [Cites] J Immunother. 2007 Nov-Dec;30(8):847-54 [18049337.001]
  • [Cites] Nat Rev Cancer. 2008 Jan;8(1):61-70 [18075512.001]
  • [Cites] Blood. 2008 Jan 1;111(1):446-52 [17916744.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Jan;14(1):50-8 [18158961.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):211-7 [18056679.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1094-100 [18003886.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1594-602 [18032710.001]
  • [Cites] Haematologica. 2008 Feb;93(2):257-64 [18223284.001]
  • [Cites] Haematologica. 2008 Feb;93(2):303-6 [18245655.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1827-33 [18048644.001]
  • [Cites] Haematologica. 2008 Mar;93(3):455-8 [18287132.001]
  • [Cites] Bone Marrow Transplant. 2008 Mar;41(5):495-503 [17952130.001]
  • [Cites] Bone Marrow Transplant. 2008 Mar;41(5):483-93 [18026156.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Apr;14(4):418-25 [18342784.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Apr;14(4):480-3 [18342792.001]
  • [Cites] Br J Haematol. 2008 Apr;141(2):235-43 [18318762.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4392-402 [17878399.001]
  • [Cites] Bone Marrow Transplant. 2008 May;41(9):779-84 [18195681.001]
  • [Cites] Leukemia. 2008 May;22(5):1007-17 [18323802.001]
  • [Cites] J Clin Oncol. 2008 May 20;26(15):2519-25 [18427150.001]
  • [Cites] Clin Immunol. 2008 Jun;127(3):280-5 [18337174.001]
  • [Cites] Blood. 2008 Jun 1;111(11):5291-7 [18334676.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Jul;14(7):817-23 [18541202.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5530-6 [18411419.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1377-86 [18418404.001]
  • [Cites] J Clin Oncol. 2008 Aug 1;26(22):3756-62 [18669463.001]
  • [Cites] Bone Marrow Transplant. 2008 Aug;42(3):201-5 [18490913.001]
  • [Cites] Bone Marrow Transplant. 2008 Aug;42(3):145-57 [18587431.001]
  • [Cites] Science. 2008 Aug 15;321(5891):974-7 [18703743.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1876-85 [18591381.001]
  • [Cites] Cancer Immunol Immunother. 2008 Nov;57(11):1705-10 [18663443.001]
  • [Cites] Br J Haematol. 2008 Sep;142(5):848-50 [18631344.001]
  • [Cites] Blood. 2008 Oct 15;112(8):3500-7 [18664621.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4912-20 [18794548.001]
  • [Cites] Biol Blood Marrow Transplant. 2008 Nov;14(11):1288-97 [18940684.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3807-17 [18599795.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3574-81 [18606875.001]
  • [Cites] Ann Oncol. 2008 Nov;19(11):1935-40 [18684698.001]
  • [Cites] J Clin Immunol. 2002 May;22(3):124-30 [12078853.001]
  • [Cites] Blood. 2002 Jul 15;100(2):397-405 [12091328.001]
  • [Cites] Blood. 2002 Jul 15;100(2):635-9 [12091358.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2289-90 [12239136.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3108-14 [12384406.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3121-7 [12384408.001]
  • [Cites] Curr Opin Hematol. 2002 Nov;9(6):503-8 [12394172.001]
  • [Cites] Biol Blood Marrow Transplant. 2002;8(11):625-32 [12463482.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):36-8 [12517774.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1637-44 [12393484.001]
  • [Cites] Br J Haematol. 2003 Feb;120(3):523-5 [12580972.001]
  • [Cites] Leukemia. 2003 Feb;17(2):468-70 [12592351.001]
  • [Cites] Cytometry B Clin Cytom. 2003 Mar;52(1):1-12 [12599176.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2742-7 [12601144.001]
  • [Cites] Bone Marrow Transplant. 2003 Feb;31(3):157-61 [12621475.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1278-84 [12663715.001]
  • [Cites] J Pediatr Hematol Oncol. 2003 Apr;25(4):327-9 [12679650.001]
  • [Cites] Leuk Lymphoma. 2002 Sep;43(9):1755-62 [12685828.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Apr;9(4):257-65 [12720218.001]
  • [Cites] Bone Marrow Transplant. 2003 May;31(9):739-46 [12732878.001]
  • [Cites] Bone Marrow Transplant. 2009 Feb;43(4):327-33 [18850014.001]
  • [Cites] Leukemia. 2009 Mar;23(3):605-7 [18784738.001]
  • [Cites] Bone Marrow Transplant. 2009 Mar;43(5):383-97 [18850012.001]
  • [Cites] J Clin Oncol. 2009 Mar 20;27(9):1492-501 [19224851.001]
  • [Cites] Blood. 2009 Mar 26;113(13):2902-5 [19179301.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 May;15(5):580-8 [19361750.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 May;15(5):610-7 [19361753.001]
  • [Cites] Leuk Lymphoma. 2009 Apr;50(4):551-8 [19373652.001]
  • [Cites] Cancer. 2009 May 1;115(9):1899-905 [19235255.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4144-52 [19168784.001]
  • [Cites] Leuk Res. 2009 Jul;33(7):e61-3 [19157550.001]
  • [Cites] Curr Opin Hematol. 2009 Mar;16(2):112-23 [19468273.001]
  • [Cites] Bone Marrow Transplant. 2009 Jun;43(11):839-43 [19151791.001]
  • [Cites] Blood. 2009 Jun 25;113(26):6567-71 [19389879.001]
  • [Cites] N Engl J Med. 2009 Jul 30;361(5):478-88 [19641204.001]
  • [Cites] Blood. 2009 Aug 13;114(7):1429-36 [19528536.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):3951-8 [19620487.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Sep 15;106(37):15825-30 [19717467.001]
  • [Cites] Bone Marrow Transplant. 2009 Nov;44(9):585-8 [19363531.001]
  • [Cites] Eur J Clin Invest. 2009 Dec;39(12):1098-109 [19744184.001]
  • [Cites] Leuk Lymphoma. 2009 Aug;50(8):1239-48 [19562639.001]
  • [Cites] Cancer. 2009 Dec 1;115(23):5490-8 [19708032.001]
  • [Cites] Cancer Treat Rev. 2009 Dec;35(8):653-61 [19682801.001]
  • [Cites] J Clin Oncol. 2009 Dec 10;27(35):6012-8 [19826119.001]
  • [Cites] Leuk Lymphoma. 2009 Dec;50(12):2075-7 [19637088.001]
  • [Cites] Biol Blood Marrow Transplant. 2010 Jan;16(1):78-85 [19744569.001]
  • [Cites] Bone Marrow Transplant. 2010 Feb;45(2):349-53 [19584825.001]
  • [Cites] Biol Blood Marrow Transplant. 2010 Mar;16(3):301-10 [19744571.001]
  • [Cites] Bone Marrow Transplant. 2010 Mar;45(3):558-64 [19633691.001]
  • [Cites] Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554.001]
  • [Cites] Mol Ther. 2010 Apr;18(4):843-51 [20179677.001]
  • [Cites] Mol Ther. 2010 Apr;18(4):666-8 [20357779.001]
  • [Cites] Bone Marrow Transplant. 2010 Apr;45(4):627-32 [19718057.001]
  • [Cites] Biol Blood Marrow Transplant. 2010 May;16(5):639-46 [20005967.001]
  • [Cites] Biol Blood Marrow Transplant. 2010 Jun;16(6):709-28 [20227509.001]
  • [Cites] Blood. 2010 May 13;115(19):3869-78 [20071660.001]
  • [Cites] Cancer Res. 2010 May 15;70(10):3915-24 [20424114.001]
  • [Cites] Br J Haematol. 2010 Aug;150(3):352-8 [20528877.001]
  • [Cites] Biol Blood Marrow Transplant. 2010 Sep;16(9):1237-44 [20302960.001]
  • [Cites] Biol Blood Marrow Transplant. 2010 Sep;16(9):1187-211 [20558311.001]
  • [Cites] Biol Blood Marrow Transplant. 2010 Oct;16(10):1325-46 [20637879.001]
  • [Cites] Blood. 2010 Oct 7;116(14):2438-47 [20595516.001]
  • [Cites] Blood. 2010 Nov 11;116(19):3875-86 [20631379.001]
  • [Cites] Leuk Lymphoma. 2010 Mar;51(3):376-89 [20141428.001]
  • (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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6. 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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7. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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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8. 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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9. 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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10. 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
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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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  • [Cites] Hematol Oncol Clin North Am. 2001 Feb;15(1):21-36 [11258387.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1469-77 [16638934.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1965-71 [12200353.001]
  • [Cites] Haematologica. 2003 Feb;88(2):227-9 [12604417.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Mar;9(3):206-12 [12652472.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1707-12 [12970768.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):685-702, x [15271400.001]
  • [Cites] J Clin Invest. 2004 Aug;114(3):379-88 [15286804.001]
  • [Cites] Blood. 1995 May 1;85(9):2632-8 [7727789.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2602-9 [9116308.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1410-4 [9269758.001]
  • [Cites] Biol Blood Marrow Transplant. 2004 Dec;10(12):883-4 [15570257.001]
  • [Cites] Blood. 2005 Jul 15;106(2):458-63 [15817679.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):460-6 [16344315.001]
  • [Cites] Nat Med. 2006 Feb;12(2):214-9 [16444265.001]
  • [Cites] Nat Med. 2006 Feb;12(2):207-13 [16444266.001]
  • [Cites] N Engl J Med. 2006 May 25;354(21):2282-4 [16723621.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1590-5 [12176876.001]
  • (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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11. Dölken G: Detection of minimal residual disease. Adv Cancer Res; 2001;82:133-85
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  • [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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12. Kobbe G, Schneider P, Rohr U, Fenk R, Neumann F, Aivado M, Dietze L, Kronenwett R, Hünerlitürkoglu A, Haas R: Treatment of severe steroid refractory acute graft-versus-host disease with infliximab, a chimeric human/mouse antiTNFalpha antibody. Bone Marrow Transplant; 2001 Jul;28(1):47-9
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  • [Title] Treatment of severe steroid refractory acute graft-versus-host disease with infliximab, a chimeric human/mouse antiTNFalpha antibody.
  • Patients with severe aGVHD not responding to treatment with steroids have a poor prognosis.
  • Patients (CML 2, MM 1, AML 1) developed grade III-IV GVHD at a median of 34 days (range 15-76) after myeloablative PBSCT (two), donor lymphocyte infusion for relapsed CML (one) or non-myeloablative PBSCT (one), respectively.
  • All patients had severe intestinal involvement in addition to skin and/or liver disease and had received treatment with high-dose steroids (four) for a median of 11 days (range 5-17) in addition to CsA (four) and MMF (three).
  • At present two patients are alive >200 days after therapy, one with limited cGVHD.
  • Infliximab is apparently an active drug for the treatment of aGVHD.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Graft vs Host Disease / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Animals. Anti-Inflammatory Agents / administration & dosage. Female. Hematologic Neoplasms / complications. Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Infliximab. Male. Mice. Middle Aged. Recombinant Fusion Proteins / administration & dosage. Salvage Therapy. Steroids / therapeutic use. Transplantation, Homologous / adverse effects. Treatment Outcome. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 11498743.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Recombinant Fusion Proteins; 0 / Steroids; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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13. 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.
  • [Cites] Genome Res. 2007 Sep;17(9):1296-303 [17675364.001]
  • [Cites] Nature. 2010 Jan 14;463(7278):191-6 [20016485.001]
  • [Cites] Cytogenet Genome Res. 2009;124(1):1-11 [19372663.001]
  • [Cites] Clin Cancer Res. 2009 Jan 15;15(2):441-51 [19147748.001]
  • [Cites] PLoS One. 2009 Sep 17;4(9):e7089 [19759907.001]
  • [Cites] Cancer Res. 2009 Nov 1;69(21):8341-8 [19826035.001]
  • [Cites] Endocr Pathol. 2006 Winter;17(4):307-17 [17525478.001]
  • [Cites] Science. 2000 Oct 6;290(5489):138-41 [11021799.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):179-87 [15013217.001]
  • [Cites] Thyroid. 2009 Dec;19(12 ):1351-61 [19895341.001]
  • [Cites] Annu Rev Genet. 1998;32:495-519 [9928489.001]
  • [Cites] Nat Rev Mol Cell Biol. 2010 Mar;11(3):171-81 [20125188.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):233-45 [17361217.001]
  • [Cites] Nat Genet. 2005 Jun;37 Suppl:S11-7 [15920524.001]
  • [Cites] Nat Genet. 2003 Aug;34(4):369-76 [12923544.001]
  • [Cites] N Engl J Med. 2003 Mar 27;348(13):1201-14 [12660384.001]
  • [Cites] Cancer. 1984 Dec 1;54(11):2409-13 [6594186.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2505-15 [18299451.001]
  • [Cites] Annu Rev Genet. 2009;43:223-49 [19686080.001]
  • [Cites] Pathol Biol (Paris). 2008 Sep;56(6):375-9 [18456424.001]
  • [Cites] Cancer Lett. 2001 May 10;166(1):1-7 [11295280.001]
  • [Cites] Oncogene. 2003 Aug 14;22(34):5374-8 [12917640.001]
  • [Cites] J Clin Invest. 2007 Aug;117(8):2067-74 [17671641.001]
  • [Cites] Mol Oncol. 2010 Aug;4(4):309-22 [20599448.001]
  • [Cites] Nature. 2008 Apr 3;452(7187):553-63 [18385729.001]
  • [Cites] Nat Med. 2009 Oct;15(10):1149-52 [19812576.001]
  • [Cites] Target Oncol. 2009 Jan;4(1):45-56 [19343301.001]
  • [Cites] Nat Rev Cancer. 2010 Jan;10 (1):59-64 [20029424.001]
  • [Cites] Cancer Lett. 2007 Aug 28;254(1):1-10 [17250957.001]
  • [Cites] Nat Rev Cancer. 2010 Feb;10(2):102-15 [20094045.001]
  • [Cites] Nat Rev Genet. 2009 Oct;10(10):704-14 [19763153.001]
  • [Cites] Am J Med Genet. 2002 Oct 30;115(3):189-93 [12407700.001]
  • [Cites] Br J Haematol. 1980 Aug;45(4):565-8 [7426437.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] Leuk Res. 1981;5(4-5):331-9 [7026904.001]
  • [Cites] Chem Biol Interact. 2010 Mar 19;184(1-2):50-7 [19958752.001]
  • [Cites] N Engl J Med. 2008 Aug 14;359(7):722-34 [18703475.001]
  • [Cites] C R Seances Acad Sci III. 1981 Nov 2;293(8):427-9 [6797692.001]
  • [Cites] Cancer Genet Cytogenet. 1981 Jun;3(4):307-15 [7260888.001]
  • [Cites] N Engl J Med. 1989 Apr 20;320(16):1047-54 [2648153.001]
  • [Cites] Nature. 2010 Feb 18;463(7283):899-905 [20164920.001]
  • [Cites] Clin Cancer Res. 2010 Jan 1;16(1):291-303 [20028749.001]
  • [Cites] J Natl Cancer Inst. 1960 Jul;25:85-109 [14427847.001]
  • [Cites] Science. 2009 Nov 27;326(5957):1230 [19933109.001]
  • [Cites] Cell. 2009 Sep 18;138(6):1051-4 [19766556.001]
  • [Cites] Br J Haematol. 1980 Aug;45(4):557-64 [7000153.001]
  • [Cites] J Natl Cancer Inst. 2006 Jul 5;98(13):897-903 [16818853.001]
  • [Cites] Curr Med Chem. 1999 Sep;6(9):775-805 [10495352.001]
  • [Cites] Am J Surg Pathol. 2008 May;32(5):656-70 [18344867.001]
  • [Cites] Blood. 2009 Nov 26;114(23):4761-70 [19745066.001]
  • [Cites] Genome Med. 2009 Apr 17;1(4):40 [19435481.001]
  • [Cites] Oncology. 2001;61 Suppl 2:22-30 [11694784.001]
  • [Cites] Haematologica. 2009 Jul;94(7):935-43 [19535347.001]
  • [Cites] Endocrinology. 2002 Jun;143(6):2025-8 [12021165.001]
  • [Cites] N Engl J Med. 1994 Aug 4;331(5):294-9 [8022439.001]
  • [Cites] Cancer Res. 1996 Jan 1;56(1):100-4 [8548747.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] J Clin Oncol. 2009 Mar 1;27(7):1026-33 [19171713.001]
  • [Cites] Nature. 1982 Jul 29;298(5873):474-6 [6806672.001]
  • [Cites] Nature. 1992 Sep 10;359(6391):162-5 [1522903.001]
  • [Cites] Science. 1992 Oct 30;258(5083):818-21 [1359641.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Med Pediatr Oncol. 2001 Jan;36(1):100-3 [11464856.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):77-82 [11900254.001]
  • [Cites] Blood. 2008 Dec 15;112(13):4808-17 [19064740.001]
  • (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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14. 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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15. 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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16. 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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  • [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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17. Yin CC, Abruzzo LV, Qiu X, Apostolidou E, Cortes JE, Medeiros LJ, Lu G: del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):18-23
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  • [Title] del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia.
  • The del(15q) chromosomal abnormality is known to occur in acute leukemias, but has rarely been described in chronic myelogenous leukemia (CML).
  • Described here are five cases of CML associated with del(15q): four men and one woman.
  • Bone marrow aspirate smears showed increased blasts in all cases at the time of del(15q) detection, in accelerated phase in two cases and myeloid blast phase in three.
  • All patients received imatinib mesylate; four received additional chemotherapy, and two had allogeneic stem cell transplantation (ASCT).
  • These findings indicate that del(15q) is a recurrent cytogenetic abnormality that may be seen at initial presentation of advanced disease or may emerge during disease progression.
  • Del(15q) appears to be associated with a poor prognosis in CML.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 15. Clone Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

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  • [Cites] Mod Pathol. 2004 Jan;17(1):96-103 [14657955.001]
  • [Cites] Cancer Genet Cytogenet. 2009 Jan 15;188(2):118-23 [19100517.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Jun;151(2):146-51 [15172752.001]
  • [Cites] Am J Clin Pathol. 2004 Jun;121(6):836-42 [15198355.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):671-84, x [15271399.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] Cancer. 1999 Dec 15;86(12):2632-41 [10594858.001]
  • [Cites] Cancer Res. 2000 Jan 1;60(1):70-3 [10646855.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] Arch Pathol Lab Med. 2001 Mar;125(3):437-9 [11231500.001]
  • [Cites] Cancer. 2002 Feb 15;94(4):1102-10 [11920481.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1266-72 [12481006.001]
  • [Cites] Int J Cancer. 2003 Aug 10;106(1):74-7 [12794759.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Jul 1;144(1):1-5 [12810248.001]
  • [Cites] Scand J Haematol. 1976 Jul;17(1):17-28 [1066809.001]
  • [Cites] Cancer. 1979 Apr;43(4):1350-7 [445335.001]
  • [Cites] Hum Genet. 1981;58(3):285-93 [6948765.001]
  • [Cites] Cancer. 1985 Feb 1;55(3):535-41 [3965107.001]
  • [Cites] Leuk Res. 1991;15(8):683-91 [1654480.001]
  • [Cites] Cancer Genet Cytogenet. 1991 Aug;55(1):35-8 [1913605.001]
  • [Cites] Leuk Lymphoma. 1993;11 Suppl 1:11-5 [8251885.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Feb;86(2):124-8 [8603337.001]
  • [Cites] Baillieres Clin Haematol. 1997 Jun;10(2):223-31 [9376661.001]
  • [Cites] Leuk Res. 1998 Sep;22(9):845-7 [9716017.001]
  • [Cites] Curr Opin Hematol. 1998 Jul;5(4):302-8 [9747637.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Am J Clin Pathol. 2005 Nov;124(5):807-14 [16203287.001]
  • [Cites] Cancer. 2006 Apr 15;106(8):1730-8 [16532439.001]
  • [Cites] J Cell Biochem. 2007 Apr 15;100(6):1376-86 [17131381.001]
  • [Cites] Cancer. 2008 May 15;112(10):2112-8 [18348294.001]
  • [Cites] Cancer. 2008 Oct 1;113(7 Suppl):1933-52 [18798533.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • (PMID = 19480932.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS627187; NLM/ PMC4167428
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18. 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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19. 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
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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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  • [Cites] J Clin Oncol. 2008 Oct 10;26(29):4806-13 [18645191.001]
  • [Cites] Blood. 2008 Aug 1;112(3):516-8 [18492956.001]
  • [Cites] Blood. 2001 Nov 15;98(10):3074-81 [11698293.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]
  • [Cites] Acta Haematol. 2002;107(2):64-75 [11919387.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1448-53 [12886230.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1423-32 [14534335.001]
  • [Cites] Br J Haematol. 2004 Jun;125(5):613-20 [15147377.001]
  • [Cites] Cancer. 1988 Apr 1;61(7):1441-6 [3162181.001]
  • [Cites] N Engl J Med. 1993 Sep 30;329(14):987-94 [8141877.001]
  • [Cites] Lancet. 1998 Oct 3;352(9134):1087-92 [9798583.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3395-400 [15705718.001]
  • [Cites] Leukemia. 2005 Apr;19(4):507-12 [15703781.001]
  • [Cites] Leukemia. 2005 Nov;19(11):1872-9 [16179913.001]
  • [Cites] Leukemia. 2006 Apr;20(4):658-63 [16467863.001]
  • [Cites] Blood. 2006 May 15;107(10):4171-6 [16449534.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] Blood. 2006 Jul 1;108(1):28-37 [16522812.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1809-20 [16709930.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2303-9 [17138817.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3540-6 [17715389.001]
  • [Cites] Lancet Oncol. 2007 Dec;8(12):1116-28 [18054881.001]
  • [Cites] Leuk Res. 2008 Mar;32(3):505-6 [17512589.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1200-6 [18401416.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3204-12 [18541900.001]
  • [Cites] J Clin Oncol. 2008 Jul 10;26(20):3358-63 [18519952.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4437-44 [18716134.001]
  • (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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20. 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


21. 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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  • [Cites] Blood. 2003 Sep 15;102(6):2236-9 [12750174.001]
  • [Cites] Biochim Biophys Acta. 2005 Jun 1;1711(1):1-11 [15904657.001]
  • [Cites] J Mol Med (Berl). 2004 Sep;82(9):579-91 [15221077.001]
  • [Cites] Nat Med. 2005 Mar;11(3):263-70 [15723075.001]
  • [Cites] Blood. 2003 Jan 15;101(2):425-32 [12393493.001]
  • [Cites] Semin Hematol. 2003 Apr;40(2 Suppl 2):15-20 [12783370.001]
  • [Cites] Curr Opin Hematol. 2005 Jan;12(1):33-9 [15604889.001]
  • [Cites] Nucleic Acids Res. 2003 Aug 1;31(15):4417-24 [12888501.001]
  • [Cites] Haematologica. 2005 Mar;90(3):326-34 [15749664.001]
  • [Cites] Nature. 2001 May 24;411(6836):494-8 [11373684.001]
  • [Cites] Ann Hematol. 2005 Aug;84(8):487-97 [15931535.001]
  • [Cites] Clin Exp Med. 2006 Mar;6(1):45-7 [16550344.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1566-9 [12393533.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1451-64 [14534339.001]
  • [Cites] Oncogene. 2002 Aug 22;21(37):5716-24 [12173041.001]
  • [Cites] J Clin Oncol. 2005 Oct 20;23(30):7697-702 [16186597.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2375-84 [8839828.001]
  • [Cites] Adv Drug Deliv Rev. 2004 Apr 23;56(7):931-46 [15066753.001]
  • [Cites] Blood. 2002 May 1;99(9):3472-5 [11964322.001]
  • [Cites] J Pharmacol Exp Ther. 2002 Dec;303(3):1334-43 [12438559.001]
  • [Cites] Leuk Lymphoma. 2006 Jan;47(1):1-7 [16321820.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2374-86 [12239145.001]
  • [Cites] Blood. 2003 Jul 1;102(1):276-83 [12623848.001]
  • [Cites] Cancer. 2004 Jan 15;100(2):321-6 [14716767.001]
  • [Cites] Br J Haematol. 2001 Jun;113(4):1072-5 [11442504.001]
  • [Cites] Biosci Rep. 2000 Oct;20(5):419-32 [11332603.001]
  • (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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22. 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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23. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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  • [Cites] Hum Mutat. 2000 Apr;15(4):385-6 [10737995.001]
  • [Cites] Cell. 1997 Aug 22;90(4):797-807 [9288758.001]
  • [Cites] Pediatr Nephrol. 2003 Sep;18(9):853-9 [12836090.001]
  • [Cites] Am J Med. 1967 Aug;43(2):227-53 [5340644.001]
  • [Cites] Arthritis Rheum. 1997 Oct;40(10):1879-85 [9336425.001]
  • [Cites] Intern Med. 2002 Mar;41(3):221-4 [11929185.001]
  • [Cites] Br J Rheumatol. 1997 Sep;36(9):1005-8 [9376975.001]
  • [Cites] Eur J Hum Genet. 2001 Jul;9(7):473-83 [11464238.001]
  • [Cites] J Rheumatol. 2002 Jun;29(6):1324-5 [12064853.001]
  • [Cites] Hum Mutat. 2003 Oct;22(4):339-40 [12955725.001]
  • [Cites] QJM. 2001 Oct;94(10 ):527-31 [11588211.001]
  • [Cites] Eur J Haematol. 1992 Apr;48(4):196-201 [1592099.001]
  • [Cites] Nat Genet. 1997 Sep;17 (1):25-31 [9288094.001]
  • (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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24. 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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25. Jameel A, Jamil SN: Safety of cytotoxic chemotherapy during pregnancy. J Pak Med Assoc; 2007 Sep;57(9):449-52
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  • [Title] Safety of cytotoxic chemotherapy during pregnancy.
  • OBJECTIVE: To To present an experience and results of treatment of pregnant cancer patients with cytotoxic chemotherapy from second trimester of pregnancy.
  • METHODS: Eighteen consecutive pregnant patients treated at Khyber Teaching Hospital, Peshawar between December 2000 and August 2006 for different types of malignancies are reported.
  • Six patients (33%) had breast cancer, four (22%) had chronic myeloid leukaemia, two (11%) had Hodgkin's disease, two (11%) had acute myeloid leukaemia and one each had recurrent ovarian carcinoma (5.7%), soft-tissue sarcoma (5.7%), acute lymphoblastic leukaemia (5.7%) and non-Hodgkin's lymphoma (5.7%).
  • RESULTS: Two patients were lost to follow-up after one course of chemotherapy while two patients chose to have therapeutic abortion.
  • Out of the remaining 14 patients, one patient had spontaneous abortion while one patient had an intra-uterine death of foetus during chemotherapy.
  • CONCLUSION: Chemotherapy during the second and third trimester of pregnancy can be safe if proper obstetric and radiologic monitoring is performed.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytotoxins / adverse effects. Drug-Related Side Effects and Adverse Reactions. Pregnancy Complications. Pregnancy Outcome
  • [MeSH-minor] Adult. Breast Neoplasms / drug therapy. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasms / drug therapy. Pregnancy. Pregnancy Trimester, Second. Prospective Studies. Time Factors

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  • (PMID = 18072640.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytotoxins
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26. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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27. 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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28. 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
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  • [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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