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1. Loh AH, Chui CH: Port-A-Cath insertions in acute leukaemia and childhood malignancies. Asian J Surg; 2007 Jul;30(3):193-9
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  • [Title] Port-A-Cath insertions in acute leukaemia and childhood malignancies.
  • METHODS: Between January 2002 and December 2004, 175 consecutive Port-A-Cath insertions were followed for a total of 75,000 days (median, 407; range, 6-1,074).
  • Incidence of catheter-related bloodstream infections (CRBSIs), other complications and CRBSI-related port removals were analysed for cases with acute leukaemia versus other malignancies.
  • While mean preoperative platelet count was 125.34 x 10(9)/L in children with acute leukaemia and 392.11 x 10(9)/L in those with other malignancies (p < 0.01), the incidence of all complications were similar between both subgroups.

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  • (PMID = 17638639.001).
  • [ISSN] 1015-9584
  • [Journal-full-title] Asian journal of surgery
  • [ISO-abbreviation] Asian J Surg
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
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2. Admirand JH, Knoblock RJ, Coombes KR, Tam C, Schlette EJ, Wierda WG, Ferrajoli A, O'Brien S, Keating MJ, Luthra R, Medeiros LJ, Abruzzo LV: Immunohistochemical detection of ZAP70 in chronic lymphocytic leukemia predicts immunoglobulin heavy chain gene mutation status and time to progression. Mod Pathol; 2010 Nov;23(11):1518-23
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  • [Title] Immunohistochemical detection of ZAP70 in chronic lymphocytic leukemia predicts immunoglobulin heavy chain gene mutation status and time to progression.
  • Zeta-associated protein-70 (ZAP70) expression measured by flow cytometry has been proposed as a surrogate marker of the somatic mutation status of the immunoglobulin heavy chain variable region (IGHV) genes in chronic lymphocytic leukemia.
  • Assessment of ZAP70 protein expression by immunohistochemistry in chronic lymphocytic leukemia tissue sections is an easy, alternative approach, although lack of quantitation and subjective interpretation of results are potential pitfalls.
  • In this study, we correlated ZAP70 protein expression, assessed by immunohistochemistry, with ZAP70 messenger RNA (mRNA) transcript expression, assessed by semi-quantitative real-time reverse transcriptase-polymerase chain reaction assay, with the somatic mutation status of the IGHV genes in previously untreated patients with chronic lymphocytic leukemia.

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  • [Cites] Cytometry B Clin Cytom. 2006 Jul 15;70(4):227-34 [16342060.001]
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  • (PMID = 20657554.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA123252-01; United States / NCI NIH HHS / CA / R01 CA123252; United States / NCI NIH HHS / CA / 5R01CA123252-3; United States / NCI NIH HHS / CA / R01 CA123252-01
  • [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 / Biomarkers, Tumor; 0 / RNA, Messenger; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
  • [Other-IDs] NLM/ NIHMS217756; NLM/ PMC2966512
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3. Pagano-Therrien J, Santacroce SJ: Bone mineral density decrements and children diagnosed with cancer. J Pediatr Oncol Nurs; 2005 Nov-Dec;22(6):328-38
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  • This integrative literature review is focused on (1) the prevalence of bone mineral density (BMD) decrements in children treated for acute lymphoblastic leukemia (ALL), and when these decrements are observed;.
  • The etiology of BMD decrements can be attributed to multiple factors including genetic endowment, lifestyle behaviors, the leukemia disease process, and treatment exposures especially to corticosteroids and cranial radiotherapy.
  • The role of pediatric oncology nurses in the management of bone disease in children with cancer across the illness trajectory is discussed.
  • [MeSH-major] Bone Density. Osteoporosis / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Survivors

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  • (PMID = 16216895.001).
  • [ISSN] 1043-4542
  • [Journal-full-title] Journal of pediatric oncology nursing : official journal of the Association of Pediatric Oncology Nurses
  • [ISO-abbreviation] J Pediatr Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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4. Xu YZ, Lou SF, Deng YJ: [Biodistribution study of 131I-gM-CSF in SCID mice bearing human leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 Oct;27(10):678-81
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  • [Title] [Biodistribution study of 131I-gM-CSF in SCID mice bearing human leukemia].
  • METHODS: The xenograft model of human leukemia was established in SCID mice.
  • In the leukemia mice, the biodistribution of 131I-GM-CSF produced by chlo amine-T method was studied.
  • RESULTS: (1)The inoculated HL-60 cells could grow in SCID mice, which developed leukemia after 4 weeks. (2) 131 I-GM-CSF was concentrated in spleen, bone marrow and tumor tissue of the mice.
  • CONCLUSIONS: 131 I-GM-CSF is able to concentrate electively in spleen, bone marrow and organs infiltrated by leukemia cells.
  • The biodistribution of 131I-GM-CSF in the leukemia mice is tissue specific.
  • [MeSH-major] Granulocyte-Macrophage Colony-Stimulating Factor / pharmacokinetics. Leukemia, Myeloid, Acute / metabolism

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  • (PMID = 17343200.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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5. Higuchi M, Nishinaka H, Yamano Y: [A case of chronic myeloid leukemia following TS-1 therapy for advanced gastric cancer]. Gan To Kagaku Ryoho; 2006 Dec;33(13):2049-52
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  • [Title] [A case of chronic myeloid leukemia following TS-1 therapy for advanced gastric cancer].
  • On the basis of these findings, the chronic phase of secondary chronic myeloid leukemia (CML) was diagnosed.
  • Although CML is rare in secondary leukemia, this is, to our knowledge, the first reported case of therapy-related CML following TS-1 treatment.
  • The present case suggested that imatinib therapy was also effective for secondary CML as well as de novo CML.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / etiology. Neoplasms, Second Primary / etiology. Oxonic Acid / adverse effects. Stomach Neoplasms / drug therapy. Tegafur / adverse effects

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  • (PMID = 17197751.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Drug Combinations; 0 / Piperazines; 0 / Pyrimidines; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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6. Karremann M, von Komorowski G, Neumaier-Probst E, Dürken M: [Hemiparesis in acute lymphoblastic leukemia]. Radiologe; 2010 Aug;50(8):706-10
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  • [Title] [Hemiparesis in acute lymphoblastic leukemia].
  • The case of an adolescent female patient with acute lymphoblastic leukemia and stroke-like hemiparesis demonstrates a typical manifestation of methotrexate-induced acute encephalopathy.
  • Diagnosis can confidently be made using cerebral MRI including diffusion-weighted imaging (DWI), so that patients can be informed about the favorable prognosis.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Methotrexate / adverse effects. Neurotoxicity Syndromes / diagnosis. Paresis / chemically induced. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 20652214.001).
  • [ISSN] 1432-2102
  • [Journal-full-title] Der Radiologe
  • [ISO-abbreviation] Radiologe
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; YL5FZ2Y5U1 / Methotrexate
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7. Sturm I, Oertel J, Oertel S, Westermann J, Pezzutto A: Successful long-term monotherapy with rituximab in a patient with chronic lymphocytic leukemia of the B-cell-lineage: a case report. J Med Case Rep; 2008;2:275
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  • [Title] Successful long-term monotherapy with rituximab in a patient with chronic lymphocytic leukemia of the B-cell-lineage: a case report.
  • INTRODUCTION: Treatment of chronic lymphocytic leukemia of the B-cell-lineage is strongly based upon clinical staging because of the heterogeneous clinical course of this disease.
  • CASE PRESENTATION: We describe a 62-year-old patient with newly diagnosed chronic lymphocytic leukemia of the B-cell-lineage who did not respond to several chemotherapy regimens including chlorambucil, fludarabine and cyclophosphamide, developing a marked neutropenia and thrombocytopenia with life-threatening infections.
  • The patient was treated with 600 mg/m2 rituximab weekly followed by eight courses of biweekly therapy and then by long-term maintenance therapy, achieving almost complete remission of the symptoms and disease control.
  • CONCLUSION: After resistance to standard chemotherapy with chlorambucil and fludarabine, a patient with chronic lymphocytic leukemia of the B-cell-lineage was successfully treated with rituximab.

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  • (PMID = 18702813.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2531126
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8. Sperr WR, Drach J, Hauswirth AW, Ackermann J, Mitterbauer M, Mitterbauer G, Foedinger M, Fonatsch C, Simonitsch-Klupp I, Kalhs P, Valent P: Myelomastocytic leukemia: evidence for the origin of mast cells from the leukemic clone and eradication by allogeneic stem cell transplantation. Clin Cancer Res; 2005 Oct 1;11(19 Pt 1):6787-92
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  • [Title] Myelomastocytic leukemia: evidence for the origin of mast cells from the leukemic clone and eradication by allogeneic stem cell transplantation.
  • PURPOSE: Myelomastocytic leukemia is a term used for patients with advanced myeloid neoplasms, in whom elevated numbers of immature atypical mast cells are found, but criteria for a primary mast cell disease are not met.
  • PATIENT AND METHODS: We have analyzed clonality of mast cells in an 18-year-old patient suffering from acute myeloid leukemia with a complex karyotype including a t(8;21) and mastocytic transformation with a huge increase in immature mast cells and elevated serum tryptase level, but no evidence for a primary mast cell disease/mastocytosis.
  • Myeloablative stem cell transplantation resulted in complete remission with consecutive disappearance of AML1/ETO transcripts, decrease of serum tryptase to normal range, and disappearance of neoplastic mast cells.
  • CONCLUSION: These data suggest that mast cells directly derive from the leukemic clone in patients with myelomastocytic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Mast Cells / cytology. Stem Cell Transplantation / methods
  • [MeSH-minor] Adolescent. Antigens, CD2 / biosynthesis. Antigens, CD34 / biosynthesis. Biomarkers, Tumor. Bone Marrow Cells / metabolism. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Flow Cytometry. Granulocyte Precursor Cells / metabolism. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male. Proto-Oncogene Proteins c-kit / biosynthesis. Receptors, Interleukin-2 / biosynthesis. Serine Endopeptidases / blood. Serine Endopeptidases / metabolism. Translocation, Genetic. Transplantation, Homologous. Tryptases

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  • (PMID = 16203765.001).
  • [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] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD2; 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / Receptors, Interleukin-2; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases
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9. Yang JS, Wu CC, Kuo CL, Yeh CC, Chueh FS, Hsu CK, Wang CK, Chang CY, Ip SW, Hsu YM, Kuo WW, Chung JG: Solanum lyratum extract affected immune response in normal and leukemia murine animal in vivo. Hum Exp Toxicol; 2010 May;29(5):359-67
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  • [Title] Solanum lyratum extract affected immune response in normal and leukemia murine animal in vivo.
  • Our previous studies have shown that the crude extract of S. lyratum Thunberg (SLE) induced apoptosis in colo 205 human colon adenocarcinoma cells; however, there is no report to show SLE affect immune responses in vivo.
  • In this study, the in vivo effects of SLE on leukemia WEHI-3 cells and immune responses such as phagocytosis and natural killer (NK) cell activity in normal and leukemia mice were investigated.
  • The SLE treatment decreases surface markers of CD3 and Mac-3 in normal and leukemia mice but promoted the cell markers of CD19 and CD11b in normal mice and CD11b in leukemia mice indicating that the precursors of T cells was inhibited and B cells and macrophage were promoted.
  • The SLE treatment promoted the activity of macrophage phagocytosis in the peripheral blood mononuclear cells (PBMC) and peritoneal cells from normal and leukemia mice.
  • The results also showed that NK cells from the normal and leukemia mice after treatment with SLE can kill the YAC-1 target cells.
  • Therefore, the SLE treatment increased macrophage and NK cell activities.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Drugs, Chinese Herbal / pharmacology. Leukemia, Experimental / drug therapy. Plant Extracts / pharmacology. Solanum / chemistry
  • [MeSH-minor] Animals. Antigens, CD3 / metabolism. Antigens, Differentiation / metabolism. B-Lymphocytes / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Killer Cells, Natural / drug effects. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / physiology. Lymphocyte Activation / drug effects. Macrophages / drug effects. Macrophages / physiology. Macrophages, Peritoneal / drug effects. Macrophages, Peritoneal / physiology. Mice. Mice, Inbred BALB C. Phagocytosis / drug effects. Phagocytosis / physiology. Phytotherapy. Spleen / drug effects. Spleen / pathology. T-Lymphocytes / drug effects

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  • (PMID = 20197453.001).
  • [ISSN] 1477-0903
  • [Journal-full-title] Human & experimental toxicology
  • [ISO-abbreviation] Hum Exp Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antigens, Differentiation; 0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / Plant Extracts; 0 / monocyte-macrophage differentiation antigen
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10. Weinel S, Malone J, Jain D, Callen JP: Leukaemia cutis in a patient treated for breast cancer. Australas J Dermatol; 2009 Feb;50(1):52-5
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  • [Title] Leukaemia cutis in a patient treated for breast cancer.
  • Biopsy of the skin lesions revealed leukaemia cutis, which led to the discovery of acute myelogenous leukaemia.
  • Treatment included induction chemotherapy in preparation for a bone marrow transplant, which resulted in the disappearance of the cutaneous lesions.
  • However, the patient later succumbed to her leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms / drug therapy. Leukemia, Myeloid, Acute / chemically induced. Neoplasms, Second Primary / chemically induced

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  • (PMID = 19178494.001).
  • [ISSN] 1440-0960
  • [Journal-full-title] The Australasian journal of dermatology
  • [ISO-abbreviation] Australas. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
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11. Boatsman EE, Fu CH, Song SX, Moore TB: Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation. J Pediatr Hematol Oncol; 2010 Mar;32(2):e57-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation.
  • INTRODUCTION: Infant acute lymphoblastic leukemia (ALL) is considered a high-risk entity.
  • By morphology, infant ALL is classified as a lymphoid lineage leukemia; however, its physiologic behavior has brought many to consider it a pathologic hybrid between lymphoid leukemia and myeloid leukemias.
  • As such, standard of care currently employs the use of chemotherapeutic agents used commonly in ALL protocols and agents typically reserved for the treatment of myelogenous lineage leukemias.
  • The role of hematopoietic stem cell transplantation and graft-versus-leukemia effect in these patients has not been well studied.
  • CASE PRESENTATION: An earlier healthy 9-week-old Hispanic male diagnosed with precursor B-cell lymphoblastic leukemia was treated with protocol P9407 and matched sibling hematopoietic stem cell transplantation.
  • Relapse was noted on posttransplant day +114 with blasts on peripheral blood smear.
  • The sole antigraft-versus-host disease (GVHD) agent, cyclosporine, was discontinued.
  • Blast clearance from the peripheral blood was obtained by posttransplant day +128 with the appearance of skin and liver GVHD at posttransplant day +181.
  • He remains disease free more than 2 years posttransplant.
  • CONCLUSION: Traditionally, graft-versus-leukemia effect was thought to contribute therapeutically little to the treatment of ALL by hematopoietic stem cell transplantation (HSCT).
  • The effects of graft-versus-leukemia immunologic phenomenon in our patient with infant acute lymphoblastic leukemia underscore the potential that infant ALL may not be entirely the same biologic entity as standard pediatric ALL and may be more responsive than understood earlier.
  • Therapeutic response and appearance of GVHD after the withdrawal of immunosuppression in this patient provides evidence that graft-versus-leukemia effect may play a role in disease control in infant ALL after HSCT.
  • This suggests that other immunotherapeutic interventions in the context of relapse may offer potential clinical benefit in this disease.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20168246.001).
  • [ISSN] 1536-3678
  • [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
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12. Zhang WG, Liu SH, Cao XM, Cheng YX, Ma XR, Yang Y, Wang YL: A phase-I clinical trial of active immunotherapy for acute leukemia using inactivated autologous leukemia cells mixed with IL-2, GM-CSF, and IL-6. Leuk Res; 2005 Jan;29(1):3-9
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  • [Title] A phase-I clinical trial of active immunotherapy for acute leukemia using inactivated autologous leukemia cells mixed with IL-2, GM-CSF, and IL-6.
  • We evaluated the efficacy and toxicity of vaccination in 29 patients with relapsed or refractory acute leukemia using inactivated autologous leukemia cells combined with interleukin-2 (IL-2), granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-6.
  • MHC-I, MHC-II, and B7-1 expression status on the surface of leukemia cells and the cytokine profile of IFN-gamma and IL-10 in serum before and after vaccination was detected.
  • RESULTS: Five achieved a complete remission (CR) and six a partial remission (PR) in this vaccination procedure.
  • The expression of MHC-I and MHC-II on leukemia cells was 100% and 90% positive, respectively.
  • The efficacy of the vaccine was statistically associated with the expression status of B7-1 on leukemia cells (P < 0.01).
  • The serum level of IL-10 reduced significantly in the five patients who achieved complete remission (CR) after vaccination as compared with when they were originally diagnosed (P < 0.01).
  • CONCLUSION: We presented here a promising immunotherapy in the treatment of acute leukemia, especially for F.A.B. M5.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Interleukin-2 / administration & dosage. Interleukin-6 / administration & dosage. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Female. Fever / etiology. Humans. Male. Middle Aged. Skin / drug effects

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  • (PMID = 15541469.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Interleukin-2; 0 / Interleukin-6; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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13. Ma XX, Wang C, Wei J, Qin YW, Yan SK, Gao YR, Cai Q: [Inhibitory effect of RNA interference on chronic myeloid leukemia bcr/abl oncogene expression]. Zhonghua Xue Ye Xue Za Zhi; 2005 Jun;26(6):359-62
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  • [Title] [Inhibitory effect of RNA interference on chronic myeloid leukemia bcr/abl oncogene expression].
  • OBJECTIVE: To investigate the inhibitory effect of RNA interference on chronic myeloid leukemia (CML) bcr/abl oncogene expression.
  • K562 cells stably expressing bcr/abl gene were transfected with the siRNA by electroporation, both the non-transfected cells and non-specific siRNAs transfected cells were taken as controls.
  • Cell proliferation was measured by MTT assay and apoptosis by Annexin V-FITC assay.
  • The synthesized siRNAs inhibited CML bcr/abl oncogene expression at both mRNA and protein levels. siRNAs could inhibit K562 cell proliferation to 47% and 56% at 24 h and 48 h after transfection, respectively, and induce cell apoptosis from 1.00% in control group to 15.05% and 19.4% at 24 h and 48 h respectively.
  • CONCLUSION: At the cell level, inhibition of CML bcr/abl oncogene expression by chemically synthesized siRNAs provides the new method for anti-leukemia study.
  • [MeSH-minor] Apoptosis / genetics. Cell Proliferation. Humans. K562 Cells. Transfection

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  • (PMID = 16185484.001).
  • [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 / RNA, Small Interfering; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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14. Savchenko VG, Liubimova LS, Parovichnikova EN, Mendeleeva LP, Mamotiuk KS, Demidova IA, Gribanova EO, Gal'tseva IV, Pokrovskaia OS, Kuz'mina LA, Zhelnova EI, Kliasova GA, Glasko EN, Kaplanskaia IB, Poreshina LP, Kut'ina RM, Shpakova AP, Shtareva EM, Varlamova SV, Kalinin NN: [Transplantations of allogenic and autologous hemopoietic stem cells in acute leukemia (results of 20-year experience)]. Ter Arkh; 2007;79(7):30-5
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  • [Title] [Transplantations of allogenic and autologous hemopoietic stem cells in acute leukemia (results of 20-year experience)].
  • AIM: To analyse results of transplantation of allogenic and autologous hemopoietic stem cells (allo-THSC and auto-THSC) with myeloablation preconditioning in patients with acute leukemia (AL) performed in 1987-2006.
  • Auto-THSC in 15 patients was for the first time followed by immunomodulating therapy aimed at prevention of AL relapses: in acute myeloid leukemia ATRA in combination with alpha-interferon, in acute lymphoblastic leukemia (ALL)--ronkoleukin, interleukin-2 preparation.
  • Results of allo-THSC conducted in the first complete remission were much better than in patients with other AL stages at the time of THSC.
  • Outcomes of allo-THSC performed in the first complete remission are much higher.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / mortality. Leukemia, Myeloid / surgery
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Female. Humans. Immunotherapy. Male. Survival Analysis. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 17802787.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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15. Kim JS, Eom JI, Cheong JW, Choi AJ, Lee JK, Yang WI, Min YH: Protein kinase CK2alpha as an unfavorable prognostic marker and novel therapeutic target in acute myeloid leukemia. Clin Cancer Res; 2007 Feb 1;13(3):1019-28
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  • [Title] Protein kinase CK2alpha as an unfavorable prognostic marker and novel therapeutic target in acute myeloid leukemia.
  • However, the clinical and biological significances of CK2 have not been elucidated in acute myeloid leukemia (AML).
  • EXPERIMENTAL DESIGN: We evaluated the biological significances of catalytic subunit of CK2 (CK2alpha) expression in leukemia cell lines and primary leukemic blasts obtained from AML patients.
  • In AML patients with normal karyotype, the disease-free survival and overall survival rates were significantly lower in the CK2alpha-high compared with the CK2alpha-low AML cases (P=0.0252 and P=0.0392, respectively).
  • Treatment of U937 cell line and primary AML blasts with selective CK2 inhibitor, tetrabromobenzotriazole or apigenin, reduced the levels of these molecules in a dose-dependent manner.
  • Apigenin-induced cell death was preferentially observed in the CK2alpha-high leukemia cell lines, HL-60 and NB4, which was accompanied by cytoplasmic release of SMAC/DIABLO and proteolytic cleavage of procaspase-9, procaspase-3, procaspase-8, and poly(ADP)ribose polymerase.
  • An induced overexpression of CK2alpha potentially enhanced the sensitivity of U937 cells to the apigenin-induced cell death.
  • Apigenin-induced cell death was significantly higher in CK2alpha-high AML compared with CK2alpha-low AML (P<0.0001) or normal bone marrow samples (P<0.0001).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Casein Kinase II / physiology. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / drug therapy. Prognosis
  • [MeSH-minor] Adolescent. Adult. Aged. Apigenin / pharmacology. Caspases / metabolism. Catalytic Domain. Cell Line, Tumor. Disease-Free Survival. Female. Humans. Karyotyping. Male. Middle Aged. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-bcl-2 / metabolism. U937 Cells


16. Cervantes F: [Chronic myeloid leukemia 2008]. Med Clin (Barc); 2008 Nov 15;131(17):658-9
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  • [Title] [Chronic myeloid leukemia 2008].
  • [Transliterated title] Leucemia mieloide crónica.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 19087793.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] Comparative Study; Editorial; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
  • [Number-of-references] 19
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17. Robak T: Current treatment options in hairy cell leukemia and hairy cell leukemia variant. Cancer Treat Rev; 2006 Aug;32(5):365-76
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  • [Title] Current treatment options in hairy cell leukemia and hairy cell leukemia variant.
  • Hairy cell leukemia (HCL) is a chronic B-cell lymphoproliferative disorder characterized by splenomegaly, pancytopenia and circulating lymphocytes displaying prominent cytoplasmic projections.
  • HCL has usually an indolent course and the patients with asymptomatic disease do not require therapy.
  • Treatment of progressive symptomatic HCL includes a variety of pharmacological approaches such as interferon-alpha (IFN-alpha), pentostatin (DCF) and cladribine (2-CdA), which have significantly improved the disease prognosis.
  • More recently high activity of anti-CD20 monoclonal antibody (rituximab) and anti-CD25 (LMB-2) and anti-CD22 (BL-22) immunotoxins have increased the number of therapeutic options for HCL.
  • However, preliminary observations suggest that monoclonal antibodies - rituximab and BL-22 immunotoxin are highly active in this disorder even refractory to 2-CdA.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Hairy Cell / therapy

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  • (PMID = 16781083.001).
  • [ISSN] 0305-7372
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / Immunotoxins
  • [Number-of-references] 119
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18. Larson RA: Three new drugs for acute lymphoblastic leukemia: nelarabine, clofarabine, and forodesine. Semin Oncol; 2007 Dec;34(6 Suppl 5):S13-20
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  • [Title] Three new drugs for acute lymphoblastic leukemia: nelarabine, clofarabine, and forodesine.
  • The search for more effective and safer anti-leukemia therapies has led to the identification of several new agents that show activity against specific types of acute lymphoblastic leukemia (ALL).
  • Of these, nelarabine has shown clinically meaningful benefit in patients with T-cell ALL, with overall response rates ranging from 33% to 60%, the induction of durable complete remissions, and an overall 1-year survival rate of 28% in adults.
  • Clofarabine has also shown promising clinical activity in pediatric patients, with an overall response rate of 30%, and some patients are able to proceed to allogeneic hematopoietic cell transplantation.
  • Forodesine is the most recent novel agent, with a unique mechanism that has shown single-agent activity in relapsed and refractory T- and B-cell leukemias and cutaneous lymphomas.
  • The rationale, pharmacology, and clinical experience to date with these agents in the treatment of patients with refractory acute leukemia are reviewed, with a highlight on ALL.
  • [MeSH-major] Adenine Nucleotides / pharmacology. Antineoplastic Agents / pharmacology. Arabinonucleosides / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Purine Nucleosides / pharmacology. Purine-Nucleoside Phosphorylase / drug effects. Pyrimidinones / pharmacology

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  • (PMID = 18086342.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 0 / Purine Nucleosides; 0 / Pyrimidinones; 426X066ELK / forodesine; 60158CV180 / nelarabine; 762RDY0Y2H / clofarabine; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase
  • [Number-of-references] 41
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19. Han TH, Tang Y, Park YH, Maynard J, Li P, Akbulut H, Petersen L, Deisseroth A: Vector prime protein boost vaccination in the setting of myeloablative-induced lymphopenia suppresses growth of leukemia and solid tumors. Bone Marrow Transplant; 2010 Mar;45(3):550-7
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  • [Title] Vector prime protein boost vaccination in the setting of myeloablative-induced lymphopenia suppresses growth of leukemia and solid tumors.
  • We have developed a vaccine, which is designed to induce tumor-associated antigen (TAA)-specific T cells and antibodies in the setting of profound lymphopenia induced by myeloablative therapy and T-cell-depleted bone marrow transplantation.
  • Test mice were injected subcutaneously (sc) with the 32DP210Bcr-Abl cell line, which is positive for the p210Bcr-Abl protein (Group 1).
  • In Group 2, 7 days after injection of the 32DP210Bcr-Abl positive cell line, the mice received 900 cGy total body irradiation (TBI) followed in 1 h by the intravenous infusion of 10 million T-cell-depleted syngeneic bone marrow cells (TCDBMT) (Group 2).
  • The leukemia-bearing group received an intravenous injection of 10 million spleen cells (donor lymphocyte infusions) from unvaccinated (Group 3) and TAA/ecdCD40L-vaccinated (Group 4) syngeneic mice 3 days after completion of the TBI and TCDBMT.
  • Vaccinated mice from Group 4, which developed complete responses, survived up to 350 days post-injection of the leukemia cells without any evidence of leukemia regrowth.
  • [MeSH-major] Cancer Vaccines / administration & dosage. Leukemia, Experimental / therapy. Neoplasms, Experimental / therapy
  • [MeSH-minor] Amino Acid Sequence. Animals. Antigens, Neoplasm / administration & dosage. Antigens, Neoplasm / genetics. Base Sequence. Bone Marrow Transplantation. CD40 Ligand / administration & dosage. CD40 Ligand / genetics. Cell Line, Tumor. DNA Primers / genetics. Genes, abl. Immunization, Secondary. Lymphocyte Depletion. Lymphopenia / etiology. Lymphopenia / immunology. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. Molecular Sequence Data. Recombinant Fusion Proteins / administration & dosage. Recombinant Fusion Proteins / genetics. Whole-Body Irradiation

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  • (PMID = 19648971.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / DNA Primers; 0 / Recombinant Fusion Proteins; 147205-72-9 / CD40 Ligand
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20. Miller CP, Rudra S, Keating MJ, Wierda WG, Palladino M, Chandra J: Caspase-8 dependent histone acetylation by a novel proteasome inhibitor, NPI-0052: a mechanism for synergy in leukemia cells. Blood; 2009 Apr 30;113(18):4289-99
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  • [Title] Caspase-8 dependent histone acetylation by a novel proteasome inhibitor, NPI-0052: a mechanism for synergy in leukemia cells.
  • Our previous work found that a novel proteasome inhibitor, NPI-0052, and HDACi synergistically induce apoptosis in leukemia cells in a caspase-8- and oxidant-dependent manner.
  • Here we extend those observations to primary leukemia cells and identify novel mechanisms of synergy.
  • Overall, our results suggest that crosstalk by NPI-0052 and HDACi are contributing, along with caspase-8 activation and oxidative stress, to their synergistic cytotoxic effects in leukemia cells, reinforcing the potential clinical utility of combining these 2 agents.
  • [MeSH-major] Caspase 8 / metabolism. Histone Deacetylase Inhibitors. Lactones / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Protease Inhibitors / pharmacology. Proteasome Inhibitors. Pyrroles / pharmacology

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  • (PMID = 19182209.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / F31 CA123645; United States / NCI NIH HHS / CA / R01 CA115811
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Boronic Acids; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Lactones; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Pyrroles; 0 / RNA, Messenger; 11062-77-4 / Superoxides; 58IFB293JI / vorinostat; 69G8BD63PP / Bortezomib; 703P9YDP7F / marizomib; EC 3.4.22.- / Caspase 8; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC2676087
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21. Quintás-Cardama A, Cortes J: Omacetaxine mepesuccinate--a semisynthetic formulation of the natural antitumoral alkaloid homoharringtonine, for chronic myelocytic leukemia and other myeloid malignancies. IDrugs; 2008 May;11(5):356-72
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  • [Title] Omacetaxine mepesuccinate--a semisynthetic formulation of the natural antitumoral alkaloid homoharringtonine, for chronic myelocytic leukemia and other myeloid malignancies.
  • ChemGenex Pharmaceuticals Ltd, in collaboration with Stragen Group, is developing omacetaxine mepesuccinate, a semisynthetic formulation of HHT, as a potential treatment for chronic myelocytic leukemia (CML), myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).
  • In preclinical studies, omacetaxine mepesuccinate induced apoptosis in leukemia cell lines.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Harringtonines / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


22. Moretta A, Pende D, Locatelli F, Moretta L: Activating and inhibitory killer immunoglobulin-like receptors (KIR) in haploidentical haemopoietic stem cell transplantation to cure high-risk leukaemias. Clin Exp Immunol; 2009 Sep;157(3):325-31
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  • [Title] Activating and inhibitory killer immunoglobulin-like receptors (KIR) in haploidentical haemopoietic stem cell transplantation to cure high-risk leukaemias.
  • Clinical data from haploidentical haematopoietic stem cell transplantation (haplo-HSCT) revealed that NK cells were responsible for remarkably favourable effects in both adult and paediatric high-risk leukaemias.
  • NK receptors specific for major histocompatibility complex (MHC) class I molecules, including killer immunoglobulin (Ig)-like receptors (KIR) and CD94/NKG2A, play a major role in the anti-leukaemia effect (mediating either inhibitory or activating signals).
  • Haplo- HSCT requires a heavy conditioning regimen for the patient and the use of large numbers of T cell-depleted HSC to be grafted.
  • After transplantation, natural killer cells develop from HSC shortly after engraftment and may include 'alloreactive' NK cells that kill leukaemic cells and prevent graft-versus-host disease (GvHD).
  • Their generation is dependent upon the existence of a KIR/HLA class I mismatch between donor and recipient.
  • Novel important information on the function and specificity of different KIR has been obtained recently by the analysis of donor-derived alloreactive NK cells in a cohort of paediatric patients given haplo-HSCT to cure acute, high-risk leukaemias.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / metabolism. Leukemia / surgery. Receptors, KIR / metabolism

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  • (PMID = 19664139.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Receptors, KIR
  • [Number-of-references] 74
  • [Other-IDs] NLM/ PMC2745025
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23. Heesch S, Goekbuget N, Stroux A, Tanchez JO, Schlee C, Burmeister T, Schwartz S, Blau O, Keilholz U, Busse A, Hoelzer D, Thiel E, Hofmann WK, Baldus CD: Prognostic implications of mutations and expression of the Wilms tumor 1 (WT1) gene in adult acute T-lymphoblastic leukemia. Haematologica; 2010 Jun;95(6):942-9
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  • [Title] Prognostic implications of mutations and expression of the Wilms tumor 1 (WT1) gene in adult acute T-lymphoblastic leukemia.
  • BACKGROUND: The role of the Wilms tumor 1 gene (WT1) in acute leukemias has been underscored by mutations found in acute myeloid leukemia identifying patients with inferior survival.
  • Furthermore, aberrant expression of WT1 in acute myeloid leukemia was associated with an increased risk of relapse.
  • No larger studies have performed a combined approach including WT1 mutation and expression analyses in acute T-lymphoblastic leukemia.
  • DESIGN AND METHODS: We analyzed the WT1 mutations and the expression status in a total of 252 consecutive adult patients with newly diagnosed T-lymphoblastic leukemia, who were registered on the GMALL 06/99 and 07/03 protocols and had sufficient material available.
  • The GMALL protocols included intensive chemotherapy as well as stem cell transplantation according to a risk-based model with indication for stem cell transplantation in first complete remission for early and mature T-lymphoblastic leukemia patients; patients with thymic T-lymphoblastic leukemia were allocated to a standard risk group and treated with intensive chemotherapy.
  • In thymic T-lymphoblastic leukemia, WT1mut patients had an inferior relapse-free survival compared to WT1 wild-type patients.
  • T-lymphoblastic leukemia patients with aberrant WT1 expression (high or negative) showed a higher relapse rate and an inferior outcome compared to patients with intermediate WT1 expression.
  • In the standard risk group of thymic T-lymphoblastic leukemia, aberrant WT1 expression was predictive for an inferior relapse-free survival as compared to patients with intermediate expression.
  • CONCLUSIONS: WT1 mutations were associated with an inferior relapse-free survival in standard risk thymic T-lymphoblastic leukemia patients.
  • Moreover, altered expression associated with inferior outcome also suggests a role of WT1 in T-lymphoblastic leukemia and the potential use of molecularly-based treatment stratification to improve outcome.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, Wilms Tumor / physiology. Mutation / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20435628.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2878792
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24. Nakahashi H, Tsukamoto N, Hashimoto Y, Koiso H, Yokohama A, Saitoh T, Uchiumi H, Handa H, Murakami H, Nojima Y, Karasawa M: Characterization of immunoglobulin heavy and light chain gene expression in chronic lymphocytic leukemia and related disorders. Cancer Sci; 2009 Apr;100(4):671-7
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  • [Title] Characterization of immunoglobulin heavy and light chain gene expression in chronic lymphocytic leukemia and related disorders.
  • The incidence of chronic lymphocytic leukemia is low in the Japanese population compared with populations in western countries, suggesting a role for genetic factors in the occurrence of this disease.
  • We have previously shown that chronic lymphocytic leukemia in Japan rarely expresses the immunoglobulin heavy chain variable region (IGHV) 1-69 gene (1 out of 43 patients, 2.3%), which is a gene most commonly expressed in chronic lymphocytic leukemia cases from western countries.
  • In the current study, we extended the previous study by examining immunoglobulin heavy chain and light chain gene expression in 80 Japanese patients with chronic lymphocytic leukemia and in 52 Japanese patients with other leukemic chronic lymphoproliferative disorders.
  • IGHV1-69 gene expression was again quite low in our cohort, found in only two patients: one with chronic lymphocytic leukemia and the other with splenic marginal zone lymphoma.
  • The IGHV4-34 gene was most frequently expressed in chronic lymphocytic leukemia (27.5%), whereas it was rarely found in leukemic chronic lymphoproliferative disorders (7.7%, P = 0.005).
  • There was also a significant difference in the expression of IGLV3-21 between chronic lymphocytic leukemia and leukemic chronic lymphoproliferative disorders (29.4 vs 4.8%, P = 0.018).
  • The IGLV3-21 gene in the majority of chronic lymphocytic leukemia cases was associated with homologous complementarity determining region 3 sequences.
  • Recent studies identified subsets of cases expressing almost identical B-cell receptors.
  • We found that two patients with chronic lymphocytic leukemia and the patient with splenic marginal zone lymphoma expressed IGHV4-39/IGKV1-39 and IGHV1-69/IGKV3-20, respectively, which belong to these subsets.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Immunoglobulin Light Chains / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoproliferative Disorders / genetics

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  • (PMID = 19220298.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD5; 0 / CCND1 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Light Chains; 0 / Immunoglobulin Variable Region; 0 / Receptors, IgE; 136601-57-5 / Cyclin D1
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25. Lee C, Lin Y, Huang M, Lin C, Liu C, Chow J, Liu HE: Increased cellular glutathione and protection by bone marrow stromal cells account for the resistance of non-acute promylocytic leukemia acute myeloid leukemia cells to arsenic trioxide in vivo. Leuk Lymphoma; 2006 Mar;47(3):521-9
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  • [Title] Increased cellular glutathione and protection by bone marrow stromal cells account for the resistance of non-acute promylocytic leukemia acute myeloid leukemia cells to arsenic trioxide in vivo.
  • Arsenic trioxide (ATO) is a novel agent for acute promylocytic leukemia (APL).
  • Studies performed in vitro have demonstrated that ATO also induces cell-cycle arrest and apoptosis in multiple cancers, including non-APL acute myeloid leukemia (AML).
  • To explore the potential use of ATO on non-APL AML, we treated the leukemic cells in vivo using a NOD/SCID animal model.
  • Mice harboring HL-60 or NB-4 leukemia or primary AML-M2 cells were treated daily with 5 mug/g ATO intraperitoneally for a maximum of 6 weeks.
  • Therefore, our study suggests that strategies to inhibit the compensatory increase of glutathione and block the interaction between leukemic cells and BM stromal cells should be employed before applying ATO to non-APL hematologic malignancies.
  • [MeSH-major] Arsenicals / administration & dosage. Bone Marrow Cells / drug effects. Drug Resistance, Neoplasm. Glutathione / metabolism. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology. Oxides / administration & dosage. Stromal Cells / drug effects
  • [MeSH-minor] Acute Disease. Animals. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacology. Buthionine Sulfoximine / pharmacology. Cell Count. Cell Line, Tumor. Coculture Techniques. Disease Models, Animal. Humans. Injections, Intraperitoneal. Mice. Mice, Inbred NOD. Mice, SCID. Treatment Failure


26. Yao J, Zhang XB, Zhang XL, Fu WL: Methylation status of oestrogen receptor alpha-A: a predictor of prognosis in leukaemias. Biosci Rep; 2010 Aug;30(4):217-22
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  • [Title] Methylation status of oestrogen receptor alpha-A: a predictor of prognosis in leukaemias.
  • Many studies have shown that epigenetic regulation of ERs (oestrogen receptors) plays a key role in the pathogenesis of leukaemia.
  • In the present study, it was found that the methylated status of ERalpha-A might serve as an epigenetic biomarker of leukaemias.
  • In this study, the protein expression and cell apoptosis, cycle, proliferation and viability with and without 5-aza-dC (5-aza-2'-deoxycytidine) were evaluated with Western blotting, 3H-TdR (3H-thymidine) incorporation, propidium iodide staining and Trypan Blue staining respectively.
  • The protein expression of ERalpha was significantly enhanced in all leukaemic cell lines using treatment with the DNA demethylation reagent 5-aza-dC.
  • And with 5-aza-dC, cell apoptosis, cell cycle, cell proliferation and viability were all inhibited significantly.
  • We also tracked 40 cases of leukaemias with ERalpha-A methylation (95%; 38 of 40) to observe the prognosis 1 year after chemotherapy treatment.
  • This result suggested that ERalpha plays a significant role in leukaemogenesis, and the methylated status of ERalpha-A not only might serve as an epigenetic biomarker of leukaemias for diagnosis, but also has the potential to serve as a predictor of prognosis in leukaemias.
  • [MeSH-major] Estrogen Receptor alpha / metabolism. Leukemia / metabolism
  • [MeSH-minor] Adult. Cell Line, Tumor. Cell Proliferation. Female. Humans. Male. Methylation. Prognosis

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  • (PMID = 19555348.001).
  • [ISSN] 1573-4935
  • [Journal-full-title] Bioscience reports
  • [ISO-abbreviation] Biosci. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha
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27. Paquette RL, Nicoll J, Chalukya M, Gondek L, Jasek M, Sawyers CL, Shah NP, Maciejewski J: Clonal hematopoiesis in Philadelphia chromosome-negative bone marrow cells of chronic myeloid leukemia patients receiving dasatinib. Leuk Res; 2010 Jun;34(6):708-13
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  • [Title] Clonal hematopoiesis in Philadelphia chromosome-negative bone marrow cells of chronic myeloid leukemia patients receiving dasatinib.
  • A clonal cytogenetic abnormality was observed in Philadelphia chromosome-negative bone marrow cells of 6/27 chronic myeloid leukemia patients (+8 in 4, -7 in 1, and 20q- in 1) with dasatinib-induced remissions.
  • The TP53 gene had a 5' splice site deletion of exon 6 that caused alternative splicing, frame shifting and introduction of a premature stop codon.
  • After three years, no patient developed myelodysplastic syndrome or acute myeloid leukemia.
  • [MeSH-major] Bone Marrow Cells / physiology. Clone Cells / pathology. Hematopoiesis / physiology. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / drug therapy. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / physiopathology. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Base Sequence. Cell Differentiation / drug effects. Cell Differentiation / genetics. Cytogenetic Analysis. Dasatinib. Female. Follow-Up Studies. Genes, p53. Humans. Male. Middle Aged. Molecular Sequence Data. Philadelphia Chromosome. Treatment Outcome

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19804904.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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28. MacMillan ML, Davies SM, Nelson GO, Chitphakdithai P, Confer DL, King RJ, Kernan NA: Twenty years of unrelated donor bone marrow transplantation for pediatric acute leukemia facilitated by the National Marrow Donor Program. Biol Blood Marrow Transplant; 2008 Sep;14(9 Suppl):16-22
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  • [Title] Twenty years of unrelated donor bone marrow transplantation for pediatric acute leukemia facilitated by the National Marrow Donor Program.
  • The National Marrow Donor Program (NMDP) has facilitated unrelated donor hematopoietic cell transplants for more than 20 years.
  • Availability of banked unrelated donor cord blood (incorporated into the NMDP registry in 2000) as a source of stem cells has become an important option for children with leukemia, offering the advantages of immediate availability for children with high-risk disease, the need for a lesser degree of HLA match, and expanding access for those with infrequent HLA haplotypes.
  • Overall survival (OS) in children with acute leukemia transplanted with unrelated donor bone marrow (BM) is markedly better in more recent years, largely attributable to less treatment-related mortality (TRM).
  • Within this cohort, 2-year survival was markedly better for patients with acute lymphoblastic leukemia (ALL) in first complete response (CR1) (74%) versus second complete response (CR2) (62%) or more advanced disease (33%).
  • Notably, this improvement over time was not observed in unmodified peripheral blood stem cell (PBSC) recipients, suggesting unmodified PBSC may not be the optimal stem cell source for children.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. National Health Programs

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  • (PMID = 18721776.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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29. Kitazawa S, Kitazawa R, Kondo T, Mori K, Matsui T, Watanabe H, Watanabe M: Fatal cardiac tamponade due to coronary sinus thrombosis in acute lymphoblastic leukaemia: a case report. Cases J; 2009;2:9095
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  • [Title] Fatal cardiac tamponade due to coronary sinus thrombosis in acute lymphoblastic leukaemia: a case report.
  • An 83-year-old man was admitted to the hospital complaining of general fatigue.
  • Laboratory examination revealed marked increase of atypical lymphoblastic cells in peripheral blood.
  • CHOP therapy was started under the diagnosis of acute lymphoblastic leukemia.
  • A condition similar to leukemia-related venous thromboembolic disease, combined with endothelial damage induced by leukemic infiltration, may cause this rare complication.

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  • [Cites] Cancer Invest. 2009;27 Suppl 1:63-74 [19291526.001]
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  • (PMID = 20062732.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2803892
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30. Fink SR, Paternoster SF, Smoley SA, Flynn HC, Geyer SM, Shanafelt TD, Lee YK, Jelinek DF, Kay NE, Dewald GW: Fluorescent-labeled DNA probes applied to novel biological aspects of B-cell chronic lymphocytic leukemia. Leuk Res; 2005 Mar;29(3):253-62
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  • [Title] Fluorescent-labeled DNA probes applied to novel biological aspects of B-cell chronic lymphocytic leukemia.
  • Fluorescent-labeled DNA probes were used to study 52 chronic lymphocytic leukemia (B-CLL) patients for (1) disease progression, (2) angiogenesis genes, (3) T-cell leukemia 1 gene (TCL1), (4) immunoglobulin heavy chain variable region (IGHv) and (5) chromosome 6q.
  • Compared to stable disease, more patients with progressive disease had > or =2 anomalies and a high percentage of neoplastic nuclei.
  • [MeSH-major] Chromosome Aberrations. DNA Probes. Leukemia, Lymphocytic, Chronic, B-Cell / classification. Leukemia, Lymphocytic, Chronic, B-Cell / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Fibroblast Growth Factor 2 / genetics. Genes, Immunoglobulin. Humans. Immunoglobulin Variable Region / genetics. In Situ Hybridization, Fluorescence. Interleukin-4 / genetics. Male. Middle Aged. Neovascularization, Pathologic / genetics. Prognosis. Proto-Oncogene Proteins / genetics. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 15661260.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 91542; United States / NCI NIH HHS / CA / CA 95241-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Probes; 0 / Immunoglobulin Variable Region; 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 207137-56-2 / Interleukin-4
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31. Weisberg E, Wright RD, McMillin DW, Mitsiades C, Ray A, Barrett R, Adamia S, Stone R, Galinsky I, Kung AL, Griffin JD: Stromal-mediated protection of tyrosine kinase inhibitor-treated BCR-ABL-expressing leukemia cells. Mol Cancer Ther; 2008 May;7(5):1121-9
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  • [Title] Stromal-mediated protection of tyrosine kinase inhibitor-treated BCR-ABL-expressing leukemia cells.
  • Clinical studies of patients with chronic myeloid leukemia revealed that a common pattern of response is a dramatic fall in the circulating population of blast cells, with a minimal or delayed decrease in marrow blasts, suggesting a protective environment.
  • Here, we present an in vivo system for monitoring relative tumor accumulation in leukemic mice and residual disease in leukemic mice treated with a tyrosine kinase inhibitor and an in vitro system for identifying integral factors involved in stromal-mediated cytoprotection.
  • Using the in vivo model, we observed high tumor burden/residual disease in tissues characterized as significant sources of hematopoiesis-promoting stroma, with bone marrow stroma most frequently showing the highest accumulation of leukemia in untreated and nilotinib-treated mice as well as partial protection of leukemic cells from the inhibitory effects of nilotinib.
  • These studies, which showed a pattern of leukemia distribution consistent with what is observed in imatinib- and nilotinib-treated chronic myeloid leukemia patients, were followed by a more in-depth analysis of stroma-leukemia cell interactions that lead to protection of leukemia cells from nilotinib-induced cytotoxicity.
  • For the latter, we used the human BCR-ABL-positive cell line, KU812F, and the human bone marrow stroma cell line, HS-5, to more closely approximate the bone marrow-associated cytoprotection observed in drug-treated leukemia patients.
  • This in vitro system helped to elucidate stromal-secreted viability factors that may play a role in stromal-mediated cytoprotection of tyrosine kinase inhibitor-treated leukemia cells.

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  • (PMID = 18445657.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA66996; United States / NCI NIH HHS / CA / CA36167; United States / NCI NIH HHS / CA / R37 CA036167; United States / NIDDK NIH HHS / DK / DK50654; United States / NCI NIH HHS / CA / P01 CA066996; United States / NIDDK NIH HHS / DK / P01 DK050654; United States / NCI NIH HHS / CA / R01 CA036167
  • [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 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS582783; NLM/ PMC4034541
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32. Forestier E, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology NOPHO: The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations. J Pediatr Hematol Oncol; 2006 Aug;28(8):486-95
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  • [Title] The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations.
  • The correlation between age and karyotype was studied in 1425, 0 to 14.9 years old children who were diagnosed with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia.
  • Almost 80% of the non-Down B-cell precursor ALL cases in the 2 to 7 years frequency peak group who had aberrant cytogenetic results had either a high-hyperdiploid clone (51 to 61 chromosomes) or a translocation t(12;21)(p13;q22).
  • Among B-cell precursor ALL cases, high white blood cell counts correlated with earlier age at diagnosis (rS=-0.23; P<0.001) being most evident for 11q23/MLL-aberrations, translocation t(12;21)(p13;q22), and high-hyperdiploidy.
  • Among acute myeloblastic leukemia patients, frequency peaks were found for those with MLL/11q23 rearrangements (peak: first year), Down syndrome (peak: second to third year), or cytogenetic abnormalities other than translocations t(8;21), t(15;17), and inv(16)/t(16;16) (peak: first to third year).
  • The epidemiology of the cytogenetic subsets of acute leukemias questions whether age as a disease-related prognostic parameter has any relevance in childhood leukemia clinical research beyond being a surrogate marker for more important, truly biologic features such as cytogenetic aberrations and white cell count at diagnosis.
  • Further research is needed to explore whether the 2 to 7 years age incidence peak in childhood ALL harbor yet unidentified cytogenetic subsets with the same natural history as the high-hyperdiploid and t(12;21)-positive leukemias.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Age Distribution. Child. Child, Preschool. Cohort Studies. Comorbidity. Cytogenetic Analysis / methods. Down Syndrome / diagnosis. Down Syndrome / epidemiology. Down Syndrome / genetics. Female. Humans. Incidence. Infant. Infant, Newborn. Karyotyping. Male. Ploidies. Recurrence. Registries / statistics & numerical data. Risk Factors. Scandinavian and Nordic Countries / epidemiology

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  • (PMID = 16912588.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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33. Liu H, Zang C, Fenner MH, Liu D, Possinger K, Koeffler HP, Elstner E: Growth inhibition and apoptosis in human Philadelphia chromosome-positive lymphoblastic leukemia cell lines by treatment with the dual PPARalpha/gamma ligand TZD18. Blood; 2006 May 1;107(9):3683-92
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  • [Title] Growth inhibition and apoptosis in human Philadelphia chromosome-positive lymphoblastic leukemia cell lines by treatment with the dual PPARalpha/gamma ligand TZD18.
  • Treatment of adult Philadelphia chromosome-positive lymphocytic leukemia is rarely successful.
  • We report here the effects of TZD18, a novel dual ligand specific for peroxisome proliferator-activated receptor alpha and gamma (PPARalpha/gamma) on Ph(+) lymphocytic leukemia cell lines BV173, SD1, and SupB-15.
  • Exposure of these cells to TZD18 resulted in growth inhibition in a dose- and time-dependent manner that was associated with G(1) cell cycle arrest.
  • Study of the key regulators of cell cycle progression by Western blot analysis showed that the expression of the cyclin-dependent kinase inhibitor (CDKI) p27(kip1), but not that of p21(cip1), was enhanced, whereas that of c-Myc, cyclin E, cyclin D2, and cyclin-dependent kinases 2 and 4 (CDK-2 and CDK-4) was decreased when these cells were treated with TZD18 (10 or 20 microM).
  • Therefore, the up-regulation of p27(kip1) and the down-regulation of CDK-2 and CDK-4 may, at least in part, account for the G(1) cell cycle arrest.
  • In addition, TZD18 enhanced the growth inhibitory effect of imatinib, a specific tyrosine kinase inhibitor therapeutically used in the treatment of Ph(+) leukemia.
  • Overall, our findings strongly suggest that TZD18 may offer a new therapeutic approach to aid in the treatment of Ph(+) lymphocytic leukemia.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Phenyl Ethers / pharmacology. Thiazolidinediones / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p27. Humans. Imatinib Mesylate. Intracellular Signaling Peptides and Proteins / metabolism. Ligands. NF-kappa B / metabolism. PPAR alpha / agonists. PPAR alpha / genetics. PPAR gamma / agonists. PPAR gamma / genetics. Piperazines / administration & dosage. Pyrimidines / administration & dosage

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  • (PMID = 16403907.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-(3-(3-(4-phenoxy-2-propylphenoxy)propoxy)phenyl)-2,4-thiazolidinedione; 0 / Benzamides; 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Ligands; 0 / NF-kappa B; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Phenyl Ethers; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazolidinediones; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 8A1O1M485B / Imatinib Mesylate
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34. Salih HR, Wintterle S, Krusch M, Kroner A, Huang YH, Chen L, Wiendl H: The role of leukemia-derived B7-H1 (PD-L1) in tumor-T-cell interactions in humans. Exp Hematol; 2006 Jul;34(7):888-94
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  • [Title] The role of leukemia-derived B7-H1 (PD-L1) in tumor-T-cell interactions in humans.
  • Recently, B7-H1 on murine leukemia cells was reported to mediate resistance to cytolytic T-cell destruction.
  • We here investigate the expression and function of the B7 homolog B7-H1 in human leukemia.
  • PATIENTS AND METHODS: Leukemia cells from 30 patients and 9 human leukemia cell lines were investigated for B7-H1 expression by flow cytometry.
  • Functional relevance of B7-H1 for tumor-immune interactions was assessed by coculture experiments using purified, alloreactive CD4 and CD8 T cells in the presence of a neutralizing anti-B7-H1 antibody.
  • RESULTS: Significant B7-H1 expression levels on leukemia cells were detected in 17 of 30 patients and in eight of nine cell lines.
  • In contrast to various other tumor entities and the data reported from a murine leukemia system, no significant inhibitory effect of leukemia-derived B7-H1 on CD4 and CD8 cytokine production (IFN-gamma, IL-2), proliferation or expression of T-cell activation markers (ICOS, CD69) was observed.
  • Furthermore, in the presence of neutralizing B7-H1 antibody (mAb 5H1) occurred no significant changes in T cell IFN-gamma or IL-2 production or proliferation.
  • CONCLUSIONS: Our data demonstrate that leukemia-derived B7-H1 seems to have no direct influence on T-cell activation, proliferation, and cytokine production in humans.
  • Further experiments are warranted to delineate factors and characterize yet-unidentified B7-H1 receptor(s) that determine inhibitory and stimulatory functions of B7-H1 in human leukemia.
  • [MeSH-major] Antigens, CD / immunology. Leukemia / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD274. Blotting, Western. Cell Line, Tumor. Coculture Techniques. Female. Flow Cytometry. Humans. Male. Middle Aged

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  • (PMID = 16797416.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human
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35. DiNardo CD, Ky B, Vogl DT, Forfia P, Loren A, Luger S, Mato A, Tsai DE: Differentiation syndrome in non-M3 acute myeloid leukemia treated with the retinoid X receptor agonist bexarotene. Med Oncol; 2008;25(3):299-302
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  • [Title] Differentiation syndrome in non-M3 acute myeloid leukemia treated with the retinoid X receptor agonist bexarotene.
  • Differentiation Syndrome, also known as all-trans retinoic acid (ATRA) syndrome, is a well-described clinical phenomenon occurring in patients with the M3 subtype of acute myeloid leukemia receiving ATRA chemotherapy.
  • We report a patient with refractory non-M3 acute promyelocytic leukemia (AML) who developed differentiation syndrome during bexarotene monotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / pathology. Retinoid X Receptors / agonists. Tetrahydronaphthalenes / adverse effects
  • [MeSH-minor] Cell Differentiation. Humans. Male. Middle Aged. Pericardial Effusion / chemically induced. Syndrome

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  • (PMID = 18181037.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Retinoid X Receptors; 0 / Tetrahydronaphthalenes; A61RXM4375 / bexarotene
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36. Cheng H, Yang Y, Dai W, Tang C, Shi M, Feng G, Kang T, Su X, Zhao G: Acute leukemia presenting with blasts first found in the cerebrospinal fluid but not in the peripheral blood. J Clin Neurosci; 2010 Oct;17(10):1252-5
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  • [Title] Acute leukemia presenting with blasts first found in the cerebrospinal fluid but not in the peripheral blood.
  • Acute leukemia presenting with central nervous system (CNS) signs and symptoms is uncommon and prone to be misdiagnosed.
  • Here, we report nine patients with acute leukemia, including five patients with acute lymphoblastic leukemia (ALL) and four patients with acute myeloid leukemia (AML).
  • Moreover, we found that all these patients unexpectedly showed the presence of blasts in the cerebrospinal fluid (CSF) but not in the peripheral blood despite repeated examinations.
  • Bone marrow examination confirmed the presence of acute leukemia in these patients.
  • Seven patients died within 18months of diagnosis and two patients developed stable disease.
  • Our findings show a novel presenting feature of acute leukemia and highlight the importance of CSF cytology in the diagnosis of acute leukemia.
  • [MeSH-major] Leukemia / cerebrospinal fluid. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Cranial Nerve Diseases / blood. Cranial Nerve Diseases / cerebrospinal fluid. Cranial Nerve Diseases / etiology. Female. Humans. Male. Retrospective Studies. Spinal Cord / pathology. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20605098.001).
  • [ISSN] 1532-2653
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
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37. Guo L, Tang YM, Shen HQ, Qian BQ, Ning BT, Zhang HZ, Zhang Y: [Reactivity of a novel monoclonal antibody ZCH-7-2D3 on leukemia cells and its clinical significance]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2006 Jul;35(4):390-3
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  • [Title] [Reactivity of a novel monoclonal antibody ZCH-7-2D3 on leukemia cells and its clinical significance].
  • OBJECTIVE: To analyze the reactive pattern and its clinical significance of ZCH-7-2D3 monoclonal antibody on leukemia cells.
  • METHODS: Bone marrow samples from 100 leukemia patients (male 59: female 41, 34 cases of children and 66 adults, aged 11 months - 77 year) were collected.
  • A CD45 gating strategy and multi-parameter flow cytometry were used to analyze the leukemia cells.
  • RESULT: The positive rate (10/31) of 2D3 antibody on acute lymphocytic leukemia (ALL) patients was significantly lower than that (39/55) of acute myelogeneous leukemia (AML) (P <0.01).
  • 2D3 was positive for all three cases of B/myeloid mixed lineage leukemia, but negative in 6 cases of chronic myelogeneous leukemia (CML), significantly lower than that in AML (39/55, P<0.01) patients.
  • There was no difference between the positive rates of chronic lymphocytic leukemia (CLL, 3/5) and B lineage ALL (9/28, P = 0.2389).
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibodies, Neoplasm / immunology. Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD45 / immunology. Antigens, Neoplasm / immunology. Child. Child, Preschool. Female. Humans. Immunophenotyping. Infant. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Male. Middle Aged

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  • (PMID = 16924702.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; EC 3.1.3.48 / Antigens, CD45
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38. Scholz C, Nimmrich I, Burger M, Becker E, Dörken B, Ludwig WD, Maier S: Distinction of acute lymphoblastic leukemia from acute myeloid leukemia through microarray-based DNA methylation analysis. Ann Hematol; 2005 Apr;84(4):236-44
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  • [Title] Distinction of acute lymphoblastic leukemia from acute myeloid leukemia through microarray-based DNA methylation analysis.
  • To investigate whether disease-specific methylation profiles exist for different entities of acute leukemia, a microarray-based DNA methylation analysis simultaneously assessing 249 CpG dinucleotides originating from 57 genes was employed.
  • Hereby, samples from precursor B-cell acute lymphoblastic leukemia (ALL) could be distinguished from cases of acute myeloid leukemia by virtue of N33, EGR4, CDC2, CCND2, or MOS hypermethylation in ALL.
  • [MeSH-major] DNA Methylation. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Base Sequence. Classification. Diagnosis, Differential. Dinucleoside Phosphates / metabolism. Humans. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic


39. Rosenblatt J, Avigan D: Can leukemia-derived dendritic cells generate antileukemia immunity? Expert Rev Vaccines; 2006 Aug;5(4):467-72
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  • [Title] Can leukemia-derived dendritic cells generate antileukemia immunity?
  • Based on the efficacy of allogeneic transplantation, acute myelogenous leukemia appears to be susceptible to cellular immune-based therapy.
  • In acute leukemia, a promising approach involves the generation of DCs from leukemic blasts via cytokine exposure ex vivo.
  • Leukemia-derived DCs potentially retain the tumor-associated antigens of the leukemic clone, which are presented in the context of the immune stimulating machinery of the mature DC.
  • However, the efficacy of this approach may be limited by intrinsic abnormalities in the malignant clone that prevent differentiation towards a normal DC phenotype.
  • [MeSH-major] Dendritic Cells / transplantation. Leukemia / immunology. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 16989627.001).
  • [ISSN] 1744-8395
  • [Journal-full-title] Expert review of vaccines
  • [ISO-abbreviation] Expert Rev Vaccines
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 57
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40. Andersen MT, Andersen MK, Christiansen DH, Pedersen-Bjergaard J: NPM1 mutations in therapy-related acute myeloid leukemia with uncharacteristic features. Leukemia; 2008 May;22(5):951-5
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  • [Title] NPM1 mutations in therapy-related acute myeloid leukemia with uncharacteristic features.
  • Frameshift mutations of the nucleophosmin gene (NPM1) were recently reported as a frequently occurring abnormality in patients with de novo acute myeloid leukemia (AML).
  • To evaluate the frequency of NPM1 mutations in patients with therapy-related myelodysplasia (t-MDS) and therapy-related AML (t-AML), and their possible association to type of previous therapy and to other gene mutations, 140 patients with t-MDS or t-AML were analyzed for mutations of NPM1.
  • The mutations were not related to any specific type of previous therapy, but they were significantly associated with a normal karyotype and mutations of FLT3 (P=0.0002 for both comparisons).
  • Only 1 of 10 patients with NPM1 mutations presented chromosome aberrations characteristic of therapy-related disease, and 7q-/-7, the most frequent abnormalities of t-MDS/t-AML, were not observed (P=0.002).
  • This raises the question whether some of the cases presenting NPM1 mutations were in fact cases of de novo leukemia.
  • The close association to class I mutations and the inverse association to class II mutations suggest mutations of NPM1 as representing a class II mutation-like abnormality in AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Neoplasms, Second Primary / genetics. Nuclear Proteins / genetics


41. Ranganathan A, Powell BL: Risk-adapted approaches to therapy for high-risk acute promyelocytic leukemia. Clin Lymphoma Myeloma Leuk; 2010 Oct;10 Suppl 3:S135-8
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  • [Title] Risk-adapted approaches to therapy for high-risk acute promyelocytic leukemia.
  • In the past decade, risk stratification based on white blood cell (WBC) and platelet counts at initial clinical presentation in patients with acute promyelocytic leukemia (APL) has allowed adjustments in intensity and type of up-front agents used in the treatment of different risk groups, thereby optimizing clinical outcomes.
  • Multiple European and North American trials have successfully attempted incorporation of risk-adapted approaches into the consolidation phase of frontline treatment; clinical data from the integration of all-trans-retinoic acid and cytarabine into therapeutic regimens for high-risk disease are discussed.
  • A positive impact of adding ATO to consolidation regimens was reported for all risk groups of APL in the North American Leukemia Intergroup C9710 trial; recent results from that trial are also reviewed.
  • In addition to therapeutic strategies, optimal management of APL, especially high-risk disease, also involves using effective supportive care measures, monitoring response to therapy, and preventing relapse.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 21115432.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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42. Jaglowski SM, Alinari L, Lapalombella R, Muthusamy N, Byrd JC: The clinical application of monoclonal antibodies in chronic lymphocytic leukemia. Blood; 2010 Nov 11;116(19):3705-14
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  • [Title] The clinical application of monoclonal antibodies in chronic lymphocytic leukemia.
  • Chronic lymphocytic leukemia (CLL) represents the most prevalent adult leukemia.
  • The introduction of therapeutic antibodies has increased the number of treatment options for this disease.
  • Alemtuzumab, a CD52 antibody, likewise has demonstrated benefit in both symptomatic, previously untreated CLL and in patients with relapsed disease but has less selectivity.
  • Development of other therapeutic antibodies targeting alternative B-cell-specific antigens in CLL has been less successful, although many promising candidate antibodies and/or small modular immune pharmaceuticals (SMIPs) are coming forward.
  • In addition, recent efforts to combine currently applied therapeutic antibodies with other biologic and targeted therapies with efficacy in CLL offers the potential to move toward alternative non-chemotherapy-based treatment approaches.

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  • (PMID = 20610811.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01-CA95426; United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / P50-CA140158; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P01 CA81534; United States / NCI NIH HHS / CA / P01 CA095426
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / ofatumumab; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab; O43472U9X8 / obinutuzumab
  • [Other-IDs] NLM/ PMC2981531
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43. Horton HM, Bernett MJ, Pong E, Peipp M, Karki S, Chu SY, Richards JO, Vostiar I, Joyce PF, Repp R, Desjarlais JR, Zhukovsky EA: Potent in vitro and in vivo activity of an Fc-engineered anti-CD19 monoclonal antibody against lymphoma and leukemia. Cancer Res; 2008 Oct 1;68(19):8049-57
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  • [Title] Potent in vitro and in vivo activity of an Fc-engineered anti-CD19 monoclonal antibody against lymphoma and leukemia.
  • CD19 is a pan B-cell surface receptor expressed from pro-B-cell development until its down-regulation during terminal differentiation into plasma cells.
  • CD19 represents an attractive immunotherapy target for cancers of lymphoid origin due to its high expression levels on the vast majority of non-Hodgkin's lymphomas and some leukemias.
  • In vitro, XmAb5574 enhanced antibody-dependent cell-mediated cytotoxicity 100-fold to 1,000-fold relative to an anti-CD19 IgG1 analogue against a broad range of B-lymphoma and leukemia cell lines.
  • Furthermore, XmAb5574 conferred antibody-dependent cell-mediated cytotoxicity against patient-derived acute lymphoblastic leukemia and mantle cell lymphoma cells, whereas the IgG1 analogue was inactive.
  • [MeSH-major] Antibodies, Monoclonal / genetics. Antibodies, Monoclonal / therapeutic use. Antigens, CD19 / immunology. Immunoglobulin Fc Fragments / genetics. Leukemia / therapy. Lymphoma / therapy

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  • (PMID = 18829563.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / Antineoplastic Agents; 0 / FCGR1A protein, human; 0 / Immunoglobulin Fc Fragments; 0 / Receptors, IgG
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44. Whitman SP, Ruppert AS, Marcucci G, Mrózek K, Paschka P, Langer C, Baldus CD, Wen J, Vukosavljevic T, Powell BL, Carroll AJ, Kolitz JE, Larson RA, Caligiuri MA, Bloomfield CD: Long-term disease-free survivors with cytogenetically normal acute myeloid leukemia and MLL partial tandem duplication: a Cancer and Leukemia Group B study. Blood; 2007 Jun 15;109(12):5164-7
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  • [Title] Long-term disease-free survivors with cytogenetically normal acute myeloid leukemia and MLL partial tandem duplication: a Cancer and Leukemia Group B study.
  • The clinical impact of MLL partial tandem duplication (MLL-PTD) was evaluated in 238 adults aged 18 to 59 years with cytogenetically normal (CN) de novo acute myeloid leukemia (AML) who were treated intensively on similar Cancer and Leukemia Group B protocols 9621 and 19808.
  • Of those, 92% achieved complete remission (CR) compared with 83% of patients without MLL-PTD (P=.39).
  • Neither overall survival nor disease-free survival significantly differed between the 2 groups (P=.67 and P=.55, respectively).
  • Thirteen MLL-PTD(+) patients relapsed within 1.4 years of achieving CR.
  • In contrast with previously reported studies, 9 (41%) MLL-PTD(+) patients continue in long-term first remission (CR1; range, 2.5-7.7 years).
  • Intensive consolidation therapy that included autologous peripheral stem-cell transplantation during CR1 may have contributed to the better outcome of this historically poor-prognosis group of CN-AML patients with MLL-PTD.

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  • (PMID = 17341662.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA102031; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / CA098933; United States / NCI NIH HHS / CA / CA089341; United States / NCI NIH HHS / CA / CA41287; United States / NCI NIH HHS / CA / R01 CA089341; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / U10 CA041287; United States / NCI NIH HHS / CA / R01 CA098933; United States / NCI NIH HHS / CA / K01 CA096887; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA096887
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1890839
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45. Ohmachi K, Ogiya D, Morita F, Kojima M, Tsuboi K, Tazume K, Komatsu M, Hayama N, Kumaki N, Ogawa Y, Ando K: Secondary pulmonary alveolar proteinosis in a patient with chronic myeloid leukemia in the accelerated phase. Tokai J Exp Clin Med; 2008 Dec;33(4):146-9
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  • [Title] Secondary pulmonary alveolar proteinosis in a patient with chronic myeloid leukemia in the accelerated phase.
  • Pulmonary alveolar proteinosis (PAP) is a rare respiratory disease the character of which is accumulation of protein consisting of surfactant in alveolar spaces.
  • PAP sometimes complicates with hematological malignancies, especially myeloid leukemia.
  • We experienced a case of PAP with chronic myeloid leukemia (CML).
  • We consider that we should try to treat to improve respiratory status not only PAP but also hematological disease.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Pulmonary Alveolar Proteinosis / etiology

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  • (PMID = 21318986.001).
  • [ISSN] 2185-2243
  • [Journal-full-title] The Tokai journal of experimental and clinical medicine
  • [ISO-abbreviation] Tokai J. Exp. Clin. Med.
  • [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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46. Milojkovic D, Apperley J: State-of-the-art in the treatment of chronic myeloid leukaemia. Curr Opin Oncol; 2008 Jan;20(1):112-21
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  • [Title] State-of-the-art in the treatment of chronic myeloid leukaemia.
  • PURPOSE OF REVIEW: To revise the current goals of therapy of chronic myeloid leukaemia and to incorporate the influence of the underlying chronic myeloid leukaemia biology on directing therapeutic management.
  • RECENT FINDINGS: The management of chronic myeloid leukaemia has been revolutionized by targeted molecular therapy that inhibits the ABL kinase activity of the BCR-ABL gene.
  • The achievement of a major molecular response with the first tyrosine kinase inhibitor to be introduced into clinical practice, imatinib, is a focus of therapeutic regimens.
  • Strategies to overcome the restoration of BCR-ABL signalling and subsequent resistance to therapy include imatinib dose escalation, a more potent tyrosine kinase inhibitor, as well as non-BCR-ABL-dependent approaches and agents in clinical development.
  • SUMMARY: Therapeutic advances in chronic myeloid leukaemia continue to circumvent the challenges of drug resistance and the minimal residual leukaemic burden providing effective strategies for future therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 18043265.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / 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
  • [Number-of-references] 96
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47. Awan H, Jønsson V, Johannesen TB, Ly B, Tjønnfjord GE: Anticipation in families with chronic lymphocytic leukemia and other lymphoproliferative disorders. Transl Oncogenomics; 2010 Mar 30;4:1-9
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  • [Title] Anticipation in families with chronic lymphocytic leukemia and other lymphoproliferative disorders.
  • Fifty-one parent-offspring pairs with chronic lymphocytic leukemia (CLL) or other lymphoproliferative disorders (nonCLL) such as malignant lymphoma, multiple myeloma, or other types of lymphocytic leukemia than CLL were ascertained independently in 38 families.
  • The median age of onset of disease was 13 years lower in the offspring than in the parents when comparing all 51 pairs (P < 0.001).
  • This difference was mainly caused by a significantly lower age at onset in offspring with parental nonCLL (P < 0.001) where paternal disease was transferred especially to sons, while affected offspring to parents with CLL have the same age at debut of disease than their parents (P = 0.130) and a nearly equal transfer to sons and daughters.
  • The low-malignant follicular small B-cell lymphoma was the predominant diagnosis within nonCLL.
  • Anticipation is pointed out as one likely mechanism behind the lower age at onset of disease in offspring than in parents, even if a part of this difference is ascribed to a generally earlier diagnosis with modern technology in offspring than in parents.

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  • (PMID = 21566766.001).
  • [ISSN] 1177-2727
  • [Journal-full-title] Translational oncogenomics
  • [ISO-abbreviation] Transl Oncogenomics
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3072649
  • [Keywords] NOTNLM ; chronic lymphocytic leukemia / epigenetic inheritance / familial clustering / malignant lymphomas / multiple myeloma
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48. Sawa M, Yamamoto K, Yokozawa T, Kiyoi H, Hishida A, Kajiguchi T, Seto M, Kohno A, Kitamura K, Itoh Y, Asou N, Hamajima N, Emi N, Naoe T: BMI-1 is highly expressed in M0-subtype acute myeloid leukemia. Int J Hematol; 2005 Jul;82(1):42-7
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  • [Title] BMI-1 is highly expressed in M0-subtype acute myeloid leukemia.
  • Here, we quantitatively examined BMI-1 expression level in samples from patients with acute myeloid leukemia (AML) and other hematologic malignancies.
  • Specimens of French-American-British classification subtype M0 showed higher relative expression of the BMI-1 transcript (median, 390.2 3 10(-3)) than the other subtypes (median, 139.0 3 10(-3)) (P < .0001).
  • Leukemia other than AML showed low to moderate expression.
  • In an M0 patient with a high BMI-1 transcript level, the INK4a-ARF transcript level fell promptly and maintained a low value after the patient achieved complete remission.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Leukemia, Myeloid / genetics. Nuclear Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Acute Disease. Bone Marrow. Case-Control Studies. Gene Expression Profiling. Humans. Polycomb Repressive Complex 1

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  • (PMID = 16105758.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 2.3.2.27 / Polycomb Repressive Complex 1
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49. Casagrande G, te Kronnie G, Basso G: The effects of siRNA-mediated inhibition of E2A-PBX1 on EB-1 and Wnt16b expression in the 697 pre-B leukemia cell line. Haematologica; 2006 Jun;91(6):765-71
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  • [Title] The effects of siRNA-mediated inhibition of E2A-PBX1 on EB-1 and Wnt16b expression in the 697 pre-B leukemia cell line.
  • BACKGROUND AND OBJECTIVES: A common non-random translocation in childhood pre-B acute lymphoblastic leukemia (ALL) is t(1;19)(q23;p13), usually resulting in the expression of the chimeric gene E2A-PBX1.
  • DESIGN AND METHODS: We tested the efficacy of anti-E2A-PBX1 siRNA in the 697 pre-B leukemia cell line.
  • RESULTS: We demonstrated efficient downregulation induced by anti-E2A-PBX1 siRNA in 697 t(1;19)-positive leukemia cells.
  • In particular, E2A-PBX1 silencing affected the EB-1 gene, which encodes for a protein that could contribute to the transformed phenotype of pre-B ALL.
  • The detected EB-1 expression was reduced to 25% of the normal expression level in non-transfected 697 cells.
  • The siRNA inhibition was followed by an increase in apoptosis and similar results were obtained in two other ALL cell lines, one with and one without the t(1;19) translocation.
  • INTERPRETATION AND CONCLUSIONS: Targeted-E2A-PBX1 inhibition leads to reduced expression of the EB-1 and Wnt16b genes; aberrant expression of these genes may be a key step in leukemogenesis in t(1;19)-positive pre-B leukemia.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Glycoproteins / genetics. Microtubule-Associated Proteins / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Small Interfering / genetics. Wnt Proteins / genetics
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 19. DNA Primers. Humans. RNA, Messenger / genetics. RNA, Neoplasm / genetics. RNA, Neoplasm / isolation & purification. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Translocation, Genetic

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  • [CommentIn] Haematologica. 2006 Jun;91(6):724 [16769568.001]
  • (PMID = 16769578.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Glycoproteins; 0 / MAPRE1 protein, human; 0 / Microtubule-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / WNT16 protein, human; 0 / Wnt Proteins
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50. Kurihara K, Harashima N, Hanabuchi S, Masuda M, Utsunomiya A, Tanosaki R, Tomonaga M, Ohashi T, Hasegawa A, Masuda T, Okamura J, Tanaka Y, Kannagi M: Potential immunogenicity of adult T cell leukemia cells in vivo. Int J Cancer; 2005 Mar 20;114(2):257-67
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  • [Title] Potential immunogenicity of adult T cell leukemia cells in vivo.
  • Experimental vaccines targeting human T cell leukemia virus type-I (HTLV-I) Tax have been demonstrated in a rat model of HTLV-I-induced lymphomas.
  • However, the scarcity of HTLV-I-expression and the presence of defective HTLV-I-proviruses in adult T cell leukemia (ATL) cells have raised controversy about the therapeutic potential of HTLV-I-targeted immunotherapy in humans.
  • In flow cytometric analysis, we found that 3 of 5 acute-type and six of fifteen chronic-type ATL patients tested showed significant induction of HTLV-I Tax and Gag in their ATL cells in a 1-day culture.
  • Representative CTL epitopes restricted by HLA-A2 or A24 were conserved in 4 of 5 acute-type ATL patients tested.
  • Furthermore, spleen T cells from rats, which had been subcutaneously inoculated with formalin-fixed uncultured ATL cells, exhibited a strong interferon gamma-producing helper T cell responses specific for HTLV-I Tax-expressing cells.
  • Our study indicated that ATL cells from about half the patients tested readily express HTLV-I antigens including Tax in vitro, and that ATL cells express sufficient amounts of Tax or Tax-induced antigens to evoke specific T cell responses in vivo.
  • [MeSH-minor] Adult. Aged. Animals. Base Sequence. DNA Primers. Female. Humans. Japan. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemia, Prolymphocytic, T-Cell / virology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology. Male. Middle Aged. Polymerase Chain Reaction. Rats. Rats, Inbred F344. Reference Values. Transplantation, Heterologous / pathology

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551352.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers
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51. Sell S: Leukemia: stem cells, maturation arrest, and differentiation therapy. Stem Cell Rev; 2005;1(3):197-205
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  • [Title] Leukemia: stem cells, maturation arrest, and differentiation therapy.
  • Human myeloid leukemias provide models of maturation arrest and differentiation therapy of cancer.
  • The genetic lesions of leukemia result in a block of differentiation (maturation arrest) that allows myeloid leukemic cells to continue to proliferate and/or prevents the terminal differentiation and apoptosis seen in normal white blood cells.
  • In chronic myeloid leukemia, the bcr-abl (t9/22) translocation produces a fusion product that is an activated tyrosine kinase resulting in constitutive activation cells at the myelocyte level.
  • In acute promyelocytic leukemia, fusion of the retinoic acid receptor-alpha with the gene coding for promyelocytic protein, the PML-RAR alpha (t15:17) translocation, produces a fusion product that blocks the activity of the promyelocytic protein, which is required for formation of the granules of promyelocytes and prevents further differentiation.
  • In one common type of acute myeloid leukemia, which results in maturation arrest at the myeloid precursor level, there is a mutation of FLT3, a transmembrane tyrosine kinase, which results in constitutive activation of the IL-3 receptor.
  • Because acute myeloid leukemias usually have mutation of more than one gene, combinations of specific inhibitors that act on the effects of different specific genetic lesions promises to result in more effective and permanent treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Differentiation / drug effects. Cell Differentiation / genetics. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Neoplastic Stem Cells / metabolism. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Leukemic / genetics. Humans. Imatinib Mesylate. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics

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  • (PMID = 17142856.001).
  • [ISSN] 1550-8943
  • [Journal-full-title] Stem cell reviews
  • [ISO-abbreviation] Stem Cell Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 90
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52. Satoh T, Li M, Nguyen JT, Kiso Y, Gustchina A, Wlodawer A: Crystal structures of inhibitor complexes of human T-cell leukemia virus (HTLV-1) protease. J Mol Biol; 2010 Aug 27;401(4):626-41
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  • [Title] Crystal structures of inhibitor complexes of human T-cell leukemia virus (HTLV-1) protease.
  • Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus associated with several serious diseases, such as adult T-cell leukemia and tropical spastic paraparesis/myelopathy.
  • For a number of years, the protease (PR) encoded by HTLV-1 has been a target for designing antiviral drugs, but that effort was hampered by limited available structural information.
  • We report a high-resolution crystal structure of HTLV-1 PR complexed with a statine-containing inhibitor, a significant improvement over the previously available moderate-resolution structure.
  • We also report crystal structures of the complexes of HTLV-1 PR with five different inhibitors that are more compact and more potent.

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  • [Copyright] Published by Elsevier Ltd.
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  • (PMID = 20600105.001).
  • [ISSN] 1089-8638
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] ENG
  • [Databank-accession-numbers] PDB/ 3LIN/ 3LIQ/ 3LIT/ 3LIV/ 3LIX/ 3LIY
  • [Grant] United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / Intramural NIH HHS / / Z01 BC010348-08; United States / PHS HHS / / 261200800001E
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protease Inhibitors; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / HTLV-1 protease
  • [Other-IDs] NLM/ NIHMS224448; NLM/ PMC2918672
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53. Jastaniah WA, Alessandri AJ, Reid GS, Schultz KR: HLA-DM expression is elevated in ETV6-AML1 translocation-positive pediatric acute lymphoblastic leukemia. Leuk Res; 2006 Apr;30(4):487-9
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  • [Title] HLA-DM expression is elevated in ETV6-AML1 translocation-positive pediatric acute lymphoblastic leukemia.
  • ETV6-AML1-positive precursor-B acute lymphoblastic leukemia (pre-B ALL) is associated with good outcome and late relapse.
  • The HLA-DR(high)/CLIP(low)/HLA-DM(high) phenotype strongly suggests that ETV6-AML1 leukemia will induce favorable immune responses and may in part explain the characteristic late relapses associated with ETV6-AML1 pre-B ALL.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. HLA-D Antigens / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic

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  • (PMID = 16191436.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / HLA-D Antigens; 0 / HLA-DM antigens; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins
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54. Abdelhameed A, Pond GR, Mitsakakis N, Brandwein J, Chun K, Gupta V, Kamel-Reid S, Lipton JH, Minden MD, Schimmer A, Schuh A, Yee K, Messner HA: Outcome of patients who develop acute leukemia or myelodysplasia as a second malignancy after solid tumors treated surgically or with strategies that include chemotherapy and/or radiation. Cancer; 2008 Apr 1;112(7):1513-21
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  • [Title] Outcome of patients who develop acute leukemia or myelodysplasia as a second malignancy after solid tumors treated surgically or with strategies that include chemotherapy and/or radiation.
  • BACKGROUND: Evaluation of therapeutic outcomes and risk factors was undertaken for patients with primary solid tumors (PST) developing acute leukemia or myelodysplasia (MDS) as a second malignancy.
  • METHODS: In all, 131 consecutive patients presenting to a single institution with leukemia or MDS after treatment for PST with surgery or chemotherapy/radiotherapy were examined.
  • Management of the secondary acute leukemia and MDS consisted either of intensive therapy including allogeneic blood and marrow transplants or supportive measures.
  • RESULTS: The time from diagnosis of PST to development of acute leukemia or MDS, the cytogenetic profile of patients, and their survival were similar irrespective of PST therapy with surgery alone or strategies involving chemotherapy and/or radiation.
  • CONCLUSIONS: Patients developing acute leukemia or MDS after PST demonstrated similar cytogenetic profiles and clinical outcomes independent of the type of treatment.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / etiology. Neoplasms / therapy. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology


55. Kong Y, Yoshida S, Saito Y, Doi T, Nagatoshi Y, Fukata M, Saito N, Yang SM, Iwamoto C, Okamura J, Liu KY, Huang XJ, Lu DP, Shultz LD, Harada M, Ishikawa F: CD34+CD38+CD19+ as well as CD34+CD38-CD19+ cells are leukemia-initiating cells with self-renewal capacity in human B-precursor ALL. Leukemia; 2008 Jun;22(6):1207-13
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  • [Title] CD34+CD38+CD19+ as well as CD34+CD38-CD19+ cells are leukemia-initiating cells with self-renewal capacity in human B-precursor ALL.
  • The presence of rare malignant stem cells supplying a hierarchy of malignant cells has recently been reported.
  • In human acute myelogenous leukemia (AML), the leukemia stem cells (LSCs) have been phenotypically restricted within the CD34+CD38- fraction.
  • To understand the origin of malignant cells in primary human B-precursor acute lymphocytic leukemia (B-ALL), we established a novel in vivo xenotransplantation model.
  • Purified CD34+CD38+CD19+, CD34+CD38-CD19+ and CD34+CD38-CD19- bone marrow (BM) or peripheral blood (PB) cells from three pediatric B-ALL patients were intravenously injected into sublethally irradiated newborn NOD/SCID/IL2rgamma(null) mice.
  • The identification of CD34+CD38+CD19+ self-renewing B-ALL cells proposes a hierarchy of leukemia-initiating cells (LICs) distinct from that of AML.
  • [MeSH-major] Antigens, CD19 / metabolism. Antigens, CD34 / metabolism. Antigens, CD38 / metabolism. Hematopoietic Stem Cells / pathology. Neoplastic Stem Cells / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Animals. Animals, Newborn. Cell Differentiation. Cell Lineage. Child. Flow Cytometry. Graft Survival. Humans. Immunophenotyping. Infant. Mice. Mice, Inbred NOD. Mice, SCID. Transplantation, Heterologous. Tumor Cells, Cultured. Whole-Body Irradiation

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  • (PMID = 18418410.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD34; EC 3.2.2.5 / Antigens, CD38
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56. Ferraz KS, Ferandes L, Carrilho D, Pinto MC, Leite Mde F, Souza-Fagundes EM, Speziali NL, Mendes IC, Beraldo H: 2-Benzoylpyridine-N(4)-tolyl thiosemicarbazones and their palladium(II) complexes: cytotoxicity against leukemia cells. Bioorg Med Chem; 2009 Oct 15;17(20):7138-44
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  • [Title] 2-Benzoylpyridine-N(4)-tolyl thiosemicarbazones and their palladium(II) complexes: cytotoxicity against leukemia cells.
  • The free thiosemicarbazones proved to be highly cytotoxic against Jurkat, HL60 and the resistant HL60.Bcl-X(L) leukemia cell lines at nanomolar concentrations, but were much less cytotoxic to HepG2human hepatoma cells.
  • Upon coordination to palladium(II) the cytotoxic activity against all studied cell lines decreases.
  • However, the high cytotoxicity of the free thiosemicarbazones against leukemia, together with their hepatotoxic profile similar to that of cisplatin suggest that N(4)-tolyl thiosemicarbazones have potential as chemotherapeutic drug candidates.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia / pathology. Palladium / chemistry. Thiosemicarbazones / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Crystallography, X-Ray. Drug Screening Assays, Antitumor. Humans. Magnetic Resonance Spectroscopy. Models, Molecular

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  • (PMID = 19773176.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-benzoylpyridine N(4)-methylthiosemicarbazone; 0 / Antineoplastic Agents; 0 / Thiosemicarbazones; 5TWQ1V240M / Palladium
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57. Rushing EJ, Sandberg GD, Horkayne-Szakaly I: High-grade astrocytomas show increased Nestin and Wilms's tumor gene (WT1) protein expression. Int J Surg Pathol; 2010 Aug;18(4):255-9
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  • Recently, WT1 protein has been considered as a molecular target of cancer immunotherapy for several solid tumors and as a tool for monitoring minimal residual disease in leukemia patients.


58. Bleakley M, Otterud BE, Richardt JL, Mollerup AD, Hudecek M, Nishida T, Chaney CN, Warren EH, Leppert MF, Riddell SR: Leukemia-associated minor histocompatibility antigen discovery using T-cell clones isolated by in vitro stimulation of naive CD8+ T cells. Blood; 2010 Jun 10;115(23):4923-33
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  • [Title] Leukemia-associated minor histocompatibility antigen discovery using T-cell clones isolated by in vitro stimulation of naive CD8+ T cells.
  • T-cell immunotherapy that targets minor histocompatibility (H) antigens presented selectively by recipient hematopoietic cells, including leukemia, could prevent and treat leukemic relapse after hematopoietic cell transplantation without causing graft-versus-host disease.
  • To provide immunotherapy that can be applied to a majority of transplantation recipients, it is necessary to identify leukemia-associated minor H antigens that result from gene polymorphisms that are balanced in the population and presented by common human leukocyte antigen alleles.
  • We show that minor H antigen-specific cytotoxic T lymphocyte precursors are found predominantly in the naive CD8(+) T-cell subset and provide an efficient strategy for in vitro priming of native T cells to generate T cells to a broad diversity of minor H antigens presented with common human leukocyte antigen alleles.
  • We used this approach to derive a panel of stable cytotoxic T lymphocyte clones for discovery of genes that encode minor H antigens and identify a novel antigen expressed on acute myeloid leukemia stem cells and minimally in graft-versus-host disease target tissues.


59. Ramakrishna R, Manoharan A: Sustained long-term remissions with weekly interferon maintenance therapy in hairy cell leukemia. Asia Pac J Clin Oncol; 2010 Sep;6(3):210-2
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  • [Title] Sustained long-term remissions with weekly interferon maintenance therapy in hairy cell leukemia.
  • AIM: This study evaluates the efficacy of weekly α-interferon (IFN) maintenance therapy in hairy cell leukaemia (HCL), a disease that remains incurable.
  • METHOD: Nine patients (six male, three female, aged 41-69 yrs) with hairy cell leukaemia (HCL) received IFN 3mU s.c. once weekly as long-term maintenance therapy after achieving optimal clinical and hematological response to initial therapy with thrice weekly IFN.
  • CONCLUSION: Our results are similar to those from three previous studies using long-term IFN maintenance therapy, bringing the total number of patients in sustained remission to 118.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Interferon-alpha / therapeutic use. Leukemia, Hairy Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Recombinant Proteins. Remission Induction

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  • (PMID = 20887503.001).
  • [ISSN] 1743-7563
  • [Journal-full-title] Asia-Pacific journal of clinical oncology
  • [ISO-abbreviation] Asia Pac J Clin Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a
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60. Wong P, Iwasaki M, Somervaille TC, Ficara F, Carico C, Arnold C, Chen CZ, Cleary ML: The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression. Cancer Res; 2010 May 1;70(9):3833-42
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  • [Title] The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression.
  • Despite advances in defining the critical molecular determinants for leukemia stem cell (LSC) generation and maintenance, little is known about the roles of microRNAs in LSC biology.
  • Here, we identify microRNAs that are differentially expressed in LSC-enriched cell fractions (c-kit(+)) in a mouse model of MLL leukemia.
  • Expression of miR-17 family microRNAs was substantially reduced concomitant with leukemia cell differentiation and loss of self-renewal, whereas forced expression of a polycistron construct encoding miR-17-19b miRNAs significantly shortened the latency for MLL leukemia development.
  • Leukemias expressing increased levels of the miR-17-19b construct displayed a higher frequency of LSCs, more stringent block of differentiation, and enhanced proliferation associated with reduced expression of p21, a cyclin-dependent kinase inhibitor previously implicated as a direct target of miR-17 microRNAs.
  • Knockdown of p21 in MLL-transformed cells phenocopied the overexpression of the miR-17 polycistron, including a significant decrease in leukemia latency, validating p21 as a biologically relevant and direct in vivo target of the miR-17 polycistron in MLL leukemia.
  • Expression of c-myc, a crucial upstream regulator of the miR-17 polycistron, correlated with miR-17-92 levels, enhanced self-renewal, and LSC potential.
  • Thus, microRNAs quantitatively regulate LSC self-renewal in MLL-associated leukemia in part by modulating the expression of p21, a known regulator of normal stem cell function.

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  • [Copyright] (c)2010 AACR.
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  • (PMID = 20406979.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL081612; United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / CA55029; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NHLBI NIH HHS / HL / R01 HL081612-05; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / CA116606; United States / NHLBI NIH HHS / HL / R01 HL081612-04; United States / NIH HHS / OD / DP1 OD006435; United States / NCI NIH HHS / CA / CA055029-18; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [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 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MicroRNAs; 0 / Mirn17 microRNA, mouse; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS185039; NLM/ PMC2862107
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61. Sjøholt G, Bedringaas SL, Døskeland AP, Gjertsen BT: Proteomic strategies for individualizing therapy of acute myeloid leukemia (AML). Curr Pharm Biotechnol; 2006 Jun;7(3):159-70
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  • [Title] Proteomic strategies for individualizing therapy of acute myeloid leukemia (AML).
  • Acute myeloid leukemia (AML) is an aggressive hematological malignancy characterized by accumulating myeloid precursor cells in the bone marrow, with approximately 2-3 months 50% survival if left untreated.
  • However, approximately half of the AML patients have no risk stratifying features, and early reports indicate that proteomic approaches may be utilized for disease classification as well as development of novel biomarkers related to prognosis, diagnosis, and choice of therapeutic regimen.
  • Proteomics, here defined as the analysis of all proteins in a cell, in a cell compartment or in a signaling pathway, has probably its greatest potential in investigating pathways that are easily targeted by small molecules or therapeutic antibodies.
  • The major methodological challenges include detection sensitivity in a limited clinical material, a problem that in some cases can be solved through designated multiplexed protein assays based on single cells or cell extracts.
  • In this review we will discuss pharmacoproteomic studies of drugs regulating leukemia specific targets like all-trans retinoic acid, histone deacetylase inhibitors, proteasome inhibitors and tyrosine kinase inhibitors, as well as studies on drug resistance and graft-versus-host studies during stem cell transplantations.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Myeloid / therapy. Neoplasm Proteins / analysis. Proteomics / methods
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Graft vs Host Disease / metabolism. Humans. Stem Cell Transplantation

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  • (PMID = 16789901.001).
  • [ISSN] 1389-2010
  • [Journal-full-title] Current pharmaceutical biotechnology
  • [ISO-abbreviation] Curr Pharm Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 143
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62. Zhang QL, Wang L, Zhang YW, Jiang XX, Yang F, Wu WL, Janin A, Chen Z, Shen ZX, Chen SJ, Zhao WL: The proteasome inhibitor bortezomib interacts synergistically with the histone deacetylase inhibitor suberoylanilide hydroxamic acid to induce T-leukemia/lymphoma cells apoptosis. Leukemia; 2009 Aug;23(8):1507-14
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  • [Title] The proteasome inhibitor bortezomib interacts synergistically with the histone deacetylase inhibitor suberoylanilide hydroxamic acid to induce T-leukemia/lymphoma cells apoptosis.
  • Interactions between inhibitors of the proteasome and histone deacetylases have been examined in human T-leukemia/lymphoma cells both in vitro and in vivo.
  • Co-exposure of cells to bortezomib and suberoylanilide hydroxamic acid (SAHA) synergistically induces T-leukemia/lymphoma cells to undergo apoptosis, consistent with a significant increase in mitochondrial injury and caspase activation.
  • Moreover, bortezomib in conjunction with SAHA efficiently induces apoptosis of primary T-leukemia/lymphoma cells and inhibits tumor growth in a murine xenograft model established with subcutaneous injection of Jurkat cells.
  • Taken together, these findings confirm the synergistic anti-tumor effect of the proteasome and histone deacetylase inhibitors, and provide an insight into the future clinical applications of bortezomib-SAHA combining regimen in treating T-cell malignancies.
  • [MeSH-major] Boronic Acids / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Leukemia, T-Cell / pathology. Lymphoma, T-Cell / pathology. Neoplasm Proteins / antagonists & inhibitors. Protease Inhibitors / pharmacology. Proteasome Inhibitors. Pyrazines / pharmacology. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bortezomib. Cell Line, Tumor / drug effects. Cell Line, Tumor / pathology. Drug Synergism. Humans. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Intracellular Signaling Peptides and Proteins / physiology. Jurkat Cells / drug effects. Jurkat Cells / enzymology. Jurkat Cells / transplantation. Mice. Mice, Nude. Protein Kinases / physiology. Xenograft Model Antitumor Assays


63. Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B, Berger U, Telford N, Aruliah S, Yin JA, Vanstraelen D, Barker HF, Taylor PC, O'Driscoll A, Benedetti F, Rudolph C, Kolb HJ, Hochhaus A, Hehlmann R, Chase A, Cross NC: The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. Cancer Res; 2005 Apr 1;65(7):2662-7
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  • [Title] The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2.
  • We have identified a t(8;9)(p21-23;p23-24) in seven male patients (mean age 50, range 32-74) with diverse hematologic malignancies and clinical outcomes: atypical chronic myeloid leukemia/chronic eosinophilic leukemia (n = 5), secondary acute myeloid leukemia (n = 1), and pre-B-cell acute lymphoblastic leukemia (n = 1).
  • Patients with PCM1-JAK2 disease are attractive candidates for targeted signal transduction therapy.
  • [MeSH-major] Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Sequence. Autoantigens. Base Sequence. Humans. Janus Kinase 2. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15805263.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; 0 / PCM1-JAK2 fusion protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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64. Gorczynski MJ, Grembecka J, Zhou Y, Kong Y, Roudaia L, Douvas MG, Newman M, Bielnicka I, Baber G, Corpora T, Shi J, Sridharan M, Lilien R, Donald BR, Speck NA, Brown ML, Bushweller JH: Allosteric inhibition of the protein-protein interaction between the leukemia-associated proteins Runx1 and CBFbeta. Chem Biol; 2007 Oct;14(10):1186-97
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  • [Title] Allosteric inhibition of the protein-protein interaction between the leukemia-associated proteins Runx1 and CBFbeta.
  • The two subunits of core binding factor (Runx1 and CBFbeta) play critical roles in hematopoiesis and are frequent targets of chromosomal translocations found in leukemia.
  • Treatment of the human leukemia cell line ME-1 with these compounds shows decreased proliferation, indicating these are good candidates for further development.
  • [MeSH-major] Allosteric Site. Cell Proliferation / drug effects. Core Binding Factor Alpha 2 Subunit / antagonists & inhibitors. Core Binding Factor beta Subunit / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Leukemia / pathology
  • [MeSH-minor] Binding Sites. Cell Line, Tumor. Fluorescence Resonance Energy Transfer. Hematopoiesis / genetics. Hematopoiesis / physiology. Humans. Magnetic Resonance Spectroscopy. Myosin Heavy Chains / chemistry. Myosin Heavy Chains / metabolism. Recombinant Fusion Proteins / chemistry. Recombinant Fusion Proteins / metabolism. Smooth Muscle Myosins / chemistry. Smooth Muscle Myosins / metabolism. Translocation, Genetic / genetics. Translocation, Genetic / physiology

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  • (PMID = 17961830.001).
  • [ISSN] 1074-5521
  • [Journal-full-title] Chemistry & biology
  • [ISO-abbreviation] Chem. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / Enzyme Inhibitors; 0 / Recombinant Fusion Proteins; EC 3.6.1.- / Smooth Muscle Myosins; EC 3.6.4.1 / Myosin Heavy Chains
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65. Deininger M, Buchdunger E, Druker BJ: The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood; 2005 Apr 1;105(7):2640-53
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  • [Title] The development of imatinib as a therapeutic agent for chronic myeloid leukemia.
  • Imatinib has revolutionized drug therapy of chronic myeloid leukemia (CML).
  • Responses in chronic phase are unprecedented, with rates of complete cytogenetic response (CCR) of more than 40% in patients after failure of interferon-alpha (IFN) and more than 80% in newly diagnosed patients, a level of efficacy that led to regulatory approval in record time.
  • While most of these responses are stable, resistance to treatment after an initial response is common in more advanced phases of the disease.
  • Patients with CCR who achieve a profound reduction of BCR-ABL mRNA have a very low risk of disease progression.
  • However, residual disease usually remains detectable with reverse transcription-polymerase chain reaction (RT-PCR), indicating that disease eradication may pose a significant challenge.
  • The mechanisms underlying the persistence of minimal residual disease are unknown.
  • In this manuscript, we review the preclinical and clinical development of imatinib for the therapy of CML, resistance and strategies that may help to eliminate resistant or residual leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use


66. Netto CD, Santos ES, Castro CP, da Silva AJ, Rumjanek VM, Costa PR: (+/-)-3,4-Dihydroxy-8,9-methylenedioxypterocarpan and derivatives: cytotoxic effect on human leukemia cell lines. Eur J Med Chem; 2009 Feb;44(2):920-5
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  • [Title] (+/-)-3,4-Dihydroxy-8,9-methylenedioxypterocarpan and derivatives: cytotoxic effect on human leukemia cell lines.
  • Naturally occurring pterocarpans 1a,b, pterocarpan 1c, isoflavane 2 and ortho-quinone 3 were synthesized in the racemic form and their cytotoxic effect was evaluated on the human leukemia cell lines K562 (resistant to oxidative stress), Lucena-1 (MDR phenotype) and HL-60.
  • Ortho-quinone 3 (IC(50)=1.5 microM, 1.8 microM and 0.2 microM, respectively) and catechol pterocarpan 1a (IC(50)=3.0 microM, 3.7 microM and 2.1 microM, respectively) were the most active compounds on these cells and were also evaluated on other human leukemia cell lines (Jurkat and Daudi).
  • Ortho-quinone 3 was 2 to 10 times more potent than pterocarpan 1a, depending on the cell line considered, however, showed a greater toxicity for lymphocytes activated by PHA.
  • [MeSH-major] Antineoplastic Agents / chemistry. Biological Products / chemical synthesis. Leukemia / drug therapy. Pterocarpans / chemical synthesis
  • [MeSH-minor] Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Inhibitory Concentration 50. Quinones

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  • (PMID = 18468732.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 3,4-dihydroxy-8,9-methylenedioxypterocarpan; 0 / Antineoplastic Agents; 0 / Biological Products; 0 / Pterocarpans; 0 / Quinones
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67. Ghoshal Gupta S, Baumann H, Wetzler M: Epigenetic regulation of signal transducer and activator of transcription 3 in acute myeloid leukemia. Leuk Res; 2008 Jul;32(7):1005-14
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  • [Title] Epigenetic regulation of signal transducer and activator of transcription 3 in acute myeloid leukemia.
  • We have demonstrated that constitutive signal transducer and activator of transcription (STAT) 3 activity, observed in approximately 50% of acute myeloid leukemia (AML) cases, is associated with adverse treatment outcome.
  • A better understanding of mechanisms of dysregulation of STAT signaling pathways may serve as a basis for designing novel therapeutic strategies that target these pathways in leukemia cells.

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  • (PMID = 18192010.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / CA85580; United States / NCI NIH HHS / CA / CA99238; United States / NCI NIH HHS / CA / R01 CA085580; United States / NCI NIH HHS / CA / R21 CA099238; United States / NCI NIH HHS / CA / R21 CA099238-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor
  • [Number-of-references] 90
  • [Other-IDs] NLM/ NIHMS49243; NLM/ PMC4629448
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68. Bartick M, Reinhold A: The burden of suboptimal breastfeeding in the United States: a pediatric cost analysis. Pediatrics; 2010 May;125(5):e1048-56
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  • It studied 3 diseases and totaled direct and indirect costs and cost of premature death.
  • The 2001 study can be updated by using current breastfeeding rates and adding additional diseases analyzed in the 2007 breastfeeding report from the Agency for Healthcare Research and Quality.
  • Excluding type 2 diabetes (because of insufficient data), we conducted a cost analysis for all pediatric diseases for which the Agency for Healthcare Research and Quality reported risk ratios that favored breastfeeding: necrotizing enterocolitis, otitis media, gastroenteritis, hospitalization for lower respiratory tract infections, atopic dermatitis, sudden infant death syndrome, childhood asthma, childhood leukemia, type 1 diabetes mellitus, and childhood obesity.
  • We used 2005 Centers for Disease Control and Prevention breastfeeding rates and 2007 dollars.

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  • [CommentIn] J Hum Lact. 2010 Aug;26(3):338-9 [20689106.001]
  • (PMID = 20368314.001).
  • [ISSN] 1098-4275
  • [Journal-full-title] Pediatrics
  • [ISO-abbreviation] Pediatrics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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69. Yu CL, Wang SF, Pan PC, Wu MT, Ho CK, Smith TJ, Li Y, Pothier L, Christiani DC, Kaohsiung Leukemia Research Group: Residential exposure to petrochemicals and the risk of leukemia: using geographic information system tools to estimate individual-level residential exposure. Am J Epidemiol; 2006 Aug 1;164(3):200-7
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  • [Title] Residential exposure to petrochemicals and the risk of leukemia: using geographic information system tools to estimate individual-level residential exposure.
  • The authors conducted a population-based, case-control study in Kaohsiung, southern Taiwan, Republic of China, to investigate the association between residential petrochemical exposure and leukemia risk among subjects 29 years of age and younger.
  • Different conditional logistic regression models were fitted for subjects aged 0-19 and 20-29 years to evaluate separately childhood versus adulthood leukemia.
  • However, residential petrochemical exposure was a significant risk factor for leukemia for the older age group.
  • [MeSH-major] Air Pollutants / adverse effects. Environmental Exposure / adverse effects. Geographic Information Systems. Leukemia / epidemiology. Petroleum / adverse effects

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  • [CommentIn] Am J Epidemiol. 2006 Aug 1;164(3):208-11 [16707652.001]
  • (PMID = 16754633.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES00002; United States / NIEHS NIH HHS / ES / ES09723
  • [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 / Air Pollutants; 0 / Petroleum
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70. Nardi V, Naveiras O, Azam M, Daley GQ: ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines. Blood; 2009 Apr 16;113(16):3813-20
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  • [Title] ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines.
  • Interferon (IFN) is effective at inducing complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an immune mechanism.
  • Here we show that the type I IFNs (alpha and beta) regulate expression of the IFN consensus sequence-binding protein (ICSBP) in BCR-ABL-transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of BCR-ABL-induced leukemia.
  • We identify the chemokines CCL6 and CCL9 as genes prominently induced by the type I IFNs and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression.

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  • (PMID = 19171873.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL066987; United States / NHLBI NIH HHS / HL / T32-HL 66987-07
  • [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 / Ccl9 protein, mouse; 0 / Chemokines, CC; 0 / Interferon Regulatory Factors; 0 / Interferon Type I; 0 / Macrophage Inflammatory Proteins; 0 / interferon regulatory factor-8; 139568-96-0 / Ccl6 protein, mouse
  • [Other-IDs] NLM/ PMC2670796
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71. Dunphy CH: Gene expression profiling data in lymphoma and leukemia: review of the literature and extrapolation of pertinent clinical applications. Arch Pathol Lab Med; 2006 Apr;130(4):483-520
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  • [Title] Gene expression profiling data in lymphoma and leukemia: review of the literature and extrapolation of pertinent clinical applications.
  • OBJECTIVES: To review the literature regarding GE data that may provide important information regarding pathogenesis and that may be extrapolated for use in diagnosing and prognosticating lymphomas and leukemias; to present GE findings in Hodgkin and non-Hodgkin lymphomas, acute leukemias, and chronic myeloid leukemia in detail; and to summarize the practical clinical applications in tables that are referenced throughout the text.
  • CONCLUSIONS: Gene expression profiling of lymphomas and leukemias aids in the diagnosis and prognostication of these diseases.
  • The extrapolation of these findings to more timely, efficient, and cost-effective methods, such as flow cytometry and immunohistochemistry, results in better diagnostic tools to manage the diseases.
  • Flow cytometric and immunohistochemical applications of the information gained from GE profiling assist in the management of chronic lymphocytic leukemia, other low-grade B-cell non-Hodgkin lymphomas and leukemias, diffuse large B-cell lymphoma, nodular lymphocyte-predominant Hodgkin lymphoma, and classic Hodgkin lymphoma.
  • For practical clinical use, GE profiling of precursor B acute lymphoblastic leukemia, precursor T acute lymphoblastic leukemia, and acute myeloid leukemia has supported most of the information that has been obtained by cytogenetic and molecular studies (except for the identification of FLT3 mutations for molecular analysis), but extrapolation of the analyses leaves much to be gained based on the GE profiling data.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia / diagnosis. Leukemia / genetics. Lymphoma / diagnosis. Lymphoma / genetics

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  • (PMID = 16594743.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  • [Number-of-references] 173
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72. Mehrany K, Weenig RH, Pittelkow MR, Roenigk RK, Otley CC: High recurrence rates of squamous cell carcinoma after Mohs' surgery in patients with chronic lymphocytic leukemia. Dermatol Surg; 2005 Jan;31(1):38-42; discussion 42
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  • [Title] High recurrence rates of squamous cell carcinoma after Mohs' surgery in patients with chronic lymphocytic leukemia.
  • BACKGROUND: Cutaneous cancers exhibit a much higher incidence in patients with chronic lymphocytic leukemia than in nonleukemic patients.
  • Squamous and basal cell carcinomas also exhibit greater subclinical tumor extension in patients with chronic lymphocytic leukemia.
  • OBJECTIVE: The purpose of this study was to estimate and compare the recurrence rates of squamous cell carcinoma after Mohs' surgery in patients with chronic lymphocytic leukemia compared with those in controls and to evaluate differences among squamous cell carcinoma size and histologic grade.
  • METHODS: We retrospectively assessed the clinical histories, postoperative notes, and surgical photographs of patients with chronic lymphocytic leukemia and controls matched (2:1) for age, sex, and surgical year.
  • Both patients and controls underwent Mohs' surgery for squamous cell carcinoma of the head and neck at the Mayo Clinic between March 1988 and April 1999.
  • RESULTS: Twenty-eight patients who underwent Mohs' surgery for 57 squamous cell carcinomas had 7 recurrences.
  • Squamous cell carcinoma was seven times more likely to recur in patients with chronic lymphocytic leukemia than in controls (p = .003).
  • CONCLUSION: The recurrence rates of squamous cell carcinoma were significantly higher in patients with chronic lymphocytic leukemia.
  • Squamous cell carcinomas in patients with chronic lymphocytic leukemia did not exhibit a significant difference in histologic grade or clinical difference in preoperative tumor size.
  • Close surveillance for squamous cell carcinoma recurrence is warranted in patients with chronic lymphocytic leukemia.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Neoplasm Recurrence, Local / epidemiology. Skin Neoplasms / pathology


73. Uckun FM, Goodman P, Ma H, Dibirdik I, Qazi S: CD22 EXON 12 deletion as a pathogenic mechanism of human B-precursor leukemia. Proc Natl Acad Sci U S A; 2010 Sep 28;107(39):16852-7
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  • [Title] CD22 EXON 12 deletion as a pathogenic mechanism of human B-precursor leukemia.
  • Here, we report that primary leukemic cells from infants with newly diagnosed B-precursor leukemia express a truncated and functionally defective CD22 coreceptor protein that is unable to transmit apoptotic signals because it lacks most of the intracellular domain, including the key regulatory signal transduction elements and all of the cytoplasmic tyrosine residues.
  • Expression of this structurally and functionally abnormal CD22 protein is associated with a very aggressive in vivo growth of patients' primary leukemia cells causing disseminated overt leukemia in SCID mice.
  • These mutations cause marked changes in the predicted secondary structures of the mutant CD22 pre-mRNA sequences that affect the target motifs for the splicing factors hnRNP-L, PTB, and PCBP that are up-regulated in infant leukemia cells.
  • Forced expression of the mutant CD22ΔE12 protein in transgenic mice perturbs B-cell development, as evidenced by B-precursor/B-cell hyperplasia, and corrupts the regulation of gene expression, causing reduced expression levels of several genes with a tumor suppressor function.
  • We further show that CD22ΔE12-associated unique gene expression signature is a discriminating feature of newly diagnosed infant leukemia patients.
  • These striking findings implicate CD22ΔE12 as a previously undescribed pathogenic mechanism in human B-precursor leukemia.
  • [MeSH-major] Exons / genetics. Gene Expression Regulation, Leukemic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sialic Acid Binding Ig-like Lectin 2 / genetics

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  • (PMID = 20841423.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ HQ225617/ HQ225618/ HQ225619/ HQ225620; GEO/ GSE23998/ GSE24000/ GSE24001
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CD22 protein, human; 0 / RNA Precursors; 0 / Sialic Acid Binding Ig-like Lectin 2
  • [Other-IDs] NLM/ PMC2947921
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74. Bayram I, Erbey F, Kömür M, Kibar F, Tanyeli A: Flow cytometry results at diagnosis and relapse in childhood acute lymphoblastic leukemia. Asian Pac J Cancer Prev; 2010;11(5):1321-4
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  • [Title] Flow cytometry results at diagnosis and relapse in childhood acute lymphoblastic leukemia.
  • INTRODUCTION: Several studies have focused on the immunophenotype of the leukemic population at the time of relapse compared to that observed at diagnosis.
  • OBJECTIVE: The question of whether differences exist between surface antigens levels on blasts at the time of diagnosis and at relapse in cases of acute lymphoblastic leukemia (ALL) was addressed.
  • RESULTS: The most frequently detected five antigens were I2 (n=21), CD10 (n=17), CD41 (n=16), CD2 (n=14) and CD7/CD19 (n=13/n=13) at the time of diagnosis and CD41 (n=21), I2 (n=20), CD10 (n=14), CD19 (n=16) and CD2 (n=12) at the time of relapse.
  • There was a significant difference only between CD41 levels at the time of diagnosis and at the time of relapse (p=0.041).
  • This condition ought to be evaluated with reference to prognosis of leukemia.
  • [MeSH-major] Antigens, CD / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 21198285.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antigens, CD
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75. Liang L, Su LP: [Etiological analysis of 67 cases of acute leukemia combined with fungal infection]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Feb;17(1):218-21
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  • [Title] [Etiological analysis of 67 cases of acute leukemia combined with fungal infection].
  • In order to study the etiological distribution characteristics of fungal infection and improve the clinical therapeutic efficacy in acute leukemia (AL) patients, the fungal infection etiological distribution, infection site and cause were retrospectively analyzed in 67 cases of AL combined with fungal infection.
  • Infection sites involved oral cavity, low respiratory tract, gastrointestinal tract, blood and urethra; susceptible factors was correlated positively to the duration of administration of broad-spectral antibiotics, glucocorticoid and agranulocytosis.
  • (3) the susceptible factors to fungal infection are agranulocytosis and administration of broad-spectral antibiotics in acute leukemia patients;.

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  • (PMID = 19236783.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Glucocorticoids
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76. González-Herrero I, Vicente-Dueñas C, Orfao A, Flores T, Jiménez R, Cobaleda C, Sánchez-García I: Bcl2 is not required for the development and maintenance of leukemia stem cells in mice. Carcinogenesis; 2010 Jul;31(7):1292-7
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  • [Title] Bcl2 is not required for the development and maintenance of leukemia stem cells in mice.
  • The existence of leukemia stem cells (LSCs) responsible for tumor maintenance has been firmly established.
  • In order to understand the role of Bcl2 in LSC generation and maintenance, we have taken advantage of our Sca1-BCRABLp210 mouse model of human chronic myeloid leukemia and bcl2 gene-targeted mice.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / pathology. Proto-Oncogene Proteins / physiology
  • [MeSH-minor] Animals. Antigens, Ly / physiology. Benzamides. Disease Models, Animal. Fusion Proteins, bcr-abl / physiology. Humans. Imatinib Mesylate. Membrane Proteins / physiology. Mice. Piperazines / therapeutic use. Proto-Oncogene Proteins c-bcl-2. Pyrimidines / therapeutic use

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  • (PMID = 20299524.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Ly; 0 / Benzamides; 0 / Ly6a protein, mouse; 0 / Membrane Proteins; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrimidines; 114100-40-2 / Bcl2 protein, mouse; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2893797
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77. Hayani A, Lampeter E, Viswanatha D, Morgan D, Salvi SN: First report of autologous cord blood transplantation in the treatment of a child with leukemia. Pediatrics; 2007 Jan;119(1):e296-300
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  • [Title] First report of autologous cord blood transplantation in the treatment of a child with leukemia.
  • We present the case of a 3-year-old girl with acute lymphoblastic leukemia who developed isolated central nervous system relapse while receiving chemotherapy 10 months after diagnosis.
  • The child achieved a second remission on retreatment with systemic and intrathecal chemotherapy.
  • She then underwent myeloablative chemotherapy and radiation therapy followed by infusion of her own umbilical cord blood, which the parents had saved after her delivery.
  • She is now doing well and is in complete remission 20 months after cord blood transplantation.
  • In this first report of autologous cord blood transplantation for treatment of childhood leukemia, we discuss the safety and feasibility of this procedure as well as some of the uncertainties surrounding autologous cord blood collection and usage.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Child. Child, Preschool. Female. Humans. Recurrence. Remission Induction. Tissue Banks. Transplantation, Autologous

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  • [CommentIn] Pediatrics. 2007 May;119(5):1042-3; author reply 1043 [17473115.001]
  • (PMID = 17200253.001).
  • [ISSN] 1098-4275
  • [Journal-full-title] Pediatrics
  • [ISO-abbreviation] Pediatrics
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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78. Skoczen S, Surmiak M, Strojny W: Survivors of acute lymphoblastic leukemia and body mass changes. Expert Opin Drug Saf; 2010 Jan;9(1):65-77
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  • [Title] Survivors of acute lymphoblastic leukemia and body mass changes.
  • Along with malnutrition, it causes increasing morbidity and mortality in the general population.
  • Survivors of pediatric leukemia are at increased risk of developing adverse body mass changes.
  • AREAS COVERED IN THIS REVIEW: The present article reviews the data from studies of leukemia survivors in the context of basic science studies and reports of nutritional situation in Europe published between 1994 and 2009.
  • TAKE HOME MESSAGE: Both underweight and overweight leukemia survivors need to be monitored for ongoing health consequences of abnormal BMI.
  • Parameters of metabolic syndrome should be included as routine assessments in outpatient clinics taking care of childhood leukemia survivors.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Body Mass Index. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Survivors

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  • (PMID = 20001758.001).
  • [ISSN] 1744-764X
  • [Journal-full-title] Expert opinion on drug safety
  • [ISO-abbreviation] Expert Opin Drug Saf
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / FTO protein, human; 0 / Proteins
  • [Number-of-references] 65
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79. Karakosta M, Tsakiridou A, Korantzis I, Manola KN: Deletion of 5q as a rare abnormality in chronic lymphocytic leukemia. Cancer Genet Cytogenet; 2010 Jul 15;200(2):175-9
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  • [Title] Deletion of 5q as a rare abnormality in chronic lymphocytic leukemia.
  • Deletions of the long arm of chromosome 5 [del(5q)] are frequent chromosome aberrations with known prognosis in myelodysplastic syndromes and acute myeloid leukemia (AML).
  • However, in chronic lymphocytic leukemia (CLL), they are rare and have been reported only as karyotypic results without known prognosis.
  • Karyotypic and fluorescence in situ hybridization analysis that used probes for the most common aberrations of CLL demonstrated that del(5q) was the sole chromosome abnormality in both patients at the time of diagnosis.
  • Both patients had disease that was still staged as Binet A at 28 and 18 months after diagnosis, respectively, without receiving any therapy because of their good clinical condition.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 5. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20620603.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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80. Kheifets L, Oksuzyan S: Exposure assessment and other challenges in non-ionizing radiation studies of childhood leukaemia. Radiat Prot Dosimetry; 2008;132(2):139-47
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  • [Title] Exposure assessment and other challenges in non-ionizing radiation studies of childhood leukaemia.
  • Studies of electromagnetic fields (EMF) and the development of childhood leukaemia face unique difficulties.
  • Childhood leukaemia and high average exposures to magnetic fields are both quite rare.
  • New approaches are needed; the most promising in the extremely low-frequency range involves a study of a highly exposed cohort of children who have lived in apartments next to built-in transformers or electrical equipment rooms.
  • [MeSH-major] Body Burden. Environmental Exposure / analysis. Environmental Exposure / statistics & numerical data. Leukemia, Radiation-Induced / epidemiology. Radiation Monitoring / methods. Radiation Monitoring / statistics & numerical data. Risk Assessment / methods

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  • (PMID = 18940819.001).
  • [ISSN] 0144-8420
  • [Journal-full-title] Radiation protection dosimetry
  • [ISO-abbreviation] Radiat Prot Dosimetry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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81. Sancho JM, Morgades M, Arranz R, Fernández-Abellán P, Deben G, Alonso N, Blanes M, Rodríguez MJ, Nicolás C, Sánchez E, Fernández de Sevilla A, Conde E, Ribera JM, QUIT Study (PETHEMA, GELTAMO and GOTEL Groups): Practice of central nervous system prophylaxis and treatment in acute leukemias in Spain. Prospective registry study. Med Clin (Barc); 2008 Oct 4;131(11):401-5
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  • [Title] Practice of central nervous system prophylaxis and treatment in acute leukemias in Spain. Prospective registry study.
  • BACKGROUND AND OBJECTIVE: Central nervous system (CNS) involvement in patients diagnosed with acute leukemias (AL) is an uncommon complication with poor prognosis.
  • For acute lymphoblastic leukemia patients (n = 158), CNS therapy was given to 12 cases (10 at diagnosis and 2 at relapse) and consisted of triple intrathecal therapy (TIT, methotrexate, cytarabine and hydrocortisone) in 11 and liposomal depot cytarabine in one.
  • In acute myeloblastic leukemia patients (n = 107), CNS therapy was administered to 17 cases (9 at diagnosis and 8 at relapse).
  • [MeSH-major] Central Nervous System Neoplasms / prevention & control. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Registries

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  • (PMID = 18928719.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antimetabolites, Antineoplastic; 0 / Liposomes; 04079A1RDZ / Cytarabine; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate
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82. Lewis RS, Ward AC: Stat5 as a diagnostic marker for leukemia. Expert Rev Mol Diagn; 2008 Jan;8(1):73-82
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  • [Title] Stat5 as a diagnostic marker for leukemia.
  • Not surprisingly, perturbation of this pathway is implicated in diseases of hematopoietic and immune origin, including leukemia, lymphoma and immune deficiencies.
  • This review examines the role of a key component of this pathway, Stat5.
  • This has been shown to be activated in a variety of leukemias and myeloproliferative disorders, including downstream of a range of key oncogenes where it has been shown to play an important role in mediating their effects.
  • Therefore, Stat5 represents a useful pan-leukemia/myeloproliferative disorder diagnostic marker and key therapeutic end point, as well as representing an attractive therapeutic target for these disorders.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia / diagnosis. STAT5 Transcription Factor / metabolism

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  • (PMID = 18088232.001).
  • [ISSN] 1744-8352
  • [Journal-full-title] Expert review of molecular diagnostics
  • [ISO-abbreviation] Expert Rev. Mol. Diagn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / STAT5 Transcription Factor
  • [Number-of-references] 144
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83. Huguet F, Leguay T, Raffoux E, Thomas X, Beldjord K, Delabesse E, Chevallier P, Buzyn A, Delannoy A, Chalandon Y, Vernant JP, Lafage-Pochitaloff M, Chassevent A, Lhéritier V, Macintyre E, Béné MC, Ifrah N, Dombret H: Pediatric-inspired therapy in adults with Philadelphia chromosome-negative acute lymphoblastic leukemia: the GRAALL-2003 study. J Clin Oncol; 2009 Feb 20;27(6):911-8
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  • [Title] Pediatric-inspired therapy in adults with Philadelphia chromosome-negative acute lymphoblastic leukemia: the GRAALL-2003 study.
  • PURPOSE: Retrospective comparisons have suggested that adolescents or teenagers with acute lymphoblastic leukemia (ALL) benefit from pediatric rather than adult chemotherapy regimens.
  • PATIENTS AND METHODS: Between 2003 and 2005, 225 adult patients (median age, 31 years; range, 15 to 60 years) with Philadelphia chromosome-negative ALL were enrolled onto the Group for Research on Adult Acute Lymphoblastic Leukemia 2003 protocol, which included several pediatric options.
  • Some adult options, such as allogeneic stem-cell transplantation for patients with high-risk ALL, were nevertheless retained.
  • RESULTS: were retrospectively compared with the historical France-Belgium Group for Lymphoblastic Acute Leukemia in Adults 94 (LALA-94) trial experience in 712 patients age 15 to 55 years.
  • Results Complete remission rate was 93.5%.
  • In older versus younger patients, there was a higher cumulative incidence of chemotherapy-related deaths (23% v 5%, respectively; P < .001) and deaths in first CR (22% v 5%, respectively; P < .001), whereas the incidence of relapse remained stable (30% v 32%, respectively).
  • Complete remission rate (P = .02), EFS (P < .001), and OS (P < .001) compared favorably with the previous LALA-94 experience.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [ErratumIn] J Clin Oncol. 2009 May 20;27(15):2574. Dosage error in article text
  • (PMID = 19124805.001).
  • [ISSN] 1527-7755
  • [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, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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84. Hasanbegović E: [Clinical and hematologic features of pediatric leukemias]. Med Arh; 2006;60(6 Suppl 2):84-6
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  • [Title] [Clinical and hematologic features of pediatric leukemias].
  • [Transliterated title] Klinicke i hematoloske karakteristike djecijih leukemija.
  • AIM OF INVESTIGATION: to present main clinical and hematologic features of pediatric leukemias treated at Hematooncologic department of Pediatric Clinic in Sarajevo during last 7 years.
  • PATIENTS AND METHODS: In retrospective study we followed up children with leukemia aged 0-15 who were treated during period of 01.01.1997-31.12.2003. at Hematooncologic department on Pediatric Clinic in Sarajevo.
  • RESULTS: A total number of patient with leukemia was 130 of them 112 (83.2%) had acute lymphoblastic leukemia (ALL), 16 (12.3%) of them had acute myeloid leukemia (AML) and 2 (1.5%) patients had chronic myeloid leukemia (CML).
  • CONCLUSION: Most frequent signs at the beginning of the illness are general symptoms like fatigue, unclear febrile state and accented bone pains.
  • Those united signs with complete blood picture finding should be enough reason for suspicion under possible leukemia.
  • [MeSH-major] Leukemia / diagnosis

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  • (PMID = 18172990.001).
  • [Journal-full-title] Medicinski arhiv
  • [ISO-abbreviation] Med Arh
  • [Language] bos
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Bosnia and Herzegovina
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85. Viale A, De Franco F, Orleth A, Cambiaghi V, Giuliani V, Bossi D, Ronchini C, Ronzoni S, Muradore I, Monestiroli S, Gobbi A, Alcalay M, Minucci S, Pelicci PG: Cell-cycle restriction limits DNA damage and maintains self-renewal of leukaemia stem cells. Nature; 2009 Jan 1;457(7225):51-6
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  • [Title] Cell-cycle restriction limits DNA damage and maintains self-renewal of leukaemia stem cells.
  • Rare cells with the properties of stem cells are integral to the development and perpetuation of leukaemias.
  • A defining characteristic of stem cells is their capacity to self-renew, which is markedly extended in leukaemia stem cells.
  • Here we demonstrate that expression of the cell-cycle inhibitor p21 is indispensable for maintaining self-renewal of leukaemia stem cells.
  • Expression of leukaemia-associated oncogenes in mouse haematopoietic stem cells (HSCs) induces DNA damage and activates a p21-dependent cellular response, which leads to reversible cell-cycle arrest and DNA repair.
  • These data unravel the oncogenic potential of p21 and suggest that inhibition of DNA repair mechanisms might function as potent strategy for the eradication of the slowly proliferating leukaemia stem cells.
  • [MeSH-major] Cell Cycle. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. DNA Damage. Leukemia / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Cell Count. Cell Division. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA Repair. Fibroblasts. Gene Expression Regulation, Neoplastic. Mice. Mice, Inbred C57BL. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Up-Regulation


86. Gerr H, Zimmermann M, Schrappe M, Dworzak M, Ludwig WD, Bradtke J, Moericke A, Schabath R, Creutzig U, Reinhardt D: Acute leukaemias of ambiguous lineage in children: characterization, prognosis and therapy recommendations. Br J Haematol; 2010 Apr;149(1):84-92
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  • [Title] Acute leukaemias of ambiguous lineage in children: characterization, prognosis and therapy recommendations.
  • Acute leukaemias of ambiguous lineage (ALAL) represent a rare type of leukaemia, expressing both myeloid and lymphoid markers.
  • This study retrospectively analyzed data from 92 children (biphenotypic n = 78, bilineal n = 6, lineage switch n = 8) with ALAL registered in the Berlin-Frankfürt-Münster (BFM) acute myeloid leukaemia (AML) and acute lymphoblastic leukaemia (ALL) studies between 1998 and 2006 (2.4% of all cases with acute leukaemia).
  • Our cohort of ALAL patients was characterized by comparatively high median age (8.9 years), high median white blood cell count (14.9 x 10(9)/l), as well as frequent hyperleucocytosis (18.5%) and central nervous system involvement (24.1%).
  • Complete remission rate was significantly lower than in ALL-BFM patients (91.8% vs. 99.1%, P < 0.001), but comparable to AML-BFM patients (87.9%).
  • Our data suggest that an intensive therapy regimen including stem cell transplantation may be favourable for bilineal or lineage switch cases, whereas patients with ETV6/RUNX1 fusion, lymphoid morphology and patients with expression of cyCD22 and cyCD79a should be treated with an ALL-directed therapy.
  • [MeSH-major] Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Chromosome Aberrations. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. Infant. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 20085575.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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87. Xie J, Ma T, Gu Y, Zhang X, Qiu X, Zhang L, Xu R, Yu Y: Berbamine derivatives: a novel class of compounds for anti-leukemia activity. Eur J Med Chem; 2009 Aug;44(8):3293-8
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  • [Title] Berbamine derivatives: a novel class of compounds for anti-leukemia activity.
  • Our previous studies showed that the natural compound berbamine, from Chinese herb Berberis amurensis, selectively induces apoptosis of imatinib (IM)-resistant-Bcr/Abl-expressing leukemia cells from the K562 cell line and CML patients.
  • Compounds 2e, 2g, 3f, 3k, 3q and 3u exhibited consistent high anti-tumor activity for imatinib-resistant K562 leukemia cells.
  • Cell cycle analysis results showed that compound 3h could reduce G0/G1 cells.
  • In particular, these compounds displayed potent inhibition of the cytoplasm-to-nucleus translocation of NF-kappaB p65 which plays a critical role in the survival of leukemia stem cells.
  • These results suggest that berbamine could be a good starting point for the development of novel lead compounds in the fight against leukemia.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Antineoplastic Agents / pharmacology. Benzylisoquinolines / chemistry. Benzylisoquinolines / pharmacology. Drug Design. Leukemia / drug therapy
  • [MeSH-minor] Animals. Benzamides. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Inhibitory Concentration 50. Piperazines / pharmacology. Pyrimidines / pharmacology

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  • (PMID = 19285759.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzylisoquinolines; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; V5KM4XJ0WM / berbamine
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88. Pieters R: [Acute lymphoblastic leukaemia in children and adolescents: chance of cure now higher than 80%]. Ned Tijdschr Geneeskd; 2010;154:A1577
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  • [Title] [Acute lymphoblastic leukaemia in children and adolescents: chance of cure now higher than 80%].
  • [Transliterated title] Behandeling van acute lymfatische leukemie bij kinderen en adolescenten. Zijn we er bijna?
  • Acute lymphoblastic leukaemia (ALL) is the most prevalent type of cancer in patients under the age of 18 years.
  • Treatment of ALL consists of chemotherapy for a period of 2 years.
  • Prognostically important factors are age at diagnosis, genetic abnormalities in the leukaemic cells and initial response to therapy.
  • It is anticipated that genomic research will lead to better classification and to more personalized therapy for individual patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Male. Neoplasm Recurrence, Local. Prognosis. Radiotherapy, Adjuvant. Stem Cell Transplantation. Survival Rate. Treatment Outcome

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  • (PMID = 20858304.001).
  • [ISSN] 1876-8784
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
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89. Nishiwaki S, Miyamura K, Kato C, Terakura S, Ohashi K, Sakamaki H, Nakao S, Harigae H, Kodera Y: Impact of post-transplant imatinib administration on Philadelphia chromosome-positive acute lymphoblastic leukaemia. Anticancer Res; 2010 Jun;30(6):2415-8
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  • [Title] Impact of post-transplant imatinib administration on Philadelphia chromosome-positive acute lymphoblastic leukaemia.
  • To evaluate the effect of post-transplant imatinib administration, 34 Philadelphia chromosome-positive acute lymphoblastic leukaemia (Ph(+)ALL) patients were retrospectively analysed, with 7 receiving post-transplant imatinib administration.
  • Overall survival was significantly better in patients with post-transplant administration (66.7% vs. 29.6% at 3 years, p=0.03), with no significant difference in leukaemia-free survival (0% vs. 29.6% at 3 years, p=0.29).
  • The median duration of negative minimal residual disease (MRD) in patients with post-transplant imatinib administration was 6 months in the pre-emptive administration group, where imatinib was administered upon detecting MRD after allogeneic stem cell transplantation (allo-SCT).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Pyrimidines / therapeutic use

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  • (PMID = 20651401.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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90. Derwich K, Sedek L, Meyer C, Pieczonka A, Dawidowska M, Gaworczyk A, Wachowiak J, Konatkowska B, Witt M, Marschalek R, Szczepański T: Infant acute bilineal leukemia. Leuk Res; 2009 Jul;33(7):1005-8
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  • [Title] Infant acute bilineal leukemia.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • There are rare cases of acute leukemia, which cannot be clearly classified, because either blasts express antigens of more than one lineage (acute biphenotypic leukemias) or distinct blast populations of two lineages co-exist (acute bilineal leukemias, aBLL).
  • We present a 10-month-old infant with de novo aBLL, characterized by blasts of monocytic and B-cell precursor lineages.
  • Despite poor initial response, both to acute lymphoblastic leukemia (ALL) induction treatment and acute myeloid leukemia induction blocks, the child reached complete clinical remission with minimal residual disease negative status and was transplanted.
  • This case report illustrates that aBLL is a very aggressive type of acute leukemia that should be individually treated and monitored, particularly in children less than 1 year of age.
  • [MeSH-major] B-Lymphocytes / pathology. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Cell Lineage. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Remission Induction. Treatment Outcome

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  • (PMID = 19286255.001).
  • [ISSN] 1873-5835
  • [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
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91. Fiegl M, Hiddemann W, Braess J: [Current therapeutic strategies in the management of acute myeloid leukemia]. Med Klin (Munich); 2007 Apr 15;102(4):309-16
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  • [Title] [Current therapeutic strategies in the management of acute myeloid leukemia].
  • Acute myeloid leukemia (AML) is a rare disease of the hematopoietic stem cell leading to uncontrolled proliferation of immature progenitor cells.
  • Diagnosis can reliably be confirmed by bone marrow aspiration, which also allows risk stratification by cytogenetic and molecular analysis.
  • Therapy of AML that should preferentially be performed in clinical studies comprises induction therapy for achievement of complete cytomorphological remission (CR) and postremission strategies consisting of consolidation and maintenance therapy for eradication of residual blasts.
  • Different regimens exist that achieve CR rates of 60-80%.
  • To date, induction therapy will be performed independently of the individual risk constellation (with the exception of acute promyelocytic leukemia); however, postremission therapy is highly dependent on individual risk stratification.
  • Besides conventional strategies, allogeneic stem cell transplantation has to be considered in certain risk groups depending on the availability of a matched donor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Anthracyclines / administration & dosage. Anthracyclines / adverse effects. Biopsy, Needle. Bone Marrow / pathology. Bone Marrow Purging. Bone Marrow Transplantation. Cytarabine / administration & dosage. Cytarabine / adverse effects. Disease-Free Survival. Hematopoietic Stem Cell Transplantation. Humans. Prognosis. Remission Induction. Retreatment

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  • (PMID = 17426934.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anthracyclines; 04079A1RDZ / Cytarabine
  • [Number-of-references] 65
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92. Zainina S, Cheong SK: Myelodysplastic syndrome transformed into Acute Lymphoblastic Leukaemia (FAB:L3). Clin Lab Haematol; 2006 Aug;28(4):282-3
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  • [Title] Myelodysplastic syndrome transformed into Acute Lymphoblastic Leukaemia (FAB:L3).
  • Myelodysplastic syndrome (MDS) is recognized as a preleukaemic disorder with a variable risk of transformation to acute myeloid leukaemia.
  • Usually the blast cells in leukaemia are transformed after MDS displays a myeloid phenotype.
  • We report a case of an elderly man who had MDS transformed into Acute Lymphoblastic Leukaemia (ALL:L3) which is a rare lymphoid transformation.
  • [MeSH-major] Anemia, Refractory / pathology. Burkitt Lymphoma / pathology. Cell Transformation, Neoplastic / pathology


93. Guo F, Sigua C, Bali P, George P, Fiskus W, Scuto A, Annavarapu S, Mouttaki A, Sondarva G, Wei S, Wu J, Djeu J, Bhalla K: Mechanistic role of heat shock protein 70 in Bcr-Abl-mediated resistance to apoptosis in human acute leukemia cells. Blood; 2005 Feb 1;105(3):1246-55
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  • [Title] Mechanistic role of heat shock protein 70 in Bcr-Abl-mediated resistance to apoptosis in human acute leukemia cells.
  • Bcr-Abl-expressing primary or cultured leukemia cells display high levels of the antiapoptotic heat shock protein (hsp) 70 and are resistant to cytarabine (Ara-C), etoposide, or Apo-2L/TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis.
  • Collectively, these findings suggest that hsp70 inhibits apoptosis upstream and downstream of the mitochondria and is a promising therapeutic target for reversing drug-resistance in chronic myeloid leukemia-blast crisis and acute myeloid leukemia cells.
  • [MeSH-minor] Cell Line, Tumor. DNA Primers. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. HL-60 Cells. Humans. Jurkat Cells. Leukemia, Myeloid, Acute. Milk Proteins / genetics. Milk Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. STAT5 Transcription Factor. Trans-Activators / genetics. Trans-Activators / metabolism. bcl-2-Associated X Protein. bcl-X Protein

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  • (PMID = 15388581.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Milk Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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94. Huang LB, Guan XQ, Zhang YC, Zhang XL, Ke ZY, Luo XQ: Current status of diagnosis and prognosis of infant acute leukemia in China. Pediatr Blood Cancer; 2009 Dec;53(6):973-7
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  • [Title] Current status of diagnosis and prognosis of infant acute leukemia in China.
  • OBJECTIVE: Treatment and outcome of infant acute leukemia (IAL) in developed countries have been well documented.
  • However, reports summarizing diagnosis and outcome of IAL in developing countries are limited.
  • METHODS: Five hundred ninety seven pediatric patients were diagnosed with acute leukemia in our hospital between January 1997 and June 2008, of which 19 were younger than 12 months.
  • RESULTS: Of the 19 cases, 14 had acute lymphoblastic leukemia (ALL) and 5 had acute myeloid leukemia (AML) based on FAB classification.
  • Two infants with immunophenotypic AML who abandoned treatment achieved spontaneous remission without chemotherapy within 2 and 4 months respectively.
  • Combining our data with those from Chinese literature, less than one third of the infants had immunophenotypic and genetic verification of leukemia and 29% (18/63) of them received treatment.
  • [MeSH-major] Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. China / epidemiology. Female. Humans. Infant. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prognosis. Treatment Outcome

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  • (PMID = 19588516.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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95. Damnjanovic T, Milicevic R, Novkovic T, Jovicic O, Bunjevacki V, Jekic B, Lukovic L, Novakovic I, Redzic D, Milasin J: Association between the methylenetetrahydrofolate reductase polymorphisms and risk of acute lymphoblastic leukemia in Serbian children. J Pediatr Hematol Oncol; 2010 May;32(4):e148-50
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  • [Title] Association between the methylenetetrahydrofolate reductase polymorphisms and risk of acute lymphoblastic leukemia in Serbian children.
  • Polymorphisms in the MTHFR gene have been associated with susceptibility to some types of cancer.
  • We investigated a possible association of MTHFR polymorphisms (677C>T and 1298A>C) and increased risk for acute lymphoblastic leukemia in 78 affected children.
  • A significant association between CT/TT individuals and reduced risk of acute lymphoblastic leukemia was found.
  • [MeSH-major] Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Case-Control Studies. Child. Child, Preschool. Female. Genetic Predisposition to Disease. Genotype. Humans. Infant. Male. Prognosis. Risk Factors. Serbia

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  • (PMID = 20445408.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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96. Seedhouse CH, Grundy M, White P, Li Y, Fisher J, Yakunina D, Moorman AV, Hoy T, Russell N, Burnett A, Pallis M, National Cancer Research Network: Sequential influences of leukemia-specific and genetic factors on p-glycoprotein expression in blasts from 817 patients entered into the National Cancer Research Network acute myeloid leukemia 14 and 15 trials. Clin Cancer Res; 2007 Dec 1;13(23):7059-66
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  • [Title] Sequential influences of leukemia-specific and genetic factors on p-glycoprotein expression in blasts from 817 patients entered into the National Cancer Research Network acute myeloid leukemia 14 and 15 trials.
  • PURPOSE: P-glycoprotein (Pgp) is a major prognostic factor for chemotherapy failure in acute myeloid leukemia (AML).
  • This study compared the influence of genetic and leukemia-specific factors on Pgp.
  • Moreover, leukemia-specific factors, such as low WBC count and poor risk cytogenetics, have a much greater effect than genetic polymorphisms on Pgp expression in AML blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. P-Glycoprotein / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Bone Marrow Cells / metabolism. Child. Clinical Trials as Topic. Haplotypes. Humans. Leukocytes, Mononuclear / metabolism. Middle Aged. P-Glycoproteins. Phenotype. Polymorphism, Genetic. Polymorphism, Restriction Fragment Length. Prospective Studies. Proto-Oncogene Proteins c-bcl-2 / blood

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  • (PMID = 18056183.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Proto-Oncogene Proteins c-bcl-2
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97. Chiu PP, Jiang H, Dick JE: Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance. Blood; 2010 Dec 9;116(24):5268-79
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  • [Title] Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with a significant risk of disease relapse, but the biological basis for relapse is poorly understood.
  • Here, we identify leukemiainitiating cells (L-ICs) on the basis of functional assays and prospective isolation and report a role for L-ICs in T-ALL disease and relapse.
  • Long-term proliferation in response to NOTCH1 activating signals in OP9-DL1 coculture system or capacity to initiate leukemia in xenografts by the CD7(+)CD1a(-) subset of primary T-ALL samples was superior to other subsets, refining the identity of T-ALL L-ICs.
  • T-ALL engraftment was improved in nonobese diabetic/severe combined immunodeficiency (NOD/scid)IL2Rγ(null) (NSG) mice compared with NOD/scid with anti-CD122 treatment (NS122), but both showed changes in leukemia immunophenotype.
  • Clonal analysis of xenografts using the TCRG locus revealed the presence of subclones of T-ALL L-ICs, some of which possess a selective growth advantage and correlated with the capacity of CD7(+)CD1a(+) xenograft cells to engraft secondary NSG mice.
  • Our results establish that primary CD1a(-) T-ALL cells are functionally distinct from CD1a(+) cells and that the CD7(+)CD1a(-) subset is enriched for L-IC activity that may be involved in mediating disease relapse after therapy.
  • [MeSH-minor] Animals. Antigens, CD1. Antigens, CD7. Antineoplastic Agents, Hormonal / pharmacology. Cell Proliferation. Clone Cells / pathology. Coculture Techniques. Dexamethasone / pharmacology. Humans. Immunophenotyping. Mice. Mice, SCID. Receptor, Notch1 / metabolism. Recurrence. Transplantation, Heterologous

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  • (PMID = 20810926.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD7; 0 / Antineoplastic Agents, Hormonal; 0 / CD1a antigen; 0 / Glucocorticoids; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 7S5I7G3JQL / Dexamethasone
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98. Ciurea SO, Rodrigues M, Giralt S, de Lima M: Aging, acute myelogenous leukemia, and allogeneic transplantation: do they belong in the same sentence? Clin Lymphoma Myeloma; 2009 Aug;9(4):289-97
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  • [Title] Aging, acute myelogenous leukemia, and allogeneic transplantation: do they belong in the same sentence?
  • Acute myelogenous leukemia is a disease of the elderly.
  • Disease biology and functional status of this patient population contribute to poorer treatment outcomes with standard therapy.
  • Allogeneic hematopoietic stem cell transplantation is associated with an immunologic "graft-versus-tumor" effect.
  • The development of reduced-intensity preparative regimens and improvements in supportive care now allow older patients with myeloid leukemia a greater opportunity for cure with transplantation.
  • Donor availability, graft-versus-host disease, delayed immune recovery, and the high prevalence of relapsed or refractory disease remain important obstacles to be overcome in the future.
  • [MeSH-major] Aging / physiology. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy


99. Santillan DA, Theisler CM, Ryan AS, Popovic R, Stuart T, Zhou MM, Alkan S, Zeleznik-Le NJ: Bromodomain and histone acetyltransferase domain specificities control mixed lineage leukemia phenotype. Cancer Res; 2006 Oct 15;66(20):10032-9
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  • [Title] Bromodomain and histone acetyltransferase domain specificities control mixed lineage leukemia phenotype.
  • A critical unanswered question about mixed lineage leukemia (MLL) is how specific MLL fusion partners control leukemia phenotype.
  • The MLL-cyclic AMP-responsive element binding protein-binding protein (CBP) fusion requires both the CBP bromodomain and histone acetyltransferase (HAT) domain for transformation and causes acute myelogenous leukemia (AML), often preceded by a myelodysplastic phase.
  • HAT, but not bromodomain, substitutions conferred enhanced proliferative capacity in vitro but lacked expression of myeloid cell surface markers normally seen with MLL-CBP.
  • Mice reconstituted with domain-swapped hematopoietic progenitors developed different disease from those with MLL-CBP.
  • This included development of lymphoid disease and lower frequency of the myelodysplastic phase in those mice developing AML.
  • We conclude that both the CBP bromodomain and HAT domain play different but critical roles in determining the phenotype of MLL-CBP leukemia.
  • Our results support an important role for MLL partner genes in determining the leukemia phenotype besides their necessity in leukemogenesis.
  • Here, we find that subtleties in MLL fusion protein domain specificity direct cells toward a specific disease phenotype.
  • [MeSH-major] Histone Acetyltransferases / physiology. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / physiology. p300-CBP Transcription Factors / physiology
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / enzymology. Hematopoietic Stem Cells / metabolism. Mice. Mice, Inbred C57BL. Molecular Sequence Data. Phenotype. Protein Structure, Tertiary. Substrate Specificity

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  • (PMID = 17047066.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA95040; United States / NIAID NIH HHS / AI / T32 AI07508
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / p300-CBP Transcription Factors
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100. Steinherz PG, Meyers PA, Steinherz LJ, Jeha S: Clofarabine induced durable complete remission in heavily pretreated adolescents with relapsed and refractory leukemia. J Pediatr Hematol Oncol; 2007 Sep;29(9):656-8
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  • [Title] Clofarabine induced durable complete remission in heavily pretreated adolescents with relapsed and refractory leukemia.
  • Current treatments for relapsed/refractory leukemias are unable to achieve extended remissions in most patients even with multiagent chemotherapy.
  • Clofarabine is a new nucleoside analog that has demonstrated clinical benefit in phase I-II studies, and is currently being studied in children and adults with leukemias and has been approved for the treatment of children with relapsed or refractory acute lymphocytic leukemia.
  • We report the experience of three adolescents, two with acute lymphocytic leukemia in 3rd relapse and one with relapsed/refractory acute myeloid leukemia, who achieved complete remission with clofarabine.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Female. Humans. Male. Recurrence. Remission Induction

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  • (PMID = 17805046.001).
  • [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 / Adenine Nucleotides; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
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