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1. Castillo-Rama M, Grande C, Martínez-Sanchez P, Olavarria E, Marín D, Paz-Artal E, Andrés A, Morales JM: [Molecular remission of chronic myeloid leukaemia in a patient with hepatitis and a second kidney transplant]. Nefrologia; 2009;29(6):604-7
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  • [Title] [Molecular remission of chronic myeloid leukaemia in a patient with hepatitis and a second kidney transplant].
  • [Transliterated title] Remisión molecular de una leucemia mieloide crónica en un paciente con segundo trasplante renal y hepatitis.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by clonal expansion of cells in the myeloid line, expressing the BCR-ABL fusion protein responsible for the oncogenic effect of CML.
  • The current frontline therapy in CML is the BCR-ABL tyrosine kinase inhibitor, Imatinib.
  • Although this drug has been shown to improve survival in CML patients, its role in the context of a transplant setting has not been widely described in the literature.
  • We report on the long term molecular remission of CML in a 55 year old man with a second renal transplant who is hepatitis C virus positive, and has associated cardiovascular and immunological risk factors.
  • [MeSH-major] Kidney Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery
  • [MeSH-minor] Hepatitis C / complications. Humans. Male. Middle Aged. Remission Induction. Reoperation


2. de Lima M, Bonamino M, Vasconcelos Z, Colares M, Diamond H, Zalcberg I, Tavares R, Lerner D, Byington R, Bouzas L, da Matta J, Andrade C, Carvalho L, Pires V, Barone B, Maciel C, Tabak D: Prophylactic donor lymphocyte infusions after moderately ablative chemotherapy and stem cell transplantation for hematological malignancies: high remission rate among poor prognosis patients at the expense of graft-versus-host disease. Bone Marrow Transplant; 2001 Jan;27(1):73-8
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  • [Title] Prophylactic donor lymphocyte infusions after moderately ablative chemotherapy and stem cell transplantation for hematological malignancies: high remission rate among poor prognosis patients at the expense of graft-versus-host disease.
  • Twelve heavily pre-treated patients with life expectancy less than 6 months were studied; none were in remission.
  • Diagnoses were AML (n = 4), MDS (n = 1), ALL (n = 3), CML (n = 3) and multiple myeloma (n = 1).
  • Two patients are in remission of CML in blast crisis and AML for more than 14 months.
  • Six patients received 12 DLIs; three patients developed acute GVHD after the first infusion and were excluded from further DLIs, but no GVHD occurred among patients receiving subsequent DLIs.
  • One patient with CML in blast crisis went into CR after the first DLI.
  • Primary causes of death were infections (n = 3), acute GVHD (n = 3), chronic GVHD (n = 1) and disease relapse (n = 2).
  • [MeSH-major] Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / adverse effects. Lymphocyte Transfusion / standards
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Cause of Death. Child. Female. Graft vs Host Disease / etiology. Graft vs Host Disease / mortality. Graft vs Leukemia Effect. Humans. Male. Middle Aged. Prognosis. Remission Induction / methods. Secondary Prevention. Transplantation Chimera

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  • (PMID = 11244440.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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3. Kataoka I, Shinagawa K, Shiro Y, Okamoto S, Watanabe R, Mori T, Ito D, Harada M: Multiple sclerosis associated with interferon-alpha therapy for chronic myelogenous leukemia. Am J Hematol; 2002 Jun;70(2):149-53
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  • [Title] Multiple sclerosis associated with interferon-alpha therapy for chronic myelogenous leukemia.
  • We report a chronic myelogenous leukemia (CML) patient in chronic phase (CP) who developed multiple sclerosis (MS) in association with interferon-alpha (IFN-alpha) administration.
  • In our patient, recombinant IFN-alpha2b therapy induced hematologically complete and cytogenetically major partial response for CML first, and sequential central nervous system dysfunction evolved, which subsided shortly after the cessation of its administration.
  • Restarting IFN-alpha therapy by changing to a natural type of IFN-alpha resulted in rapid exacerbation of MS.
  • The patient's neurological symptoms progressed gradually, but partial hematologic response persisted without any IFN-alpha derivatives or anti-cancer agents until a matched unrelated donor transplant procedure was performed.
  • Myeloablative therapy led to lasting stable state of MS and finally to complete cytogenetic remission of CML.
  • [MeSH-major] Interferon-alpha / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Multiple Sclerosis / chemically induced
  • [MeSH-minor] Adult. Bone Marrow Transplantation. Female. Humans. Immunity, Cellular / drug effects. Magnetic Resonance Imaging. Recombinant Proteins

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12111789.001).
  • [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 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b
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4. Zhang B, Strauss AC, Chu S, Li M, Ho Y, Shiang KD, Snyder DS, Huettner CS, Shultz L, Holyoake T, Bhatia R: Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate. Cancer Cell; 2010 May 18;17(5):427-42
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  • [Title] Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate.
  • Imatinib mesylate (IM) induces remission in chronic myelogenous leukemia (CML) patients but does not eliminate leukemia stem cells (LSCs), which remain a potential source of relapse.
  • Here we investigated the ability of HDAC inhibitors (HDACis) to target CML stem cells.
  • Treatment with HDACis combined with IM effectively induced apoptosis in quiescent CML progenitors resistant to elimination by IM alone, and eliminated CML stem cells capable of engrafting immunodeficient mice.
  • In vivo administration of HDACis with IM markedly diminished LSCs in a transgenic mouse model of CML.
  • HDACi treatment represents an effective strategy to target LSCs in CML patients receiving tyrosine kinase inhibitors.

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  • [Copyright] (c) 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20478526.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE20876
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095684-07; United States / NHLBI NIH HHS / HL / R01 HL077847; United States / NHLBI NIH HHS / HL / R01 HL77847; United States / NCI NIH HHS / CA / P30 CA034196; United States / NCRR NIH HHS / RR / 5M01 RR00043; United States / NHLBI NIH HHS / HL / R01 HL077847-04; United States / NCI NIH HHS / CA / CA095684-07; None / None / / R01 HL077847-04; United States / NCI NIH HHS / CA / CA34196; United States / NCRR NIH HHS / RR / M01 RR000043; United States / NCI NIH HHS / CA / R01 CA095684; United States / NCI NIH HHS / CA / R01 CA95684
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Histone Deacetylase Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS193347; NLM/ PMC2873971
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5. Colombat M, Fort MP, Chollet C, Marit G, Roche C, Preudhomme C, Reiffers J, Praloran V, Mahon FX: Molecular remission in chronic myeloid leukemia patients with sustained complete cytogenetic remission after imatinib mesylate treatment. Haematologica; 2006 Feb;91(2):162-8
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  • [Title] Molecular remission in chronic myeloid leukemia patients with sustained complete cytogenetic remission after imatinib mesylate treatment.
  • BACKGROUND AND OBJECTIVES: Imatinib mesylate induces a complete cytogenetic response (CCR) in many patients with chronic myeloid leukemia (CML).
  • However, the ultimate goal of therapy for CML is complete elimination of Philadelphia chromosome positive cells or BCR-ABL rearrangements.
  • We studied molecular responses in CML patients in CCR after imatinib treatment.
  • DESIGN AND METHODS: Real-time quantitative reverse transcriptase polymerase chain reaction analysis were used to monitor BCR-ABL levels in 59 CCR patients.
  • Patients were considered in complete molecular remission if they had four undetectable analyses from two separate samples taken three months apart.
  • The median BCR-ABL/ABL ratio at the time of CCR was 0.3 % (0-9.88).
  • Patients were split into two groups: group A (n=43) comprised patients with a detectable BCR-ABL/ABL ratio throughout the follow-up and group B (n=16) included those with an undetectable level of BCR-ABL/ABL (< 10(-5)) i.e. in complete molecular remission.
  • By Cox regression analysis the best factor for predicting the probability of achieving molecular remission was having a CCR at 6 months (p=0.038) or at 3 months (p=0.024).
  • INTERPRETATION AND CONCLUSIONS: Molecular remission after imatinib treatment, i.e.
  • BCR-ABL/ABL< 10-5 in peripheral blood, is not a rare event, particularly in patients achieving CCR at 6 months.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Cytogenetic Analysis. Female. Fusion Proteins, bcr-abl / analysis. Humans. Imatinib Mesylate. Male. Middle Aged. Polymerase Chain Reaction. Remission Induction / methods


6. Kebriaei P, Detry MA, Giralt S, Carrasco-Yalan A, Anagnostopoulos A, Couriel D, Khouri IF, Anderlini P, Hosing C, Alousi A, Champlin RE, de Lima M: Long-term follow-up of allogeneic hematopoietic stem-cell transplantation with reduced-intensity conditioning for patients with chronic myeloid leukemia. Blood; 2007 Nov 1;110(9):3456-62
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  • [Title] Long-term follow-up of allogeneic hematopoietic stem-cell transplantation with reduced-intensity conditioning for patients with chronic myeloid leukemia.
  • Allogeneic hematopoietic stem-cell transplantation (HSCT) remains an effective strategy for inducing durable remission in chronic myeloid leukemia (CML).
  • We evaluated outcomes of 64 CML patients with advanced-phase disease (80% beyond first chronic phase), not eligible for myeloablative preparative regimens due to older age or comorbid conditions, who were treated with fludarabine-based RIC regimens.
  • Donor type was matched related (n =30), 1 antigen-mismatched related (n =4), or matched unrelated (n =30).
  • Incidence of treatment-related mortality (TRM) was 33%, 39%, and 48% at 100 days, and 2 and 5 years after HSCT, respectively.
  • In multivariate analysis, only disease stage at time of HSCT was significantly predictive for both OS and PFS.
  • RIC HSCT provides adequate disease control in chronic-phase CML patients, but alternative treatment strategies need to be explored in patients with advanced disease.
  • TRM rates are acceptable in this high-risk population but increase over time.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Transplantation Conditioning / methods. Transplantation, Homologous
  • [MeSH-minor] Adolescent. Adult. Aged. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Follow-Up Studies. Graft vs Host Disease / etiology. Graft vs Host Disease / mortality. Humans. Male. Melphalan / administration & dosage. Middle Aged. Myeloablative Agonists / administration & dosage. Recurrence. Retrospective Studies. Survival Analysis. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives


7. Chou CJ, O'Hare T, Lefebvre S, Alvarez D, Tyner JW, Eide CA, Druker BJ, Gottesfeld JM: Growth arrest of BCR-ABL positive cells with a sequence-specific polyamide-chlorambucil conjugate. PLoS One; 2008;3(10):e3593
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  • [Title] Growth arrest of BCR-ABL positive cells with a sequence-specific polyamide-chlorambucil conjugate.
  • Chronic myeloid leukemia (CML) is characterized by the presence of a constitutively active Abl kinase, which is the product of a chimeric BCR-ABL gene, caused by the genetic translocation known as the Philadelphia chromosome.
  • Imatinib, a selective inhibitor of the Bcr-Abl tyrosine kinase, has significantly improved the clinical outcome of patients with CML.
  • However, subsets of patients lose their response to treatment through the emergence of imatinib-resistant cells, and imatinib treatment is less durable for patients with late stage CML.
  • Although alternative Bcr-Abl tyrosine kinase inhibitors have been developed to overcome drug resistance, a cocktail therapy of different kinase inhibitors and additional chemotherapeutics may be needed for complete remission of CML in some cases.
  • Chlorambucil has been used for treatment of B cell chronic lymphocytic leukemia, non-Hodgkin's and Hodgkin's disease.
  • Here we report that a DNA sequence-specific pyrrole-imidazole polyamide-chlorambucil conjugate, 1R-Chl, causes growth arrest of cells harboring both unmutated BCR-ABL and three imatinib resistant strains.

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  • (PMID = 18974832.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA107311; United States / NCI NIH HHS / CA / CA107311; United States / Howard Hughes Medical Institute / /
  • [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 / Antineoplastic Agents, Alkylating; 0 / Benzamides; 0 / Nylons; 0 / Piperazines; 0 / Pyrimidines; 18D0SL7309 / Chlorambucil; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2571993
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8. Egyed M, Kollár B, Rumi G, Keller E, Vass J, Fekete S: Effect of retinoic acid treatment on cytogenetic remission of chronic myeloid leukaemia. Acta Haematol; 2003;109(2):84-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of retinoic acid treatment on cytogenetic remission of chronic myeloid leukaemia.
  • The cytogenetic responses during the first chronic phase of 11 patients with chronic myeloid leukaemia (CML) treated with all-trans retinoic acid (ATRA) + interferon (IFN) were compared with those of 9 other CML patients treated with IFN alone.
  • The preliminary results suggest that the ATRA + IFN combination may be superior in achieving cytogenetic remission in the first chronic phase of CML.
  • [MeSH-major] Cytogenetic Analysis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Remission Induction. Tretinoin / therapeutic use
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Female. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / therapeutic use. Male. Middle Aged. Recombinant Proteins. Recurrence

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  • [Copyright] Copyright 2003 S. Karger AG, Basel
  • (PMID = 12624492.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Controlled Clinical Trial; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 47RRR83SK7 / interferon alfa-2a; 5688UTC01R / Tretinoin
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9. Savani BN, Montero A, Kurlander R, Childs R, Hensel N, Barrett AJ: Imatinib synergizes with donor lymphocyte infusions to achieve rapid molecular remission of CML relapsing after allogeneic stem cell transplantation. Bone Marrow Transplant; 2005 Dec;36(11):1009-15
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 synergizes with donor lymphocyte infusions to achieve rapid molecular remission of CML relapsing after allogeneic stem cell transplantation.
  • Donor lymphocyte infusions (DLI) have been the mainstay of treatment for chronic myeloid leukemia (CML) relapsing after allogeneic stem cell transplantation (allo-SCT).
  • However, advanced phase relapse (APRel) responds poorly with either treatment.
  • To test the possibility that combinations of DLI and IM might be more effective, 37 patients with CML relapsing after allo-SCT between August 1994 and May 2004 were studied.
  • Thirty (81%) patients responded (actuarial survival and current leukemia-free survival of 80.6 +/- 6.7% and 69.1 +/- 7.7%).
  • Of 30 patients, 26 are in molecular remission (MR), median follow-up of 1,226 days (range 249-3257) since relapse.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Drug Synergism. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Recurrence. Remission Induction / methods. Retrospective Studies. Survival Analysis. Transplantation, Homologous

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  • (PMID = 16205732.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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11. Matsuda M, Morita Y, Shimada T, Miyatake J, Hirase C, Tanaka M, Tatsumi Y, Maeda Y, Kanamaru A: Extramedullary blast crisis derived from 2 different clones in the central nervous system and neck during complete cytogenetic remission of chronic myelogenous leukemia treated with imatinib mesylate. Int J Hematol; 2005 May;81(4):307-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extramedullary blast crisis derived from 2 different clones in the central nervous system and neck during complete cytogenetic remission of chronic myelogenous leukemia treated with imatinib mesylate.
  • We describe a patient with Philadelphia chromosome (Ph)-positive chronic myelogenous leukemia (CML) who developed an extramedullary blast crisis in the central nervous system (CNS) and then a subcutaneous tumor of the neck during treatment with imatinib mesylate.
  • Administered 400 mg of imatinib mesylate after the diagnosis of chronic-phase CML, the patient achieved a complete cytogenetic remission 4 months later.
  • However, he developed a mixed myeloid/B-cell blast crisis with additional karyotype abnormalities only in the CNS during a complete cytogenetic remission in the bone marrow.
  • Several doses of intrathecal chemotherapy and whole-brain irradiation were effective in treating the blast crisis in the CNS.
  • After 7 months of complete cytogenetic remission, the patient experienced a subcutaneous tumor in the right neck.
  • A biopsy of the tumor revealed a mixed myeloid/T-cell blast crisis.
  • This case suggests that the development of a clone resistant to imatinib mesylate is not always detected in the bone marrow and that multiple Ph-positive clones have the potential to become transformed into a blast crisis.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / genetics. Central Nervous System Neoplasms / genetics. Central Nervous System Neoplasms / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • [Cites] Br J Haematol. 2002 Jun;117(3):623-5 [12028032.001]
  • [Cites] Leuk Lymphoma. 1999 Apr;33(3-4):399-402 [10221523.001]
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  • (PMID = 15914360.001).
  • [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
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12. Du QF, Liu XL, Liu QF, Li R, Chen Q, Zhou SY: [Quantitative analysis of Sokal's risk index in relation to 2 therapy protocols: their respective impact on clinical remission of chronic myeloid leukemia]. Di Yi Jun Yi Da Xue Xue Bao; 2002 Aug;22(8):729-30
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  • [Title] [Quantitative analysis of Sokal's risk index in relation to 2 therapy protocols: their respective impact on clinical remission of chronic myeloid leukemia].
  • OBJECTIVE: To quantitatively evaluate the impact of Sokal's risk index and that of 2 therapy protocols on the clinical outcome of patients with chronic myeloid leukemia (CML).
  • METHODS: With the assistance of Access 2000 database of CML, 94 patients with CML were grouped on the basis of either different therapy protocols utilizing harringtonine plus Ara-C (HA) vs hydroxyurea (Hu) or Sokal scores, and the impact of therapy protocol and risk profile were quantitatively evaluated respectively.
  • RESULT: Treatment protocol utilizing HA was incapable of lengthening the duration of chronic phase (DCP) of CML, regardless of its better short-term effect than that of Hu.
  • The impact of risk profile of the patients on clinical remission rate and DCP was more significant than that of the therapy protocols.
  • CONCLUSION: HA should not be used as the first-line protocol in the treatment of CML patients in chronic phase who have not received any previous medical intervention.
  • Patients should be categorized according to the risk profile for choosing appropriate treatment protocol and making better clinical judgement.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cytarabine / therapeutic use. Harringtonines / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Outcome Assessment (Health Care). Treatment Outcome


13. Orciuolo E, Fazzi R, Galimberti S, Testi C, Azzara' A, Carulli G, Petrini M: Chronic myeloid leukaemia and hairy cell leukaemia coexisting in a single patient: difficulties at diagnosis and rational of the therapeutic strategy. Leuk Res; 2006 Mar;30(3):349-53
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  • [Title] Chronic myeloid leukaemia and hairy cell leukaemia coexisting in a single patient: difficulties at diagnosis and rational of the therapeutic strategy.
  • Chronic myeloid leukemia (CML) and hairy cell leukemia (HCL) are two distinct haematological disorders.
  • We present a second case of coexistence at diagnosis, indicating the diagnostic procedures involving morphological, immunophenotyping, and molecular testing.
  • We decided to use Interferon as common first-line therapy and Imatinib and Rituximab (anti-CD20 monoclonal antibody), to improve the first-line therapy result, obtaining a complete molecular remission for CML and clinical remission with molecular minimal residual disease for HCL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Hairy Cell / diagnosis. Leukemia, Hairy Cell / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasms, Second Primary / diagnosis. Neoplasms, Second Primary / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / administration & dosage. Benzamides. Humans. Imatinib Mesylate. Interferons / administration & dosage. Male. Middle Aged. Neoplasm, Residual. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Remission Induction. Rituximab. Treatment Outcome

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  • (PMID = 16182365.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 4F4X42SYQ6 / Rituximab; 8A1O1M485B / Imatinib Mesylate; 9008-11-1 / Interferons
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14. Agis H, Sotlar K, Valent P, Horny HP: Ph-Chromosome-positive chronic myeloid leukemia with associated bone marrow mastocytosis. Leuk Res; 2005 Oct;29(10):1227-32
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  • [Title] Ph-Chromosome-positive chronic myeloid leukemia with associated bone marrow mastocytosis.
  • The concurrent development of chronic myeloid (CML) or myelomonocytic (CMML) leukemia in patients with systemic mastocytosis (SM) is a well recognized phenomenon.
  • Although the leukemia often resembles CML in morphological and in clinical terms, a Ph-Chromosome-positive variant has not been reported in SM so far.
  • We here describe a 43-year-old female patient with typical Ph-Chromosome-positive CML in whom a co-existing bone marrow mastocytosis, a special subvariant of SM, was diagnosed.
  • RT-PCR analysis revealed the typical p210 kDa form of BCR/ABL in leukemic cells.
  • The diagnosis SM was based on the typical focal aggregates of spindle-shaped mast cells (MC) in the bone marrow, expression of CD25 in MC, and the c-kit mutation D816V, which was detectable in microdissected bone marrow MC, but not in microdissected leukemic cells, suggesting the presence of two different (sub)clones of neoplastic cells.
  • Therapy with the BCR/ABL-targeting drug Imatinib (STI571) resulted in complete cytogenetic remission of CML.
  • The exact knowledge of the pathology and target-profile of the associated leukemias in SM have important therapeutic implications.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Mastocytosis, Systemic / etiology
  • [MeSH-minor] Adult. Benzamides. Female. Fusion Proteins, bcr-abl / physiology. Humans. Imatinib Mesylate. Piperazines / therapeutic use. Proto-Oncogene Proteins c-kit / metabolism. Pyrimidines / therapeutic use


15. Sanborn RE, Blanke CD: Gastrointestinal stromal tumors and the evolution of targeted therapy. Clin Adv Hematol Oncol; 2005 Aug;3(8):647-57
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  • [Title] Gastrointestinal stromal tumors and the evolution of targeted therapy.
  • Gastrointestinal stromal tumors (GISTs) historically have differed from other soft-tissue sarcomas in demonstrating a particularly grim prognosis.
  • GISTs have an extraordinarily high rate of recurrence after surgical resection and are highly resistant to radiation and standard chemotherapy.
  • The discovery that constitutive activation of the c-kit gene drives malignant behavior in GISTs exposed a weakness that was soon exploited through the application of the novel targeted therapy imatinib, a small-molecule tyrosine kinase inhibitor of Bcr-Abl, KIT, and the platelet-derived growth factor receptor-alpha and -beta.
  • Imatinib had shown unparalleled results in patients with advanced chronic myelogenous leukemia (remission rates approaching 98%), and the first GIST patients treated with imatinib demonstrated dramatic response rates unseen with other therapeutic modalities.
  • The gains that have been made in the treatment of GIST through the use of imatinib have helped to open the door to a new era of development of targeted therapeutic agents in oncology.
  • Whether this new era of targeted therapy will provide the same advances in more common malignancies will be determined only through the ongoing application and development of clinical trials.
  • [MeSH-major] Gastrointestinal Stromal Tumors / drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-kit / metabolism. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Clinical Trials as Topic. Combined Modality Therapy / methods. Combined Modality Therapy / trends. Drug Delivery Systems / methods. Drug Delivery Systems / trends. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Receptor, Platelet-Derived Growth Factor alpha / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Receptor, Platelet-Derived Growth Factor beta / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor beta / metabolism

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  • (PMID = 16167051.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 108
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16. Skorta I, Oren M, Markwardt C, Gutekunst M, Aulitzky WE, van der Kuip H: Imatinib mesylate induces cisplatin hypersensitivity in Bcr-Abl+ cells by differential modulation of p53 transcriptional and proapoptotic activity. Cancer Res; 2009 Dec 15;69(24):9337-45
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  • [Title] Imatinib mesylate induces cisplatin hypersensitivity in Bcr-Abl+ cells by differential modulation of p53 transcriptional and proapoptotic activity.
  • Imatinib is highly effective in inducing remission in chronic myelogenous leukemia (CML).
  • Inhibition of Bcr-Abl by imatinib induced a hypersensitive phenotype both in Bcr-Abl(+) cell lines and in CD34(+) cells from CML patients.
  • Importantly, cisplatin sensitivity of leukemic cells harboring an inactive Bcr-Abl greatly exceeded that of Bcr-Abl(-) parental cells.
  • The cisplatin response of Bcr-Abl(+) cells treated with imatinib was characterized by an impaired G(2)-M arrest and by rapid induction of mitochondrial cell death after the first passage through G(2).
  • Imatinib abrogated ATM activation on cisplatin selectively in Bcr-Abl(+) cells.
  • Furthermore, p53 accumulated predominantly in the cytoplasm in Bcr-Abl(+) cells treated with imatinib and cisplatin.
  • Silencing of p53 significantly reduced sensitivity to cisplatin in imatinib-treated Bcr-Abl(+) cells, indicating that p53 retains its proapoptotic activity.
  • We conclude that imatinib sensitizes Bcr-Abl(+) cells to cisplatin by simultaneous inhibition of p53 transactivation, induction of p53 accumulation predominantly in the cytoplasm, and reduction of Bcl-x(L).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cisplatin / pharmacology. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / pharmacology. Pyrimidines / pharmacology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Ataxia Telangiectasia Mutated Proteins. Benzamides. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Cycle Proteins / antagonists & inhibitors. Cell Cycle Proteins / metabolism. DNA Damage / drug effects. DNA-Binding Proteins / antagonists & inhibitors. DNA-Binding Proteins / metabolism. Drug Synergism. Enzyme Activation / drug effects. Humans. Imatinib Mesylate. K562 Cells. Mice. Myeloid Cells / drug effects. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / metabolism. Transcription, Genetic / drug effects. Tumor Suppressor Proteins / antagonists & inhibitors. Tumor Suppressor Proteins / metabolism. bcl-X Protein / antagonists & inhibitors. bcl-X Protein / metabolism

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  • (PMID = 19934315.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Benzamides; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Piperazines; 0 / Pyrimidines; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / bcl-X Protein; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; Q20Q21Q62J / Cisplatin
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17. Reuben JM, Lee BN, Johnson H, Fritsche H, Kantarjian HM, Talpaz M: Restoration of Th1 cytokine synthesis by T cells of patients with chronic myelogenous leukemia in cytogenetic and hematologic remission with interferon-alpha. Clin Cancer Res; 2000 May;6(5):1671-7
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  • [Title] Restoration of Th1 cytokine synthesis by T cells of patients with chronic myelogenous leukemia in cytogenetic and hematologic remission with interferon-alpha.
  • Chronic myelogenous leukemia (CML) is a disorder of the hematopoietic stem cell that results in malignant expansion of myeloid cells with a cytogenetic abnormality, the translocation between chromosomes 9 and 22 known as the Philadelphia chromosome.
  • Treatment with IFN-alpha has proven to be an effective therapy, inducing cytogenetic remission in CML patients.
  • However, it is unknown whether IFN-alpha can restore normal immune function for patients who achieve a complete cytogenetic remission.
  • To address this question, we used a method of intracellular staining and flow cytometric analysis to ascribe the syntheses of Th1 or Th2 cytokines to T-cell subsets of patients in chronic, in accelerated, and in blast crisis phases as well as patients who had achieved a complete cytogenetic remission with IFN-alpha.
  • We assessed the cytoplasmic synthesis of cytokine in phorbol ester (phorbol 12-myristate 13-acetate)-activated CD4+ and CD8+ T-cell subsets of 81 patients with various stages of CML and 21 normal controls.
  • The percentages of CD4+ and CD8+ T cells from patients in chronic, in accelerated, and in blast crisis phases that synthesized Th1 cytokines interleukin (IL)-2, IFN-gamma, and tumor necrosis factor-alpha were significantly lower than those of remission patients and normal controls.
  • Conversely, the percentages of CD4+ and CD8+ T cells of patients in chronic, in accelerated, and in blast crisis phases of CML preferentially synthesized the Th2 cytokine IL-10.
  • Patients who achieved a durable complete cytogenetic remission for >2 years without maintenance IFN-alpha therapy restored their preference for a Th1 cytokine profile that is necessary for efficient cytotoxic T-cell function.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cytokines / biosynthesis. Interferon-alpha / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. T-Lymphocytes / metabolism
  • [MeSH-minor] CD8-Positive T-Lymphocytes / drug effects. CD8-Positive T-Lymphocytes / metabolism. Flow Cytometry. Humans. Interferon-gamma / biosynthesis. Interleukin-10 / biosynthesis. Interleukin-2 / biosynthesis. Lymphocyte Activation / drug effects. Remission Induction. Tetradecanoylphorbol Acetate / pharmacology. Th1 Cells / metabolism. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 10815885.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Interferon-alpha; 0 / Interleukin-2; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 82115-62-6 / Interferon-gamma; NI40JAQ945 / Tetradecanoylphorbol Acetate
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18. Khouri S, Kotliroff A, Lishner M, Amital H: Imatinib-lnduced agranulocytosis in a patient with chronic myelogenous leukemia in remission. Isr Med Assoc J; 2008 Apr;10(4):320-1
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  • [Title] Imatinib-lnduced agranulocytosis in a patient with chronic myelogenous leukemia in remission.
  • [MeSH-major] Agranulocytosis / chemically induced. Antineoplastic Agents / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / adverse effects. Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects

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  • (PMID = 18548994.001).
  • [ISSN] 1565-1088
  • [Journal-full-title] The Israel Medical Association journal : IMAJ
  • [ISO-abbreviation] Isr. Med. Assoc. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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19. Barbany G, Höglund M, Simonsson B, Swedish CML Group: Complete molecular remission in chronic myelogenous leukemia after imatinib therapy. N Engl J Med; 2002 Aug 15;347(7):539-40
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  • [Title] Complete molecular remission in chronic myelogenous leukemia after imatinib therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Male. Middle Aged. Polymerase Chain Reaction. RNA, Messenger / analysis. Remission Induction

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  • (PMID = 12181416.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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20. Ruiz-Argüelles GJ: What is the dose of STI-571 needed to induce a molecular remission in chronic myeloid leukemia? Haematologica; 2002 Mar;87(3):ELT15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] What is the dose of STI-571 needed to induce a molecular remission in chronic myeloid leukemia?
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Benzamides. Dose-Response Relationship, Drug. Fusion Proteins, bcr-abl / analysis. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. RNA, Messenger / analysis. Remission Induction

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  • (PMID = 11869961.001).
  • [ISSN] 0390-6078
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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21. Lange T, Bumm T, Mueller M, Otto S, Al-Ali HK, Grommisch L, Musiol S, Franke C, Krahl R, Niederwieser D, Deininger MW: Durability of molecular remission in chronic myeloid leukemia patients treated with imatinib vs allogeneic stem cell transplantation. Leukemia; 2005 Jul;19(7):1262-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Durability of molecular remission in chronic myeloid leukemia patients treated with imatinib vs allogeneic stem cell transplantation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Stem Cell Transplantation
  • [MeSH-minor] Benzamides. Cohort Studies. Follow-Up Studies. Humans. Imatinib Mesylate. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Homologous






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