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1. 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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2. 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


3. 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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4. 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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5. 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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6. 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


7. 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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8. Oztop I, Yaren A, Demirpence M, Alacacioglu I, Tuna B, Piskin O, Yilmaz U: The development of metachronous prostate cancer and chronic myeloid leukemia in a patient with metastatic rectal cancer. J BUON; 2008 Apr-Jun;13(2):267-70
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  • [Title] The development of metachronous prostate cancer and chronic myeloid leukemia in a patient with metastatic rectal cancer.
  • We report herein an unusual case of metachronous triple cancers (rectum, prostate and Philadelphia(+) [Ph(+)] chronic myeloid leukemia [CML]).
  • A metastatic rectal cancer was diagnosed in a 76-year-old male patient, who was treated with transanal tumor resection and chemotherapy.
  • Thirty months from the initial rectal cancer diagnosis, prostate cancer was diagnosed and the patient was administered maximal androgen blockade and received palliative radiotherapy to the lumbar spine because of painful bone metastases.
  • Thirty months after the diagnosis of rectal cancer and 12 months after the diagnosis of prostate cancer the patient developed Ph(+) CML and imatinib treatment was started.
  • After one-year period in remission, CML evolved into accelerated phase and the patient died of intracranial hemorrhage.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplasms, Multiple Primary / pathology. Prostatic Neoplasms / pathology. Rectal Neoplasms / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Aged. Benzamides. Blast Crisis. Bone Neoplasms / drug therapy. Bone Neoplasms / radiotherapy. Bone Neoplasms / secondary. Fatal Outcome. Humans. Imatinib Mesylate. Male. Philadelphia Chromosome. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use


9. 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


10. 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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  • [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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  • (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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