[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 61 of about 61
1. Myojo T, Hino N: Complete remission from chronic myelogenous leukemia--blastic crisis caused by reduced intensity stem cell transplantation following partial remission due to imatinib. Intern Med; 2004 Feb;43(2):126-30
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete remission from chronic myelogenous leukemia--blastic crisis caused by reduced intensity stem cell transplantation following partial remission due to imatinib.
  • We report a 55-year-old man who showed no change after chemotherapy for chronic myelogenous leukemia-blastic crisis (CML-BC) in 1998.
  • There are still no established radical methods of treating CML-BC.
  • Thus, therapy by allograft after the patient has entered hematological remission with imatinib is considered a new way of dealing with cases of CML-BC.
  • [MeSH-major] Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Peripheral Blood Stem Cell Transplantation / methods. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15005255.001).
  • [ISSN] 0918-2918
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
  •  go-up   go-down


2. Lee SA, Lim J, Kim M, Kim Y, Han K: [A case of t(3;3)(q21;q26.2) associated with severe multilineage dysplasia and multi-drug resistance in blastic crisis of chronic myelogenous leukemia]. Korean J Lab Med; 2010 Dec;30(6):595-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of t(3;3)(q21;q26.2) associated with severe multilineage dysplasia and multi-drug resistance in blastic crisis of chronic myelogenous leukemia].
  • Patients with these cytogenetic abnormalities show extremely poor prognosis even with aggressive anti-leukemic therapy.
  • We report a case of blastic crisis of CML with both t(3;3)(q21;q26.2) and t(9;22)(q34;q11.2) and associated severe multilineage dysplasia.
  • The patient showed a poor response to imatinib, dasatinib and aggressive induction therapy.
  • When both t(3;3)(q21;q26.2) and t(9;22)(q34;q11.2) are observed in cases of leukemia with increased blasts, they are best considered as aggressive phases of CML with t(3;3)(q21;q26.2), rather than AML with t(9;22)(q34;q11.2) by 2008 WHO classification.
  • [MeSH-major] Blast Crisis / diagnosis. Chromosomes, Human, Pair 3. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Translocation, Genetic
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Benzamides. Bone Marrow Cells / pathology. Dasatinib. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Karyotyping. Male. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21157145.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  •  go-up   go-down


3. Wadhwa J, Szydlo RM, Apperley JF, Chase A, Bua M, Marin D, Olavarria E, Kanfer E, Goldman JM: Factors affecting duration of survival after onset of blastic transformation of chronic myeloid leukemia. Blood; 2002 Apr 1;99(7):2304-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Factors affecting duration of survival after onset of blastic transformation of chronic myeloid leukemia.
  • We analyzed factors having an impact on response to treatment and survival in 78 consecutive patients with chronic myeloid leukemia (CML) in blastic transformation (BT) referred to the Hammersmith Hospital from January 1995 to December 2000.
  • BT was defined as the presence of at least 30% blasts in blood or marrow or extramedullary blastic deposits.
  • Initial treatment varied; 41 patients received cytotoxic drugs, 8 underwent allogeneic or autologous transplantation procedures, 21 received STI571 (imatinib mesylate, Gleevec), 1 received radiotherapy, and 7 received no therapy.
  • Of the 25 (32%) patients who achieved a "second chronic phase" with first therapy, 6 of 21 (29%) were treated with STI571 and 19 of 50 (38%) were treated with chemotherapy, transplantation, or radiotherapy.
  • Patients who achieved a second chronic phase survived longer than those who did not (median time from onset of BT 12.0 months versus 6.3 months, P =.0004).
  • We speculate that the combined use of STI571 with cytotoxic drugs may offer additional benefit.
  • [MeSH-major] Blast Crisis / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Child. Disease-Free Survival. Humans. Leukocyte Count. Middle Aged. Platelet Count. Predictive Value of Tests. Prognosis. Survival Rate. Time Factors


Advertisement
4. Karbasian Esfahani M, Morris EL, Dutcher JP, Wiernik PH: Blastic phase of chronic myelogenous leukemia. Curr Treat Options Oncol; 2006 May;7(3):189-99
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Blastic phase of chronic myelogenous leukemia.
  • Chronic myelogenous leukemia (CML), also known as chronic myelocytic or chronic myeloid leukemia, is a clonal disorder of hematopoiesis that arises in a hematopoietic stem cell or early progenitor cell.
  • Eventually, in spite of the term chronic, there is progression to acute leukemia, usually of the myeloid variety, which is highly resistant to current therapies.
  • Despite recent improvements in the treatment of early-stage disease, CML blast crisis (CMLBC) remains a therapeutic challenge.
  • CMLBC is highly refractory to standard induction chemotherapy, with a response rate in myeloid blast crisis of less than 30%.
  • Conventional chemotherapy has been much less successful in this disease compared with de novo acute leukemia, with a mean survival after diagnosis of blast crisis of only 2 to 4 months for nonresponders.
  • Although imatinib was evaluated in patients with CMLBC, most CMLBC cases today arise in patients already on imatinib-based therapy and developing blastic phase on that therapy; thus there is no standard therapy for patients with CMLBC.
  • Further studies of the mechanisms of transformation of chronic-phase CMLBC at a molecular level, and methods to target these molecular abnormalities, will determine the future direction of new treatment modalities.
  • The prognosis of CML in blast crisis remains disappointing, despite great efforts.
  • Currently, the most successful strategy for improving survival in CML is by prolonging the chronic phase and delaying the onset of blast crisis.
  • [MeSH-major] Blast Crisis / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 1988 Aug 15;62(4):672-6 [3165046.001]
  • [Cites] Br J Haematol. 2002 Sep;118(4):1048-54 [12199784.001]
  • [Cites] Blood. 2003 Nov 15;102(10):3765-74 [12893773.001]
  • [Cites] Trends Cell Biol. 1999 May;9(5):179-86 [10322452.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4674-81 [14581336.001]
  • [Cites] Neoplasma. 2001;48(3):203-7 [11583290.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] J Natl Cancer Inst. 1986 Jun;76(6):1295-9 [3520071.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):753-74, xii [15271404.001]
  • [Cites] Ai Zheng. 2004 Dec;23(12):1696-9 [15601563.001]
  • [Cites] Blood. 2002 May 15;99(10):3547-53 [11986206.001]
  • [Cites] Leuk Res. 1997 May;21(5):375-80 [9225062.001]
  • [Cites] Haematologica. 2004 Apr;89(4):ECR11 [15075103.001]
  • [Cites] Clin Adv Hematol Oncol. 2005 Jul;3(7):547-52 [16167037.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4163-9 [15687234.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1965-71 [12200353.001]
  • [Cites] Leuk Lymphoma. 2005 Mar;46(3):377-85 [15621827.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Leuk Res. 1996 Nov-Dec;20(11-12):905-8 [9009247.001]
  • [Cites] Am J Med. 1987 Sep;83(3):445-54 [3477958.001]
  • [Cites] Ann Hematol. 1999 Feb;78(2):49-64 [10089019.001]
  • [Cites] Leuk Lymphoma. 2004 Feb;45(2):401-3 [15101732.001]
  • [Cites] Blood. 2004 Oct 1;104(7):1979-88 [15198956.001]
  • [Cites] Haematologia (Budap). 2002;32(1):49-57 [12243555.001]
  • [Cites] J Clin Invest. 2000 Jan;105(1):3-7 [10619854.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1451-64 [14534339.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Ann Intern Med. 2003 May 20;138(10):819-30 [12755554.001]
  • [Cites] Haematologica. 2003 Nov;88(11):1213-20 [14607749.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:188-94 [16304379.001]
  • [Cites] Blood. 2000 Feb 1;95(3):738-43 [10648381.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Leukemia. 1992 Aug;6(8):770-5 [1379312.001]
  • [Cites] Curr Treat Options Oncol. 2000 Apr;1(1):51-62 [12057061.001]
  • [Cites] N Engl J Med. 1986 Jan 23;314(4):202-7 [3510388.001]
  • [Cites] Blood. 2004 Jul 15;104(2):509-18 [15039284.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):545-68, vii-viii [15271392.001]
  • [Cites] Br J Haematol. 2002 Oct;119(1):15-24 [12358949.001]
  • [Cites] Leukemia. 1998 Jul;12(7):1037-40 [9665187.001]
  • [Cites] Haematologica. 2002 Sep;87(9):979-88 [12217811.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4100-9 [15867198.001]
  • [Cites] Blood. 2003 Jun 15;101(12):5010-3 [12595307.001]
  • [Cites] J Clin Invest. 1992 Oct;90(4):1232-41 [1383271.001]
  • [Cites] J Clin Oncol. 1992 Mar;10(3):398-405 [1740679.001]
  • [Cites] Cancer Treat Rep. 1982 Feb;66(2):267-71 [6173123.001]
  • [Cites] Drug Resist Updat. 2003 Oct;6(5):231-8 [14643293.001]
  • [Cites] N Engl J Med. 1986 Dec 4;315(23):1433-8 [2431313.001]
  • [Cites] Ann Intern Med. 1999 Aug 3;131(3):207-19 [10428738.001]
  • [Cites] Int J Hematol. 2004 Jun;79(5):420-33 [15239391.001]
  • [Cites] Br J Haematol. 1998 Jan;100(1):123-8 [9450800.001]
  • [Cites] Blood. 2002 May 15;99(10):3530-9 [11986204.001]
  • [Cites] Nature. 1987 Jul 23-29;328(6128):342-4 [3474529.001]
  • [Cites] Blood. 2002 Jan 1;99(1):319-25 [11756187.001]
  • [Cites] Med Oncol. 2010 Sep;27(3):728-35 [19697165.001]
  • (PMID = 16615875.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 60
  •  go-up   go-down


5. Giles FJ, Cortes JE, Kantarjian HM, O'Brien SM: Accelerated and blastic phases of chronic myelogenous leukemia. Hematol Oncol Clin North Am; 2004 Jun;18(3):753-74, xii
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Accelerated and blastic phases of chronic myelogenous leukemia.
  • Chronic myelogenous leukemia (CML) may have a biphasic or triphasic course, whereby patients who were initially diagnosed in the chronic phase (CP) develop more aggressive disease, frequently pass through an intermediate or accelerated phase (AP), and finally evolve into an acute leukemia like blastic phase (BP).
  • A slowing in the rate of development of AP or BP has accompanied successive improvements in therapy for patients who have CP CML.
  • The management of patients in AP or BP consistently has been less effective than the management of those inCP for all modalities of therapy.
  • This article reviews the current diagnostic criteria, therapeutic strategies, outcomes, and investigational therapies for AP and BP CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Blast Crisis / diagnosis. Blast Crisis / drug therapy. Clone Cells / pathology. Humans. Leukemia, Myeloid, Accelerated Phase / diagnosis. Leukemia, Myeloid, Accelerated Phase / drug therapy. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15271404.001).
  • [ISSN] 0889-8588
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 177
  •  go-up   go-down


6. Fujimaki K, Maruta A, Yoshida M, Yamazaki E, Matsuzaki M, Fujisawa S, Kanamori H, Ishigatsubo Y: [Complete cytogenetic response obtained with unrelated donor lymphocyte infusion for relapse of chronic myeloid leukemia in blastic crisis after allogeneic bone marrow transplantation]. Rinsho Ketsueki; 2001 Mar;42(3):204-8
MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Complete cytogenetic response obtained with unrelated donor lymphocyte infusion for relapse of chronic myeloid leukemia in blastic crisis after allogeneic bone marrow transplantation].
  • A 35-year-old man with chronic myeloid leukemia (CML) in blastic crisis (BC) received an allogeneic bone marrow transplant from an unrelated donor in October 1998 after three cycles of chemotherapy.
  • BC relapse developed on day 349 after transplantation.
  • After one cycle of chemotherapy and treatment with interferon, the patient received donor lymphocyte infusion (DLI), and this resulted in a complete cytogenetic response 21 days later.
  • Grade III acute graft-versus-host disease developed on day 25 after DLI, but this was resolved after administration of prednisolone.
  • Disease relapse occurred at extramedullary sites on day 162 after DLI, and the patient died of sepsis after receiving chemotherapy.
  • This case illustrates that unrelated DLI can induce remission successfully in patients with relapse of CML in BC through a graft-versus-leukemia effect.
  • [MeSH-major] Blast Crisis. Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Male. Remission Induction. Tissue Donors


7. Hamaki T, Kami M, Momomura S, Mineishi S, Kusumi E, Kanda Y, Ueyama J, Miyakoshi S, Morinaga S, Takaue Y, Mutou Y: Sustained molecular remission in a patient with CML in blastic crisis receiving dose-reduced hematopoietic stem-cell transplantation followed by early withdrawal of cyclosporine and prophylactic use of interferon-alpha. Am J Hematol; 2002 Nov;71(3):196-9
Hazardous Substances Data Bank. CYCLOSPORIN A .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sustained molecular remission in a patient with CML in blastic crisis receiving dose-reduced hematopoietic stem-cell transplantation followed by early withdrawal of cyclosporine and prophylactic use of interferon-alpha.
  • A 54-year-old man with chronic myelocytic leukemia in blastic phase received reduced-intensity transplantation (RIST) from an HLA-identical unrelated donor.
  • To induce GVHD and augment a graft-versus-leukemia effect, we initiated interferon-alpha therapy on day 80 to a maximum dosage of three million units five times a week.
  • This case suggests that early withdrawal of cyclosporine and the prophylactic use of interferon-alpha are promising in RIST for high-risk leukemia.
  • [MeSH-major] Blast Crisis / surgery. Cyclosporine / administration & dosage. Hematopoietic Stem Cell Transplantation / methods. Immunosuppressive Agents / administration & dosage. Interferon-alpha / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Neoplasm Recurrence, Local / prevention & control
  • [MeSH-minor] Drug Administration Schedule. Graft vs Host Disease / physiopathology. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Remission Induction

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12410575.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Interferon-alpha; 83HN0GTJ6D / Cyclosporine
  •  go-up   go-down


8. Oki Y, Kantarjian HM, Gharibyan V, Jones D, O'brien S, Verstovsek S, Cortes J, Morris GM, Garcia-Manero G, Issa JP: Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia. Cancer; 2007 Mar 1;109(5):899-906
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia.
  • BACKGROUND: Resistance to imatinib is a frequent clinical problem in advanced phase chronic myelogenous leukemia (CML).
  • A Phase II study was performed on low-dose decitabine, a DNA methyltransferase inhibitor, in combination with imatinib in patients with CML in accelerated phase (AP) and myeloid blastic phase (BP).
  • CONCLUSIONS: Combination therapy with decitabine and imatinib is well tolerated and active in advanced phase CML without BCR-ABL kinase mutations.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy
  • [MeSH-minor] Adult. Aged. Azacitidine / administration & dosage. Azacitidine / analogs & derivatives. Benzamides. DNA Methylation. Female. Genes, abl. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / administration & dosage. Polymerase Chain Reaction. Pyrimidines / administration & dosage. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17236224.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01-CM-62202; United States / NCI NIH HHS / CA / P50CA100632
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 776B62CQ27 / decitabine; 8A1O1M485B / Imatinib Mesylate; M801H13NRU / Azacitidine
  •  go-up   go-down


9. Axdorph U, Stenke L, Grimfors G, Carneskog J, Hansen J, Linder O, Ljungman P, Löfvenberg E, Malm C, Simonsson B, Turesson I, Vilén L, Udén AM, Björkholm M, Swedish CML Group: Intensive chemotherapy in patients with chronic myelogenous leukaemia (CML) in accelerated or blastic phase--a report from the Swedish CML Group. Br J Haematol; 2002 Sep;118(4):1048-54
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intensive chemotherapy in patients with chronic myelogenous leukaemia (CML) in accelerated or blastic phase--a report from the Swedish CML Group.
  • In attempting to restore the chronic phase (CP) of chronic myelogenous leukaemia (CML), the Swedish CML group utilized an intensive chemotherapy protocol for 83 patients (aged 16-79 years) in accelerated (AP, n = 22) or blastic phase (BC, n = 61).
  • Responding patients < 65 years were eligible for ablative chemotherapy followed by an allogeneic (SCT) or a double autologous stem cell transplant (ASCT).
  • In conclusion, approximately half of the patients achieved a CP2/PR after intensive chemotherapy, with a clear survival advantage for responders vs non-responders.
  • Novel therapeutic options for CML patients in AP/BP are needed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Blast Crisis. Combined Modality Therapy. Cytarabine / administration & dosage. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Prognosis. Remission Induction. Statistics, Nonparametric. Stem Cell Transplantation. Survival Rate

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12199784.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone
  •  go-up   go-down


10. Dutcher JP, Wiernik PH: Accelerated and blastic phase of chronic myeloid leukemia. Curr Treat Options Oncol; 2000 Apr;1(1):51-62
MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Accelerated and blastic phase of chronic myeloid leukemia.
  • There is currently no standard treatment for the blastic phase of chronic myeloid leukemia (CML-BC), which is a chemoresistant form of acute leukemia.
  • Current approaches include using standard acute myeloid leukemia (AML) regimens in an effort to induce remission, variations of these approaches with drugs that seem more active in this specific leukemia, and the direct entry of patients into studies of investigational agents.
  • Although the likelihood of achieving remission is small, immediate bone marrow transplantation in remission should be considered because it provides the only opportunity for long-term survival at this time.
  • Often, however, the duration of chemotherapy-induced remission of blast crisis is very short and may preclude entry into a transplant program.
  • Again, there is no standard treatment, and clinical trials are recommended as first-line therapy.
  • Treatment in the accelerated phase includes standard AML chemotherapy regimens, combinations of new agents, and the combination of cytostatic agents with interferon.
  • Patients whose accelerated phase reverts to chronic phase after treatment may become candidates for bone marrow transplantation.
  • [MeSH-major] Blast Crisis / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Combined Modality Therapy. Diet. Humans. Life Style. Middle Aged. Radiotherapy. Survival Rate. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 1984 Apr;2(4):329-35 [6368762.001]
  • [Cites] Cancer. 1988 Aug 15;62(4):672-6 [3165046.001]
  • [Cites] Leukemia. 1991 Jun;5(6):504-9 [2056773.001]
  • [Cites] N Engl J Med. 1991 May 16;324(20):1385-93 [1850498.001]
  • [Cites] Leuk Lymphoma. 1995 Sep;19(1-2):153-7 [8574162.001]
  • [Cites] Leuk Res. 1997 May;21(5):375-80 [9225062.001]
  • [Cites] Ann Hematol. 1999 Nov;78(11):507-13 [10602894.001]
  • [Cites] Neoplasma. 1973;20(3):303-9 [4125219.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3668-77 [10572078.001]
  • [Cites] Leukemia. 1990 Nov;4(11):755-7 [2232887.001]
  • [Cites] Blood. 1994 Dec 15;84(12):4368-73 [7527674.001]
  • [Cites] Cancer. 1999 Dec 15;86(12):2632-41 [10594858.001]
  • [Cites] Blood. 1988 Aug;72(2):567-72 [3165295.001]
  • [Cites] J Clin Oncol. 1999 Jun;17(6):1858-68 [10561226.001]
  • [Cites] Leukemia. 1992 Aug;6(8):770-5 [1379312.001]
  • [Cites] N Engl J Med. 1998 Nov 5;339(19):1341-8 [9801394.001]
  • [Cites] Blut. 1988 Sep;57(3):131-7 [3166389.001]
  • [Cites] Leukemia. 1998 Jul;12(7):1037-40 [9665187.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3960-2 [10627126.001]
  • [Cites] Cancer. 1976 Jul;38(1):36-41 [59627.001]
  • [Cites] J Clin Invest. 1985 Jul;76(1):365-9 [3160729.001]
  • [Cites] Blood. 1997 May 1;89(9):3354-60 [9129042.001]
  • [Cites] Blood. 1968 Sep;32(3):445-59 [4970948.001]
  • [Cites] J Clin Oncol. 1992 Mar;10(3):398-405 [1740679.001]
  • [Cites] Cancer Treat Rep. 1982 Feb;66(2):267-71 [6173123.001]
  • [Cites] N Engl J Med. 1986 Dec 4;315(23):1433-8 [2431313.001]
  • [Cites] Ann Intern Med. 1999 Aug 3;131(3):207-19 [10428738.001]
  • (PMID = 12057061.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 33
  •  go-up   go-down


11. Turgut B, Vural O, Demir M, Kaldir M: Candida arthritis in a patient with chronic myelogenous leukemia (CML) in blastic transformation, unresponsive to fluconazole, but treated effectively with liposomal amphotericin B. Ann Hematol; 2002 Sep;81(9):529-31
Hazardous Substances Data Bank. FLUCONAZOLE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Candida arthritis in a patient with chronic myelogenous leukemia (CML) in blastic transformation, unresponsive to fluconazole, but treated effectively with liposomal amphotericin B.
  • We report a case of Candida arthritis, which occurred in a patient with chronic myelogenous leukemia (CML) in blastic transformation.
  • Aggressive chemotherapy and broad-spectrum antibiotics for a prolonged period for febrile neutropenia had been given to the patient.
  • Despite treatment with fluconazole, no clinical or microbiological improvement was obtained.
  • [MeSH-major] Amphotericin B / administration & dosage. Arthritis, Infectious / drug therapy. Candidiasis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Phosphatidylcholines / administration & dosage. Phosphatidylglycerols / administration & dosage
  • [MeSH-minor] Blast Crisis. Drug Combinations. Drug Resistance. Fatal Outcome. Female. Fluconazole / administration & dosage. Humans. Middle Aged. Opportunistic Infections / drug therapy. Opportunistic Infections / etiology

  • Genetic Alliance. consumer health - Arthritis.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Infectious Arthritis.
  • MedlinePlus Health Information. consumer health - Yeast Infections.
  • Hazardous Substances Data Bank. AMPHOTERICIN B .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12373355.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Phosphatidylcholines; 0 / Phosphatidylglycerols; 0 / liposomal amphotericin B; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole
  •  go-up   go-down


12. Sugiyama K, Usui N, Asai O, Saito T, Yano S, Okawa Y, Takahara S, Takei Y, Uno S, Dobashi N, Kobayashi M: [Successful induction of complete cytogenetic response with high-dose imatinib mesylate and subsequent allogeneic stem cell transplantation for CML blastic crisis]. Rinsho Ketsueki; 2003 Jun;44(6):386-90
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful induction of complete cytogenetic response with high-dose imatinib mesylate and subsequent allogeneic stem cell transplantation for CML blastic crisis].
  • We diagnosed Philadelphia chromosome-positive chronic myelogenous leukemia (CML) in a blast crisis and started imatinib mesylate therapy at a dose of 800 mg/day on March 9th, 2002.
  • This case suggested the usefulness of imatinib mesylate in the management of the CML-associated blast crisis.
  • [MeSH-major] Blast Crisis / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Peripheral Blood Stem Cell Transplantation. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Benzamides. Combined Modality Therapy. Humans. Imatinib Mesylate. Male. Pulse Therapy, Drug. Remission Induction. Treatment Outcome

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12884817.001).
  • [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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


13. Jiang Q, Chen SS, Jiang B, Jiang H, Qiu JY, Liu YR, Zhang Y, Qin YQ, Lu Y, Huang XJ, Lu DP: [The efficacy of imatinib mesylate for 124 patients with chronic myeloid leukemia in accelerated and blastic phase]. Zhonghua Xue Ye Xue Za Zhi; 2007 Nov;28(11):721-6
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The efficacy of imatinib mesylate for 124 patients with chronic myeloid leukemia in accelerated and blastic phase].
  • OBJECTIVES: To evaluate the efficacy and safety of imatinib mesylate (imatinib) for patients with Philadelphia chromosome-positive (Ph+ ) chronic myeloid leukemia (CML) in accelerated and blastic phase.
  • METHODS: Seventy-five Ph+ CML patients in accelerated phase and 49 in blastic phase were treated with 400 mg or 600 mg of imatinib once daily.
  • For patients in blastic phase, the cumulative HR rate was 63.3%, including CHR rate 44.9%, and RCP rate 18.4% in a median follow-up of 4.5 (0.3 -63.0) months.
  • CONCLUSIONS: The efficiency of imatinib was decreasing, and severer hematological toxicities increasing with the disease progressing in patients with Ph+ CML.
  • The response duration in majority of blastic phase patients is short, and the relapse rate is high.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Female. Follow-Up Studies. Humans. Imatinib Mesylate. Male. Middle Aged. Prognosis. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18457260.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


14. Gotoh M, Tauchi T, Yoshizawa S, Kitahara T, Kiguchi T, Kimura Y, Ohyashiki K: Successful prior treatment with dasatinib followed by stem cell transplantation in a patient with CML in blastic crisis with a BCR-ABL mutation. Int J Hematol; 2010 Jan;91(1):128-31
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful prior treatment with dasatinib followed by stem cell transplantation in a patient with CML in blastic crisis with a BCR-ABL mutation.
  • We report a case of imatinib- and nilotinib-resistant Ph-positive chronic myeloid leukemia (CML) in blast crisis in which successful pretreatment with dasatinib with cord blood transplantation resulted in molecular remission.
  • Before dasatinib therapy, the patient was found to have a F359V BCR-ABL mutation.
  • This successful case indicates that reduction of tumor burden by second-generation tyrosine kinase inhibitors, in combination with stem cell transplantation, might be effective to treat CML, even in the advanced phase.
  • [MeSH-major] Blast Crisis / drug therapy. Fusion Proteins, bcr-abl / genetics. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2009 Jan;23(1):190-4 [18596746.001]
  • [Cites] Leuk Res. 2010 Feb;34(2):143-7 [19481800.001]
  • [Cites] Int J Hematol. 2009 Jun;89(5):679-88 [19449194.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2309-15 [17496201.001]
  • [Cites] Int J Hematol. 2009 May;89(4):482-8 [19343480.001]
  • [Cites] J Clin Oncol. 2009 Jan 20;27(3):469-71 [19075254.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4437-44 [18716134.001]
  • [Cites] Leuk Lymphoma. 2007 Dec;48(12):2461-4 [18067026.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2828-37 [17626839.001]
  • [Cites] Expert Opin Investig Drugs. 2008 Jun;17(6):865-78 [18491988.001]
  • (PMID = 20047099.001).
  • [ISSN] 1865-3774
  • [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 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  •  go-up   go-down


15. Hirose Y, Kiyoi H, Iwai M, Yokozawa T, Ito M, Naoe T: Successful treatment with imatinib mesylate of a CML patient in megakaryoblastic crisis with severe fibrosis. Int J Hematol; 2002 Nov;76(4):349-53
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment with imatinib mesylate of a CML patient in megakaryoblastic crisis with severe fibrosis.
  • The prognosis of patients with chronic myeloid leukemia in blastic crisis (CML-BC) remains extremely poor, and multiagent chemotherapy regimens commonly used to treat acute leukemia offer only short-term benefits.
  • Therefore, the advent of the novel molecularly targeted anticancer agent imatinib mesylate is a breakthrough in CML therapy.
  • We present a CML patient in megakaryoblastic crisis with severe myelofibrosis, who was treated with imatinib at a dosage of 400 mg/day and achieved complete remission together with a marked regression of myelofibrosis after 1 month.
  • The effect of imatinib on the long-term prognosis remains unclear, although the agent is clearly a promising drug for treating CML-BC even in cases of myelofibrosis.
  • [MeSH-major] Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Primary Myelofibrosis / drug therapy. Pyrimidines / administration & dosage

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Hematol. 2001 Apr;73(3):278-91 [11345193.001]
  • [Cites] J Natl Cancer Inst. 1999 Jan 20;91(2):163-8 [9923858.001]
  • [Cites] Blood. 2000 Aug 1;96(3):925-32 [10910906.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] Cancer. 1991 Sep 15;68(6):1201-7 [1873771.001]
  • [Cites] Blood. 2002 May 15;99(10):3547-53 [11986206.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] Br J Haematol. 2000 Jan;108(1):64-71 [10651725.001]
  • [Cites] J Clin Oncol. 2001 Jun 15;19(12 ):2994-3009 [11408494.001]
  • [Cites] Blood. 2002 May 15;99(10):3854-6 [11986248.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):2558-62 [7708684.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Semin Hematol. 2001 Jul;38(3 Suppl 8):9-14 [11526596.001]
  • [Cites] Br J Haematol. 2000 Jul;110(1):2-11 [10930974.001]
  • [Cites] J Clin Invest. 2000 Jan;105(1):3-7 [10619854.001]
  • [Cites] Ann Hematol. 2001 Sep;80(9):516-20 [11669299.001]
  • [Cites] Cancer. 1999 Dec 15;86(12):2632-41 [10594858.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3691-8 [9345054.001]
  • [Cites] Blood Cells Mol Dis. 1997 Dec;23(3):380-94 [9446752.001]
  • [Cites] Blood. 1997 Dec 15;90(12):4947-52 [9389713.001]
  • [Cites] Cancer Res. 1996 Jan 1;56(1):100-4 [8548747.001]
  • [Cites] Lancet. 2002 Feb 9;359(9305):487-91 [11853795.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2246-53 [10979973.001]
  • [Cites] Blood. 2002 Jan 1;99(1):381-3 [11756197.001]
  • [Cites] J Pharmacol Exp Ther. 2000 Oct;295(1):139-45 [10991971.001]
  • [Cites] Am J Clin Pathol. 1971 Jul;56(1):24-31 [5556211.001]
  • [Cites] Blood. 2000 Nov 1;96(9):3195-9 [11050003.001]
  • [Cites] J Natl Cancer Inst. 1997 Nov 5;89(21):1616-20 [9362160.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] Blood. 2002 May 15;99(10):3530-9 [11986204.001]
  • [Cites] Lancet. 2002 Feb 9;359(9305):481-6 [11853794.001]
  • [Cites] Thromb Haemost. 1997 Aug;78(2):892-6 [9268191.001]
  • (PMID = 12463599.001).
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


16. Robak T, Góra-Tybor J: Cladribine combined with mitoxantrone in the treatment of blastic phase of chronic myeloid leukemia. Neoplasma; 2001;48(3):203-7
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cladribine combined with mitoxantrone in the treatment of blastic phase of chronic myeloid leukemia.
  • A phase II clinical study was performed to evaluate the effectiveness and toxicity of cladribine (2-CdA) combined with mitoxantrone (CM regimen) in the treatment of chronic myeloid leukemia in blastic phase (CML BP).
  • A total of 12 adult patients with CML BP were included in this study.
  • Infections occurred in 4 patients (33.3%) and 2 of them died of sepsis shortly after CM treatment.
  • This preliminary results in a small group of patients suggest that CM programme has limited value in pre-treated patients with CML BP.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cladribine / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mitoxantrone / therapeutic use
  • [MeSH-minor] Adult. Aged. Blast Crisis / drug therapy. Drug Administration Schedule. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Treatment Outcome


17. Altintas A, Cil T, Kilinc I, Kaplan MA, Ayyildiz O: Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: a case report. J Neurooncol; 2007 Aug;84(1):103-5
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: a case report.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by a reciprocal translocation between chromosomes 9 and 22.
  • Imatinib is a first choice of treatment of chronic phase CML.
  • It has also shown activity in patients with CML in accelerated or blastic phases.
  • However, the penetration of the drug and its active metabolites into the central nervous system (CNS) is poor.
  • Herein, we report a patient with CML in accelerated phase that developed central nervous system disease while on imatinib mesylate therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Central Nervous System Neoplasms / secondary. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Sarcoma, Myeloid / drug therapy
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Blood-Brain Barrier / drug effects. Blood-Brain Barrier / metabolism. Cytarabine / administration & dosage. Dexamethasone / administration & dosage. Humans. Imatinib Mesylate. Magnetic Resonance Imaging. Male. Methotrexate / administration & dosage. Protein-Tyrosine Kinases / antagonists & inhibitors. Treatment Outcome


18. Kakihana K, Mizuchi D, Yamaguchi M, Sakashita C, Fukuda T, Yamamoto K, Miki T, Tohda S, Koyama T, Murakami N, Miura O: [Hypercalcemia mediated by parathyroid hormone-related protein in the blastic phase of chronic myelogenous leukemia]. Rinsho Ketsueki; 2002 Feb;43(2):102-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Hypercalcemia mediated by parathyroid hormone-related protein in the blastic phase of chronic myelogenous leukemia].
  • A 45-year-old man with chronic myelogenous leukemia (CML) in the accelerated phase was admitted to our hospital because of lower back pain and hypercalcemia.
  • Splenomegaly recurred after cessation of the chemotherapy, and examination of the peripheral blood showed 31% blasts, positive for both CD13 and CD33, on which basis myeloid blastic transformation was diagnosed.
  • Furthermore, RT-PCR analysis revealed that the patient's CML cells expressed PTHrP mRNA, and a high level of PTHrP was detected in the supernatant of cultured mononuclear cells derived from the patient's peripheral blood.
  • Several cases of PTHrP. mediated hypercalcemia associated with CML have been reported previously, and are reviewed here.
  • [MeSH-major] Blast Crisis. Hypercalcemia / etiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Protein Biosynthesis

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11925871.001).
  • [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; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / PTHLH protein, human; 0 / Parathyroid Hormone-Related Protein; 0 / Proteins
  • [Number-of-references] 8
  •  go-up   go-down


19. Tedeschi A, Montillo M, Ferrara F, Nosari A, Mele G, Copia C, Leoni P, Morra E: Treatment of chronic myeloid leukemia in the blastic phase with fludarabine, cytosine arabinoside and G-CSF (FLAG). Eur J Haematol; 2000 Mar;64(3):182-7
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of chronic myeloid leukemia in the blastic phase with fludarabine, cytosine arabinoside and G-CSF (FLAG).
  • The present study was undertaken to evaluate the efficacy of the association of fludarabine plus Ara-C and G-CSF (FLAG) in the treatment of 15 patients with chronic myeloid leukemia in the blastic phase (CML-BP).
  • Patients were then submitted to an individualized program of treatment depending on age and suitable donors.
  • Overall seven patients achieved CR (46.7%), three (20%) showed a primary resistant disease, while three (20%) died during remission induction therapy.
  • Five of them received a consolidation therapy; in two cases further treatment was not performed because of severe toxicity.
  • FLAG proved to be effective in achieving a high CR rate in patients with CML-BP.
  • Nevertheless, the treatment was well tolerated even in a group of heavily pretreated patients, allowing further transplantation opportunities in younger patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Cytarabine / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Vidarabine / administration & dosage

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10997884.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] DENMARK
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FLAG protocol
  •  go-up   go-down


20. Morimoto A, Ogami A, Chiyonobu T, Takanashi M, Sugimoto T, Imamura T, Ishida H, Yoshihara T, Imashuku S: Early blastic transformation following complete cytogenetic response in a pediatric chronic myeloid leukemia patient treated with imatinib mesylate. J Pediatr Hematol Oncol; 2004 May;26(5):320-2
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Early blastic transformation following complete cytogenetic response in a pediatric chronic myeloid leukemia patient treated with imatinib mesylate.
  • This article reports early blastic transformation of chronic myeloid leukemia (CML) in a child following a complete cytogenetic response induced by imatinib mesylate.
  • A 14-year-old Japanese boy was diagnosed with t(9;22) cryptic CML in the chronic phase and treated with imatinib.
  • His response to treatment was slow, but a major cytogenetic response was obtained at 142 days of therapy.
  • However, he developed lymphoid blastic transformation at 9 months.
  • He attained remission with acute lymphoblastic leukemia-type chemotherapy and then successfully received a non-T-cell-depleted allogeneic stem cell transplantation (allo-SCT) with his mother's two loci-mismatched donor cells.
  • A sudden blastic transformation may occur even with a complete cytogenetic response induced by imatinib.
  • CML patients who respond slowly to imatinib may still be candidates for allo-SCT, even when a major cytogenetic response is obtained.
  • [MeSH-major] Blast Crisis / therapy. Leukemia, Myeloid, Chronic-Phase / drug therapy. Lymphocyte Activation. Piperazines / therapeutic use. Pyrimidines / therapeutic use

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15111787.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


21. Fang B, Song Y, Han Z, Wei X, Lin Q, Zhu X, Yang R, Sun J, Tian G, Liu X, Cao G, Shi Y, Nie N, Li D, Zhao RC: Synergistic interactions between 12-0-tetradecanoylphorbol-13-acetate (TPA) and imatinib in patients with chronic myeloid leukemia in blastic phase that is resistant to standard-dose imatinib. Leuk Res; 2007 Oct;31(10):1441-4
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synergistic interactions between 12-0-tetradecanoylphorbol-13-acetate (TPA) and imatinib in patients with chronic myeloid leukemia in blastic phase that is resistant to standard-dose imatinib.
  • We have demonstrated that 12-0-tetradecanoylphorbol-13-acetate (TPA) combined with vitamin D(3) (VD(3)) and cytosine arabinoside (Ara C) is effective and feasible for chronic myelogenous leukemia (CML) in blastic phase (BP).
  • In the current study, the efficacy of TPA combined with inhibitor imatinib mesylate (imatinib) was investigated in patients with CML in BP that was resistant to standard-dose imatinib (400mg/day).
  • So this approach deserves further evaluation as frontline therapy for newly diagnosed CML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Adult. Benzamides. Drug Synergism. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Tetradecanoylphorbol Acetate / administration & dosage. Treatment Outcome


22. Voglová J, Maisnar V, Beránek M, Chrobák L: [Combination of imatinib and anagrelide in treatment of chronic myeloid leukemia in blastic phase]. Vnitr Lek; 2006 Sep;52(9):819-22
SciCrunch. DrugBank: Data: Chemical .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Combination of imatinib and anagrelide in treatment of chronic myeloid leukemia in blastic phase].
  • Chronic myeloid leukemia in blast phase (BP) is resistant to chemotherapy and majority of patients die within 6 months.
  • Inhibitor Bcr-Abl tyrosine kinase imatinib mesylate dramatically improved outcome of patients in chronic phase (CP) and is also effective in BP of CML.
  • High platelet counts are often observed at diagnosis or in the subsequent course of the CML in about 25% of patients.
  • Anagrelide selectively reduces circulating platelets and is used in treatment of thrombocythemia in chronic myeloproliferative disorders.
  • Efficacy and safety of combination imatinib mesylate with anagrelide was demonstrated in chronic and accelerated phase of CML.
  • 51-year-old white man with CML presented in blast phase was followed for 4 years.
  • Imatinib mesylate in dose of 600 mg p.o. qd. was administered after the failure of initial chemotherapy.
  • The patient tolerated the combination of imatinib and anagrelide well and long-term survival gave him the chance of treatment with the new tyrosin kinase inhibitor (dasatinib).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Platelet Aggregation Inhibitors / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Quinazolines / administration & dosage. Thrombocytosis / drug therapy


23. Takahashi N, Maruta A, Hashimoto C, Kato K, Tanabe J, Kodama F, Oba R, Harada H, Omine M: [Successful allogeneic bone marrow transplantation following fungal liver abscess treatment in a patient with chronic myeloid leukemia in blastic crisis]. Rinsho Ketsueki; 2000 Dec;41(12):1247-53
Hazardous Substances Data Bank. FLUCONAZOLE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful allogeneic bone marrow transplantation following fungal liver abscess treatment in a patient with chronic myeloid leukemia in blastic crisis].
  • A 40-year-old man was diagnosed as having chronic myeloid leukemia (CML) in December 1990 and received busulfan and hydroxyurea.
  • He developed myeloid blast crisis in February 1996.
  • After DCMP combination chemotherapy, his disease reverted to chronic phase, but right hypochondrial pain developed and low-grade fever persisted.
  • Acute grade III GVHD developed, but there was no evidence of reactivation of the liver abscesses.
  • This case demonstrates that a prior fungal liver abscess is not an absolute contraindication for BMT if prophylactic antifungal drugs are administered and careful observation is conducted.
  • [MeSH-major] Blast Crisis. Bone Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Liver Abscess / drug therapy. Mycoses / drug therapy
  • [MeSH-minor] Adult. Amphotericin B / administration & dosage. Antifungal Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fluconazole / therapeutic use. Humans. Male. Transplantation, Homologous


24. Sureda A, Carrasco M, de Miguel M, Martínez JA, Conde E, Sanz MA, Díaz-Mediavilla J, Sierra J: Imatinib mesylate as treatment for blastic transformation of Philadelphia chromosome positive chronic myelogenous leukemia. Haematologica; 2003 Nov;88(11):1213-20
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imatinib mesylate as treatment for blastic transformation of Philadelphia chromosome positive chronic myelogenous leukemia.
  • BACKGROUND AND OBJECTIVES: Imatinib mesylate (STI571) is a selective inhibitor of the bcr/abl tyrosine kinase with therapeutic potential in the blast crisis (BC) of chronic myelogenous leukemia (CML).
  • DESIGN AND METHODS: We report the characteristics and clinical outcome of 30 patients [16 males and 14 females, median age 50 (range, 18 to 72) years] with CML in BC included in a phase II international multicenter extended trial of treatment with imatinib.
  • RESULTS: Eighteen patients (60%) achieved a sustained hematologic remission (SHR) at a median time of 4 weeks (range, 2-14) after starting therapy.
  • Four patients (13%) achieved a cytogenetic remission at a median time of 8 weeks (range, 6-10) after beginning imatinib therapy.
  • In univariate analysis, the achievement of a SHR was more frequent in patients without a complex karyotype and in those receiving imatinib without having had previous chemotherapy.
  • A long interval between the diagnosis of BC and imatinib therapy (> or = 9.5 weeks) (p=0.0011), the presence of additional cytogenetic abnormalities (p=0.015), and extramedullary involvement (p=0.02) were associated with significantly shorter EFS.
  • Multivariate analyses indicated that the time interval between the diagnosis of BC and the beginning of imatinib therapy was the only significant prognostic factor for both EFS and OS.
  • INTERPRETATION AND CONCLUSIONS: STI571 therapy produces a high percentage of SHR in patients with CML in BC; a minority of the patients also obtain some degree of cytogenetic response.
  • Nevertheless, these responses are transient and additional therapy should be offered.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Disease-Free Survival. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / blood. Humans. Imatinib Mesylate. Karyotyping. Male. Middle Aged. Neoplasm Proteins / antagonists & inhibitors. Neoplasm Proteins / blood. Neutropenia / chemically induced. Remission Induction. Survival Analysis. Thrombocytopenia / chemically induced. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14607749.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


25. Zaucha JM, Wyrowinska E, Prejzner W, Calbecka M, Hellmann A: Imatinib-associated neutropenia may not be overcome by filgrastim treatment in patients with blastic phase of chronic myeloid leukaemia. Clin Lab Haematol; 2006 Jun;28(3):208-10
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imatinib-associated neutropenia may not be overcome by filgrastim treatment in patients with blastic phase of chronic myeloid leukaemia.
  • Imatinib mesylate is a very effective treatment in patients with Philadelphia (Ph)-positive chronic myeloid leukaemia (CML).
  • However, in patients with advanced phase CML, it is still unclear whether, in the presence of myelosuppression, therapy with imatinib should be continued.
  • It has been reported that intermittent filgrastim treatment may overcome imatinib-associated neutropenia and allow improved delivery of imatinib.
  • Such combined sequential treatment is theoretically attractive as it may lead to better disease response.
  • Here, we report a patient with blastic phase CML who developed severe and prolonged myelosuppression during imatinib treatment.
  • Despite cessation of imatinib and 2 months of filgrastim therapy neither recurrence of Ph-positive or Ph-negative cells occurred.
  • We conclude that filgrastim treatment may not always reverse imatinib-associated neutropenia therefore the decision of continued imatinib therapy in patients with advanced CML should be taken with caution.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Blast Crisis / drug therapy. Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neutropenia / drug therapy. Piperazines / adverse effects. Pyrimidines / adverse effects

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. Filgrastim .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16706939.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; PVI5M0M1GW / Filgrastim
  •  go-up   go-down


26. Ilaria RL Jr: Pathobiology of lymphoid and myeloid blast crisis and management issues. Hematology Am Soc Hematol Educ Program; 2005;:188-94
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathobiology of lymphoid and myeloid blast crisis and management issues.
  • Despite recent improvements in the treatment of early-stage disease, the blastic phase of chronic myeloid leukemia (CML) remains a therapeutic challenge.
  • For imatinib-naïve patients, imatinib provided encouraging hematologic and cytogenetic benefits; however, the vast majority of CML blast crisis cases today arise in patients already on imatinib-based therapy.
  • Clonal evolution and duplication of the Philadelphia chromosome continue to be associated with blastic phase transformation, but recent studies have identified BCR/ABL kinase domain mutations in 30%-40% of blast crisis patients.
  • This implies that BCR-ABL-targeted therapy might have influenced the molecular road map to blastic transformation.
  • In this review, we will examine the effect of imatinib on primitive CML progenitors and how this might influence the pathophysiology of blast crisis.
  • A rational framework for deciding how best to integrate stem cell transplantation, traditional chemotherapy, imatinib, and other BCR-ABL kinase inhibitors in the care of blast crisis patients will also be discussed.

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16304379.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


27. Kwatra KS, Prabhakar BR, Arora Y: Bilateral granulocytic sarcoma (chloroma) of the breast in CML in blast crisis: a case report. Indian J Pathol Microbiol; 2004 Jan;47(1):66-8
MedlinePlus Health Information. consumer health - Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral granulocytic sarcoma (chloroma) of the breast in CML in blast crisis: a case report.
  • A 35 year old lady was diagnosed as having chronic myeloid leukemia in May 1999 and thereafter started on chemotherapy.
  • The peripheral blood picture showed blastic transformation.
  • [MeSH-major] Blast Crisis / pathology. Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15471137.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  •  go-up   go-down


28. Zang C, Liu H, Waechter M, Eucker J, Bertz J, Possinger K, Koeffler HP, Elstner E: Dual PPARalpha/gamma ligand TZD18 either alone or in combination with imatinib inhibits proliferation and induces apoptosis of human CML cell lines. Cell Cycle; 2006 Oct;5(19):2237-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dual PPARalpha/gamma ligand TZD18 either alone or in combination with imatinib inhibits proliferation and induces apoptosis of human CML cell lines.
  • Despite progress in the treatment of early-stage chronic myeloid leukemia (CML), the accelerated and blastic phases of CML still remain a therapeutic challenge.
  • Persistence of BCR-ABL-positive (bcr-abl(+)) cells or secondary resistance during imatinib therapy frequently occurs.
  • In this study, we investigated the activity of a novel dual ligand specific for peroxisome proliferator-activated receptor alpha and gamma (PPARalpha/gamma) against CML blast crisis cell lines.
  • Exposure of these cell lines (K562, KU812 and KCL22) to TZD18 resulted in a growth inhibition in a dose- and time-dependent manner.
  • Overall, our findings strongly suggest that either TZD18, either alone or in combination with imatinib may be beneficial for the treatment of CML in myeloid blast crisis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Phenyl Ethers / pharmacology. Piperazines / pharmacology. Pyrimidines / pharmacology. Thiazolidinediones / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Humans. Imatinib Mesylate. PPAR alpha / agonists. PPAR gamma / agonists

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17102607.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-(3-(3-(4-phenoxy-2-propylphenoxy)propoxy)phenyl)-2,4-thiazolidinedione; 0 / Benzamides; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Phenyl Ethers; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazolidinediones; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


29. Goto H, Tsurumi H, Hara T, Moriwaki H: Lymphoid blast crisis during interferon-alpha therapy in a patient with chronic myelogenous leukemia in myeloid blast crisis. Int J Hematol; 2000 Dec;72(4):474-6
MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lymphoid blast crisis during interferon-alpha therapy in a patient with chronic myelogenous leukemia in myeloid blast crisis.
  • It was determined that she had chronic myelogenous leukemia (CML) in myeloid blast crisis.
  • Hydroxyurea was started initially, and the blasts completely disappeared from peripheral blood on day 9 of therapy.
  • Treatment with adriamycin, vincristine, and prednisolone (AdVP) was immediately started, which rapidly reduced the lymphoblasts.
  • The ratio between myeloblasts and lymphoblasts depended on the treatment (IFN-alpha or AdVP).
  • This patient may have had an underlying bipotential blastic clone that evolved differently in response to IFN-alpha or AdVP.
  • In some CML patients, IFN-alpha may induce lymphoid blast crisis.
  • [MeSH-major] Blast Crisis / chemically induced. Interferon-alpha / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Clone Cells / drug effects. Clone Cells / pathology. Fatal Outcome. Female. Humans. Middle Aged. Myeloid Cells / drug effects. Myeloid Cells / pathology

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11197215.001).
  • [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] Ireland
  • [Chemical-registry-number] 0 / Interferon-alpha
  •  go-up   go-down


30. Dutcher JP, Lee S, Gallagher RE, Makary AZ, Hines JD, Londer H, Farnen JP, Bennett JM, Paietta E, Rowe JM, Goloubeva O, Wiernik PH, Eastern Cooperative Oncology Group: Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993). Leuk Lymphoma; 2005 Mar;46(3):377-85
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993).
  • The aims of this study were to evaluate the safety and efficacy of all-trans retinoic acid (ATRA) in the treatment of the accelerated and blastic phase of chronic myeloid leukemia (CML) and to evaluate in vitro correlates of biological activity.
  • ATRA was administered in an intermittent schedule to patients with CML in the accelerated or blastic phases for a 6 week induction period, which was continued if there was evidence of clinical response or stable disease.
  • Laboratory correlative studies were performed prior to treatment and at intervals during treatment to evaluate effects on maturation and differentiation, and on CML progenitor cell growth by assessment of colony-forming cells (CFC).
  • Laboratory data for the responders demonstrated high sensitivity of primary CFC to ATRA prior to treatment and low serial CFC counts on ATRA therapy.
  • ATRA demonstrated clinical and hematological activity in 5 of 18 patients with the accelerated phase of CML, and there was evidence of a biological effect in laboratory studies of 3 of the 5 patients' progenitor cells.
  • Combination therapy with other differentiating agents may be useful in this disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Tretinoin / administration & dosage
  • [MeSH-minor] Adult. Aged. Blast Crisis. Combined Modality Therapy. Cytogenetic Analysis. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Male. Middle Aged. Recombinant Proteins. Survival Analysis. Time Factors

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15621827.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 11083; United States / NCI NIH HHS / CA / CA 14548; United States / NCI NIH HHS / CA / CA 14958; United States / NCI NIH HHS / CA / CA 23318; United States / NCI NIH HHS / CA / CA 66636; United States / NCI NIH HHS / CA / CA21115
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 5688UTC01R / Tretinoin; 76543-88-9 / interferon alfa-2a
  •  go-up   go-down


31. Matsuo T, Tomonaga M: [Chemotherapy and radiation therapy]. Nihon Rinsho; 2001 Dec;59(12):2364-8
Hazardous Substances Data Bank. BUSULFAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chemotherapy and radiation therapy].
  • Stem cell transplantation and interferon-based treatment are major strategies in chronic phase CML and chemotherapy is one of limited therapeutic options when they are not available or ineffective.
  • Homoharringtonine, a plant alkaloid, has shown cytogenetic response in one third of patients who were resistant to interferon therapy, and a better response rate in combination with cytarabine and interferon alfa.
  • There have been no improvement of clinical outcome in treatment of accelerated phase and blastic crisis although many trials including decitabine are going on.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Azacitidine / analogs & derivatives. Hydroxyurea / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / radiotherapy
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Agents, Phytogenic / therapeutic use. Busulfan / therapeutic use. Harringtonines / therapeutic use. Humans

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11766340.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 0 / Harringtonines; 6FG8041S5B / homoharringtonine; 776B62CQ27 / decitabine; G1LN9045DK / Busulfan; M801H13NRU / Azacitidine; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 13
  •  go-up   go-down


32. Higashi T, Tsukada J, Kato C, Iwashige A, Mizobe T, Machida S, Morimoto H, Ogawa R, Toda Y, Tanaka Y: Imatinib mesylate-sensitive blast crisis immediately after discontinuation of imatinib mesylate therapy in chronic myelogenous leukemia: report of two cases. Am J Hematol; 2004 Jul;76(3):275-8
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imatinib mesylate-sensitive blast crisis immediately after discontinuation of imatinib mesylate therapy in chronic myelogenous leukemia: report of two cases.
  • Although imatinib mesylate has shown encouraging activity in chronic myelogenous leukemia (CML), disease progression during therapy has been observed, manifested by clonal expansion of imatinib mesylate-resistant leukemia cells.
  • On the other hand, myelosuppression related to treatment of imatinib mesylate is often managed with temporary interruption of treatment or dose reduction.
  • We here report two CML patients who had imatinib mesylate-sensitive blast crisis (BC) immediately after discontinuation of imatinib mesylate therapy.
  • The patients discontinued therapy because of neutropenia.
  • Although there was no evidence of blastic phase during therapy, BC occurred 2 weeks after the withdrawal of treatment in both cases.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 15224366.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


33. Alimena G, Breccia M, Latagliata R, Carmosino I, Russo E, Biondo F, Diverio D, Mancini M, Nanni M, Mandelli F: Sudden blast crisis in patients with Philadelphia chromosome-positive chronic myeloid leukemia who achieved complete cytogenetic remission after imatinib therapy. Cancer; 2006 Sep 1;107(5):1008-13
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sudden blast crisis in patients with Philadelphia chromosome-positive chronic myeloid leukemia who achieved complete cytogenetic remission after imatinib therapy.
  • BACKGROUND: Most patients with Philadelphia chromosome (Ph)-positive chronic myeloid leukemia (CML) in chronic phase (CP) who receive treatment with imatinib achieve complete cytogenetic remission (CCR), which is correlated tightly with long-term progression-free survival.
  • In these patients, the occurrence of blastic crisis (BC) is rare, and its clinical biologic characteristics are not well known.
  • METHODS: Among 164 patients who received imatinib and were followed for a median of 35 months, 11 patients (6.7%) developed a BC; this was sudden (i.e., it occurred within 3 months of a documented CCR) in 6 patients (54.5%).
  • RESULTS: At the time of diagnosis, there were 3 low-risk patients and 3 intermediate-risk patients; 4 patients had received pretreatment with interferon, and 2 patients received only imatinib.
  • The median CP was 18 months, and the median duration of imatinib therapy was 7 months.
  • The median time to CCR was 3 months, and the median time from CCR to BC was 4 months.
  • CONCLUSIONS: Sudden BC generally is an uncommon phenomenon that may be relatively frequent in patients with CML who receive imatinib.
  • Clinical and biologic features also seem to characterize this peculiar type of abrupt disease evolution, which intervenes in patients' response to this drug.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Pyrimidines / therapeutic use


34. Neviani P, Santhanam R, Oaks JJ, Eiring AM, Notari M, Blaser BW, Liu S, Trotta R, Muthusamy N, Gambacorti-Passerini C, Druker BJ, Cortes J, Marcucci G, Chen CS, Verrills NM, Roy DC, Caligiuri MA, Bloomfield CD, Byrd JC, Perrotti D: FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia. J Clin Invest; 2007 Sep;117(9):2408-21
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia.
  • Blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph1-positive) acute lymphocytic leukemia (ALL) are 2 fatal BCR/ABL-driven leukemias against which Abl kinase inhibitors fail to induce a long-term response.
  • We recently reported that functional loss of protein phosphatase 2A (PP2A) activity is important for CML blastic transformation.
  • We assessed the therapeutic potential of the PP2A activator FTY720 (2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propanediol hydrochloride), an immunomodulator in Phase III trials for patients with multiple sclerosis or undergoing organ transplantation, in CML-BC and Ph1 ALL patient cells and in in vitro and in vivo models of these BCR/ABL+ leukemias.
  • Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.
  • Furthermore, pharmacologic doses of FTY720 remarkably suppress in vivo p210/p190(BCR/ABL)-driven [including p210/p190(BCR/ABL)(T315I)] leukemogenesis without exerting any toxicity.
  • Altogether, these results highlight the therapeutic relevance of rescuing PP2A tumor suppressor activity in Ph1 leukemias and strongly support the introduction of the PP2A activator FTY720 in the treatment of CML-BC and Ph1 ALL patients.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Genet. 2002 Jan;30(1):48-58 [11753385.001]
  • [Cites] Leuk Res. 2002 Mar;26(3):301-10 [11792420.001]
  • [Cites] Br J Pharmacol. 2004 Nov;143(5):581-9 [15466446.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] Science. 1990 Feb 16;247(4944):824-30 [2406902.001]
  • [Cites] Mol Cell Biol. 1991 Apr;11(4):1988-95 [1706474.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3589-93 [1708885.001]
  • [Cites] J Biol Chem. 1991 Aug 5;266(22):14486-90 [1860857.001]
  • [Cites] Nature. 1991 Sep 12;353(6340):170-3 [1716348.001]
  • [Cites] Blood. 1992 Dec 15;80(12):2983-90 [1467514.001]
  • [Cites] J Biol Chem. 1993 Jul 25;268(21):15523-30 [8393446.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1929-36 [8400243.001]
  • [Cites] Leukemia. 1994 Jan;8(1):186-9 [8289486.001]
  • [Cites] Transplant Proc. 1998 Aug;30(5):2210-3 [9723444.001]
  • [Cites] J Exp Med. 1999 May 3;189(9):1399-412 [10224280.001]
  • [Cites] J Biol Chem. 1999 Sep 24;274(39):27351-8 [10488065.001]
  • [Cites] Carcinogenesis. 2004 Dec;25(12):2397-405 [15297371.001]
  • [Cites] Yonsei Med J. 2004 Dec 31;45(6):991-7 [15627289.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):12-9 [15671523.001]
  • [Cites] J Biol Chem. 2005 Feb 18;280(7):6238-44 [15569672.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1478-84 [16627756.001]
  • [Cites] Br J Haematol. 1997 Jan;96(1):111-6 [9012696.001]
  • [Cites] Cancer Res. 2002 Mar 1;62(5):1410-9 [11888913.001]
  • [Cites] J Am Soc Nephrol. 2002 Apr;13(4):1073-83 [11912269.001]
  • [Cites] J Biol Chem. 2002 Jun 14;277(24):21453-7 [11967257.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1965-71 [12200353.001]
  • [Cites] J Clin Invest. 2003 Mar;111(5):659-69 [12618520.001]
  • [Cites] Br J Pharmacol. 2003 Apr;138(7):1303-12 [12711631.001]
  • [Cites] Biochim Biophys Acta. 2003 May 12;1640(2-3):97-104 [12729918.001]
  • [Cites] Blood. 2003 May 15;101(10):4122-30 [12531792.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2038-44 [8161775.001]
  • [Cites] Leuk Res. 1995 Jun;19(6):389-96 [7596151.001]
  • [Cites] Blood. 1995 Dec 15;86(12):4603-11 [8541551.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] J Biol Chem. 1996 May 10;271(19):11059-62 [8626647.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2375-84 [8839828.001]
  • [Cites] Oncogene. 1997 Nov 6;15(19):2333-42 [9393877.001]
  • [Cites] J Urol. 2003 Jun;169(6):2372-7 [12771800.001]
  • [Cites] Leuk Res. 2003 Aug;27(8):709-17 [12801529.001]
  • [Cites] Cancer. 2003 Oct 1;98(7):1337-54 [14508819.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5962-9 [14522923.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7389-95 [14576846.001]
  • [Cites] Transplant Proc. 2004 Mar;36(2 Suppl):531S-543S [15041402.001]
  • [Cites] J Clin Pharmacol. 2004 May;44(5):532-7 [15102874.001]
  • [Cites] J Org Chem. 2004 May 28;69(11):3950-2 [15153030.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Prostaglandins Other Lipid Mediat. 2004 Jan;73(1-2):29-45 [15165029.001]
  • [Cites] Am J Transplant. 2004 Jul;4(7):1019-25 [15196057.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):545-68, vii-viii [15271392.001]
  • [Cites] Nat Rev Cancer. 2004 Aug;4(8):604-16 [15286740.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 12;101(41):14788-93 [15466700.001]
  • [Cites] IDrugs. 2005 Mar;8(3):236-53 [15772896.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2640-53 [15618470.001]
  • [Cites] Circ Res. 2005 Apr 29;96(8):913-20 [15802614.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4500-5 [15930265.001]
  • [Cites] Nat Med. 2005 Jun;11(6):630-7 [15908956.001]
  • [Cites] Clin Sci (Lond). 2005 Jul;109(1):13-25 [15966868.001]
  • [Cites] Mol Cell Biol. 2005 Aug;25(15):6464-74 [16024784.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7478-84 [16103102.001]
  • [Cites] J Immunol. 2005 Sep 1;175(5):2913-24 [16116177.001]
  • [Cites] Mol Cancer Ther. 2005 Sep;4(9):1430-8 [16170036.001]
  • [Cites] J Clin Pharmacol. 2005 Nov;45(11):1268-78 [16239360.001]
  • [Cites] Cancer Cell. 2005 Nov;8(5):355-68 [16286244.001]
  • [Cites] Pharmacol Ther. 2005 Dec;108(3):308-19 [15951022.001]
  • [Cites] Clin Cancer Res. 2005 Dec 1;11(23):8458-66 [16322309.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1454-8 [16223773.001]
  • [Cites] NeuroRx. 2005 Oct;2(4):638-49 [16489371.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2507-16 [16293596.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] Blood. 2000 Feb 1;95(3):1007-13 [10648416.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10832-7 [10995457.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Feb 23;281(2):282-8 [11181042.001]
  • [Cites] Biochem J. 2001 Feb 1;353(Pt 3):417-39 [11171037.001]
  • [Cites] Cell Signal. 2001 Jan;13(1):7-16 [11257442.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] J Interferon Cytokine Res. 2001 Jun;21(6):369-78 [11440634.001]
  • (PMID = 17717597.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / P30 CA016058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Propylene Glycols; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC1950458
  •  go-up   go-down


35. Kroschinsky F, Friedrich K, Hanel M, Mohr B, Langer T, Meinhardt M, Thiede C, Bornhauser M, Baretton G, Ehninger G: Extramedullary blast crisis of chronic myeloid leukemia after allogeneic hematopoietic stem cell transplantation mimicking aggressive, translocation t(14;18)-positive B-cell lymphoma. Ann Hematol; 2003 Jan;82(1):47-52
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extramedullary blast crisis of chronic myeloid leukemia after allogeneic hematopoietic stem cell transplantation mimicking aggressive, translocation t(14;18)-positive B-cell lymphoma.
  • We report the case of a 42-year-old male patient who was diagnosed with a large tumor of the right thoracic aperture 30 months after unrelated hematopoietic stem cell transplantation (HSCT) for accelerated phase of Philadelphia chromosome (Ph)-positive chronic myeloid leukemia (CML).
  • Biopsy revealed an immature lymphoid neoplasia with blastic tumor cell morphology and immunoreactivity for CD34, CD79a, CD43, and CD30 as well as slight positivity for TdT and CD20.
  • Neither radiation nor intensive chemotherapy was capable of achieving a tumor remission, and the patient died from progressive disease 6 months later.
  • We conclude that lymphoid neoplasia occurring in our patient should be interpreted as an extramedullary, very immature blast crisis of CML expressing lymphoid differentiation markers rather than a true de novo NHL.
  • [MeSH-major] Blast Crisis / diagnosis. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 18. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphoma, B-Cell / diagnosis. Lymphoma, B-Cell / genetics. Thoracic Neoplasms / diagnosis. Thoracic Neoplasms / genetics. Translocation, Genetic


36. Park SJ, Kim DW, Kim HJ, Eom HS, Min CK, Lee JW, Min WS, Kim CC: Topotecan-based combination chemotherapy in patients with transformed chronic myelogenous leukemia and advanced myelodysplastic syndrome. Korean J Intern Med; 2000 Jul;15(2):122-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topotecan-based combination chemotherapy in patients with transformed chronic myelogenous leukemia and advanced myelodysplastic syndrome.
  • BACKGROUND: Patients with transformed chronic myelogenous leukemia(CML) and advanced myelodysplastic syndrome(MDS) have poor prognosis.
  • The aim of this study is to evaluate the feasibility of second chronic phase induction in accelerated phase(CML-AP) or blastic crisis of CML(CML-BC) and remission induction in advanced MDS by combining topoisomerase I inhibitor (topotecan) with topoisomerase II inhibitor(mitoxantrone).
  • Eighteen patients with transformed CML(7 CML-AP, 11 CML-BC) and 6 patients with advanced MDS were treated.
  • Four of 7 patients with CML-AP(57%), 2 of 4 patients with CML-lymphoid blastic crisis (-LBC)(50%) and 2 of 6 patients with advanced MDS(33%) had CR lasting more than 45 days(45 to 400 days).
  • There was no CR in the patients with CML-myeloid blastic crisis(-MBC).
  • In patients who recovered their neutrophil count, the absolute neutrophil count(ANC) remained below 500/microL for a period of 13 to 58 days(median 21 days) and the time to ANC recovery was associated with pretreatment severity of bone marrow fibrosis(mainly CML patients).
  • CONCLUSION: The combination of topotecan-mitoxantrone has shown modest activity in CML-AP, CML-LBC and advanced MDS with acceptable toxicities.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Myelodysplastic Syndromes / drug therapy. Topotecan / administration & dosage


37. Avery S, Nadal E, Marin D, Olavarria E, Kaeda J, Vulliamy T, Brito Babapulle F, Goldman JM, Apperley JF: Lymphoid transformation in a CML patient in complete cytogenetic remission following treatment with imatinib. Leuk Res; 2004 May;28 Suppl 1:S75-7
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lymphoid transformation in a CML patient in complete cytogenetic remission following treatment with imatinib.
  • We describe here a patient with Philadelphia (Ph) chromosome-positive chronic myeloid leukemia who achieved a complete cytogenetic response following treatment with imatinib and then progressed abruptly to lymphoid blastic transformation.
  • The sequence of events suggests that at least in some cases patients who respond well to imatinib may still harbor residual leukemia progenitor or 'stem' cells that are susceptible to acquisition of molecular events that underlie progression to advanced phase disease.
  • The case highlights the need for molecular monitoring of responders and the need to develop strategies for reducing to a minimum or totally eradicating leukemia cells.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Aged. Benzamides. Blast Crisis / etiology. Blast Crisis / pathology. Cytogenetic Analysis. Female. Humans. Imatinib Mesylate. Neoplastic Stem Cells / pathology. Remission Induction

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15036946.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


38. Larghero J, Leguay T, Mourah S, Madelaine-Chambrin I, Taksin AL, Raffoux E, Bastie JN, Degos L, Berthaud P, Marolleau JP, Calvo F, Chomienne C, Mahon FX, Rousselot P: Relationship between elevated levels of the alpha 1 acid glycoprotein in chronic myelogenous leukemia in blast crisis and pharmacological resistance to imatinib (Gleevec) in vitro and in vivo. Biochem Pharmacol; 2003 Nov 15;66(10):1907-13
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relationship between elevated levels of the alpha 1 acid glycoprotein in chronic myelogenous leukemia in blast crisis and pharmacological resistance to imatinib (Gleevec) in vitro and in vivo.
  • The Abl tyrosine kinase inhibitor imatinb is becoming a standard for the treatment of chronic myelogenous leukemia (CML).
  • We aimed to investigate if alpha 1 acid glycoprotein (AGP), an acute phase drug binding protein, could be a biological marker for pharmacological resistance to imatinib in nine patients in acute phase CML.
  • No mutation in the adenosine triphosphate domain of Abl were detected before the initiation of imatinib therapy.
  • By using in vitro tests combining various imatinib concentrations (1-10 microM) with purified human AGP (1 and 3 mg/mL), we demonstrate that imatinib-induced apoptosis of K562 or fresh leukemic CML cells is abrogated or reduced.
  • In patients with CML in blastic phase, AGP levels could reflect pharmacological resistance to imatinib, suggesting that increased dosage of imatinib or the use of a competitor to drug binding should be recommended to optimize the therapeutic effect of the drug.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Blast Crisis / pathology. Drug Resistance, Neoplasm / physiology. Orosomucoid / metabolism. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Apoptosis. Benzamides. Humans. Imatinib Mesylate. K562 Cells. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14599548.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Orosomucoid; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


39. Kawai Y, Ueda T: [Imatinib therapy for patients with chronic myelogenous leukemia]. Nihon Rinsho; 2004 Jul;62(7):1325-31
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Imatinib therapy for patients with chronic myelogenous leukemia].
  • Imatinib mesylate (imatinib), a selective inhibitor of BCR-ABL tyrosine kinase, has shown excellent efficacy in patients with chronic myelogenous leukemia (CML) in the chronic phase, however, it does not in those in the accelerated phase or blastic crisis.
  • In patients with CML who have undergone allogeneic stem cell transplantation, imatinib has the capability to induce hematological and even molecular response, and provides a prolonged survival among those in the chronic and accelerated phases.
  • Polyclonal cells which harbor distinct mutations in a single patient seemed to be selected in vivo under the selective pressure of imatinib, indicating the rationale of combined treatment with other types of agents.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Humans. Imatinib Mesylate

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15283151.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 21
  •  go-up   go-down


40. Rosti G, Palandri F, Castagnetti F, Breccia M, Levato L, Gugliotta G, Capucci A, Cedrone M, Fava C, Intermesoli T, Cambrin GR, Stagno F, Tiribelli M, Amabile M, Luatti S, Poerio A, Soverini S, Testoni N, Martinelli G, Alimena G, Pane F, Saglio G, Baccarani M, GIMEMA CML Working Party: Nilotinib for the frontline treatment of Ph(+) chronic myeloid leukemia. Blood; 2009 Dec 3;114(24):4933-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nilotinib for the frontline treatment of Ph(+) chronic myeloid leukemia.
  • Nilotinib has a higher binding affinity and selectivity for BCR-ABL with respect to imatinib and is an effective treatment of chronic myeloid leukemia (CML) after imatinib failure.
  • In a phase 2 study, 73 early chronic-phase, untreated, Ph(+) CML patients, received nilotinib at a dose of 400 mg twice daily.
  • During the first year, the treatment was interrupted at least once in 38 patients (52%).
  • One patient progressed to blastic crisis after 6 months; one went off-treatment for lipase increase grade 4 (no pancreatitis).
  • Nilotinib is safe and very active in early chronic-phase CML.
  • These data support a role for nilotinib for the frontline treatment of CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Fusion Proteins, bcr-abl / drug effects. Humans. Male. Middle Aged. Treatment Outcome. Young Adult


41. Bulum J, Labar B, Mikulić M, Bogdanić V, Sertić D, Nemet D, Krecak-Gverić V, Kovacević J, Serventi-Seiwerth R, Mrsić-Davidović S, Zadro R, Boban D: [Treatment of chronic myeloid leukemia with imatinib in the accelerated stage of the disease]. Lijec Vjesn; 2003 Jul-Aug;125(7-8):176-9
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of chronic myeloid leukemia with imatinib in the accelerated stage of the disease].
  • Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML), in advanced stage of disease, is resistant to standard chemotherapy.
  • Nine of them were in accelerated phase and 6 in blastic crisis of Ph+ CML.
  • After a 9-month follow up Ph+ CML progressed in 9 patients (60%) and 4 of them died.
  • Imatinib mesylate has a substantial, but short term activity in the accelerated phase and blastic crisis of the Ph+ CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14692090.001).
  • [ISSN] 0024-3477
  • [Journal-full-title] Lijec̆nic̆ki vjesnik
  • [ISO-abbreviation] Lijec Vjesn
  • [Language] hrv
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
  •  go-up   go-down


42. Kantarjian HM, O'Brien S, Cortes J, Giles FJ, Faderl S, Issa JP, Garcia-Manero G, Rios MB, Shan J, Andreeff M, Keating M, Talpaz M: Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia. Cancer; 2003 Aug 1;98(3):522-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of decitabine (5-aza-2'deoxycytidine) therapy in 130 patients with chronic myelogenous leukemia.
  • BACKGROUND: General and site-specific DNA methylation is associated with tumor progression and resistance in several cancers, including chronic myelogenous leukemia (CML).
  • Decitabine is a hypomethylating agent that has shown encouraging preliminary anti-CML activity.
  • This study evaluated the activity and toxicity of decitabine in different phases of CML.
  • METHODS: One hundred and thirty patients with CML were treated: 123 with Philadelphia chromosome (Ph)-positive CML (64 blastic, 51 accelerated, 8 chronic) and 7 with Ph-negative CML.
  • Of 64 patients in the CML blastic phase, 18 patients (28%) achieved objective responses.
  • Of seven patients treated for Ph-negative CML, four (57%) had objective responses.
  • The estimated 3-year survival rate was less than 5% in the blastic phase and 27% in the accelerated phase.
  • With decitabine 50-75 mg/m(2), the median time to granulocyte recovery above 0.5 x 10(9)/L was about 4 weeks.
  • CONCLUSIONS: Decitabine appears to have significant anti-CML activity.
  • Future studies should evaluate lower-dose, longer-exposure decitabine schedules alone in imatinib-resistant CML, as well as combinations of decitabine and imatinib in different CML phases.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / analogs & derivatives. Azacitidine / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Blast Crisis. DNA Modification Methylases / antagonists & inhibitors. Drug Administration Schedule. Female. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. AZACITIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 American Cancer Society.DOI 10.1002/cncr.11543
  • (PMID = 12879469.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  •  go-up   go-down


43. 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
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • 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

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


44. Kantarjian H, Shah NP, Hochhaus A, Cortes J, Shah S, Ayala M, Moiraghi B, Shen Z, Mayer J, Pasquini R, Nakamae H, Huguet F, Boqué C, Chuah C, Bleickardt E, Bradley-Garelik MB, Zhu C, Szatrowski T, Shapiro D, Baccarani M: Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med; 2010 Jun 17;362(24):2260-70
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia.
  • BACKGROUND: Treatment with dasatinib, a highly potent BCR-ABL kinase inhibitor, has resulted in high rates of complete cytogenetic response and progression-free survival among patients with chronic myeloid leukemia (CML) in the chronic phase, after failure of imatinib treatment.
  • We assessed the efficacy and safety of dasatinib, as compared with imatinib, for the first-line treatment of chronic-phase CML.
  • METHODS: In a multinational study, 519 patients with newly diagnosed chronic-phase CML were randomly assigned to receive dasatinib at a dose of 100 mg once daily (259 patients) or imatinib at a dose of 400 mg once daily (260 patients).
  • The rate of major molecular response was higher with dasatinib than with imatinib (46% vs. 28%, P<0.0001), and responses were achieved in a shorter time with dasatinib (P<0.0001).
  • Progression to the accelerated or blastic phase of CML occurred in 5 patients who were receiving dasatinib (1.9%) and in 9 patients who were receiving imatinib (3.5%).
  • The safety profiles of the two treatments were similar.
  • Since achieving complete cytogenetic response within 12 months has been associated with better long-term, progression-free survival, dasatinib may improve the long-term outcomes among patients with newly diagnosed chronic-phase CML. (ClinicalTrials.gov number, NCT00481247. )
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Blast Crisis / prevention & control. Dasatinib. Disease Progression. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Kaplan-Meier Estimate. Male. Middle Aged. Young Adult

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Massachusetts Medical Society
  • [CommentIn] Expert Opin Pharmacother. 2011 Jan;12(1):157-63 [21108601.001]
  • [CommentIn] N Engl J Med. 2010 Jun 17;362(24):2314-5 [20525994.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672; author reply 1673-5 [20961253.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973146.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973145.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672-3; author reply 1673-5 [20973144.001]
  • (PMID = 20525995.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00481247
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  •  go-up   go-down


45. Auewarakul CU, Huang S, Yimyam M, Boonmoh S: Natural history of Southeast Asian chronic myeloid leukemia patients with different BCR-ABL gene variants. Acta Haematol; 2006;116(2):114-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natural history of Southeast Asian chronic myeloid leukemia patients with different BCR-ABL gene variants.
  • Little evidence exists regarding the prognostic impact of the major BCR-ABL gene variants (e13a2 and e14a2) in chronic myeloid leukemia (CML) patients diagnosed and treated in the developing Asian countries.
  • In this study, 139 Thai CML patients were followed for a median period of 3 years (range 18-43 months).
  • All patients received oral chemotherapy and 13% underwent allogeneic stem cell transplantation.
  • In the conventional chemotherapy group, the overall survival (OS) rate was slightly better in e14a2+ than in e13a2+ patients (p = n.s.).
  • The type of blastic crisis in e14a2+ and e13a2+ patients was similar, being predominantly myeloid.
  • In conclusion, CML patients in Thailand, despite being much younger, had a comparable OS with those in the Western countries, with no different OS between e14a2+ and e13a2+ patients.
  • Future studies should focus on the impact of novel oral BCR-ABL tyrosine kinase inhibitors on the outcome of Thai CML patients with different BCR-ABL gene variants.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Genes, abl. Genetic Variation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Female. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Stem Cell Transplantation. Thailand. Transplantation, Homologous


46. Zhang Y, Jiang Q, Qiu JY, Chen SS, Jiang B, Huang XJ: [The prognostic implications of secondary chromosomal aberrations in Philadelphia chromosome-positive chronic myeloid leukemia patients after imatinib mesylate treatment]. Zhonghua Nei Ke Za Zhi; 2007 Aug;46(8):648-50
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The prognostic implications of secondary chromosomal aberrations in Philadelphia chromosome-positive chronic myeloid leukemia patients after imatinib mesylate treatment].
  • OBJECTIVE: To investigate the change of Philadelphia chromosome-positive clone with secondary chromosomal aberrations after imatinib mesylate (IM) treatment in patients with chronic myeloid leukemia (CML) and its relation with prognosis.
  • METHODS: 37 cases of CML in accelerated phase and blastic phase were collected and chromosome specimens of bone marrow cells were prepared by with 24-hour culture.
  • The percentage of Philadelphia chromosome-positive clone with secondary chromosomal aberrations showed the following 4 types of change; amplification, no change, decrease and complete remission after treatment with IM.
  • 2 of the 24 cases in CML in accelerated phase gained complete cytogenetic response (CCyR) and 2 of the 13 in blastic phase did so.
  • CONCLUSION: The percentage of Philadelphia chromosome-positive clone with secondary chromosomal aberrations may drop in some CML patients after IM treatment and the patients may gain CCyR with accompanied prolonged survival.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Benzamides. Blast Crisis. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Female. Follow-Up Studies. Humans. Imatinib Mesylate. Karyotyping. Male. Middle Aged. Philadelphia Chromosome. Prognosis

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17967235.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


47. Salesi N, Bossone G, Della Longa G, Di Cocco B: [A new drug in the therapy of chronic myeloid leukemia: ST1571]. Minerva Med; 2003 Apr;94(2):71-6
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A new drug in the therapy of chronic myeloid leukemia: ST1571].
  • The therapy of chronic myeloid leukemia, characterized by the presence of the Philadelphia chromosome in the clonal hematopoietic stem cells, has changed dramatically in the last years with the development of a specific inhibitor of the BCR-ABL tyrosine kinase: tyrosine kinase inhibitor imatinib mesylate (formerly STI571, [Glivec]).
  • The majority (88%) of interferon-alpha-resistant or intolerant patients in chronic-phase CML, achieved a complete hematologic response to imatinib mesylate.
  • Furthermore, 21% of patients in accelerated-phase CML and 13.5% of patients in blastic-phase CML (patient populations with typically poor prognosis before the advent of imatinib mesylate) achieved major cytogenetic responses.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Blast Crisis / drug therapy. Clinical Trials, Phase I as Topic. Humans. Imatinib Mesylate


48. Kantarjian HM, Cortes J, O'Brien S, Giles FJ, Albitar M, Rios MB, Shan J, Faderl S, Garcia-Manero G, Thomas DA, Resta D, Talpaz M: Imatinib mesylate (STI571) therapy for Philadelphia chromosome-positive chronic myelogenous leukemia in blast phase. Blood; 2002 May 15;99(10):3547-53
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imatinib mesylate (STI571) therapy for Philadelphia chromosome-positive chronic myelogenous leukemia in blast phase.
  • Molecular abnormalities caused by the hybrid Bcr-Abl gene are causally associated with the development and progression of Philadelphia chromosome-positive (Ph(+)) chronic myelogenous leukemia (CML).
  • Imatinib mesylate (STI571), a specific Bcr-Abl tyrosine-kinase signal-transduction inhibitor, has shown encouraging activity in phase I and II studies of CML.
  • Here, we describe the use of imatinib mesylate to treat 75 patients in blast-phase CML (median age, 53 years; 65 with nonlymphoid and 10 with lymphoid blasts), and compare the results with those of a historical control group treated with standard cytarabine-based therapy.
  • Imatinib mesylate was given as oral doses at 300 to 1000 mg per day and was the first salvage therapy for 47 patients.
  • The objective response rate was 52% (39 of 75 patients: 16 had complete and 3 had partial hematologic response; 12 had hematologic improvement; 7 returned to second chronic phase; and 1 had a complete response in extramedullary blastic disease).
  • Response to therapy (landmark analysis at 8 weeks) was associated with survival prolongation.
  • Compared with standard cytarabine combinations, imatinib mesylate therapy was less toxic and produced a higher response rate (55% versus 29%, P =.001), longer median survival (7 versus 4 months, P =.04), and lower 4-week induction mortality (4% versus 15%, P =.07).
  • Imatinib mesylate is currently being tested in combination with other drugs to improve the prognosis for blast-phase CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Benzamides. Blood Cell Count. Cytarabine / therapeutic use. Cytogenetic Analysis. Enzyme Inhibitors / adverse effects. Enzyme Inhibitors / therapeutic use. Follow-Up Studies. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Middle Aged. Prognosis. Survival Rate. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11986206.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


49. Tanaka H, Tanaka K, Oguma N, Ito K, Ito T, Kyo T, Dohy H, Kimura A: Effect of interferon-alpha on chromosome abnormalities in treated chronic myelogenous leukemia patients. Cancer Genet Cytogenet; 2004 Sep;153(2):133-43
Hazardous Substances Data Bank. BUSULFAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of interferon-alpha on chromosome abnormalities in treated chronic myelogenous leukemia patients.
  • To investigate the relationship of chromosomal aberrations at blastic crisis (BC) in chronic myelogenous leukemia (CML), with previous therapies and with atomic bomb (AB) exposure, we studied 114 CML patients who developed BC, including 23 AB survivors in Hiroshima.
  • Occurrence of major-route abnormality was not associated with either duration of chronic phase or survival time after BC.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Chromosome Aberrations. Interferon-alpha / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / therapeutic use. Female. Humans. Japan. Karyotyping. Male. Middle Aged. Neoplasms, Radiation-Induced / genetics. Nuclear Warfare

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15350303.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; G1LN9045DK / Busulfan
  •  go-up   go-down


50. Zitella L: Tyrosine kinase inhibitors: a cure for chronic myeloid leukemia? Clin J Oncol Nurs; 2000 Sep-Oct;4(5):227-9
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tyrosine kinase inhibitors: a cure for chronic myeloid leukemia?
  • Chronic myeloid leukemia (CML), a malignant transformation of hematopoietic cells, accounts for one-fifth of all leukemias and will be diagnosed in 4,400 individuals in the United States this year.
  • CML has three phases: chronic, accelerated, and blastic.
  • Interferon, hydroxyurea, busulfan, and bone marrow and stem cell transplantation are used to treat CML, but individuals who are in the accelerated phases or blast crisis usually respond poorly to treatment.
  • Further research is needed to determine the rate of response and survival data, but STI 571 holds great promise in the treatment of CML.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11111454.001).
  • [ISSN] 1092-1095
  • [Journal-full-title] Clinical journal of oncology nursing
  • [ISO-abbreviation] Clin J Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
  •  go-up   go-down


51. Giles FJ, Cortes JE, Baker SD, Thomas DA, O'Brien S, Smith TL, Beran M, Bivins C, Jolivet J, Kantarjian HM: Troxacitabine, a novel dioxolane nucleoside analog, has activity in patients with advanced leukemia. J Clin Oncol; 2001 Feb 01;19(3):762-71
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Troxacitabine, a novel dioxolane nucleoside analog, has activity in patients with advanced leukemia.
  • PURPOSE: To investigate the toxicity profile, activity, and pharmacokinetics of a novel L-nucleoside analog, troxacitabine (BCH-4556), in patients with advanced leukemia.
  • PATIENTS AND METHODS: Patients with refractory or relapsed acute myeloid (AML) or lymphocytic (ALL) leukemia, myelodysplastic syndromes (MDS), or chronic myelogenous leukemia in blastic phase (CML-BP).
  • RESULTS: Forty-two patients (AML: 31 patients; MDS: six patients [five MDS + one CMML]; ALL: four patients; CML-BP: one patient) were treated.
  • Approximately 69% of troxacitabine was excreted as unchanged drug in the urine.
  • A patient with CML-BP achieved a return to chronic phase disease.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytosine / adverse effects. Cytosine / analogs & derivatives. Dioxolanes / adverse effects. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Blast Crisis / drug therapy. Blast Crisis / metabolism. Dose-Response Relationship, Drug. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Middle Aged. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11157029.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dioxolanes; 60KQZ0388Y / troxacitabine; 8J337D1HZY / Cytosine
  •  go-up   go-down


52. Olavarria E, Ottmann OG, Deininger M, Clark RE, Bandini G, Byrne J, Lipton J, Vitek A, Michallet M, Siegert W, Ullmann A, Wassmann B, Niederwieser D, Fischer T, Chronic Leukaemia Working Party of the European Group of Bone and Marrow Transplantation (EBMT): Response to imatinib in patients who relapse after allogeneic stem cell transplantation for chronic myeloid leukemia. Leukemia; 2003 Sep;17(9):1707-12
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Response to imatinib in patients who relapse after allogeneic stem cell transplantation for chronic myeloid leukemia.
  • We studied 128 patients with chronic myeloid leukemia (CML) relapsing after allogeneic stem cell transplantation (SCT).
  • Disease at the time of treatment with Imatinib was in chronic phase (CP) in 51 patients, accelerated phase (AP) in 31 and blastic crisis (BC) in 46.
  • The median interval between relapse and Imatinib therapy was 5 months (0-65).
  • A total of 50 patients had failed treatment with donor lymphocyte infusions prior to Imatinib.
  • We conclude that Imatinib has significant activity against CML in relapse after allogeneic SCT.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Female. Graft vs Leukemia Effect. Humans. Imatinib Mesylate. Male. Middle Aged. Retrospective Studies. Salvage Therapy. Survival Rate. Transplantation, Homologous. Treatment Outcome


53. Morel F, Bris MJ, Herry A, Calvez GL, Marion V, Abgrall JF, Berthou C, Braekeleer MD: Double minutes containing amplified bcr-abl fusion gene in a case of chronic myeloid leukemia treated by imatinib. Eur J Haematol; 2003 Apr;70(4):235-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Double minutes containing amplified bcr-abl fusion gene in a case of chronic myeloid leukemia treated by imatinib.
  • Amplification of the bcr-abl fusion gene has recently been associated with resistance to imatinib therapy in chronic myeloid leukemia (CML).
  • A 55-yr-old man was diagnosed with Philadelphia (Ph) chromosome-positive CML.
  • Resistance to interferon treatment and occurrence of blastic phase lead to the decision of imatinib therapy.
  • A second blastic phase occurred 4 months after transplantation, of which the patient died.
  • To the best of our knowledge, dmin containing amplified bcr-abl gene has never been reported in patients with CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / genetics. Drug Resistance, Neoplasm / genetics. Enzyme Inhibitors / therapeutic use. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Neoplasm Proteins / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Aneuploidy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Chromosome Aberrations. Chromosome Painting. Combined Modality Therapy. Cytarabine / administration & dosage. Fatal Outcome. Humans. Hydroxyurea / administration & dosage. Imatinib Mesylate. Interferon-alpha / administration & dosage. Karyotyping. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Philadelphia Chromosome. Transplantation, Autologous


54. Lewandowski K, Warzocha K, Hellmann A, Skotnicki A, Prejzner W, Foryciarz K, Sacha T, Gniot M, Majewski M, Solarska I, Nowak G, Wasag B, Kobelski M, Scibiorski C, Siemiatkowski M, Lewandowska M, Komarnicki M: Frequency of BCR-ABL gene mutations in Polish patients with chronic myeloid leukemia treated with imatinib: a final report of the MAPTEST study. Pol Arch Med Wewn; 2009 Dec;119(12):789-94
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequency of BCR-ABL gene mutations in Polish patients with chronic myeloid leukemia treated with imatinib: a final report of the MAPTEST study.
  • INTRODUCTION: The presence of BCR-ABL oncogene mutations in patients with chronic myeloid leukemia (CML) may be responsible for the failure of tyrosine kinase inhibitor treatment.
  • OBJECTIVES: The aim of the study was to evaluate the frequency of BCR-ABL gene mutations in patients with CML (the MAPTEST study) treated with imatinib (IM).
  • The mean time of IM treatment was 18 months.
  • At the time of the analysis, 75 patients were in the first chronic phase (CP), 4 in the second CP, 5 in the acceleration and 8 in the blastic phase.
  • Inclusion criteria were based on the European Leukemia Net definitions for failure and suboptimal response to IM.
  • RESULTS: Twelve mutations were detected in 11 of 92 patients, including 4 mutations (36.7%) diagnosed during CP, 3 (27.3%) in acceleration, and 4 (36.7%) in blast crisis.
  • In 1 patient with lymphoid blast crisis of CML coexisting F359V and Y253F mutations were detected.
  • CONCLUSIONS: The study confirmed the usefulness of BCR-ABL gene mutation screening in patients with CML resistant to IM therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Chromatography, High Pressure Liquid. DNA Mutational Analysis. Dose-Response Relationship, Drug. Female. Gene Expression Regulation, Leukemic. Humans. Imatinib Mesylate. Male. Middle Aged. Neoplasm Staging. Poland. Treatment Outcome. Young Adult


55. Iványi JL, Marton E, Kereskai L, Kiss Z, Pajor L: [Molecular biology follow-up of interferon therapy in patients with chronic myeloid leukemia]. Orv Hetil; 2000 Nov 19;141(47):2527-33
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Molecular biology follow-up of interferon therapy in patients with chronic myeloid leukemia].
  • In a prospective survey clinical haematological and molecular biological data of 31 patients with chronic myelogenous leukaemia (chronic phase, CML) observed in their haematological outpatient department were analyzed.
  • During the follow-up period of 33 months from the 31 patients with CML (16 males, 15 females) 25 ones were treated with human recombinant interferon-alpha (IFN), however, six others were getting only hydroxyurea (HU).
  • During this period in three patients allogen bone marrow transplantation was performed and seven ones expired (six out of them of blastic crisis).
  • The quality of therapeutic response at cytogenetical level was determined by decrease of the bcr-abl level due to the treatment (non-responders, major, minor and complete cytogenetic remission groups).
  • In nine patients (five from the IFN-group, four from the HU-group) achieved no cytogenetic therapeutic response (non-responders, 29%).
  • The improvement of the overall survival of patients with CML, the postpone of the fatal accelerated-blastic phase could be expected only from the early introduced, in individually adjusted and given in maximally tolerated dosage of interferon (3-5 million UI/m2/day).
  • The qualitative (RT-PCR) and quantitative (FISH) detections of the Philadelphia chromosome are reliably reproducible up-to-date molecular biological methods getting relevant results, which could be very helpful in the planning, monitoring, in setting of optimal dosage of the interferon therapy of patients with CML, in addition in the judgement of the effectiveness of the therapy, in the reduction of adverse effects, as well as in forecasting of the cytogenetic progression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Genes, abl / genetics. Interferon Type I / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Philadelphia Chromosome
  • [MeSH-minor] Female. Gene Expression Regulation, Neoplastic. Humans. In Situ Hybridization, Fluorescence. Male. Recombinant Proteins. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic. Treatment Outcome


56. Cortes J, Albitar M, Thomas D, Giles F, Kurzrock R, Thibault A, Rackoff W, Koller C, O'Brien S, Garcia-Manero G, Talpaz M, Kantarjian H: Efficacy of the farnesyl transferase inhibitor R115777 in chronic myeloid leukemia and other hematologic malignancies. Blood; 2003 Mar 1;101(5):1692-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of the farnesyl transferase inhibitor R115777 in chronic myeloid leukemia and other hematologic malignancies.
  • We investigated the clinical activity of the farnesyl transferase inhibitor R115777 in 22 patients with chronic myelogenous leukemia (CML) in chronic, accelerated, or blastic phase and in 8 patients with myelofibrosis (MF) and 10 patients with multiple myeloma (MM).
  • Seven patients with CML (6 in chronic phase, 1 in advanced phase) achieved complete or partial hematologic response.
  • Two patients discontinued therapy because of toxicity while in complete hematologic response.
  • Patients who responded to therapy had significantly higher plasma vascular endothelial growth factor (VEGF) concentrations prior to treatment than nonresponders.
  • Plasma concentrations decreased significantly during therapy among responders.
  • R115777 showed clinical activity in patients with CML and MF.
  • [MeSH-major] Alkyl and Aryl Transferases / antagonists & inhibitors. Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Multiple Myeloma / drug therapy. Neoplasm Proteins / antagonists & inhibitors. Primary Myelofibrosis / drug therapy. Quinolones / therapeutic use
  • [MeSH-minor] Adult. Aged. Blast Crisis / blood. Blast Crisis / drug therapy. Drug Administration Schedule. Drug Eruptions / etiology. Endothelial Growth Factors / blood. Farnesyltranstransferase. Fatigue / chemically induced. Female. Fibroblast Growth Factor 2 / blood. Hepatocyte Growth Factor / blood. Humans. Intercellular Signaling Peptides and Proteins / blood. Interferon-alpha / blood. Leukemia, Myeloid, Accelerated Phase / blood. Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / blood. Leukemia, Myeloid, Chronic-Phase / drug therapy. Lymphokines / blood. Male. Middle Aged. Nausea / chemically induced. Salvage Therapy. Treatment Outcome. Tumor Necrosis Factor-alpha / analysis. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12411300.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R21-CA91518A
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Endothelial Growth Factors; 0 / Enzyme Inhibitors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interferon-alpha; 0 / Lymphokines; 0 / Neoplasm Proteins; 0 / Quinolones; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2; 192185-72-1 / tipifarnib; 67256-21-7 / Hepatocyte Growth Factor; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase
  •  go-up   go-down


57. Olsson-Strömberg U, Simonsson B, Ahlgren T, Björkholm M, Carlsson K, Gahrton G, Hast R, Löfvenberg E, Linder O, Ljungman P, Malm C, Paul C, Rödjer S, Turesson I, Udén AM, Wahlin A, Killander A, Wadman B, Westin J, Vikrot O, Zettervall O, Oberg G, Swedish CML Study Group: Comparison of busulphan, hydroxyurea and allogeneic bone marrow transplantation (BMT) in chronic myeloid leukaemia: BMT prolongs survival. Hematol J; 2004;5(6):462-6
Hazardous Substances Data Bank. BUSULFAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • INTRODUCTION: Whether busulphan-treated patients develop blastic transformation earlier than hydroxyurea treated has been a controversial issue.
  • In a randomised prospective study, we examined the busulphan versus hydroxyurea influence on time to blast crisis and on survival.
  • When we opened our study in 1984, the clinical benefit of allogeneic bone marrow transplantation (BMT) was not well known; to follow up the long-time outcome of this treatment was therefore of great interest.
  • MATERIALS AND METHODS: Previously untreated CML patients were randomly started on either hydroxyurea (30 mg/kg/day) or busulphan (0.1 mg/kg/day).
  • The end points of the study were overall survival and time to blast crisis.
  • RESULTS: A total of 179 patients were randomised, 90 of hydroxyurea, and 89 to busulphan treatment.
  • In all, 85 of the patients were subsequently diagnosed with blast crisis, 41 in the busulphan and 44 in the hydroxyurea group.
  • CONCLUSION: We did not find any difference between hydroxyurea and busulphan treatment, either in overall survival or in blast crisis-free survival; transplanted patients survived significantly longer than nontransplanted patients.

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • Hazardous Substances Data Bank. HYDROXYUREA .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15570285.001).
  • [ISSN] 1466-4860
  • [Journal-full-title] The hematology journal : the official journal of the European Haematology Association
  • [ISO-abbreviation] Hematol. J.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] G1LN9045DK / Busulfan; X6Q56QN5QC / Hydroxyurea
  •  go-up   go-down


58. Yamada O, Kawauchi K, Akiyama M, Ozaki K, Motoji T, Adachi T, Aikawa E: Leukemic cells with increased telomerase activity exhibit resistance to imatinib. Leuk Lymphoma; 2008 Jun;49(6):1168-77
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Imatinib mesylate (imatinib), previously known as STI571 (Gleevec), is currently utilized in the treatment of chronic myeloid leukemia (CML).
  • The telomerase activity of primary leukemic cells from CML patients in blastic crisis showed less suppression than that of cells from patients in chronic phase.
  • These results suggest a novel mechanism in the antitumor activity of imatinib and may provide a basis for future development of anti-telomerase therapies, as well as leading to better understanding of the regulation of telomerase in leukemic cells.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Telomerase / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Blast Crisis. Female. Gene Expression Regulation, Leukemic. Humans. Imatinib Mesylate. Male. Middle Aged. Promoter Regions, Genetic. Protein-Tyrosine Kinases / antagonists & inhibitors. Telomere / genetics. Transcription, Genetic / drug effects. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Lymphoma. 2008 Jun;49(6):1022-3 [18452091.001]
  • (PMID = 18569639.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] 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; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  •  go-up   go-down


59. Raiola AM, Van Lint MT, Valbonesi M, Lamparelli T, Gualandi F, Occhini D, Bregante S, di Grazia C, Dominietto A, Soracco M, Romagnani C, Vassallo F, Casini M, Bruno B, Frassoni F, Bacigalupo A: Factors predicting response and graft-versus-host disease after donor lymphocyte infusions: a study on 593 infusions. Bone Marrow Transplant; 2003 Apr;31(8):687-93
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patients were analyzed after stratification for type of relapse: (1).
  • chronic phase of chronic myeloid leukemia (CML) or complete remission of other disease post chemotherapy (n=24), (4).
  • CML in accelerated/blastic phase (n=14), (5).
  • resistant disease not responding to chemotherapy (n=36).
  • Factors predicting response by multivariate analysis were type of relapse (P<0.0001), post-DLI GvHD (P=0.005), pancytopenia (P=0.008), and a diagnosis of CML (P=0.04).
  • The actuarial probability of treatment-related mortality was 9% for HLA identical siblings and 44% for alternative donor transplants (P=0.006).
  • [MeSH-major] Bone Marrow Transplantation / immunology. Graft vs Host Disease / epidemiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion. Transplantation, Homologous
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD / blood. Antigens, CD3 / blood. Blast Crisis / therapy. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Probability. Prognosis. Recurrence. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12692609.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3
  •  go-up   go-down


60. Uchida M, Watanabe T, Kunitama M, Mori M, Kikuchi S, Yoshida K, Kirito K, Nagai T, Ozawa K, Komatsu N: Erythropoietin overcomes imatinib-induced apoptosis and induces erythroid differentiation in TF-1/bcr-abl cells. Stem Cells; 2004;22(4):609-16
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Targeting BCR-ABL tyrosine kinase by treatment with the selective inhibitor imatinib (formerly STI571, Gleevec) has proved to be highly efficient for inhibiting leukemic growth in vitro.
  • In addition, in clinical trials, imatinib has produced high response rates in patients with chronic myeloid leukemia (CML) in chronic phase and blastic crisis.
  • However, episodes of severe cytopenia were also frequently observed, leading to discontinuation of therapy in some cases.
  • In this study, we examine the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (EPO) on TF-1/bcr-abl (which was generated by transduction of a bcr-abl fusion gene into the TF-1 cell line) as a model system for CML with blastic crisis.
  • Taken together, imatinib-treated CML cells may differentiate into mature cells in the presence of differentiation-inducing cytokines such as EPO.
  • [MeSH-major] Apoptosis / physiology. Cell Differentiation / drug effects. Erythropoietin / pharmacology. Fusion Proteins, bcr-abl / drug effects. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Neoplasm Proteins / drug effects. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Apoptosis Regulatory Proteins. Benzamides. Cell Line, Tumor. Hemoglobins / biosynthesis. Humans. Imatinib Mesylate. Leukemia, Lymphocytic, Chronic, B-Cell. Protein-Tyrosine Kinases / antagonists & inhibitors

  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15277706.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Benzamides; 0 / Hemoglobins; 0 / Neoplasm Proteins; 0 / PDCD5 protein, human; 0 / Piperazines; 0 / Pyrimidines; 11096-26-7 / Erythropoietin; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  •  go-up   go-down


61. Tolo-Diebkilé A, Koffi KG, Sawadogo GD, Ndiaye FS, Nanho DC, Sékongo YM, Kouakou B, Méité N, Ayemou R, Sanogo I: [Therapeutic impact of alpha interferon in chronic myelogenous leukaemia]. Mali Med; 2010;25(1):22-7
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Therapeutic impact of alpha interferon in chronic myelogenous leukaemia].
  • [Transliterated title] Impact therapeutique de l'interferon alpha dans la prise en charge des patients atteints de leucemie myeloide chronique.
  • CONTEXT: Ten years after the use of alpha interferon in chronic myelogenous (CML) leukaemia treatment, we review this treatment.
  • OBJECTIVE: We propose through this study to evaluate the therapeutic answer of the patients reached of CML in chronic phase and to study its impact on survival.
  • On the evolutionary level, it was noted 27.5% of deaths related to a blastic transformation.
  • The age, socioeconomic level, delay of treatment started, therapeutic protocol, length and regularity of treatment influenced the therapeutic response.
  • CONCLUSION: Many factors influence the treatment response.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy
  • [MeSH-minor] Adult. Blast Crisis / etiology. Cytarabine / administration & dosage. Female. Fusion Proteins, bcr-abl / blood. Humans. Hydroxyurea / administration & dosage. Immunologic Factors / adverse effects. Immunologic Factors / therapeutic use. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Retrospective Studies. Socioeconomic Factors. Virus Activation. Young Adult

  • Hazardous Substances Data Bank. HYDROXYUREA .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21436004.001).
  • [ISSN] 1993-0836
  • [Journal-full-title] Le Mali médical
  • [ISO-abbreviation] Mali Med
  • [Language] fre
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] Mali
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interferon-alpha; 04079A1RDZ / Cytarabine; EC 2.7.10.2 / Fusion Proteins, bcr-abl; X6Q56QN5QC / Hydroxyurea
  •  go-up   go-down






Advertisement