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1. Kolmannskog S, Flaegstad T, Helgestad J, Hellebostad M, Zeller B, Glomstein A: [Childhood acute lymphoblastic leukemia in Norway 1992-2000]. Tidsskr Nor Laegeforen; 2007 May 31;127(11):1493-5
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  • [Title] [Childhood acute lymphoblastic leukemia in Norway 1992-2000].
  • BACKGROUND: Acute lymphoblastic leukemia is the most common malignancy in childhood.
  • Four of 6 infants with acute lymphoblastic leukemia and all 4 with mature B-cell leukemia are alive.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Neoplasm Recurrence, Local. Norway / epidemiology. Risk Factors. Stem Cell Transplantation. Treatment Outcome

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  • (PMID = 17551551.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Norway
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2. De Keersmaecker K, Graux C, Odero MD, Mentens N, Somers R, Maertens J, Wlodarska I, Vandenberghe P, Hagemeijer A, Marynen P, Cools J: Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32). Blood; 2005 Jun 15;105(12):4849-52
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  • [Title] Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32).
  • The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL).
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 9. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Fusion Proteins, bcr-abl / chemistry. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, T-Cell / pathology. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Base Sequence. Benzamides. Blotting, Western. Cell Line. Cell Survival. DNA, Complementary / metabolism. DNA-Binding Proteins / metabolism. Female. Gene Deletion. Genes, abl. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Karyotyping. Microtubules / metabolism. Milk Proteins / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Models, Genetic. Molecular Sequence Data. Open Reading Frames. Phenotype. Phosphorylation. Piperazines / pharmacology. Polymerase Chain Reaction. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Protein-Tyrosine Kinases / metabolism. Pyrimidines / pharmacology. Recombinant Fusion Proteins / metabolism. Retroviridae. Reverse Transcriptase Polymerase Chain Reaction. STAT5 Transcription Factor. Signal Transduction. Time Factors. Trans-Activators / metabolism

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  • (PMID = 15713800.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / EML1-ABL1 fusion protein, human; 0 / Milk Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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3. Cui W, Kong NR, Ma Y, Amin HM, Lai R, Chai L: Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia. Mod Pathol; 2006 Dec;19(12):1585-92
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  • [Title] Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia.
  • Previously, we reported that SALL4 was constitutively expressed in acute myeloid leukemia and SALL4 transgenic mice developed acute myeloid leukemia.
  • In this study, we aimed to survey SALL4 protein expression in benign and neoplastic hematopoietic tissues in addition to acute myeloid leukemia using immunostaining with a polyclonal anti-SALL4 antibody.
  • Reverse transcription-polymerase chain reaction was also performed to detect SALL4 mRNA expression on eight precursor B-cell lymphoblastic leukemia/lymphomas, 10 benign hematopoietic tissues, and seven hematopoietic cancer cell lines.
  • Of the benign tissues, SALL4 expression was detectable only in CD34+ hematopoietic stem/progenitor cells (2/2 at protein level, 3/3 at RNA level).
  • In neoplastic tissues, only precursor B-cell lymphoblastic leukemia/lymphomas had detectable SALL4 (12/16 at protein level, 7/8 at RNA level), similar to that observed in acute myeloid leukemia.
  • Of the seven cell lines examined, only those derived from acute myeloid leukemia and precursor B-cell lymphoblastic leukemia/lymphomas were positive.
  • The persistence of SALL4 expression in leukemic blasts in precursor B-cell lymphoblastic leukemia/lymphomas resembles to what we observed in acute myeloid leukemia, and correlates with the maturation arrest of these cells.
  • We have shown in our previous study that the constitutive expression of SALL4 in mice can lead to acute myeloid leukemia development.
  • The similar expression pattern of SALL4 in acute myeloid leukemia and B-cell lymphoblastic leukemia/lymphomas suggests that these two disease entities may share similar biological features and/or mechanisms of leukemogenesis.
  • More definite studies to investigate the role of SALL4 in the pathogenesis of B-cell lymphoblastic leukemia/lymphomas are needed in the future to address this question.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma / genetics. Plasmacytoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Antigens, CD34 / metabolism. Biomarkers, Tumor / metabolism. Cell Line, Tumor. Cell Separation. Flow Cytometry. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Humans. Immunoenzyme Techniques. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16998462.001).
  • [ISSN] 0893-3952
  • [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 / NIDDK NIH HHS / DK / K08 DK063220
  • [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 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / SALL4 protein, human; 0 / Transcription Factors
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4. Lin TL, Wang QH, Brown P, Peacock C, Merchant AA, Brennan S, Jones E, McGovern K, Watkins DN, Sakamoto KM, Matsui W: Self-renewal of acute lymphocytic leukemia cells is limited by the Hedgehog pathway inhibitors cyclopamine and IPI-926. PLoS One; 2010 Dec 28;5(12):e15262
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  • [Title] Self-renewal of acute lymphocytic leukemia cells is limited by the Hedgehog pathway inhibitors cyclopamine and IPI-926.
  • Recent data suggests that Hh signaling plays a role in normal B-cell development, and we hypothesized that Hh signaling may be important in precursor B-cell acute lymphocytic leukemia (B-ALL).
  • We found that the expression of Hh pathway components was common in human B-ALL cell lines and clinical samples.

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  • (PMID = 21203400.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL075826; United States / NCI NIH HHS / CA / P01 CA015396; United States / NCI NIH HHS / CA / R01 CA127574; United States / NCI NIH HHS / CA / R01CA127574; United States / NCI NIH HHS / CA / R01 CA127574-05; United States / NHLBI NIH HHS / HL / HL83077; United States / NHLBI NIH HHS / HL / HL75826; United States / NHLBI NIH HHS / HL / R01 HL083077; United States / NHLBI NIH HHS / HL / T32 HL086345; United States / NCI NIH HHS / CA / P01CA15396
  • [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 / Antigens, CD19; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / IPI-926; 0 / Receptors, G-Protein-Coupled; 0 / SMO protein, human; 0 / Veratrum Alkaloids; EC 1.2.1.3 / Aldehyde Dehydrogenase; ZH658AJ192 / cyclopamine
  • [Other-IDs] NLM/ PMC3011010
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5. Chunsong H, Yuling H, Li W, Jie X, Gang Z, Qiuping Z, Qingping G, Kejian Z, Li Q, Chang AE, Youxin J, Jinquan T: CXC chemokine ligand 13 and CC chemokine ligand 19 cooperatively render resistance to apoptosis in B cell lineage acute and chronic lymphocytic leukemia CD23+CD5+ B cells. J Immunol; 2006 Nov 15;177(10):6713-22
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  • [Title] CXC chemokine ligand 13 and CC chemokine ligand 19 cooperatively render resistance to apoptosis in B cell lineage acute and chronic lymphocytic leukemia CD23+CD5+ B cells.
  • We have investigated expression and functions of CXCL13/CXCR5 and CCL19/CCR7 in CD23+CD5+ and CD23+CD5- B cells from cord blood (CB) and patients with B cell lineage acute or chronic lymphocytic leukemia (B-ALL or B-CLL).
  • Therefore, we suggest that normal lymphocytes, especially naive B and T cells, use CXCL13/CXCR5 and CCL19/CCR7 for migration, homing, maturation, and cell homeostasis as well as secondary lymphoid tissues organogenesis.
  • [MeSH-major] Apoptosis / immunology. B-Lymphocyte Subsets / immunology. B-Lymphocyte Subsets / metabolism. Burkitt Lymphoma / immunology. Chemokines, CC / physiology. Chemokines, CXC / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] Antigens, CD5 / biosynthesis. Cell Lineage / immunology. Chemokine CCL19. Chemokine CXCL13. Fetal Blood / cytology. Fetal Blood / immunology. Fetal Blood / metabolism. Humans. Lymphocyte Count. Proteins / metabolism. Proteins / physiology. Receptors, CCR7. Receptors, CXCR5. Receptors, Chemokine / biosynthesis. Receptors, IgE / biosynthesis

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  • (PMID = 17082584.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / CCL19 protein, human; 0 / CCR7 protein, human; 0 / CXCL13 protein, human; 0 / CXCR5 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CXCL13; 0 / Chemokines, CC; 0 / Chemokines, CXC; 0 / PEG10 protein, human; 0 / Proteins; 0 / Receptors, CCR7; 0 / Receptors, CXCR5; 0 / Receptors, Chemokine; 0 / Receptors, IgE
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6. Vallera DA, Oh S, Chen H, Shu Y, Frankel AE: Bioengineering a unique deimmunized bispecific targeted toxin that simultaneously recognizes human CD22 and CD19 receptors in a mouse model of B-cell metastases. Mol Cancer Ther; 2010 Jun;9(6):1872-83
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  • [Title] Bioengineering a unique deimmunized bispecific targeted toxin that simultaneously recognizes human CD22 and CD19 receptors in a mouse model of B-cell metastases.
  • The aims were to reduce toxin immunogenicity using mutagenesis, measure the ability of mutated drug to elicit antitoxin antibody responses, and show that mutated drug was effective against systemic B-cell lymphoma in vivo.
  • Site-specific mutagenesis was used to mutate amino acids in seven key epitopic toxin regions that dictate B-cell generation of neutralizing antitoxin antibodies.
  • Finally, a powerful genetically altered luciferase xenograft model was used that could be imaged in real time to determine the effect on systemic malignant human B-cell lymphoma, Raji-luc.
  • Patient B-lineage acute lymphoblastic leukemia, B-cell chronic lymphocytic leukemia, and B lymphoma were high in CD22 and CD19 expression.

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  • (PMID = 20530709.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108637; United States / NCI NIH HHS / CA / R01 CA082154; United States / NCI NIH HHS / CA / CA036725-25; United States / NCI NIH HHS / CA / CA108637-05; United States / NCI NIH HHS / CA / R01 CA036725; United States / NCI NIH HHS / CA / R01-CA36725; United States / NCI NIH HHS / CA / R01-CA082154; United States / NCI NIH HHS / CA / R01 CA108637-05; United States / NCI NIH HHS / CA / R01 CA036725-25
  • [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 / Antibodies, Bispecific; 0 / Antigens, CD19; 0 / Bacterial Toxins; 0 / Exotoxins; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / Virulence Factors; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa
  • [Other-IDs] NLM/ NIHMS198461; NLM/ PMC2884080
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7. Salerni BL, Bates DJ, Albershardt TC, Lowrey CH, Eastman A: Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed. Mol Cancer Ther; 2010 Apr;9(4):791-802
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed.
  • Inhibition of the extracellular signal-regulated kinase by PD98059 dramatically accelerates vinblastine-mediated apoptosis in ML-1 leukemia with cells dying in 4 hours from all phases of the cell cycle.
  • Inhibition of protein synthesis by cycloheximide also markedly accelerated vinblastine-induced apoptosis, showing that the proteins required for this acute apoptosis are constitutively expressed.
  • We also investigated the response of 13 other leukemia and lymphoma cell lines and cells from seven chronic lymphocytic leukemia patients.
  • Four cell lines and all chronic lymphocytic leukemia cells were killed in 6 hours by vinblastine alone.
  • Two additional cell lines were sensitized to vinblastine by PD98059, which suppressed Mcl-1.
  • This acute apoptosis either alone or in combination with PD98059 required vinblastine-mediated activation of c-Jun-NH(2)-terminal kinase.
  • PD98059 did not suppress Mcl-1 in other cell lines whereas sorafenib did, but this did not sensitize the cells to vinblastine, suggesting that the acute apoptosis varies depending on which Bcl-2 protein mediates protection.
  • Most of the cell lines were sensitized to vinblastine by cycloheximide, suggesting that inhibition of a short-lived protein in addition to Mcl-1 can acutely sensitize cells.

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  • (PMID = 20371726.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009658-17; United States / NCI NIH HHS / CA / CA23108; United States / NCI NIH HHS / CA / CA009658-17; United States / NCI NIH HHS / CA / T32 CA009658; United States / NCI NIH HHS / CA / R01 CA050224; United States / NCI NIH HHS / CA / P30 CA023108-315657; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / CA023108-315657; United States / NCI NIH HHS / CA / CA050224-14; United States / NCI NIH HHS / CA / R01 CA050224-14; United States / NCI NIH HHS / CA / CA50224
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 5V9KLZ54CY / Vinblastine; 98600C0908 / Cycloheximide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS184304; NLM/ PMC2852489
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8. Zhu L, Wang HX, Lui J, Yan HM, Xue M: [Acute leukemia relapse of donor origin in two cases after haploidentical bone marrow transplantation]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):400-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute leukemia relapse of donor origin in two cases after haploidentical bone marrow transplantation].
  • To investigate the leukemia relapse of AL patients after HLA haploidentical bone marrow transplantation (HLA HBMT), 2 relapsed leukemia patients received HLA HBMT were studied, peripheral blood simples and bone marrow smear were examined, morphologic change of bone marrow cells was observed, while the HLA genotype and chromosome karyotye were analyzed by PCR and routine G-banding methods, respectively.
  • The results indicated that the two cases were diagnosed primarily as acute lymphocytic leukemia (common cell subtype) and acute megakaryocytic leukemia, in which chromosome abnormalities or activation of protooncogene in leukemic cells were observed.
  • The complete hematopuietie reconstitution of donor origin was obtained in these 2 cases after HLA HBMT, but the leukemic cells in these 2 leukemia patients were confirmed to be donor origin after relapse, their blood groups and HLA genotype were found to be originated from donor.
  • These 2 relapsed leukemia patients were diagnosed as acute lymphocytic leukemia (B cell subtype) and acute megakaryocytic leukemia.
  • It is suggested that high-dose of immunosuppressive agents used in transplantation may contribute to leukemia relapse of donor origin in these patients.
  • Abnormalities in hematopoietic microenvironment may be also involved in the leukemia development.
  • Donor-cell leukemia after allogeneic hematopoietic stem cell transplantation can be an ideal model to investigate the related events in human leukemogenesis.

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  • (PMID = 16638225.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HLA Antigens
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9. Miao K, Li J, Qiu H, Zhang R, Chen L, Wu H, Wang R, Zhang J: The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia. Onkologie; 2010;33(7):385-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia.
  • BACKGROUND: Cytogenetic abnormalities are the most important independent prognostic factors of acute leukemia and imply the potential molecular mechanism of the disease.
  • Translocation (11;14)(p13;q11) has been predominantly found in T-cell acute lymphocytic leukemia (ALL) but is rare in B-cell ALL.
  • CASE REPORT: We present the case of a 30-year-old male patient, who presented with symptomatic anemia, thrombocytopenia and leukocytosis.
  • CONCLUSIONS: Translocation (11;14) (p13;q11) in B-cell ALL is rare, but it is worth exploring the molecular mechanisms and discovering the prognostic value in more B-cell ALL patients.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Leukemia, B-Cell / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosome Banding. Disease Progression. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male. Prognosis. Remission Induction

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20631486.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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10. Catusse J, Wollner S, Leick M, Schröttner P, Schraufstätter I, Burger M: Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells. J Cell Physiol; 2010 Nov;225(3):792-800
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells.
  • Elevated levels of CCL18 have been described in various diseases including childhood acute lymphocytic leukemia (ALL) but its functions remain poorly characterized.
  • CXCL12 is a pivotal chemokine for hematopoiesis and B cell homing processes.
  • We demonstrate that CCL18 interferes with CXCL12-mediated pre-B ALL cell activation.
  • CXCL12-induced calcium mobilization, chemotaxis, pseudo-emperipolesis and cellular proliferation could be significantly reduced by CCL18 in pre-B ALL cell lines.
  • [MeSH-major] Chemokines, CC / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology. Receptors, CXCR4 / metabolism. Signal Transduction
  • [MeSH-minor] Animals. Apoptosis. COS Cells. Calcium Signaling. Cell Line, Tumor. Cell Proliferation. Cercopithecus aethiops. Chemokine CXCL12 / metabolism. Chemotaxis, Leukocyte. Estradiol / metabolism. Estrogen Antagonists / pharmacology. Humans. Ligands. Lymphocyte Activation. Receptors, Estrogen. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Recombinant Proteins / metabolism. Transfection

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20568229.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL18 protein, human; 0 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CC; 0 / Estrogen Antagonists; 0 / GPER protein, human; 0 / Ligands; 0 / Receptors, CXCR4; 0 / Receptors, Estrogen; 0 / Receptors, G-Protein-Coupled; 0 / Recombinant Proteins; 4TI98Z838E / Estradiol
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11. Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M: Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin. Int J Oncol; 2008 Aug;33(2):371-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.
  • The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.
  • During normal hematopoiesis B203.13 is expressed on a fraction of CD34+ cells, while on mature cells it is only present on B-lymphocytes.
  • We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).
  • The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.
  • We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18636158.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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12. Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B: V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):725-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.
  • Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

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  • (PMID = 19455608.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases
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13. Kraigher-Krainer E, Lackner H, Sovinz P, Schwinger W, Benesch M, Urban C: Numb chin syndrome as initial manifestation in a child with acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):426-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Numb chin syndrome as initial manifestation in a child with acute lymphoblastic leukemia.
  • We report on an 11-year-old male who presented with NCS as initial manifestation of acute lymphoblastic leukemia of B-cell type.
  • [MeSH-major] Chin / pathology. Hypesthesia / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18506757.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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14. Song JH, Schnittke N, Zaat A, Walsh CS, Miller CW: FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias. Leuk Res; 2008 Nov;32(11):1751-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.
  • Engineered FBXW7 null cells display cell cycle and chromosome stability defects.
  • Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-cell acute lymphocytic leukemias.
  • Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.
  • As expected, mutations were found in T-cell acute lymphocytic leukemias.
  • However mutations of FBXW7 were also found in four of 118 B-cell acute lymphocytic leukemias and one of 24 adult T-cell leukemia samples.
  • These observations suggest that disruption of FBXW7 has a role in several forms of lymphocytic leukemias and not exclusively T-cell acute lymphocytic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 18485478.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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15. Saxena A, Rai A, Raina V, Seth T, Mitra DK: Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells. Cancer Immunol Immunother; 2010 Jan;59(1):125-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells.
  • Expression of cell surface CD13 in acute B-cell leukemia (ALL-B) is often viewed, as an aberrant expression of a myeloid lineage marker.
  • Here, we attempted to study the stage specific expression of CD13 on ALL-B blasts and understand its role in leukemogenesis as pertaining to stage of B-cell ontogeny.
  • Among 68 cases of early B-cell ALL, 22 cases with distinct immunophenotype was identified as immature B-cell ALL.
  • This strongly indicates leukemogenesis at an early stage of B-cell development.
  • We also identified, the existence of a subpopulation of cells with remarkably similar phenotype in non-leukemic marrow from healthy subjects (expressing CD10, CD19, CD22, CD24, Tdt together with the co-expression of CD13).
  • By blocking their cell surface CD13 in leukemic blasts with monoclonal antibody we were able to inhibit their proliferation.
  • CD13 may thus be an important target for novel molecular therapy of early stage acute B-cell leukemia.
  • [MeSH-major] Antigens, CD13 / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19562339.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.4.11.2 / Antigens, CD13
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16. Bhatia S, Kaul D, Varma N: Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia. Mol Cell Biochem; 2010 Jul;340(1-2):97-106
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia.
  • Keeping in view the fact that genes coding microRNAs (miRNAs) have been found to be localized in chromosomal regions susceptible to genetic translocations, this study was addressed to identify and characterize the miRNAs that are present near/within the regions involved in genetic translocations characteristic of B-cell acute lymphoblastic leukemia (B-cell ALL).
  • Out of six such identified miRNAs miR-196b was not only found to be significantly down-regulated in both EB-3 cell line as well as B-cell ALL patients as compared to that found in the corresponding controls, but also had the inherent capacity to down-regulate the highly expressed c-myc gene, a consequence of genetic translocation characteristic of EB-3 cells at both transcriptional and translational level.
  • Also down-regulation of c-myc gene was accompanied by decreased expressions of c-myc effector genes coding for hTERT, Bcl-2, and AATF.
  • Based upon these results, we propose for the first time that miR-196b has the inherent capacity to down-regulate the overamplified c-myc gene recognized as a common pathognomonic feature leading to cancer in general and B-cell ALL in particular.
  • Hence miR-196b can be assigned with the tumor suppressor function and can be of therapeutic importance in paving the way toward the treatment of B-cell ALL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. MicroRNAs / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Algorithms. Apoptosis / genetics. Apoptosis Regulatory Proteins / genetics. Case-Control Studies. Cell Line, Tumor. Cell Proliferation. Computational Biology. Down-Regulation. Humans. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics. Repressor Proteins / genetics. Telomerase / genetics. Transcription, Genetic. Transfection

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  • (PMID = 20549547.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AATF protein, human; 0 / Apoptosis Regulatory Proteins; 0 / MIRN196 microRNA, human; 0 / MYC protein, human; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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17. Luong NV, Kantarjian HM, Faderl SH, Thomas DA, Vu KD: Occurence of venothromboembolism (VTE) in patients (pts) with acute lymphocytic leukemia (ALL), Burkitt's leukemia/lymphoma (BL), or lymphoblastic leukemia (LL). J Clin Oncol; 2009 May 20;27(15_suppl):7059

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Occurence of venothromboembolism (VTE) in patients (pts) with acute lymphocytic leukemia (ALL), Burkitt's leukemia/lymphoma (BL), or lymphoblastic leukemia (LL).
  • Although neoplastic diseases are known risk factors for the development of VTE, little is known about the incidence and predisposing factors of VTE among leukemia patients (pts).
  • In addition to traditional risk factors, disease-specific features may also predispose pts to higher VTE risk.
  • Further studies should be done in other leukemias to establish guidelines in the prevention and management of VTE in pts with leukemia.

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  • (PMID = 27961450.001).
  • [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] Journal Article
  • [Publication-country] United States
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18. Teachey DT, Felix CA: Development of cold agglutinin autoimmune hemolytic anemia during treatment for pediatric acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2005 Jul;27(7):397-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of cold agglutinin autoimmune hemolytic anemia during treatment for pediatric acute lymphoblastic leukemia.
  • Those most often associated with AIHA include chronic lymphocytic leukemia, B-cell lymphomas, and Burkitt-type acute lymphoblastic leukemia (ALL) and are clonal populations of mature B cells.
  • There have been no reports of patients with B-cell precursor ALL who developed AIHA while undergoing chemotherapy, but AIHA has been reported in a few patients with ALL after hematopoietic stem cell transplant.
  • The authors describe a child with B-cell precursor ALL who developed cold agglutinin AIHA during maintenance treatment while in remission after infection with influenza B.
  • [MeSH-major] Agglutinins. Anemia, Hemolytic / chemically induced. Anemia, Hemolytic, Autoimmune / etiology. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16012332.001).
  • [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 / Agglutinins; 0 / Autoantibodies; 0 / Cryoglobulins; 0 / cold agglutinins
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19. Luo SD, Wu Y, Chen JH, Liu HK, Chen YZ: [Gene expression profile of human TGF-beta signal transduction pathway of B cell type acute lymphocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Aug;16(4):742-5
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  • [Title] [Gene expression profile of human TGF-beta signal transduction pathway of B cell type acute lymphocytic leukemia].
  • This study was aimed to investigate the gene expression profile of TGF-beta signal transduction pathway in B-cell type acute lymphocytic leukemia (B-ALL).
  • The gene expression profiles in B-ALL primary cells and cell lines (NALM6 cells, Raji cells), B-lymphocyte of control were detected by cDNA microarray including 113 different genes in human TGF-beta/BMP signal transduction pathway, and TGF-beta(1) mRNA expression was detected by real time RT-PCR.
  • The B lymphocytes in peripheral blood of heacthy persons sorted by flow cytometry were used as control.
  • The results showed that as compared with B lymphocytes in peripheral blood of heacthy persons, the TGF-beta(1) expression in B-ALL cells, NALM6 cells and Raji cells were down-regulationed, myc and smad1 gene expressions were up-regulated, IL-6, smad 7 gene expressions were down-regulated.
  • It is concluded that TGF-beta signal transduction is abnormal in B-cell type acute lymphocytic leukemia.

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  • (PMID = 18718051.001).
  • [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 / RNA, Messenger; 0 / Transforming Growth Factor beta
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20. Li LX, Tang YM, Gu WZ, Tang HF, Qian BQ, Shen HQ, Luo CF: [Establishment of animal model with B lineage acute leukemia in nude mice for evaluation of new therapeutic agents]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2008 Sep;37(5):511-4
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  • [Title] [Establishment of animal model with B lineage acute leukemia in nude mice for evaluation of new therapeutic agents].
  • OBJECTIVE: To establish an acute leukemia animal model for testing new therapeutic agents in vivo.
  • METHODS: Nude mice were intraperitoneally injected with 2 mg cyclophosphamide, 24 h later 5 x 10(6) acute B-cell leukemia Nalm-6 cells was inoculated via the tail vein, then monitored daily.
  • CONCLUSION: B lineage acute leukemia animal model has been successfully established in the nude mice, which is suitable for testing new therapeutic agents.
  • [MeSH-major] Disease Models, Animal. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 18925721.001).
  • [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] 8N3DW7272P / Cyclophosphamide
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21. Hatakeyama N, Tamura Y, Sahara H, Suzuki N, Suzuki K, Hori T, Mizue N, Torigoe T, Tsutsumi H, Sato N: Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells. Exp Hematol; 2006 Feb;34(2):197-207

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells.
  • OBJECTIVE: Several studies have demonstrated that dendritic cells (DCs) pulsed with tumor lysate or apoptotic tumor cells can elicit effective T-cell responses.
  • We applied this approach to induce HLA class I- and class II-restricted T-cell responses directed against autologous acute lymphocytic leukemia (B-ALL) cell line NH-1.
  • METHODS: Autologous T cells were stimulated by apoptotic tumor cell-loaded DCs generated from a patient with ALL.
  • The stimulated and expanded T cells were isolated into CD8(+) T-cell line and CD4(+) T-cell line, and each of them was examined as to their functions.
  • RESULTS: Both CD8(+) and CD4(+) T-cell lines demonstrated cytotoxicity against NH-1 in an major histocompatibility complex-dependent manner.
  • Finally, we established two independent CD4(+) T-cell clones restricted to HLA-DR.
  • The CD4(+) T-cell line responded strongly to autologous Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCL) but not to autologous normal cells.
  • Furthermore, the T-cell clones also responded to allogeneic EBV-LCLs and B-ALL cell lines in the context of the HLA-DRB1( *)04051 molecule.
  • Interestingly, 293T and COS-7 cells, which had been transfected with the HLA-DRB1( *)04051, were also recognized by T-cell clones.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Fusion. Dendritic Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Apoptosis / immunology. Cell Line, Tumor. Cytotoxicity Tests, Immunologic. Epitopes / immunology. Epstein-Barr Virus Nuclear Antigens / immunology. Female. HLA-DR Antigens / classification. HLA-DR Antigens / immunology. Histocompatibility Antigens Class II / immunology. Histocompatibility Antigens Class II / pharmacology. Humans. Infant. Lymphocyte Activation

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  • (PMID = 16459188.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Epitopes; 0 / Epstein-Barr Virus Nuclear Antigens; 0 / HLA-DR Antigens; 0 / Histocompatibility Antigens Class II
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22. Takenokuchi M, Saigo K, Nakamachi Y, Kawano S, Hashimoto M, Fujioka T, Koizumi T, Tatsumi E, Kumagai S: Troglitazone inhibits cell growth and induces apoptosis of B-cell acute lymphoblastic leukemia cells with t(14;18). Acta Haematol; 2006;116(1):30-40
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  • [Title] Troglitazone inhibits cell growth and induces apoptosis of B-cell acute lymphoblastic leukemia cells with t(14;18).
  • Peroxisome proliferator-activated receptor-gamma (PPARgamma), a member of the nuclear receptor superfamily, has been detected in several human leukemia cells.
  • Recent studies reported that PPARgamma ligands inhibit cell proliferation and induce apoptosis in both normal and malignant B-lineage cells.
  • We investigated the expression of PPARgamma and the effects of PPARgamma ligands on UTree-O2, Bay91 and 380, three B-cell acute lymphoblastic leukemia (B-ALL) cell lines with t(14;18), which show a poor prognosis, accompanying c-myc abnormality.
  • Western blot analysis identified expression of PPARgamma protein and real-time PCR that of PPARgamma mRNA on the three cell lines.
  • Troglitazone (TGZ), a synthetic PPARgamma ligand, inhibited cell growth in these cell lines in a dose-dependent manner, which was associated with G(1) cell cycle arrest and apoptosis.
  • We assessed the expression of c-myc, an apoptosis-regulatory gene, since c-myc abnormality was detected in most B-ALL cells with t(14;18).
  • TGZ was found to dose-dependently downregulate the expression of c-myc mRNA and c-myc protein in the three cell lines.
  • These results suggest that TGZ inhibits cell growth via induction of G(1) cell cycle arrest and apoptosis in these cell lines and that TGZ-induced apoptosis, at least in part, may be related to the downregulation of c-myc expression.
  • Moreover, the downregulation of c-myc expression by TGZ may depend on a PPARgamma-independent mechanism.
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Female. Gene Expression Regulation, Leukemic / drug effects. Humans. Ligands. Male. Prognosis. Proto-Oncogene Proteins c-myc / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16809887.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chromans; 0 / Ligands; 0 / MYC protein, human; 0 / PPAR gamma; 0 / Proto-Oncogene Proteins c-myc; 0 / Thiazolidinediones; I66ZZ0ZN0E / troglitazone
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23. Zhang X, Wang M, Zhou C, Chen S, Wang J: The expression of iASPP in acute leukemias. Leuk Res; 2005 Feb;29(2):179-83
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  • [Title] The expression of iASPP in acute leukemias.
  • To examine the role of iASPP in acute leukemia (AL), we analyzed iASPP mRNA expression in AL by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).
  • There was no significant difference between acute lymphocytic leukemia (ALL) cells and acute myeloid leukemia (AML) cells (P = 0.593).
  • The expression level of iASPP gene and its overexpression in M3 and M4EO were significantly lower than in other subtypes of AML.
  • However, iASPP gene expression in AL cells was not associated with gender, age, initial white blood cell count or p53 type, but was associated with CD34 expression.
  • The results of the present study suggest that iASPP gene overexpression may play an important role in the leukemogenesis and/or disease progression of AL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Female. Humans. Male. Mutation. Repressor Proteins. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / antagonists & inhibitors. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Up-Regulation

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  • (PMID = 15607367.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / PPP1R13L protein, human; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53
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24. Wang ZY, Chen QS: [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Apr;13(2):169-73
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  • [Title] [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial].
  • One of the important approaches for further prolonging remission duration and eradicating minimal residual disease in acute leukemia is immunotherapy.
  • Four kinds of immunotherapy for acute leukemia are under investigation:.
  • (1) monoclonal antibodies, among them, Mylotarg (cytotoxic antibiotic calicheamicin linked to CD33 Mab) is given for the treatment of refractory or relapsed acute myeloid leukemia and molecular relapse in acute promyelocytic leukemia with good results, Campath-1H (antiCD52 Mab) is administered in the treatment of prolymphocytic leukemia and Rituximab (anti-CD20 Mab) in B-PLL with high complete remission rates.
  • Other Mabs under preclinical and clinical trials include anti-IL-2 receptor Mab for the treatment of acute T lymphocytic leukemia, anti-220 kD Mab-6G7 for acute leukemias, recombinant immune toxin BL22 (anti-CD22) for hairy cell leukemia and Mabs labeled with radio-isotopes for different types of acute leukemias;.
  • (2) adoptive cellular immunotherapy using cytokine-induced killer cell, alloreactive NK cells, allogeneic or autologous leukemic-specific CD8(+) cytotoxic T lymphocytes, and other immune effector cells;.
  • (4) leukemia vaccines of several different formulations including antigen-specific, leukemia cell-based, leukemia antigen-pulsed dendritic cell (DC) and leukemia-derived DC vaccines, the latter two formulations are more attractive.
  • In conclusion, up to now, the most effective example of immunotherapy in acute leukemia is provided by the administration of Mabs, and the majority of other approaches in immunotherapy for acute leukemia although promising, need further studies.

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  • (PMID = 15854271.001).
  • [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] Editorial; English Abstract
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines
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25. Paietta E: Surrogate marker profiles for genetic lesions in acute leukemias. Best Pract Res Clin Haematol; 2010 Sep;23(3):359-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surrogate marker profiles for genetic lesions in acute leukemias.
  • While cytogenetic and molecular aberrancies currently are accepted prognostic predictors in acute leukemias, single antigen expression and even antigenic profiles rarely impact on prognosis.
  • This chapter will focus on established surrogate marker profiles, such as those for PML/RARα, AML1/ETO, FLT3-gene mutated acute lymphocytic leukemia (ALL), and BCR/ABL(POS) ALL.
  • [MeSH-major] Biomarkers, Tumor / genetics. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Drug Delivery Systems / methods. Humans

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21112035.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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26. Kiss F, Buslig J, Szegedi I, Scholtz B, Kappelmayer J, Kiss C: Early relapse after rituximab chemoimmunotherapy. Pediatr Blood Cancer; 2008 Feb;50(2):372-5
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  • In relapsed/refractory childhood acute lymphoblastic leukemia (ALL) of the B-cell lineage rituximab, a monoclonal anti-CD20 antibody was used successfully in some cases.
  • We report on a 15-year-old female with relapsed CD20-positive B-cell progenitor ALL treated with rituximab because of positive minimal residual disease signals after chemotherapy, as checked by flow cytometry and real time quantitative-PCR.
  • The patient died with fulminant aspergillosis before hematopoietic stem cell transplantation could be performed.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Flow Cytometry. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Humans. Neoplasm, Residual / pathology. Recurrence. Rituximab

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17973316.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
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27. Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF: Clinical characteristics and outcome of children with biphenotypic acute leukemia. Haematologica; 2009 Dec;94(12):1682-90
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  • [Title] Clinical characteristics and outcome of children with biphenotypic acute leukemia.
  • BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of biphenotypic acute leukemia in children is limited.
  • DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with biphenotypic acute leukemia diagnosed and treated over an 8-year period.
  • According to the EGIL scoring system 24 (3.7%) of 633 patients with acute leukemia were classified as having biphenotypic acute leukemia.
  • The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the diagnosis of leukemia of ambiguous lineage.
  • Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having mixed phenotype acute leukemia.
  • Patients received therapy based on a treatment regimen for acute lymphocytic leukemia regimen, which included myeloid-effective agents.
  • The survival of those patients who underwent hematopoietic stem cell transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).
  • The outcome of the 11 patients who were retrospectively classified as having mixed phenotype acute leukemia according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.
  • CONCLUSIONS: An acute lymphocytic leukemia type of induction therapy, using agents that are active against lymphoid and myeloid leukemias, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.
  • Hematopoietic stem cell transplantation may not be necessary for all patients in first complete remission.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy
  • [MeSH-minor] Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies

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  • [Cites] Am J Clin Pathol. 2002 Mar;117(3):380-9 [11888077.001]
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  • (PMID = 19713227.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Other-IDs] NLM/ PMC2791935
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28. Ning BT, Tang YM, Chen YH, Shen HQ, Qian BQ: Comparison between CD19 and CD20 expression patterns on acute leukemic cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):943-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison between CD19 and CD20 expression patterns on acute leukemic cells.
  • In order to provide the evidences for CD19 as a better antibody targeting molecule for B lineage acute leukemias than CD20 through the multi-parameter flow-cytometry analysis of leukemia cells, the samples from 321 patients with acute leukemia (AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.
  • The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with B lineage acute lymphoblastic leukemia (B lineage ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with B lineage/Myeloid (B/My) acute mixed lineage leukemia (AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).
  • Both of the two antigens were negative in 29 patients with acute T lymphoblastic leukemia and 7 patients with T/My AMLL.
  • The positive rates of CD19 and CD20 in 152 patients with acute myeloid leukemia (AML) were 7.2% and 2.0%, respectively.
  • The specificity of CD19 and CD20 in B lymphocytic lineage was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).
  • It is concluded that CD19 continuously and steadily express on almost all subtypes of B lineage leukemic cells with homogeneous pattern while only a small number of leukemias express CD20.
  • These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-lineage acute leukemia.

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  • (PMID = 16403255.001).
  • [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] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20
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29. Teuffel O, Stanulla M, Cario G, Ludwig WD, Rottgers S, Schafer BW, Zimmermann M, Schrappe M, Niggli FK: Anemia and survival in childhood acute lymphoblastic leukemia. Haematologica; 2008 Nov;93(11):1652-7
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  • [Title] Anemia and survival in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Several studies have demonstrated that patients with childhood acute lymphoblastic leukemia presenting with mild anemia at diagnosis have an increased risk of poor outcome compared to patients with more severe anemia.
  • However, it has not been reported whether there is any correlation between degree of anemia and leukemia subtype.
  • DESIGN AND METHODS: In a cohort of 1162 patients with childhood acute lymphoblastic leukemia we analyzed whether there was a correlation between degree of anemia and leukemia subtype.
  • The degree of anemia was significantly different for three distinct groups of patients compared to the remaining patients (mean hemoglobin; T-cell leukemia: 106 g/L versus 76 g/L (precursor B-cell acute lymphoblastic leukemia); within precursor B-cell ALL: TEL-AML1 positive: 68 g/L versus 79 g/L; BCR-ABL positive: 93 g/L versus 76 g/L; each p<0.05).
  • Furthermore, in contrast to the entire study group, patients with T-cell leukemia, TEL-AML1(+), and BCR-ABL(+) precursor B-cell leukemia had a more favorable prognosis if presenting with a higher hemoglobin level (>/=80 g/L).
  • CONCLUSIONS: These observations indicate that the formerly reported direct correlation between severity of anemia and survival in childhood acute lymphoblastic leukemia mainly reflects differences in the degree of anemia between distinct biological subgroups with different treatment outcomes.
  • On the other hand, the inverse relationship between severity of anemia and survival found within specific subgroups suggests that very low hemoglobin levels at diagnosis are associated with more advanced disease in these subgroups.
  • [MeSH-major] Anemia / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Burkitt Lymphoma / complications. Burkitt Lymphoma / genetics. Burkitt Lymphoma / mortality. Child. Cohort Studies. Core Binding Factor Alpha 2 Subunit / genetics. Disease-Free Survival. Fusion Proteins, bcr-abl / genetics. Hemoglobins / metabolism. Homeodomain Proteins / genetics. Humans. Leukemia, T-Cell / complications. Leukemia, T-Cell / genetics. Leukemia, T-Cell / mortality. Leukocyte Count. Mutation. Oncogene Proteins, Fusion / genetics. Risk Factors. Survival Analysis. Treatment Outcome


30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. Robazzi TC, Barreto JH, Silva LR, Santiago MB, Mendonça N: Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil. J Pediatr Hematol Oncol; 2007 Sep;29(9):622-6
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  • [Title] Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil.
  • OBJECTIVE: This study was to determine the prevalence and characteristics of the osteoarticular manifestations on initial clinical presentation of acute leukemias (ALs) on childhood in the state of Bahia, Brazil.
  • RESULTS: Acute lymphocytic leukemia (ALL) was diagnosed in 313 (77.1%) patients and acute myeloid leukemia (AML), in 93 (22.9%) patients, including 241 males (59.4%) and 165 females (40.6%).
  • Prior referral to our center, the most frequent initial diagnosis was anemia (15.8%), leukemia (15.0%), amygdalitis (3.7%), and rheumatic fever (2.7%).
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Osteoarthritis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Brazil. Child. Child, Preschool. Female. Humans. Infant. Male

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  • (PMID = 17805037.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Robazzi TC, Silva LR, Mendonça N, Barreto JH: Gastrointestinal manifestations as initial presentation of acute leukemias in children and adolescents. Acta Gastroenterol Latinoam; 2008 Jun;38(2):126-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastrointestinal manifestations as initial presentation of acute leukemias in children and adolescents.
  • OBJECTIVE: this study aimed to determine the prevalence and characteristics of gastrointestinal manifestations on initial clinical presentation of acute leukemias (AL) in childhood.
  • RESULTS: acute lymphoid leukemia (ALL) was diagnosed in 273 (77.1%) patients and acute non-lymphocytic leukemia (AML) in 81 (22.9%).
  • CONCLUSIONS: gastrointestinal symptoms are not very well-documented as initial manifestation of leukemia in children and should be considered on the differential diagnosis of gastrointestinal symptoms of unknown etiology in children.
  • [MeSH-major] Gastrointestinal Diseases / etiology. Leukemia, Myeloid, Acute / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 18697407.001).
  • [ISSN] 0300-9033
  • [Journal-full-title] Acta gastroenterologica Latinoamericana
  • [ISO-abbreviation] Acta Gastroenterol. Latinoam.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Argentina
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33. Wiemels JL, Kang M, Chang JS, Zheng L, Kouyoumji C, Zhang L, Smith MT, Scelo G, Metayer C, Buffler P, Wiencke JK: Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia. Blood Cells Mol Dis; 2010 Oct 15;45(3):186-91
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  • [Title] Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy is the single largest subtype of childhood acute lymphoblastic leukemia (ALL) and is defined by the presence of 51-68 chromosomes in a karyotype.
  • We screened for RAS mutations among 517 acute childhood leukemias (including 437 lymphocytic, of which 393 were B-cell subtypes) and found mutations in 30% of high hyperdiploids compared to only 10% of leukemias of other subtypes (P<0.0001).
  • While RAS mutations were previously associated with prior chemical exposures in childhood and adult leukemias, in this study RAS-mutated cases were not significantly associated with parental smoking when compared to study controls.
  • IGH rearrangements were backtracked in three RAS-positive patients (which were negative for KRAS mutation at birth) and found to be evident before birth, confirming a prenatal origin for the leukemia clone.
  • We posit a natural history for hyperdiploid leukemia in which prenatal mitotic catastrophe is followed by a postnatal RAS mutation to produce the leukemic cell phenotype.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20688547.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NCI NIH HHS / CA / R25-CA112355; United States / NIEHS NIH HHS / ES / R01-ES09137; United States / NIEHS NIH HHS / ES / P01 ES018172; United States / NCI NIH HHS / CA / R01-CA089032; United States / NIEHS NIH HHS / ES / P01-ES018172; United States / NIEHS NIH HHS / ES / R01 ES009137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS224426; NLM/ PMC2943008
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34. Zeng Z, Samudio IJ, Munsell M, An J, Huang Z, Estey E, Andreeff M, Konopleva M: Inhibition of CXCR4 with the novel RCP168 peptide overcomes stroma-mediated chemoresistance in chronic and acute leukemias. Mol Cancer Ther; 2006 Dec;5(12):3113-21
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  • [Title] Inhibition of CXCR4 with the novel RCP168 peptide overcomes stroma-mediated chemoresistance in chronic and acute leukemias.
  • Using peptide-based CXCR4 inhibitors derived from the chemokine viral macrophage inflammatory protein II, we tested the hypothesis that the inhibition of CXCR4 increases sensitivity to chemotherapy by interfering with stromal/leukemia cell interactions.
  • Results showed that the polypeptide RCP168 had the strongest antagonistic effect on the SDF-1alpha- or stromal cell-induced chemotaxis of leukemic cells.
  • Finally, RCP168 significantly enhanced chemotherapy-induced apoptosis in stroma-cocultured Jurkat, primary chronic lymphocytic leukemia, and in a subset of acute myelogenous leukemia cells harboring Flt3 mutation.
  • Our data therefore suggest that the SDF-1alpha/CXCR4 interaction contributes to the resistance of leukemia cells to chemotherapy-induced apoptosis.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Peptides / pharmacology. Pyridines / pharmacology. Receptors, CXCR4 / antagonists & inhibitors

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  • (PMID = 17172414.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / CA55164
  • [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 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / N-(1,4,8,11- tetraazacyclotetradecanyl-1,4-phenylenebis(methylene))-2-(aminomethyl)- pyridine; 0 / Peptides; 0 / Pyridines; 0 / Receptors, CXCR4; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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35. Stachel D, Albert M, Meilbeck R, Paulides M, Schmid I: Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia. Oncol Rep; 2007 Jan;17(1):147-52
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  • [Title] Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia.
  • Pathological angiogenesis is increasingly recognized to be an important feature of pathogenesis in solid tumors and also in leukemias.
  • Vascular endothelial growth factor (VEGF) seems to play a central role in tumor angiogenesis and is associated with a poor prognosis in both solid tumors and adult leukemias.
  • In pediatric acute lymphocytic leukemia however, the expression of angiogenic molecules and its relation to prognosis and relapse are unknown.
  • Therefore, we prospectively analyzed 46 pediatric patients with precursor B cell acute lymphocytic leukemia by semi-quantitative RT-PCR for expression of the angiogenic molecules VEGF, VEGF-C, iNOS and TGF-beta and correlated relapse and survival data with the expression of these factors.
  • Angiogenic factors are expressed in the bone marrow of patients with pediatric B cell precursor ALL and VEGF is a potential candidate for therapeutic intervention as it is significantly higher expressed in children with late relapses.
  • The mRNA expression of iNOS in the surviving children possibly reflects an increased activity of the immune system against the leukemia which leads to a superior survival.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Burkitt Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17143492.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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36. Dunwell TL, Dickinson RE, Stankovic T, Dallol A, Weston V, Austen B, Catchpoole D, Maher ER, Latif F: Frequent epigenetic inactivation of the SLIT2 gene in chronic and acute lymphocytic leukemia. Epigenetics; 2009 May 16;4(4):265-9
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  • [Title] Frequent epigenetic inactivation of the SLIT2 gene in chronic and acute lymphocytic leukemia.
  • Recently a mouse model of T/natural killer acute lymphoblastic leukemia was used to assess global promoter methylation across the mouse genome using the restriction landmark genomic scanning technique.
  • We have previously demonstrated that SLIT2 is frequently inactivated in lung, breast, colorectal and glioma tumors by hypermethylation of a CpG island in its promoter region, whilst inactivating somatic mutations are rare.
  • In this report we determined the methylation status of the SLIT2 gene in leukemias (CLL and ALL).
  • SLIT2 was methylated in all ten leukemia cell lines analyzed (eight completely and two partially methylated).
  • Methylation results in leukemia cell lines and ALL and CLL primary samples were confirmed by direct sequencing of bisulfite modified DNA.
  • [MeSH-major] DNA Methylation. Intercellular Signaling Peptides and Proteins / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Nerve Tissue Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Bone Marrow / metabolism. Cell Line, Tumor. CpG Islands / genetics. Humans

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  • (PMID = 19550140.001).
  • [ISSN] 1559-2308
  • [Journal-full-title] Epigenetics
  • [ISO-abbreviation] Epigenetics
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / Slit homolog 2 protein
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37. Zanette DL, Rivadavia F, Molfetta GA, Barbuzano FG, Proto-Siqueira R, Silva-Jr WA, Falcão RP, Zago MA: miRNA expression profiles in chronic lymphocytic and acute lymphocytic leukemia. Braz J Med Biol Res; 2007 Nov;40(11):1435-40
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  • [Title] miRNA expression profiles in chronic lymphocytic and acute lymphocytic leukemia.
  • MicroRNAs (miRNAs) are a class of small endogenous RNAs that play important regulatory roles by targeting mRNAs for cleavage or translational repression. miRNAs act in diverse biological processes including development, cell growth, apoptosis, and hematopoiesis, suggesting their association with cancer.
  • We determined the miRNA expression profile of chronic and acute lymphocytic leukemias (CLL and ALL) using the TaqMan MicroRNA Assays Human Panel (Applied Biosystems).
  • Pooled leukemia samples were compared to pooled CD19+ samples from healthy individuals (calibrator) by the 2-DD Ct method.
  • One of its putative targets, SOCS1, promotes STAT activation, which is a known mediator of cell proliferation and survival, suggesting the possibility of an association between miR-331 and these processes.

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  • (PMID = 17934639.001).
  • [ISSN] 1414-431X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / MicroRNAs
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38. Pérez-Campos-Mayoral L, Ruiz-Argüelles A, Pérez-Romano B, Zenteno E, Hernández-Cruz P, Martínez-Cruz R, Martínez-Cruz M, Pina-Canseco S, Pérez-Campos E: Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia. Tohoku J Exp Med; 2008 Jan;214(1):11-6
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  • [Title] Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia is the most common form of cancer in children.
  • Lectins are proteins or glycoproteins from plants or animals that recognize oligossacharides on the cell surface and have been used to characterize the structural changes of oligosaccharides in leukemias.
  • In this study, we used the lectin from the freshwater prawn Macrobrachium (M. rosenbergii), specific for acetyl groups in sialylated glycans, because increased sialylation of glycoproteins and glycolipids has been identified in lymphoblastic leukemias.
  • We compared the specificity of the M. rosenbergii lectin for lymphoblastic leukemias with the specificities of the lectins from Triticum vulgaris, Solanum tuberosum, Arachis hipogaea, and Phytolacca americana.
  • By morphologic and phenotype characterization with a panel of monoclonal antibodies, we identified four types of leukemias from 106 leukemia patients: 11 cases of T-cell acute lymphoblastic leukemia, 61 cases of B-cell acute lymphoblastic leukemia, 24 cases of acute myeloblastic leukemia, and 10 cases of acute biphenotypic leukemia.
  • As determined by cytofluorometric assays, nine of the eleven cases with T-cell acute lymphoblastic leukemia (8 +/- 3 years old) were specifically identified with the lectin from M. rosenbergii.
  • In contrast, only six cases of B-cell leukemia, one case of myeloblastic leukemia, and 2 cases of biphenotypic leukemia were identified with this M. rosenbergii lectin.
  • The other lectins tested showed no capacity to differentiate, in a significant manner, any of the four types of leukemias tested.
  • Thus, the lectin from M. rosenbergii could be considered a useful tool for the diagnosis and study of T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Lectins. Leukemia, Biphenotypic, Acute / diagnosis. Palaemonidae / chemistry
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Antigens, CD45 / analysis. Antigens, Neoplasm / immunology. Child. Diagnosis, Differential. Flow Cytometry. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Phenotype

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  • (PMID = 18212483.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45
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39. Kozlov I, Beason K, Yu C, Hughson M: CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity. Cancer Genet Cytogenet; 2005 Nov;163(1):62-7
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  • [Title] CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity.
  • Acute leukemias that express antigens associated with more than one lineage have been classified as acute lymphocytic leukemia with myeloid markers, acute myeloid leukemia with lymphoid markers, or biphenotypic acute leukemia (BAL).
  • CD79a functions in and has a high degree of specificity for B-cell differentiation.
  • It has only recently begun to be reported in biphenotypic acute leukemias.
  • Cases of acute leukemia submitted to the flow cytometry laboratory were retrospectively reviewed beginning from the time analysis for cytoplasmic CD79a was added to leukemia and lymphoma panels.
  • Nevertheless, the cytogenetic and FISH findings indicate that CD79a, despite its specificity for B-cell differentiation, represented the aberrant presence of a B-cell antigen in leukemias of distinct myeloid linage.
  • [MeSH-major] Antigens, CD79 / genetics. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / genetics. Antigens, CD / immunology. B-Lymphocytes / immunology. Blast Crisis. Bone Marrow Cells / pathology. Cytarabine / therapeutic use. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. T-Lymphocytes / immunology

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  • [CommentIn] Cancer Genet Cytogenet. 2007 Apr 1;174(1):76-7 [17350472.001]
  • (PMID = 16271957.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 04079A1RDZ / Cytarabine
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40. Aleskog A, Larsson R, Höglund M, Kristensen J, Nygren P, Lindhagen E: In vitro drug resistance in B cell chronic lymphocytic leukemia: a comparison with acute myelocytic and acute lymphocytic leukemia. Anticancer Drugs; 2005 Mar;16(3):277-83
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  • [Title] In vitro drug resistance in B cell chronic lymphocytic leukemia: a comparison with acute myelocytic and acute lymphocytic leukemia.
  • The aim of the study was to evaluate cellular drug resistance in B cell chronic lymphocytic leukemia (B-CLL) in vitro, and compare it with that in acute myelocytic leukemia (AML) and acute lymphocytic leukemia (ALL).
  • In vitro drug resistance was analyzed by the fluorometric microculture cytotoxicity assay (FMCA) in all samples from patients with leukemia sent to our laboratory between 1992 and 2001.
  • For all drugs, there was a good agreement between the activity in vitro and the known clinical disease-specific activity.
  • The study also demonstrated an acquired cellular drug resistance in B-CLL, but not in the acute leukemias.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


41. Malani AK, Gupta C, Rangineni R, Singh J, Ammar H: Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia. Acta Oncol; 2007;46(2):247-9
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  • [Title] Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia.
  • T-cell large granular lymphocyte leukemia (T-LGL) also known as T-cell chronic lymphocytic leukemia is rare and comprises a small minority of all small lymphocytic leukemias.
  • The concomitant presentation of T-LGL with acute myeloid leukemia (AML) has not been previously reported.
  • We present an elderly gentleman with concomitant T-LGL and AML (non-M3) diagnosed by a combination of morphologic evaluation, immunophenotyping by flow cytometry, and T-cell gene rearrangement studies.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Prolymphocytic, T-Cell / diagnosis
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Antigens, CD / analysis. Flow Cytometry. Humans. Male

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  • (PMID = 17453377.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 17
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42. Strick R, Zhang Y, Emmanuel N, Strissel PL: Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias. Hum Genet; 2006 Jun;119(5):479-95
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  • [Title] Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
  • The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia.
  • Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.
  • Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.
  • In this report, using cell lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.
  • Although MLL2 was expressed in all cell lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.
  • A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.
  • [MeSH-major] Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics. Leukemia / genetics. Leukemia / metabolism. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cells, Cultured. Chronic Disease. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic

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  • (PMID = 16572268.001).
  • [ISSN] 0340-6717
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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43. Ostrowska H, Hempel D, Holub M, Sokolowski J, Kloczko J: Assessment of circulating proteasome chymotrypsin-like activity in plasma of patients with acute and chronic leukemias. Clin Biochem; 2008 Nov;41(16-17):1377-83
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  • [Title] Assessment of circulating proteasome chymotrypsin-like activity in plasma of patients with acute and chronic leukemias.
  • OBJECTIVE: We evaluated whether the proteasomal chymotrypsin-like (ChT-L) activity is increased in plasma of patients with acute lymphoblastic (ALL), acute myeloblastic (AML) and chronic lymphocytic (CLL) leukemias.
  • CONCLUSIONS: Plasma proteasome ChT-L activity can be a useful bio-marker for patients with acute leukemia at the blast stage.
  • [MeSH-major] Chymotrypsin / blood. Leukemia / blood. Proteasome Endopeptidase Complex / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Female. Humans. Hydrolysis / drug effects. L-Lactate Dehydrogenase / blood. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Male. Middle Aged. Oligopeptides / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Proteasome Inhibitors. Protein Subunits / metabolism. Sodium Dodecyl Sulfate / pharmacology

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  • (PMID = 18773885.001).
  • [ISSN] 1873-2933
  • [Journal-full-title] Clinical biochemistry
  • [ISO-abbreviation] Clin. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Proteasome Inhibitors; 0 / Protein Subunits; 134381-21-8 / epoxomicin; 368GB5141J / Sodium Dodecyl Sulfate; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.4.21.1 / Chymotrypsin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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44. Belson M, Kingsley B, Holmes A: Risk factors for acute leukemia in children: a review. Environ Health Perspect; 2007 Jan;115(1):138-45
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  • [Title] Risk factors for acute leukemia in children: a review.
  • Although overall incidence is rare, leukemia is the most common type of childhood cancer.
  • Within this population, acute lymphocytic leukemia (ALL) occurs approximately five times more frequently than acute myelogenous leukemia (AML) and accounts for approximately 78% of all childhood leukemia diagnoses.
  • Epidemiologic studies of acute leukemias in children have examined possible risk factors, including genetic, infectious, and environmental, in an attempt to determine etiology.
  • Most environmental risk factors have been found to be weakly and inconsistently associated with either form of acute childhood leukemia.
  • Our review focuses on the demographics of childhood leukemia and the risk factors that have been associated with the development of childhood ALL or AML.
  • Knowledge of these particular risk factors can be used to support measures to reduce potentially harmful exposures and decrease the risk of disease.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Child. Communicable Diseases / complications. Environmental Exposure. Genetic Predisposition to Disease. Humans. Risk Factors

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  • (PMID = 17366834.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 145
  • [Other-IDs] NLM/ PMC1817663
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45. Sait SN, Claydon MA, Conroy JM, Nowak NJ, Barcos M, Baer MR: Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):143-6
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  • [Title] Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia.
  • Reciprocal chromosomal translocations involving the MLL gene at chromosome region 11q23 are recurring cytogenetic abnormalities in both de novo and therapy-related acute myeloid leukemia (AML) and in acute lymphoblastic leukemia.
  • We report a t(4;11)(p12;q23) with rearrangement of MLL and FRYL (also known as AF4p12), a human homolog to the furry gene of Drosophila, in an adult patient with therapy-related AML after fludarabine and rituximab therapy for small lymphocytic lymphoma and radiation therapy for breast carcinoma.
  • Both of the previous patients had therapy-related leukemias after exposure to topoisomerase II inhibitors, whereas our patient had received cytotoxic therapy that did not include a topoisomerase II inhibitor.
  • Thus, t(4;11)(p12;q23) with MLL and FRYL involvement represents a new recurring 11q23 translocation, to date seen only in therapy-related acute leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. DNA-Binding Proteins / genetics. Gene Rearrangement. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Middle Aged. Rituximab. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17854671.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; 4F4X42SYQ6 / Rituximab; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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46. Kawahara T, Kawaguchi-Ihara N, Okuhashi Y, Itoh M, Nara N, Tohda S: Cyclopamine and quercetin suppress the growth of leukemia and lymphoma cells. Anticancer Res; 2009 Nov;29(11):4629-32
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  • [Title] Cyclopamine and quercetin suppress the growth of leukemia and lymphoma cells.
  • BACKGROUND: Hedgehog (Hh) and Wnt signaling pathways are involved in the stimulation of growth of leukemia and lymphoma cells.
  • In the present study, whether or not the Hh inhibitor, cyclopamine, and the Wnt inhibitor, quercetin, suppress cell growth was investigated.
  • MATERIALS AND METHODS: The effects of cyclopamine and quercetin on the in vitro growth and protein expression of ten acute leukemia and B-cell lymphoma cell lines were examined.
  • RESULTS: Cyclopamine and quercetin suppressed cell growth and induced apoptosis in seven and eight cell lines respectively.
  • Cyclopamine decreased the level of Gli1 protein, a target gene product of Hh signaling.
  • Quercetin decreased the level of Notch1 protein and its active fragment in the DND-41 T-lymphoblastic leukemia cell line with constitutive Notch activation.
  • CONCLUSION: Cyclopamine and quercetin suppress the growth of a number of leukemia and lymphoma cells.
  • This finding suggests the potential use of these compounds in molecularly-targeted therapy for leukemia and lymphoma.
  • [MeSH-major] Leukemia / drug therapy. Lymphoma / drug therapy. Quercetin / pharmacology. Veratrum Alkaloids / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. Protein Biosynthesis / drug effects. Receptor, Notch1 / biosynthesis. Transcription Factors / biosynthesis

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  • (PMID = 20032413.001).
  • [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 / GLI1 protein, human; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Transcription Factors; 0 / Veratrum Alkaloids; 9IKM0I5T1E / Quercetin; ZH658AJ192 / cyclopamine
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47. Wang W, Ji P, Steffen B, Metzger R, Schneider PM, Halfter H, Schrader M, Berdel WE, Serve H, Müller-Tidow C: Alterations of lymphoid enhancer factor-1 isoform expression in solid tumors and acute leukemias. Acta Biochim Biophys Sin (Shanghai); 2005 Mar;37(3):173-80
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  • [Title] Alterations of lymphoid enhancer factor-1 isoform expression in solid tumors and acute leukemias.
  • The highest expression level of LEF-1 was found in carcinoma samples whereas brain cancer samples expressed little.
  • For example, the mRNA level of LEF-1 was lower in testicular tumor samples compared with tumor-free control samples.
  • In hematological malignancies, overall LEF-1 level was higher in lymphocytic leukemias compared with myeloid leukemias and normal hematopoiesis.
  • However, acute myeloid leukemia and acute lymphocytic leukemia showed a significantly increased fraction of the oncogenic LEF-1 compared with chronic lymphocytic leukemia and chronic myeloid leukemia.
  • Taken together, these data suggest that LEF-1 is abundantly expressed in human tumors and the ratio of the oncogenic and the dominant negative short isoform altered not only in carcinomas but also in leukemia.
  • [MeSH-minor] Humans. Leukemia / genetics. Leukemia / metabolism. Lymphoid Enhancer-Binding Factor 1. Protein Isoforms / genetics. Protein Isoforms / metabolism

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  • (PMID = 15756419.001).
  • [ISSN] 1672-9145
  • [Journal-full-title] Acta biochimica et biophysica Sinica
  • [ISO-abbreviation] Acta Biochim. Biophys. Sin. (Shanghai)
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Neoplasm Proteins; 0 / Protein Isoforms; 0 / Transcription Factors
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48. Desouki MM, Post GR, Cherry D, Lazarchick J: PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms. Clin Med Res; 2010 Jul;8(2):84-8
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  • PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy.
  • The lack of PAX-5 expression in most CD30-positive non-hematopoietic malignancies (embryonal carcinoma and seminoma) and T-cell lymphomas, such as anaplastic large cell lymphoma (ALCL), suggests that the absence of PAX-5 may be used to confirm non-B-cell lineage.
  • RESULTS: Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5).
  • PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8).
  • Non-neoplastic bone marrow sections showed scattered nuclear staining in small B-cell lymphocytes/hematogones.
  • CONCLUSION: Overall, our results demonstrate that including PAX-5 in a panel with other immunomarkers helps establish B-cell lineage and increases diagnostic yield.
  • [MeSH-major] B-Cell-Specific Activator Protein / analysis. Biomarkers, Tumor / analysis. Lymphoma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Hodgkin Disease / diagnosis. Humans. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

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  • (PMID = 20660931.001).
  • [ISSN] 1554-6179
  • [Journal-full-title] Clinical medicine & research
  • [ISO-abbreviation] Clin Med Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ PMC2910102
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49. Cardone M, Kandilci A, Carella C, Nilsson JA, Brennan JA, Sirma S, Ozbek U, Boyd K, Cleveland JL, Grosveld GC: The novel ETS factor TEL2 cooperates with Myc in B lymphomagenesis. Mol Cell Biol; 2005 Mar;25(6):2395-405
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  • The human ETS family gene TEL2/ETV7 is highly homologous to TEL1/ETV6, a frequent target of chromosome translocations in human leukemia and specific solid tumors.
  • Although TEL2 is infrequently up-regulated in human sporadic Burkitt's lymphoma, analysis of pediatric B-cell acute lymphocytic leukemia (B-ALL) samples showed increased coexpression of TEL2 and MYC and/or MYCN in over one-third of B-ALL patients.
  • Therefore, TEL2 and MYC also appear to cooperate in provoking a cadre of human B-cell malignancies.

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  • (PMID = 15743832.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076379; United States / NCI NIH HHS / CA / R01 CA76379-07; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01-CA72999-08
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ETV7 protein, human; 0 / Proto-Oncogene Proteins c-ets; 0 / Proto-Oncogene Proteins c-myc; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC1061619
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50. Attarbaschi A, Mann G, König M, Steiner M, Strehl S, Schreiberhuber A, Schneider B, Meyer C, Marschalek R, Borkhardt A, Pickl WF, Lion T, Gadner H, Haas OA, Dworzak MN: Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity. Clin Cancer Res; 2006 May 15;12(10):2988-94
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  • [Title] Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity.
  • PURPOSE: Mixed lineage leukemia (MLL) abnormalities occur in approximately 50% of childhood pro-B acute lymphoblastic leukemia (ALL).
  • RESULTS: We found that 15 of 29 pro-B ALL, 7 of 11 CD10- pre-B ALL, and 1 of 2 French-American-British classification L1 mature B-cell leukemia cases had a MLL rearrangement.
  • CONCLUSIONS: The striking similarities between the two CD10- ALL subsets imply that CD10- pre-B ALL variants may represent pro-B ALL cases that maintained the propensity to rearrange and express their immunoglobulin heavy chain rather than actual pre-B ALL forms transformed at this later stage of B-cell differentiation.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. B-Lymphocytes. Child. Child, Preschool. Female. Humans. Immunoglobulin Heavy Chains. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Male. Neprilysin. Phenotype. Prognosis. Retrospective Studies. Sensitivity and Specificity

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  • (PMID = 16707593.001).
  • [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 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
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51. Waldmann TA, Morris JC: Development of antibodies and chimeric molecules for cancer immunotherapy. Adv Immunol; 2006;90:83-131
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  • Monoclonal antibodies targeting non-Hodgkin's lymphoma (NHL), Her-2/neu highly expressing metastatic breast cancer, colorectal cancer, acute myelogenous leukemia, and B-cell chronic lymphocytic leukemia (CLL) have received FDA approval.

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  • (PMID = 16730262.001).
  • [ISSN] 0065-2776
  • [Journal-full-title] Advances in immunology
  • [ISO-abbreviation] Adv. Immunol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Blocking; 0 / Antibodies, Monoclonal; 0 / Recombinant Fusion Proteins
  • [Number-of-references] 194
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52. Orlowski RZ, Voorhees PM, Garcia RA, Hall MD, Kudrik FJ, Allred T, Johri AR, Jones PE, Ivanova A, Van Deventer HW, Gabriel DA, Shea TC, Mitchell BS, Adams J, Esseltine DL, Trehu EG, Green M, Lehman MJ, Natoli S, Collins JM, Lindley CM, Dees EC: Phase 1 trial of the proteasome inhibitor bortezomib and pegylated liposomal doxorubicin in patients with advanced hematologic malignancies. Blood; 2005 Apr 15;105(8):3058-65
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  • However, due to frequent dose reductions and delays at this level, 1.30 and 30 mg/m2 are recommended for further study.
  • Antitumor activity was seen against multiple myeloma, with 8 of 22 evaluable patients having a complete response (CR) or near-CR, including several with anthracycline-refractory disease, and another 8 having partial responses (PRs).
  • One patient with relapsed/refractory T-cell non-Hodgkin lymphoma (NHL) achieved a CR, whereas 2 patients each with acute myeloid leukemia and B-cell NHL had PRs.

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  • (PMID = 15626743.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30-CA16086; United States / NCI NIH HHS / CA / R01 CA102278; United States / NCRR NIH HHS / RR / RR00046
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Boronic Acids; 0 / Liposomes; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 30IQX730WE / Polyethylene Glycols; 69G8BD63PP / Bortezomib; 80168379AG / Doxorubicin
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53. van Zelm MC, van der Burg M, de Ridder D, Barendregt BH, de Haas EF, Reinders MJ, Lankester AC, Révész T, Staal FJ, van Dongen JJ: Ig gene rearrangement steps are initiated in early human precursor B cell subsets and correlate with specific transcription factor expression. J Immunol; 2005 Nov 1;175(9):5912-22
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  • [Title] Ig gene rearrangement steps are initiated in early human precursor B cell subsets and correlate with specific transcription factor expression.
  • The role of specific transcription factors in the initiation and regulation of Ig gene rearrangements has been studied extensively in mouse models, but data on normal human precursor B cell differentiation are limited.
  • We purified five human precursor B cell subsets, and assessed and quantified their IGH, IGK, and IGL gene rearrangement patterns and gene expression profiles.
  • Transcripts of the RAG1 and RAG2 genes and earlier defined transcription factors, such as E2A, early B cell factor, E2-2, PAX5, and IRF4, were specifically up-regulated at stages undergoing Ig gene rearrangements.
  • Based on the combined Ig gene rearrangement status and gene expression profiles of consecutive precursor B cell subsets, we identified 16 candidate genes involved in initiation and/or regulation of Ig gene rearrangements.
  • These analyses provide new insights into early human precursor B cell differentiation steps and represent an excellent template for studies on oncogenic transformation in precursor B acute lymphoblastic leukemia and B cell differentiation blocks in primary Ab deficiencies.
  • [MeSH-minor] Adolescent. Cell Separation. Child. Child, Preschool. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Gene Rearrangement, B-Lymphocyte, Light Chain. Humans

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  • [ErratumIn] J Immunol. 2006 Jun 15;176(12):7787
  • (PMID = 16237084.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors
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54. Blum W, Phelps MA, Klisovic RB, Rozewski DM, Ni W, Albanese KA, Rovin B, Kefauver C, Devine SM, Lucas DM, Johnson A, Schaaf LJ, Byrd JC, Marcucci G, Grever MR: Phase I clinical and pharmacokinetic study of a novel schedule of flavopiridol in relapsed or refractory acute leukemias. Haematologica; 2010 Jul;95(7):1098-105
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  • [Title] Phase I clinical and pharmacokinetic study of a novel schedule of flavopiridol in relapsed or refractory acute leukemias.
  • BACKGROUND: A pharmacokinetically derived schedule of flavopiridol administered as a 30 min intravenous bolus followed by 4-hour continuous intravenous infusion (IVB/CIVI) is active in fludarabine-refractory chronic lymphocytic leukemia, but no studies examining the feasibility and maximum tolerated dose of this schedule have been reported in acute leukemia.
  • DESIGN AND METHODS: We conducted a phase I dose escalation trial of single-agent flavopiridol in adults with relapsed/refractory acute leukemias, utilizing a modification of the intravenous bolus/continuous intravenous infusion approach, intensifying treatment for administration on days 1, 2, and 3 of 21-day cycles.
  • RESULTS: Twenty-four adults with relapsed/refractory acute myeloid leukemia (n=19) or acute lymphoblastic leukemia (n=5) were enrolled.
  • One refractory acute myeloid leukemia patient had short-lived complete remission with incomplete count recovery.
  • CONCLUSIONS: Flavopiridol as a single agent given by intravenous bolus/continuous intravenous infusion causes marked, immediate cytoreduction in relapsed/refractory acute leukemias, but objective clinical responses were uncommon.
  • [MeSH-major] Flavonoids / administration & dosage. Leukemia / drug therapy. Piperidines / administration & dosage
  • [MeSH-minor] Acute Disease. Adult. Aged. Drug Administration Schedule. Female. Humans. Male. Maximum Tolerated Dose. Middle Aged. Pharmacokinetics. Salvage Therapy / methods. Treatment Outcome. Young Adult

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  • (PMID = 20460644.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00101231
  • [Grant] United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / K23 CA120708; United States / NCI NIH HHS / CA / U01 CA 76576; United States / NCI NIH HHS / CA / K23CA120708; United States / NCI NIH HHS / CA / U01 CA076576; United States / NCRR NIH HHS / RR / UL1 RR025755
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Piperidines; 45AD6X575G / alvocidib
  • [Other-IDs] NLM/ PMC2895033
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55. Au WY, Wong KY, Leung RY, Tong AC: Isolated gingival relapse of acute lymphoblastic leukemia after transplantation. J Oral Pathol Med; 2008 Apr;37(4):249-51
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  • [Title] Isolated gingival relapse of acute lymphoblastic leukemia after transplantation.
  • A patient with a history of precursor B-cell leukemia presented with an isolated ulcerating gum lesion 8 years after allogeneic stem cell transplantation with severe graft versus host disease.
  • Molecular studies confirmed clonal relationship between the gum lesion with the original marrow disease, despite the anatomical, histological and chronological separations.
  • [MeSH-major] Gingival Neoplasms / pathology. Graft vs Leukemia Effect. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adult. Bone Marrow Neoplasms / surgery. Fatal Outcome. Female. Graft vs Host Disease / etiology. Hematopoiesis, Extramedullary. Humans. Recurrence. Stem Cell Transplantation / adverse effects

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  • (PMID = 18321346.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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56. Tigay JH: A comparison of acute lymphoblastic leukemia in Down syndrome and non-Down syndrome children: the role of trisomy 21. J Pediatr Oncol Nurs; 2009 Nov-Dec;26(6):362-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparison of acute lymphoblastic leukemia in Down syndrome and non-Down syndrome children: the role of trisomy 21.
  • Among the many aberrations caused by DS, including shortened stature and distorted facies, are several blood dyscrasias, including childhood leukemias-namely, acute myeloid leukemia (AML) and acute lymphoblastic, or lymphocytic, leukemia (ALL).
  • Other mutations are the gene fusion at TEL/AML1, and a new mutation found, which labels the Janus Kinase gene or JAK2 as on oncogenic precursor, which when associated with the B-cell precursor gene or BCP is highly leukomogenic.
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


57. Lucas DM, Edwards RB, Lozanski G, West DA, Shin JD, Vargo MA, Davis ME, Rozewski DM, Johnson AJ, Su BN, Goettl VM, Heerema NA, Lin TS, Lehman A, Zhang X, Jarjoura D, Newman DJ, Byrd JC, Kinghorn AD, Grever MR: The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo. Blood; 2009 May 7;113(19):4656-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo.
  • Therapeutic options for advanced B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are limited.
  • Available treatments can also deplete T lymphocytes, leaving patients at risk of life-threatening infections.
  • In the National Cancer Institute cell line screen, the structurally unique natural product silvestrol produces an unusual pattern of cytotoxicity that suggests activity in leukemia and selectivity for B cells.
  • We investigated silvestrol efficacy using primary human B-leukemia cells, established B-leukemia cell lines, and animal models.
  • In vivo, silvestrol causes significant B-cell reduction in Emu-Tcl-1 transgenic mice and significantly extends survival of 697 xenograft severe combined immunodeficient (SCID) mice without discernible toxicity.
  • These data indicate silvestrol has efficacy against B cells in vitro and in vivo and identify translational inhibition as a potential therapeutic target in B-cell leukemias.

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  • (PMID = 19190247.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U19 CA052956; United States / NCI NIH HHS / CA / P01CA125066; United States / NCI NIH HHS / CA / P01 CA125066; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / CA52956
  • [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 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tcl1 protein, mouse; 0 / Triterpenes; 0 / silvestrol
  • [Other-IDs] NLM/ PMC2680369
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58. Kern W, Kohlmann A, Schoch C, Schnittger S, Haferlach T: Comparison of mRNA abundance quantified by gene expression profiling and percentage of positive cells using immunophenotyping for diagnostic antigens in acute and chronic leukemias. Cancer; 2006 Nov 15;107(10):2401-7
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  • [Title] Comparison of mRNA abundance quantified by gene expression profiling and percentage of positive cells using immunophenotyping for diagnostic antigens in acute and chronic leukemias.
  • BACKGROUND: Microarray analysis is considered a future diagnostic tool in leukemias.
  • Whereas data accumulate on specific gene expression patterns in biologically defined leukemia entities, data on the correlation between flow cytometrically determined protein expression, which are essential in the diagnostic setting today, and microarray results are limited.
  • METHODS: The results obtained by microarray analysis were compared using the Affymetrix GeneChip HG-U133 system in parallel with flow cytometric findings of 36 relevant targets in 814 patients with newly diagnosed acute and chronic leukemias as well as in normal bone marrow samples.
  • RESULTS: In a total of 21,581 individual comparisons between signal intensities obtained by microarray analysis and percentages of positive cell as determined by flow cytometry, coefficients of correlation in the range of 0.171 to 0.807 were obtained.
  • They are in favor of a future application of the microarray technology as a robust diagnostic tool in leukemias.
  • [MeSH-major] Antigens, Surface / analysis. Biomarkers, Tumor / analysis. Immunophenotyping. Leukemia / diagnosis. Microarray Analysis. Molecular Diagnostic Techniques / methods. RNA, Messenger / analysis
  • [MeSH-minor] Antigens, CD / analysis. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Flow Cytometry. Gene Expression Profiling. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 17041886.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Surface; 0 / Biomarkers, Tumor; 0 / RNA, Messenger
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59. Lapucci A, Lulli M, Amedei A, Papucci L, Witort E, Di Gesualdo F, Bertolini F, Brewer G, Nicolin A, Bevilacqua A, Schiavone N, Morello D, Donnini M, Capaccioli S: zeta-Crystallin is a bcl-2 mRNA binding protein involved in bcl-2 overexpression in T-cell acute lymphocytic leukemia. FASEB J; 2010 Jun;24(6):1852-65
Archivio Istituzionale della Ricerca Unimi. Full text from AIR - Univ. Milan .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] zeta-Crystallin is a bcl-2 mRNA binding protein involved in bcl-2 overexpression in T-cell acute lymphocytic leukemia.
  • The human antiapoptotic bcl-2 gene has been discovered in t(14;18) B-cell leukemias/lymphomas because of its overexpression caused at a transcriptional control level by the bcl-2/IgH fusion gene.
  • An increased Bcl-2 level observed in normal phytohemagglutinin (PHA)-activated T lymphocytes, acute lymphatic leukemia (ALL) T-cell lines, and T cells of patients with leukemia in comparison with normal non-PHA-activated T lymphocytes was concomitant with an increase in zeta-crystallin level.
  • The specific association of zeta-crystallin with the bcl-2 ARE was significantly enhanced in T cells of patients with ALL, which accounts for the higher stability of bcl-2 mRNA and suggests a possible contribution of zeta-crystallin to bcl-2 overexpression occurring in this leukemia.
  • [MeSH-major] 3' Untranslated Regions / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / metabolism. zeta-Crystallins / metabolism
  • [MeSH-minor] Blotting, Western. Cytoplasm / drug effects. Cytoplasm / metabolism. Female. Gene Expression Regulation. Humans. Immunoprecipitation. Male. Middle Aged. Phytohemagglutinins. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. T-Lymphocytes / drug effects. T-Lymphocytes / pathology

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  • (PMID = 20103721.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA052443; United States / NCI NIH HHS / CA / R01 CA052443; United States / NCI NIH HHS / CA / R01 CA052443-16
  • [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 / 3' Untranslated Regions; 0 / Phytohemagglutinins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / zeta-Crystallins
  • [Other-IDs] NLM/ PMC2874474
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60. Kotani A, Ha D, Schotte D, den Boer ML, Armstrong SA, Lodish HF: A novel mutation in the miR-128b gene reduces miRNA processing and leads to glucocorticoid resistance of MLL-AF4 acute lymphocytic leukemia cells. Cell Cycle; 2010 Mar 15;9(6):1037-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel mutation in the miR-128b gene reduces miRNA processing and leads to glucocorticoid resistance of MLL-AF4 acute lymphocytic leukemia cells.
  • MLL-AF4 acute lymphocytic leukemia has a poor prognosis, and the mechanisms by which these leukemias develop are not understood despite intensive research based on well-known concepts and methods.

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  • (PMID = 20237425.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK068348-05; United States / NIDDK NIH HHS / DK / DK068348-06A1; United States / NIDDK NIH HHS / DK / R56 DK068348-06A1; United States / NIDDK NIH HHS / DK / R01 DK068348-05; United States / NIDDK NIH HHS / DK / R56 DK068348; United States / NIDDK NIH HHS / DK / R01 DK068348
  • [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 / Glucocorticoids; 0 / MIRN128 microRNA, human; 0 / MIRN221 microRNA, human; 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS277523; NLM/ PMC3096720
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61. Neviani P, Santhanam R, Oaks JJ, Eiring AM, Notari M, Blaser BW, Liu S, Trotta R, Muthusamy N, Gambacorti-Passerini C, Druker BJ, Cortes J, Marcucci G, Chen CS, Verrills NM, Roy DC, Caligiuri MA, Bloomfield CD, Byrd JC, Perrotti D: FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia. J Clin Invest; 2007 Sep;117(9):2408-21
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia.
  • Blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph1-positive) acute lymphocytic leukemia (ALL) are 2 fatal BCR/ABL-driven leukemias against which Abl kinase inhibitors fail to induce a long-term response.
  • We assessed the therapeutic potential of the PP2A activator FTY720 (2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propanediol hydrochloride), an immunomodulator in Phase III trials for patients with multiple sclerosis or undergoing organ transplantation, in CML-BC and Ph1 ALL patient cells and in in vitro and in vivo models of these BCR/ABL+ leukemias.
  • Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.
  • Altogether, these results highlight the therapeutic relevance of rescuing PP2A tumor suppressor activity in Ph1 leukemias and strongly support the introduction of the PP2A activator FTY720 in the treatment of CML-BC and Ph1 ALL patients.

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  • (PMID = 17717597.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / P30 CA016058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Propylene Glycols; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC1950458
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62. Wang X, Yuling H, Yanping J, Xinti T, Yaofang Y, Feng Y, Ruijin X, Li W, Lang C, Jingyi L, Zhiqing T, Jingping O, Bing X, Li Q, Chang AE, Sun Z, Youxin J, Jinquan T: CCL19 and CXCL13 synergistically regulate interaction between B cell acute lymphocytic leukemia CD23+CD5+ B Cells and CD8+ T cells. J Immunol; 2007 Sep 1;179(5):2880-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CCL19 and CXCL13 synergistically regulate interaction between B cell acute lymphocytic leukemia CD23+CD5+ B Cells and CD8+ T cells.
  • In a previous study, we have reported that ligation of CCL19-CCR7 and CXCL13-CXCR5 activates paternally expressed gene 10 (PEG10), resulting in an enhancement of apoptotic resistance in B-cell acute lymphocytic leukemia (B-ALL) CD23+CD5+ B cells.
  • Here, we report that B-ALL CD23+CD5+ B cells produce IL-10 at high level, which can be further elevated by costimulation with CCL19 and CXCL13.
  • CCL19/CXCL13-activated B-ALL CD23+CD5+ B cells, in turn, increase IL-10 expression in syngeneic CD8+ T cells in a B cell-derived IL-10-dependent manner and requiring a cell-cell contact.
  • Moreover, using a short hairpin RNA to knockdown PEG10, we provide direct evidence that increased expression of PEG10 in B-ALL CD23+CD5+ B cells is involved in malignant B-T cell interaction, contributing to the up-regulation of IL-10 expression, as well as to the impairment of cytotoxicity of syngeneic CD8+ T cells.
  • [MeSH-major] B-Lymphocytes / immunology. Burkitt Lymphoma / immunology. CD8-Positive T-Lymphocytes / immunology. Chemokine CCL19 / physiology. Chemokine CXCL13 / physiology. Immunologic Surveillance / immunology

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  • [ErratumIn] J Immunol. 2007 Nov 15;179(10):7184
  • (PMID = 17709502.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / CXCL13 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CXCL13; 0 / PEG10 protein, human; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Receptors, IgE; 130068-27-8 / Interleukin-10
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63. Crespo M, Villamor N, Giné E, Muntañola A, Colomer D, Marafioti T, Jones M, Camós M, Campo E, Montserrat E, Bosch F: ZAP-70 expression in normal pro/pre B cells, mature B cells, and in B-cell acute lymphoblastic leukemia. Clin Cancer Res; 2006 Feb 1;12(3 Pt 1):726-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 expression in normal pro/pre B cells, mature B cells, and in B-cell acute lymphoblastic leukemia.
  • PURPOSE: The ZAP-70 gene is normally expressed in T and natural killer cells, where it is required for the T-cell receptor (TCR) signaling.
  • More recently, it has been described that ZAP-70 contributes to the B-cell development at early stages of B-cell differentiation in mice.
  • The purpose was to investigate the presence of ZAP-70 in normal pro/pre B cells and mature B cells and in tumoral cells from B-acute lymphoblastic leukemias (B-ALL).
  • Among tumoral cells, ZAP-70 was expressed in 56% of B-ALLs with pro/pre B-cell phenotype and in 4 of 6 Burkitt/ALL lymphomas.
  • CONCLUSIONS: Among normal B-cell subsets, ZAP-70 was found expressed in normal pro/pre B cells but not in a significant proportion of normal B cells with mature phenotype.
  • The lack of ZAP-70 expression in normal mature B cells suggests that its expression in mature-derived neoplasms with different cellular origin, such as Burkitt's lymphoma and chronic lymphocytic leukemia, might be due to an aberrant phenomenon.
  • [MeSH-major] B-Lymphocytes / metabolism. Burkitt Lymphoma / genetics. Gene Expression Regulation. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / metabolism. ZAP-70 Protein-Tyrosine Kinase / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. DNA Mutational Analysis. Humans. Middle Aged. Phenotype. Phosphorylation. Receptors, Antigen, T-Cell / metabolism

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  • (PMID = 16467082.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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64. Wang YF, Chen BG, Luo WD, Zheng R, Li BL: [Expression of CD123 in lymphocytic leukemia and its significance for monitoring minimal residual diseases.]. Zhonghua Xue Ye Xue Za Zhi; 2010 Apr;31(4):244-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of CD123 in lymphocytic leukemia and its significance for monitoring minimal residual diseases.].
  • OBJECTIVE: To investigate the expression of CD123 and its significance in lymphocytic leukemia.
  • METHODS: CD123 expression in 139 lymphocytic leukemia patients and in lymphocytes from 10 normal bone marrows (BM) was analyzed by multi-parameter flow cytometry.
  • Cytogenetic and minimal residual disease (MRD) analysis were performed in acute B-lymphocytic leukemia (B-ALL) patients.
  • RESULTS: CD123 expression was absent in B lymphoid lineage stem-progenitor cells, mature B and T lymphocytes from 10 normal BM.
  • Among 139 lymphocytic leukemia patients, CD123 was negative in 5 T-ALL and 23 B-CLL patients.
  • A statistically significant difference in relapse rate within 12 months (MRD positive group: 63.04% vs MRD negative group 21.56%)and in disease free survival (DFS) time was found beween patients with MRD\[(36.06 +/- 2.62)%\] or not \[(48.23 +/- 1.82)%\] (P < 0.01).
  • [MeSH-major] Neoplasm, Residual. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Flow Cytometry. Humans. Leukemia, Lymphocytic, Chronic, B-Cell. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 20510041.001).
  • [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
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65. Bastida Vilá P, Palacio García C, Solsona Riera M, Ortega Aramburu JJ, Sánchez de Toledo Codina J: [Minimal residual disease in acute lymphoblastic leukemia: a new concept of complete remission]. An Pediatr (Barc); 2005 Nov;63(5):390-5
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  • [Title] [Minimal residual disease in acute lymphoblastic leukemia: a new concept of complete remission].
  • [Transliterated title] Leucemia mínima residual: nuevo concepto de remisión completa.
  • INTRODUCTION: Early response to induction treatment is one of the most important prognostic factors in children with acute lymphoblastic leukemia (ALL).
  • More sensitive techniques are required to measure residual leukemia and establish a new definition of complete remission.
  • OBJECTIVE: To identify minimal residual disease (MRD) by immunological techniques and define its prognostic impact in children with ALL.
  • All the children achieved complete cytological remission (< 5 %) with the induction treatment and had at least one useful phenotype for follow-up: 11 % were T phenotype, one was biphenotypic and the remainder were B cell leukemias.
  • Continued sequential monitoring may predict recurrence before the onset of clinical or hematologic manifestations.
  • [MeSH-major] Neoplasm, Residual / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 16266612.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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66. 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.
  • 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.
  • 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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67. Kazemi T, Asgarian-Omran H, Memarian A, Shabani M, Sharifian RA, Vossough P, Ansaripour B, Rabbani H, Shokri F: Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia. Cancer Immunol Immunother; 2009 Jun;58(6):989-96
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  • [Title] Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia.
  • Recent studies have demonstrated expression of Fc receptor-like (FCRL) molecules, a newly identified family with preferential B-cell lineage expression, in some chronic B-cell leukemias with possible implication for classification and/or targeted immunotherapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cell Surface / genetics. Receptors, Fc / genetics. Receptors, Immunologic / genetics

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  • (PMID = 18802695.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / FCRL2 protein, human; 0 / FCRL4 protein, human; 0 / FCRL5 protein, human; 0 / FCRLA protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Fc; 0 / Receptors, Immunologic
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68. Poitras JL, Dal Cin P, Aster JC, Deangelo DJ, Morton CC: Novel SSBP2-JAK2 fusion gene resulting from a t(5;9)(q14.1;p24.1) in pre-B acute lymphocytic leukemia. Genes Chromosomes Cancer; 2008 Oct;47(10):884-9
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  • [Title] Novel SSBP2-JAK2 fusion gene resulting from a t(5;9)(q14.1;p24.1) in pre-B acute lymphocytic leukemia.
  • In addition, less common aberrations (particularly gene fusions) involving JAK2 have been described in acute leukemias.
  • In this report, we identify SSBP2 as a new JAK2 fusion partner in a patient with pre-B cell acute lymphocytic leukemia.
  • This finding adds to the expanding compendium of JAK2 aberrations found in various hematopoietic malignancies, as well as the potential need for a diagnostic FISH analysis in the appropriate clinical setting.
  • [MeSH-major] Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 9 / genetics. DNA-Binding Proteins / genetics. Janus Kinase 2 / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Humans. In Situ Hybridization, Fluorescence. Male. Mutation. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18618714.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA066996-11A1
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / SSBP2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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69. Dubowy R, Graham M, Hakami N, Kletzel M, Mahoney D, Newman E, Ravindranath Y, Camitta B: Sequential oral hydroxyurea and intravenous cytosine arabinoside in refractory childhood acute leukemia: a pediatric oncology group phase 1 study. J Pediatr Hematol Oncol; 2008 May;30(5):353-7
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  • [Title] Sequential oral hydroxyurea and intravenous cytosine arabinoside in refractory childhood acute leukemia: a pediatric oncology group phase 1 study.
  • At concentrations >0.1 mM, hydroxyurea (HU) enhances the accumulation of cytosine arabinoside (ara-C) in leukemia cells in vitro.
  • This study of children with refractory acute leukemia was designed to take advantage of this biochemical modulation.
  • Thirty-three children [26 acute lymphocytic leukemia (ALL), 7 acute nonlymphocytic leukemia] were treated; 29 received at least 1 full course.
  • There were 6 complete responses (5 ALL), 5 partial responses (3 ALL), and 19 patients with no response or progressive disease.
  • There was no dosage effect for response with 2 complete responses occurring at the lowest ara-C level.
  • Twenty of twenty-six patients achieved a peak serum HU level >0.5 mM by 2 hours after the HU dose.
  • The mean level at 2 hours was 0.57 mM (range: 0.21 to 0.99 mM).
  • This combination of HU and ara-C is tolerable and has efficacy in refractory leukemias.
  • Responses at the lowest ara-C dose level suggests synergism.
  • [MeSH-major] Cytarabine / toxicity. Hydroxyurea / toxicity. Leukemia / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Humans. Infection / epidemiology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / mortality. Liver / drug effects. Liver / pathology. Skin / drug effects. Skin / pathology. Survival Analysis

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  • (PMID = 18458568.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; X6Q56QN5QC / Hydroxyurea
  • [Other-IDs] NLM/ NIHMS721202; NLM/ PMC4601800
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70. Cooper TM: Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Ther Clin Risk Manag; 2007 Dec;3(6):1135-41
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  • [Title] Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.
  • T-cell malignancies have distinct biochemical, immunologic, and clinical features which set them apart from non-T-cell malignancies.
  • In the past, T-cell leukemia portended a worse prognosis than leukemia of B-cell origin.
  • Cure rates have improved with intensification of therapy and advanced understanding of the molecular genetics of T-cell malignancies.
  • Further advances in the treatment of T-cell leukemia will require the development of novel agents that can target specific malignancies without a significant increase in toxicity.
  • Nelarabine is water soluble and rapidly converted to ara-G, which is specifically cytotoxic to T-lymphocytes and T-lymphoblastoid cells.
  • Clinical and pharmacokinetic investigations have established that nelarabine is active as a single agent which has led to exploration of an expanded role in the treatment of T-cell hematologic malignances.

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  • (PMID = 18516261.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2387290
  • [Keywords] NOTNLM ; 9-β-D-arabinofuranosylguanine / T-cell acute lymphoblastic leukemia / nelarabine
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71. Haferlach C, Rieder H, Lillington DM, Dastugue N, Hagemeijer A, Harbott J, Stilgenbauer S, Knuutila S, Johansson B, Fonatsch C: Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes. Genes Chromosomes Cancer; 2007 May;46(5):494-9
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  • [Title] Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes.
  • Therefore, laboratory techniques have to be optimized to provide reliable results for optimal patient care.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Acute Disease. Chromosome Aberrations. Diagnosis, Differential. Humans. Karyotyping


72. Schubauer-Berigan MK, Daniels RD, Fleming DA, Markey AM, Couch JR, Ahrenholz SH, Burphy JS, Anderson JL, Tseng CY: Risk of chronic myeloid and acute leukemia mortality after exposure to ionizing radiation among workers at four U.S. nuclear weapons facilities and a nuclear naval shipyard. Radiat Res; 2007 Feb;167(2):222-32
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  • [Title] Risk of chronic myeloid and acute leukemia mortality after exposure to ionizing radiation among workers at four U.S. nuclear weapons facilities and a nuclear naval shipyard.
  • A nested case-control study was conducted among workers at five U.S. nuclear facilities to evaluate leukemia mortality risk (excluding chronic lymphocytic) from ionizing radiation using worksite doses and adjusting for potential confounding.
  • Adjusting for sex and benzene, the RR of leukemia for workers receiving more than 10 mSv was higher compared to those receiving lower or no dose; however, the risk increase was attenuated in the highest dose group.
  • The ERR per 10 mSv was 1.44% (95% CI: < -1.03%, 7.59%) but was higher for workers born after 1921 compared to workers born earlier or when excluding leukemias of uncertain type.
  • The results suggest that risks among these nuclear workers are comparable to those observed in high-dose populations, although no evidence was observed of a positive quadratic dose-response term in this study.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / etiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / mortality. Neoplasms, Radiation-Induced / mortality


73. 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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74. Bloomfield CD, Mrózek K, Caligiuri MA: Cancer and leukemia group B leukemia correlative science committee: major accomplishments and future directions. Clin Cancer Res; 2006 Jun 1;12(11 Pt 2):3564s-71s
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  • [Title] Cancer and leukemia group B leukemia correlative science committee: major accomplishments and future directions.
  • The Cancer and Leukemia Group B (CALGB) Leukemia Correlative Science Committee (LCSC) has a remarkable history of outstanding productivity and has been at the cutting edge of correlative science for adult leukemia for almost 25 years.
  • Its work, initially focused on the use of immunophenotyping for diagnosis and prognosis of acute lymphoblastic leukemia and acute myeloid leukemia, has, for the last 15 years, focused on the clinical use of cytogenetic and molecular genetic markers in acute myeloid leukemia and acute lymphoblastic leukemia as well as in chronic lymphocytic leukemia.
  • Numerous CALGB LCSC studies have had a major effect on the way we currently diagnose, predict outcome, select appropriate treatment, document complete remission, and monitor residual disease in adults with acute leukemia.
  • In part as a result of the work of the CALGB LCSC, we are increasingly moving toward molecularly targeted therapy in acute and chronic leukemias.
  • In this report, we briefly review those contributions from the CALGB LCSC that have had, or are likely to have in the future, a major effect on how we currently manage leukemia and outline directions of ongoing and future research conducted by the CALGB LCSC.
  • [MeSH-major] Cytogenetics / trends. Leukemia / genetics. Molecular Biology / trends. Societies, Medical / trends

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  • (PMID = 16740786.001).
  • [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; Review
  • [Publication-country] United States
  • [Number-of-references] 80
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75. Reichardt VL, Brossart P: Current status of vaccination therapy for leukemias. Curr Hematol Rep; 2005 Jan;4(1):73-6
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  • [Title] Current status of vaccination therapy for leukemias.
  • Acute and chronic leukemias are common diseases in the clinical practice but few vaccination protocols have found their way to phase I trials in leukemias.
  • Therapeutic vaccination protocols share the goal of inducing or augmenting leukemia-specific immune responses in the tumor-bearing host in order to potentially achieve therapeutical benefit in these otherwise fatal diseases.
  • Major interest has been drawn to the use of dendritic cell (DC-based immunotherapy protocols relying on the unique properties of these most powerful antigen-presenting cells.
  • With the bcr-abl oncogene a target of specific immunotherapy has been determined in chronic myelogenous leukemia (CML), while there is a limited information on leukemia-specific tumor antigens in acute myelogenous and lymphoblastic leukemias.
  • This review will focus on immunotherapy development in acute and chronic leukemias and will discuss published clinical trials in acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL) and CML.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Leukemia / therapy. Vaccination
  • [MeSH-minor] Acute Disease. Clinical Trials as Topic. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Treatment Outcome

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  • (PMID = 15610663.001).
  • [ISSN] 1541-0714
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines
  • [Number-of-references] 29
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76. Altieri A, Castro F, Bermejo JL, Hemminki K: Number of siblings and the risk of lymphoma, leukemia, and myeloma by histopathology. Cancer Epidemiol Biomarkers Prev; 2006 Jul;15(7):1281-6
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  • [Title] Number of siblings and the risk of lymphoma, leukemia, and myeloma by histopathology.
  • Epidemiologic evidence indicates that several markers of exposure to childhood infections are inversely associated with the risk of childhood leukemia and lymphomas.
  • We used the Swedish Family-Cancer Database to assess the effects of number of siblings on the risk of non-Hodgkin's (n = 7,007) and Hodgkin's lymphomas (n = 3,115), leukemias (n = 7,650), and multiple myeloma (n = 1,492) by histopathology.
  • Having four or more siblings compared with none was associated with an excess risk of childhood acute lymphoblastic leukemia [ALL; rate ratio (RR), 2.11; P(trend) = 0.001], acute monocytic leukemia (RR, 2.51; P(trend) = 0.002), and multiple myeloma (RR, 1.34; P(trend) = 0.006).
  • Having three or more older siblings compared with none decreased the risk of acute monocytic leukemia (RR, 0.35; P(trend) = 0.001) and childhood ALL (RR, 0.69; P(trend) = 0.01).
  • Acute myeloid leukemia, chronic lymphocytic leukemia, and other lymphoproliferative malignancies were not associated with number of siblings.
  • In conclusion, we found an excess risk of childhood ALL and acute monocytic leukemia in large families.
  • However, for ALL, acute monocytic leukemia, and Hodgkin's lymphoma, younger siblings were strongly protected compared with older siblings.
  • The remarkable protective effect of number of older siblings on acute monocytic leukemia is a novel finding of potential interest.
  • Possible interpretations of our findings in the context of a putative infectious etiology are discussed.
  • [MeSH-major] Birth Order. Hodgkin Disease / etiology. Leukemia / etiology. Multiple Myeloma / etiology. Siblings
  • [MeSH-minor] Adolescent. Adult. Age of Onset. Aged. Child. Child, Preschool. Family Characteristics. Female. Humans. Incidence. Infant. Infant, Newborn. Male. Middle Aged. Registries. Risk Factors. Sweden / epidemiology

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  • (PMID = 16835324.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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77. 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.
  • 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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78. Mai YJ, Qiu LG, Li ZJ, Yu Z, Li CH, Wang YF, Wang GR, Li Q: [The expression of beta-catenin and its significance in leukemia cells]. Zhonghua Xue Ye Xue Za Zhi; 2007 Aug;28(8):541-4
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  • [Title] [The expression of beta-catenin and its significance in leukemia cells].
  • OBJECTIVE: To investigate the expression of beta-catenin in patients with leukemia and explore its significance in leukemias.
  • METHODS: RT-PCR was used to detect the expression of beta-catenin in bone marrow mononuclear cells (BMMNCs) from patients with leukemia.
  • RESULTS: Expression of beta-catenin was statistically higher in acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) samples than in normal donors (P = 0.001 and 0.016 respectively) and chronic phase chronic myeloid leukemia (CML) patients (P = 0.001 and P = 0.008 respectively), while there was no statistic difference between AML and ALL patients (P = 0.58).
  • Immunocytochemical analysis revealed that BMMNCs from normal donors expressed beta-catenin on the plasma membrane and cytoplasma, while those from acute leukemia expressed beta-catenin to varying degrees in the nucleus as well.
  • The expression of beta-catenin gene statistically showed the highest level in M5 (n = 15) and the lowest level in M3 (n = 18).
  • No clinical features, such as, age, initial WBC count, therapy response rate, blast cell numbers or cytogenetic risk was found to be correlated with the expression of beta-catenin excepting for CD34+ positive rate (P = 0.004) in AML.
  • CONCLUSION: As a key mediator of Wnt signal transduction way, overexpression of beta-catenin in leukemia cells indicates that it might be aberrantly activated in acute leukemia, accelerated or blastic phase of CML.
  • [MeSH-major] Leukemia / metabolism. beta Catenin / metabolism

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  • (PMID = 18078131.001).
  • [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 / RNA, Messenger; 0 / beta Catenin
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79. Yamamoto JF, Goodman MT: Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control; 2008 May;19(4):379-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
  • OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.
  • Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
  • METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.
  • RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.
  • The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).
  • Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.
  • African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.
  • A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.
  • CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.
  • Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.
  • [MeSH-major] Leukemia / ethnology

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  • (PMID = 18064533.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
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80. Small D: Targeting FLT3 for the treatment of leukemia. Semin Hematol; 2008 Jul;45(3 Suppl 2):S17-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting FLT3 for the treatment of leukemia.
  • FLT3 is a receptor tyrosine kinase with important roles in hematopoietic stem/progenitor cell survival and proliferation.
  • It is frequently overexpressed in acute leukemias and is frequently mutated in acute myeloid leukemia (AML).
  • Anti-FLT3 antibodies may also prove to be an excellent way of targeting FLT3 in AML and acute lymphocytic leukemia (ALL) by inhibiting signaling and through antibody-dependent cell-mediated cytotoxicity.

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  • (PMID = 18760705.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090668; United States / NCI NIH HHS / CA / P01 CA070970; United States / NCI NIH HHS / CA / R01 CA090668-01A1; United States / NCI NIH HHS / CA / CA090668-01A1; United States / NCI NIH HHS / CA / P01 CA070970-10A16432; United States / NCI NIH HHS / CA / CA070970-10A16432
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 34
  • [Other-IDs] NLM/ NIHMS69701; NLM/ PMC2597087
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81. Henrich S, Crossett B, Christopherson RI: Differentially expressed nuclear proteins in human CCRF-CEM, HL-60, MEC-1 and Raji cells correlate with cellular properties. Proteomics Clin Appl; 2007 Oct;1(10):1252-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The human cell lines CCRF-CEM (T-cell acute lymphocytic leukemia), HL-60 (acute myeloid leukemia), MEC-1 (B-cell chronic lymphocytic leukemia) and Raji (Burkitt's B-cell lymphoma) have been analysed for differences in their nuclear proteomes.
  • Using 2-D DIGE, 55 nuclear proteins have been identified that are differentially expressed (p<0.025) between the four cell lines, including proteins associated with transcription, proliferation, DNA repair and apoptosis.
  • Of these 55 proteins, 22 were over-expressed in just one cell line, and four were down-regulated in one cell line.
  • Proteins uniquely over-expressed between myeloid and lymphoid cell lines include those that may have use as markers for diagnosis, disease progression and B-cell maturation and differentiation.
  • Expression of various proliferation-associated nuclear proteins correlated with relative growth rates of the cell lines, giving these proteins potential diagnostic applications for distinction of chronic versus acute subtypes of haematological malignancies.
  • Identification of these differentially expressed nuclear proteins should facilitate elucidation of the molecular mechanisms underlying leukocyte differentiation and transformation to leukemias and lymphomas.
  • The nuclear expression profiles should enable classification of subtypes of leukemia, and identify potential nuclear protein targets for development of diagnostic and therapeutic strategies.

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  • [Copyright] Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21136623.001).
  • [ISSN] 1862-8346
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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82. Figueroa ME, Reimers M, Thompson RF, Ye K, Li Y, Selzer RR, Fridriksson J, Paietta E, Wiernik P, Green RD, Greally JM, Melnick A: An integrative genomic and epigenomic approach for the study of transcriptional regulation. PLoS One; 2008 Mar 26;3(3):e1882
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The molecular heterogeneity of acute leukemias and other tumors constitutes a major obstacle towards understanding disease pathogenesis and developing new targeted-therapies.
  • We predicted that integration of different genome-wide epigenetic regulatory marks along with gene expression levels would provide greater power in capturing biological differences between leukemia subtypes.
  • Gene expression, cytosine methylation and histone H3 lysine 9 (H3K9) acetylation were measured using high-density oligonucleotide microarrays in primary human acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) specimens.
  • We found that DNA methylation and H3K9 acetylation distinguished these leukemias of distinct cell lineage, as expected, but that an integrative analysis combining the information from each platform revealed hundreds of additional differentially expressed genes that were missed by gene expression arrays alone.

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  • (PMID = 18365023.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104348; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NIGMS NIH HHS / GM / GM007288
  • [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 / DNA Primers; 0 / Histones
  • [Other-IDs] NLM/ PMC2266992
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83. Su X, Della-Valle V, Delabesse E, Azgui Z, Berger R, Merle-Béral H, Bernard OA, Nguyen-Khac F: Transcriptional activation of the cardiac homeobox gene CSX1/NKX2-5 in a B-cell chronic lymphoproliferative disorder. Haematologica; 2008 Jul;93(7):1081-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional activation of the cardiac homeobox gene CSX1/NKX2-5 in a B-cell chronic lymphoproliferative disorder.
  • Study of T-cell acute lymphoblastic leukemia identified the related non-clustered homeobox transcription factors, TLX1 and TLX3, as frequently ectopically expressed as a result of chromosomal translocations.
  • We report the deregulation of a non-clustered homeobox gene in a new type of t(5;14)(q35;q11) translocation in a mature peripheral B-cell leukemia.
  • Our study establishes that deregulation of homeobox encoding genes is not restricted to acute leukemic proliferations, but is also observed in chronic malignant diseases.
  • [MeSH-major] B-Lymphocytes / metabolism. Gene Expression Regulation. Homeodomain Proteins / genetics. Lymphoproliferative Disorders / genetics. Lymphoproliferative Disorders / pathology. Transcription Factors / genetics. Transcriptional Activation
  • [MeSH-minor] Cell Proliferation. Chronic Disease. Cytogenetics. Female. Humans. Middle Aged. Models, Biological. Mutation. Sequence Analysis, DNA. Translocation, Genetic

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  • (PMID = 18492690.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NKX2-5 protein, human; 0 / Transcription Factors
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84. Taniguchi A, Nemoto Y, Yokoyama A, Kotani N, Imai S, Shuin T, Daibata M: Promoter methylation of the bone morphogenetic protein-6 gene in association with adult T-cell leukemia. Int J Cancer; 2008 Oct 15;123(8):1824-31
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  • [Title] Promoter methylation of the bone morphogenetic protein-6 gene in association with adult T-cell leukemia.
  • Bone morphogenetic proteins (BMP), belonging to the transforming growth factor-beta superfamily, are multifunctional regulators of cell proliferation, differentiation and apoptosis in various types of malignant cells.
  • In this study, we investigated BMP-6 promoter methylation in patients with various types of leukemias.
  • The BMP-6 methylation was found preferentially in adult T-cell leukemia (ATL) (49 of 60, 82%) compared with other types of leukemias studied including acute myeloid leukemia (3 of 67, 5%), acute lymphoblastic leukemia (6 of 38, 16%) and chronic lymphocytic leukemia (1 of 21, 5%).
  • Among subtypes of ATL, the BMP-6 gene was more frequently methylated in aggressive ATL forms of acute (96%) and lymphoma (94%) types than less malignant chronic ATL (44%) and smoldering ATL (20%).
  • These findings suggested that BMP-6 promoter methylation is likely to be a common epigenetic event at later stages of ATL and that the methylation profiles may be useful for the staging of ATL as well as for evaluation of the individual risk of developing the disease.
  • [MeSH-major] Bone Morphogenetic Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 18688853.001).
  • [ISSN] 1097-0215
  • [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 / BMP6 protein, human; 0 / Bone Morphogenetic Protein 6; 0 / Bone Morphogenetic Proteins; 0 / RNA, Messenger; 0 / Sulfites; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine; OJ9787WBLU / hydrogen sulfite
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85. Grüllich C, Friske V, Finke J: Ex vivo detection of primary leukemia cells resistant to granule cytotoxin-induced cell death: a rapid isolation method to study granzyme-B-mediated cell death. Ann Hematol; 2008 Sep;87(9):701-8
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  • [Title] Ex vivo detection of primary leukemia cells resistant to granule cytotoxin-induced cell death: a rapid isolation method to study granzyme-B-mediated cell death.
  • Cytotoxic T lymphocytes and natural killer cells (CTL/NK) induce cell death in leukemia cells by the granzyme B (grB)-dependent granule cytotoxin (GC) pathway.
  • Resistance to GC may be involved in immune evasion of leukemia cells.
  • We developed a rapid method for the isolation of GC to investigate GC-mediated cell death in primary leukemia cells.
  • We isolated GC containing grB, grB complexes and PFN by detergent free hypotonic lysis of the human NK cell leukemia line YT.
  • The human leukemia cell lines KG-1, U937, K562 (myeloid leukemia), Jurkat, Daudi, and BV173 (lymphoblastic leukemia) treated with GC internalized grB and underwent cell death.
  • In primary leukemia cells analyzed ex vivo, we found GC-resistant leukemia cells in three out of seven patients with acute myeloid leukemia and one out of six patients with acute lymphoblastic leukemia.
  • We conclude that our method is fast (approximately 1 h) and yields active GC that induce grB-dependent cell death.
  • Furthermore, resistance to GC can be observed in acute leukemias and may be an important mechanism contributing to leukemia cell immune evasion.
  • [MeSH-major] Cell Death / drug effects. Cytotoxins / toxicity. Granzymes / toxicity. Leukemia / pathology
  • [MeSH-minor] Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. K562 Cells / drug effects. K562 Cells / pathology. Killer Cells, Natural / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Myeloid, Acute / pathology. Perforin / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. T-Lymphocytes, Cytotoxic / immunology. U937 Cells / drug effects. U937 Cells / pathology

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  • (PMID = 18437383.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytotoxins; 126465-35-8 / Perforin; EC 3.4.21.- / Granzymes
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86. Arbel Y, Swartzon M, Justo D: QT prolongation and Torsades de Pointes in patients previously treated with anthracyclines. Anticancer Drugs; 2007 Apr;18(4):493-8
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  • [Title] QT prolongation and Torsades de Pointes in patients previously treated with anthracyclines.
  • Anthracyclines reduce myocardial repolarization reserve and might increase the risk for Torsades de Pointes a long time after treatment.
  • We studied all the publications concerning Torsades de Pointes in patients previously treated with anthracyclines to investigate the clinical circumstances leading to this rare life-threatening complication.
  • Our literature search yielded nine reports of 11 patients who had developed Torsades de Pointes anywhere from weeks to years following treatment with anthracyclines.
  • Risk factors and triggers for Torsades de Pointes, among other clinical aspects, were analyzed in each report.
  • Most patients (n=10; 90.9%) were previously treated with anthracyclines owing to acute leukemias: acute myelogenous leukemia (n=5), acute lymphocytic leukemia (n=3) and acute promyelocytic leukemia (n=2).
  • The most prevalent triggers for Torsades de Pointes were the administration of a QT-prolonging agent (n=10; 90.9%) and hypokalemia (n=9; 81.8%).
  • Azole derivatives were the most prevalent of the QT-prolonging agents that triggered Torsades de Pointes (n=5; 45.5%).
  • Although four patients suffered from anthracycline-induced left ventricular dysfunction and five other patients had only one or two questionable triggers for Torsades de Pointes, in only two of these cases the authors considered previous treatment with anthracyclines as a risk factor for Torsades de Pointes.
  • Previous treatment with anthracycline is an underestimated risk factor for Torsades de Pointes.
  • [MeSH-major] Anthracyclines / adverse effects. Antineoplastic Agents / adverse effects. Long QT Syndrome / chemically induced. Torsades de Pointes / chemically induced

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  • (PMID = 17351403.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Meta-Analysis
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents; BZ114NVM5P / Mitoxantrone
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87. Tasca S, Carli E, Caldin M, Menegazzo L, Furlanello T, Gallego LS: Hematologic abnormalities and flow cytometric immunophenotyping results in dogs with hematopoietic neoplasia: 210 cases (2002-2006). Vet Clin Pathol; 2009 Mar;38(1):2-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Based on cell morphology and phenotype, cases were classified as: acute lymphoblastic leukemia (ALL, n=51), acute myeloid leukemia (AML, n=33), chronic lymphocytic leukemia (CLL, n=61), and leukemic high-grade lymphoma (L-HGL, n=65).
  • Most cases of ALL (47/51) and L-HGL (41/65) had a B-cell phenotype, while most cases of CLL (54/61) had a T-cell phenotype, with a high prevalence of the large granular lymphocyte subtype (49/61).
  • Neutropenia was seen in 64-78% of acute leukemias (AML and ALL) in contrast to no cases of CLL and 11% of L-HGL.
  • Thrombocytopenia was seen in 88-90% of acute leukemias in contrast to 15% of CLL and 40% of L-HGL.
  • Thrombocytopenia was more prevalent (71% vs 22%) and significantly more severe in T-cell vs B-cell L-HGL.

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  • (PMID = 19171020.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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88. Staratschek-Jox A, Classen S, Gaarz A, Debey-Pascher S, Schultze JL: Blood-based transcriptomics: leukemias and beyond. Expert Rev Mol Diagn; 2009 Apr;9(3):271-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Blood-based transcriptomics: leukemias and beyond.
  • In 1999, Golub et al. proposed for the first time microarray-based transcriptional profiling to be used as a new technology for the differential diagnosis of acute myeloid leukemias and acute lymphocytic leukemias.
  • This very preliminary study sparked great enthusiasm beyond the leukemias.
  • Here we highlight the advances in the field of blood transcriptomics during the last 10 years and also critically discuss the issues that need to be resolved before blood transcriptomics will become part of daily diagnostics in the leukemias, as well as in other diseases showing involvement of peripheral blood.
  • [MeSH-major] Blood. Gene Expression Profiling / methods. Leukemia / diagnosis. Leukemia / genetics. Oligonucleotide Array Sequence Analysis / methods

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  • (PMID = 19379085.001).
  • [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
  • [Number-of-references] 57
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89. Luczyński W, Krawczuk-Rybak M, Stasiak-Barmuta A: [Experimental and selected clinical aspects of active immunotherapy in leukemia]. Postepy Hig Med Dosw (Online); 2006;60:379-86
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  • [Title] [Experimental and selected clinical aspects of active immunotherapy in leukemia].
  • The aim of the review is to summarize current knowledge concerning active immunotherapy in leukemia.
  • The molecular mechanisms and selected clinical implications of different cancer vaccines used in pediatric and adult leukemias are discussed.
  • Cells of acute lymphoblastic leukemia and chronic lymphocytic leukemia can be induced into antigen-presenting cells with the CD40 ligation system.
  • In many studies it was confimed that these cells stimulate auto- and/or allogeneic T-cell response.
  • Similar effects using different cytokines such as GM-CSF, TNF-alpha, and IL-4 can be observed in acute myeloid leukemia and myelodysplastic syndromes.

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  • (PMID = 16885908.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Cancer Vaccines
  • [Number-of-references] 51
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90. Sternberg DW, Licht JD: Therapeutic intervention in leukemias that express the activated fms-like tyrosine kinase 3 (FLT3): opportunities and challenges. Curr Opin Hematol; 2005 Jan;12(1):7-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic intervention in leukemias that express the activated fms-like tyrosine kinase 3 (FLT3): opportunities and challenges.
  • PURPOSE OF REVIEW: The fms-like tyrosine kinase 3 (FLT3) receptor tyrosine kinase is now recognized to be a critical mediator in the pathogenesis of myeloid and some lymphoid leukemias.
  • This article reviews recent efforts to disrupt FLT3 signaling in acute myelogenous leukemia and to identify potential therapeutic challenges posed by the acquisition of resistance mutations in these malignancies.
  • Although the agents are well tolerated by patients, clinical responses in relapsed or refractory acute myelogenous leukemia (AML) are limited and transient.
  • SUMMARY: FLT3 is widely expressed in AML and some cases of acute lymphocytic leukemia.
  • The development of FLT3 small molecule kinase inhibitors follows from research efforts to understand signal transduction and profiles of gene expression in leukemia pathogenesis.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / genetics

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  • (PMID = 15604885.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA82261; United States / NCI NIH HHS / CA / R01 CA59936
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 69
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91. Lü SQ, Yang JM, Wang JM: [Effects of proteasome inhibitors on leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):896-900
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  • [Title] [Effects of proteasome inhibitors on leukemias].
  • A lot of studies on effects of proteasome inhibitors on leukemias, including plasma cell leukemia; chronic lymphocytic leukemia, adult T cell lymphoma/leukemia, chronic myeloid leukemia and acute myeloid leukemia, were reviewed in this article.

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  • (PMID = 17708829.001).
  • [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; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 27
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92. Clark BR, Ferketich AK, Fisher JL, Ruymann FB, Harris RE, Wilkins JR 3rd: Evidence of population mixing based on the geographical distribution of childhood leukemia in Ohio. Pediatr Blood Cancer; 2007 Nov;49(6):797-802
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  • [Title] Evidence of population mixing based on the geographical distribution of childhood leukemia in Ohio.
  • BACKGROUND: This ecologic study examined the geographic distribution of childhood leukemias in Ohio, 1996-2000, among children aged 0-19 for evidence that population mixing may be a factor.
  • RESULTS: Of the 585 cases, 73.3% were acute lymphocytic leukemia (ALL), 16.6% acute myelogenous leukemia (AML), 3.2% acute monocytic leukemia (AMoL), and 2.6% chronic myelogenous leukemia (CML).
  • Rates for total leukemia burden were significantly below national levels for all races (P = 0.00001), likely due to poor ascertainment of cases.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Population Density. Population Dynamics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Rural Population. Urban Population


93. Grzybowska-Izydorczyk O, Smolewski P: [The role of the inhibitor of apoptosis protein (IAP) family in hematological malignancies]. Postepy Hig Med Dosw (Online); 2008 Feb 14;62:55-63
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  • The apoptotic mode of cell death is a major regulatory process in all complex organisms.
  • The low proliferative index and slow accumulation of malignant cells in chronic lymphocytic leukemia (CLL), the most frequent type of leukemia in Europe and North America, suggests that the disease is caused by a defect in apoptosis regulation.
  • Overexpression of several IAPs has been detected in various hematological malignancies, including acute leukemias, myelodysplastic syndrome (MDS), chronic myeloid leukemia (CML), and many types of lymphoid malignancies, such as chronic lymphocytic leukemia (CLL) and diffuse large B-cell lymphoma (DLBCL).
  • Many publications revealed significant correlation between a high level of IAPs, especially of XIAP and survivin, and tumor progression.
  • It seems that overexpression of XIAP in acute myeloid leukemia (AML) and survivin in acute lymphoblastic leukemia (ALL) and DLBCL could become a new unfavorable prognostic factor.

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  • (PMID = 18283236.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Inhibitor of Apoptosis Proteins
  • [Number-of-references] 67
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94. Kara IO, Sahin B, Gunesacar R: Levels of serum and cerebrospinal fluid soluble CD27 in the diagnosis of leptomeningeal involvement of hematolymphoid malignancies. Adv Ther; 2007 Jul-Aug;24(4):741-7
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  • Reportedly, soluble CD27 (sCD27) is a sensitive and specific marker for leptomeningeal involvement (LI) of CD27-expressing lymphoproliferations, such as B-cell non-Hodgkin's lymphoma and chronic B-lymphocytic leukemia.
  • On morphologic analysis of cerebrospinal fluid (CSF), one third of patients suspected of LI have false negatives, so a diagnostic marker for LI in B-cell non-Hodgkin's lymphoma or B-lymphocytic leukemia would be extremely valuable. sCD27 was detected in the serum and CSF samples from 35 selected patients in whom 18 cases of acute lymphoblastic leukemia (ALL) (3 with LI), 7 of non-Hodgkin's lymphoma, and 5 of acute myelogenous leukemia (3 with LI) were submitted for (immuno)morphologic detection of malignant cells and intrathecal therapy, along with samples from 5 control patients (2 submitted for epidural hemorrhage, 3 for lumbar disc protrusion).
  • The cutoff value was 350 U/mL.
  • Serum and CSF-sCD27 concentrations above the cutoff value were not detected.
  • [MeSH-minor] Biomarkers, Tumor / blood. Biomarkers, Tumor / cerebrospinal fluid. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / cerebrospinal fluid. Leukemia, Myeloid, Acute / pathology. Lymphoma, Non-Hodgkin / blood. Lymphoma, Non-Hodgkin / cerebrospinal fluid. Lymphoma, Non-Hodgkin / pathology. Meninges / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / cerebrospinal fluid. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Predictive Value of Tests

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  • (PMID = 17901023.001).
  • [ISSN] 0741-238X
  • [Journal-full-title] Advances in therapy
  • [ISO-abbreviation] Adv Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Biomarkers, Tumor
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95. Schmitt A, Hus I, Schmitt M: Dendritic cell vaccines for leukemia patients. Expert Rev Anticancer Ther; 2007 Mar;7(3):275-83
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  • [Title] Dendritic cell vaccines for leukemia patients.
  • The graft-versus-leukemia effect observed after allogeneic stem cell transplantation strongly suggests that T lymphocytes play a major role in the rejection of leukemic cells.
  • This graft-versus-leukemia effect might be enhanced through dendritic cell vaccination.
  • The characterization of leukemia-specific antigens eliciting immune responses in the autologous host has prompted researchers and clinicians to broaden the spectrum of dendritic cell vaccines to hematological malignancies.
  • Recently, the focus is on acute myeloid leukemia and chronic lymphocytic leukemia.
  • This review summarizes data on the administration of autologous and allogeneic dendritic cells to leukemia patients as an interesting approach in cellular therapy of leukemias.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Dendritic Cells / transplantation. Immunotherapy, Active. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Animals. Antigen Presentation. Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Cell Adhesion. Cell Differentiation / drug effects. Cells, Cultured / immunology. Cells, Cultured / transplantation. Clinical Trials as Topic. Cytokines / pharmacology. Humans. Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myeloid / therapy. Lymphocyte Activation. Mice. Models, Immunological. Neoplastic Stem Cells / cytology. Neoplastic Stem Cells / drug effects. T-Lymphocyte Subsets / immunology. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 17338648.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Cytokines
  • [Number-of-references] 66
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96. Smith MT, McHale CM, Wiemels JL, Zhang L, Wiencke JK, Zheng S, Gunn L, Skibola CF, Ma X, Buffler PA: Molecular biomarkers for the study of childhood leukemia. Toxicol Appl Pharmacol; 2005 Aug 07;206(2):237-45
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  • [Title] Molecular biomarkers for the study of childhood leukemia.
  • Various specific chromosome rearrangements, including t(8;21), t(15;17), and inv(16), are found in acute myeloid leukemia (AML) and in childhood acute lymphocytic leukemia (ALL), t(12;21) and t(1;19) are common.
  • These findings show that most childhood leukemias begin before birth and that maternal and perinatal exposures such as chemical and infectious agents are likely to be critical.
  • Indeed, we have reported that exposure to indoor pesticides during pregnancy and the first year of life raises leukemia risk, but that later exposures do not.
  • We have also examined aberrant gene methylation in different cytogenetic subgroups and have found striking differences between them, suggesting that epigenetic events are also important in the development of some forms of childhood leukemia.
  • Further, at least two studies now show that the inactivating NAD(P)H:quinone acceptor oxidoreductase (NQO1) C609T polymorphism is positively associated with leukemias arising in the first 1-2 years of life and polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene have been associated with adult and childhood ALL.
  • Thus, low folate intake and compounds that are detoxified by NQO1 may be important in elevating leukemia risk in children.
  • Finally, we are exploring the use of proteomics to subclassify leukemia, because cytogenetic analysis is costly and time-consuming.
  • Several proteins have been identified that may serve as useful biomarkers for rapidly identifying different forms of childhood leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15967214.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES0098137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 935E97BOY8 / Folic Acid; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  • [Number-of-references] 55
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97. Adams H, Schmid P, Dirnhofer S, Tzankov A: Cytokeratin expression in hematological neoplasms: a tissue microarray study on 866 lymphoma and leukemia cases. Pathol Res Pract; 2008;204(8):569-73
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  • [Title] Cytokeratin expression in hematological neoplasms: a tissue microarray study on 866 lymphoma and leukemia cases.
  • Using tissue microarray technology, we tested 1059 lymphoma and acute leukemia cases, covering the most common disease entities, for aberrant CK expression, using CK22.
  • In total, 866 of the arrayed cases were evaluable (80%), and 13 positive cases (1.5%) were found: 1 out of 230 Hodgkin lymphomas (0.4%), 1 plasma cell myeloma, 2 out of 326 diffuse large B-cell lymphomas (0.6%), 5 out of 18 mantle cell lymphomas (26%), 3 out of 70 small cell lymphomas/chronic lymphocytic leukemias (4%) and 1 out of 27 peripheral T-cell lymphomas, not otherwise specified (4%).
  • All CK22-positive cases, except for one mantle cell lymphoma, expressed the specific simple epithelial CK8 but not the basal/stratified epithelial CK5/6.
  • Aberrant CK expression can be encountered in a small subset of otherwise characteristic B- and T-cell lymphomas, but not in acute leukemias, which should be considered in difficult differential diagnostic settings.
  • [MeSH-major] Keratins / analysis. Leukemia / metabolism. Lymphoma / chemistry. Tissue Array Analysis

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  • (PMID = 18436389.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Germany
  • [Chemical-registry-number] 68238-35-7 / Keratins
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98. Svecová D, Pallová A, Chmurová N, Babal P: Paraneoplastic vasculitis associated with hairy cell leukemia. Prague Med Rep; 2008;109(1):83-7
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  • [Title] Paraneoplastic vasculitis associated with hairy cell leukemia.
  • Hairy cell leukemia (HCL) is a rare B-cell lymphoproliferative disease, accounting for about 2-3% of all leukemias in adults.
  • Vasculitis in lymphoproliferative disease is relatively uncommon and may predate the diagnosis of lymphoproliferative disease.
  • A 54-year old female with one month history of general symptoms and sudden onset of maculopapular exanthema on the skin, suffered from anemia, leukopenia and thrombocytopenia.
  • Examination of the skin biopsy revealed lymphocytic vasculitis.
  • Immunophenotyping of the skin biopsy revealed cell population with CD45RO, and small groups with CD20, partly DBA44 positivity.
  • The diagnosis of HCL was confirmed by flow cytometry of the bone marrow and of the peripheral blood cells that revealed pathological cell population with expression of CD11c, CD19, CD25, CD103.
  • The patient with acute vasculitis should be screened and monitored for possible lymphoproliferative diseases.
  • Skin manifestation of acute vasculitis accompanied with hairy cells may be the first manifestation of HCL.
  • [MeSH-major] Leukemia, Hairy Cell / complications. Paraneoplastic Syndromes / complications. Vasculitis / complications

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  • (PMID = 19097393.001).
  • [ISSN] 1214-6994
  • [Journal-full-title] Prague medical report
  • [ISO-abbreviation] Prague Med Rep
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Czech Republic
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99. Bourette RP, Grasset MF, Mouchiroud G: E2a/Pbx1 oncogene inhibits terminal differentiation but not myeloid potential of pro-T cells. Oncogene; 2007 Jan 11;26(2):234-47
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  • E2a/Pbx1 is a fusion oncoprotein resulting from the t(1;19) translocation found in human pre-B acute lymphocytic leukemia and in a small number of acute T-lymphoid and myeloid leukemias.
  • To address this question, we introduced the receptor of the macrophage-colony-stimulating factor (M-CSF-R) in pro-T cells immortalized by a conditional, estradiol-dependent, E2a/Pbx1-protein, and continuously proliferating in response to stem cell factor and interleukin-7.
  • We asked whether M-CSF-R would be functional in an early T progenitor cell and influence the fate of E2a/Pbx1-immortalized cells.
  • This demonstrated that M-CSF-R is functional for proliferation and differentiation signaling in a T-lymphoid progenitor cell, which, in addition, unveiled myeloid potential of pro-T progenitors.
  • [MeSH-major] Cell Differentiation. Cell Lineage. Cell Transformation, Neoplastic. Homeodomain Proteins / physiology. Oncogene Proteins, Fusion / physiology. T-Lymphocytes / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Proliferation. Estradiol / pharmacology. Female. Flow Cytometry. Genes, fms / genetics. Genes, fms / physiology. Green Fluorescent Proteins / metabolism. Interleukin-7 / pharmacology. Lymphocytes / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Myeloid Cells / metabolism. Phagocytosis. Receptor, Macrophage Colony-Stimulating Factor / genetics. Receptor, Macrophage Colony-Stimulating Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Stem Cell Factor / pharmacology. Stem Cells / metabolism. Stem Cells / pathology

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  • (PMID = 16819510.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Interleukin-7; 0 / Oncogene Proteins, Fusion; 0 / Stem Cell Factor; 0 / enhanced green fluorescent protein; 146150-85-8 / E2A-Pbx1 fusion protein; 147336-22-9 / Green Fluorescent Proteins; 4TI98Z838E / Estradiol; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
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100. Garcia-Manero G, Yang H, Bueso-Ramos C, Ferrajoli A, Cortes J, Wierda WG, Faderl S, Koller C, Morris G, Rosner G, Loboda A, Fantin VR, Randolph SS, Hardwick JS, Reilly JF, Chen C, Ricker JL, Secrist JP, Richon VM, Frankel SR, Kantarjian HM: Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes. Blood; 2008 Feb 1;111(3):1060-6
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  • [Title] Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes.
  • Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor active clinically in cutaneous T-cell lymphoma and preclinically in leukemia.
  • Patients with relapsed or refractory leukemias or myelodysplastic syndromes (MDS) and untreated patients who were not candidates for chemotherapy were eligible.
  • Of 41 patients, 31 had acute myeloid leukemia (AML), 4 chronic lymphocytic leukemia, 3 MDS, 2 acute lymphoblastic leukemia, and 1 chronic myelocytic leukemia.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Histone Deacetylase Inhibitors. Hydroxamic Acids / therapeutic use. Leukemia / drug therapy. Leukemia / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology






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