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1. Calin GA, Croce CM: Chronic lymphocytic leukemia: interplay between noncoding RNAs and protein-coding genes. Blood; 2009 Nov 26;114(23):4761-70
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  • [Title] Chronic lymphocytic leukemia: interplay between noncoding RNAs and protein-coding genes.
  • MicroRNAs (miRNAs), small regulatory ncRNAs, are involved in the pathogenesis of all types of human cancers, including leukemias, mainly via dysregulation of expression of cancer genes.
  • Researchers first identified this new paradigm of molecular oncology in patients with chronic lymphocytic leukemia (CLL).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Neoplasm Proteins / physiology. RNA, Untranslated / physiology
  • [MeSH-minor] Animals. Apoptosis / genetics. B-Lymphocyte Subsets / metabolism. B-Lymphocyte Subsets / pathology. Cell Hypoxia / genetics. Chromosome Aberrations. Conserved Sequence. Disease Progression. Drug Delivery Systems. Forecasting. Gene Regulatory Networks. Genes, Tumor Suppressor. Humans. Mammals / genetics. MicroRNAs / genetics. MicroRNAs / physiology. Neovascularization, Pathologic / genetics. Oncogenes. Signal Transduction / genetics

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  • (PMID = 19745066.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Untranslated
  • [Number-of-references] 92
  • [Other-IDs] NLM/ PMC2786287
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2. Catellani S, Poggi A, Bruzzone A, Dadati P, Ravetti JL, Gobbi M, Zocchi MR: Expansion of Vdelta1 T lymphocytes producing IL-4 in low-grade non-Hodgkin lymphomas expressing UL-16-binding proteins. Blood; 2007 Mar 1;109(5):2078-85
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  • [Title] Expansion of Vdelta1 T lymphocytes producing IL-4 in low-grade non-Hodgkin lymphomas expressing UL-16-binding proteins.
  • Data on 23 patients with low-grade non-Hodgkin lymphomas (NHLs), 4 mantle (MT), 4 marginal zone (MZ), and 15 follicular (FL), were analyzed and compared with 10 high-risk (HR) B-cell chronic lymphocytic leukemias (B-CLLs) with lymph node involvement and 4 diffuse large-cell lymphomas (DLCLs).
  • A significant increase in circulating Vdelta1 T lymphocytes producing interleukin-4 (IL-4) was found in patients with FL, MT, and MZ NHL, at variance with DLCL and HR B-CLL.
  • In 19 of the 23 patients with NHL with increased circulating Vdelta1 T lymphocytes, B cells expressing the UL-16-binding proteins (ULBPs) ULBP2 or ULBP3 or both were found in peripheral blood, bone marrow, or lymph nodes.
  • Of note, in HR B-CLL or in DLCL, where leukemic cells were negative for ULBPs, no Vdelta1 T-cell increase was found.
  • Moreover, Vdelta1 T lymphocytes from patients with FL NHL proliferate in response to ULBP2+ and ULBP3+ lymphoma cells.
  • Finally, patients with high expression of ULBPs, increased circulating Vdelta1 T lymphocytes, and high levels of serum IL-4 showed stable disease in a 1-year follow-up in contrast to patients with low circulating Vdelta1 T cells and undetectable IL-4 or ULBPs.
  • [MeSH-major] Carrier Proteins / metabolism. Histocompatibility Antigens Class I / metabolism. Immunoglobulin delta-Chains / metabolism. Interleukin-4 / biosynthesis. Lymphoma, Non-Hodgkin / metabolism. Lymphoma, Non-Hodgkin / pathology. T-Lymphocytes / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Proliferation. Cells, Cultured. Disease Progression. Female. Follow-Up Studies. GPI-Linked Proteins. Humans. Intercellular Signaling Peptides and Proteins. Male. Middle Aged. Neoplasm Staging. Protein Binding. Transcription, Genetic / genetics

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  • (PMID = 16973957.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / GPI-Linked Proteins; 0 / Histocompatibility Antigens Class I; 0 / Immunoglobulin delta-Chains; 0 / Intercellular Signaling Peptides and Proteins; 0 / ULBP2 protein, human; 0 / ULBP3 protein, human; 207137-56-2 / Interleukin-4
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3. Richmond J, Bryant R, Trotman W, Beatty B, Lunde J: FISH detection of t(14;18) in follicular lymphoma on Papanicolaou-stained archival cytology slides. Cancer; 2006 Jun 25;108(3):198-204
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  • METHODS: Cases included 35 FL, 6 small lymphocytic lymphomas/chronic lymphocytic leukemias (SLL/CLL), 4 mantle cell lymphomas (MCL), 4 marginal zone lymphomas (MZL), 1 lymphoplasmacytic lymphoma (LPL), and 10 reactive lymphoid tissues (RLT).
  • [MeSH-minor] Biopsy, Fine-Needle. Humans. In Situ Hybridization, Fluorescence. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphoid Tissue / pathology. Lymphoma, Mantle-Cell / diagnosis. Lymphoma, Mantle-Cell / genetics. Lymphoma, Mantle-Cell / pathology. Staining and Labeling

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  • (PMID = 16671111.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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4. 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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  • 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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5. Swerdlow SH: T-cell and NK-cell posttransplantation lymphoproliferative disorders. Am J Clin Pathol; 2007 Jun;127(6):887-95
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  • [Title] T-cell and NK-cell posttransplantation lymphoproliferative disorders.
  • Posttransplantation lymphoproliferative disorders (PTLDs) of T-cell or natural killer (NK)-cell origin are an uncommon heterogeneous group of lymphoid proliferations that fulfill the criteria for one of the T- or NK-cell lymphomas/leukemias.
  • This report summarizes 130 T/NK-cell PTLDs reported in the literature or presented at the Society for Hematopathology/European Association for Haematopathology Workshop on T/NK-cell malignancies.
  • The T/NK-cell PTLDs occur at a median of 66 months following transplantation and are usually extranodal.
  • The most common types reported are peripheral T-cell lymphoma, unspecified, and hepatosplenic T-cell lymphoma.
  • EBV+ cases have a significantly longer survival than EBV- cases, even when indolent T-cell large granular lymphocytic leukemias are included among the EBV- cases.
  • Many T/NK-cell PTLDs have been treated with chemotherapy, often together with decreased immunosuppression, but there are infrequent patients who have done well without chemotherapy or radiation.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoproliferative Disorders / pathology. Organ Transplantation / adverse effects. T-Lymphocytes / pathology
  • [MeSH-minor] Epstein-Barr Virus Infections / complications. Humans. Lymphoma, T-Cell, Peripheral / etiology. Lymphoma, T-Cell, Peripheral / mortality. Lymphoma, T-Cell, Peripheral / pathology. Postoperative Complications. Survival Rate

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  • (PMID = 17509986.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Congresses
  • [Publication-country] United States
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6. Messmer BT, Messmer D, Allen SL, Kolitz JE, Kudalkar P, Cesar D, Murphy EJ, Koduru P, Ferrarini M, Zupo S, Cutrona G, Damle RN, Wasil T, Rai KR, Hellerstein MK, Chiorazzi N: In vivo measurements document the dynamic cellular kinetics of chronic lymphocytic leukemia B cells. J Clin Invest; 2005 Mar;115(3):755-64
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  • [Title] In vivo measurements document the dynamic cellular kinetics of chronic lymphocytic leukemia B cells.
  • Due to its relatively slow clinical progression, B cell chronic lymphocytic leukemia (B-CLL) is classically described as a disease of accumulation rather than proliferation.
  • We used a nonradioactive, stable isotopic labeling method to measure B-CLL cell kinetics in vivo.
  • Those patients with birth rates greater than 0.35% per day were much more likely to exhibit active or to develop progressive disease than those with lower birth rates Thus, B-CLL is not a static disease that results simply from accumulation of long-lived lymphocytes.
  • A correlation between birth rates and disease activity and progression appears to exist, which may help identify patients at risk for worsening disease in advance of clinical deterioration.

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  • (PMID = 15711642.001).
  • [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 / R01 CA087956; United States / NCI NIH HHS / CA / R01 CA81554; United States / NCRR NIH HHS / RR / M01 RR018535; United States / NCI NIH HHS / CA / R01 CA081554; United States / NCI NIH HHS / CA / R01 CA87956
  • [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] 059QF0KO0R / Water; 9007-49-2 / DNA; AR09D82C7G / Deuterium
  • [Other-IDs] NLM/ PMC548318
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7. Deaglio S, Aydin S, Vaisitti T, Bergui L, Malavasi F: CD38 at the junction between prognostic marker and therapeutic target. Trends Mol Med; 2008 May;14(5):210-8
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  • CD38 is an ectoenzyme involved in transmembrane signaling and cell adhesion and is used as a disease marker for leukemias and myeloma.
  • CD38 is a dependable negative prognostic marker for chronic lymphocytic leukemia (CLL).
  • In conjunction with chemokines and their receptors, CD38 also influences cell migratory responses.
  • [MeSH-major] Antigens, CD38 / biosynthesis. Antigens, CD38 / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / chemistry. Cell Movement. Gene Expression Regulation, Leukemic. Humans. Immunotherapy / methods. Ligands. Models, Biological. Prognosis

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  • (PMID = 18403265.001).
  • [ISSN] 1471-4914
  • [Journal-full-title] Trends in molecular medicine
  • [ISO-abbreviation] Trends Mol Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Ligands; EC 3.2.2.5 / Antigens, CD38
  • [Number-of-references] 88
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8. Willenbrock K, Jungnickel B, Hansmann ML, Küppers R: Human splenic marginal zone B cells lack expression of activation-induced cytidine deaminase. Eur J Immunol; 2005 Oct;35(10):3002-7
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  • Moreover, the lack of AID-positive MZ B cells questions the recent speculation that B cell chronic lymphocytic leukemias with mutated V genes are derived from mutating MZ B cells.
  • [MeSH-major] B-Lymphocytes / immunology. Cytosine Deaminase / biosynthesis. Spleen / cytology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Lineage / immunology. Cytidine Deaminase. Female. Humans. Immunohistochemistry. Male. Middle Aged. Somatic Hypermutation, Immunoglobulin / immunology

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  • [CommentIn] Eur J Immunol. 2005 Oct;35(10):2789-92 [16180256.001]
  • (PMID = 16180254.001).
  • [ISSN] 0014-2980
  • [Journal-full-title] European journal of immunology
  • [ISO-abbreviation] Eur. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.1 / Cytosine Deaminase; EC 3.5.4.5 / Cytidine Deaminase
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9. Tamura K, Arai H, Ueno E, Saito C, Yagihara H, Isotani M, Ono K, Washizu T, Bonkobara M: Comparison of dendritic cell-mediated immune responses among canine malignant cells. J Vet Med Sci; 2007 Sep;69(9):925-30
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  • [Title] Comparison of dendritic cell-mediated immune responses among canine malignant cells.
  • Dendritic cell (DC) vaccination is one of the most attractive immunotherapies for malignancies in dogs.
  • To examine the differences in DC-mediated immune responses from different types of malignancies in dogs, we vaccinated dogs using autologous DCs pulsed with keyhole limpet hemocyanin (KLH) and cell lysate prepared from squamous cell carcinoma SCC2/88 (SCC-KLH-DC), histiocytic sarcoma CHS-5 (CHS-KLH-DC), or B cell leukemia GL-1 (GL-KLH-DC) in vitro.
  • By contrast, neither CD8 nor CD4 T cell infiltration was found at the DTH challenge site in the dogs vaccinated with CHS-KLH-DC or GL-KLH-DC.
  • These findings may reflect that the efficacy of immune induction by DC vaccination varies among tumor types and that immune responses could be inducible in squamous cell carcinoma.
  • Our results encouraged further investigation of therapeutic vaccination for dogs with advanced squamous cell carcinoma in clinical trials.

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  • (PMID = 17917377.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cancer Vaccines
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10. Suljagic M, Longo PG, Bennardo S, Perlas E, Leone G, Laurenti L, Efremov DG: The Syk inhibitor fostamatinib disodium (R788) inhibits tumor growth in the Eμ- TCL1 transgenic mouse model of CLL by blocking antigen-dependent B-cell receptor signaling. Blood; 2010 Dec 2;116(23):4894-905
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  • [Title] The Syk inhibitor fostamatinib disodium (R788) inhibits tumor growth in the Eμ- TCL1 transgenic mouse model of CLL by blocking antigen-dependent B-cell receptor signaling.
  • Inhibition of antigen-dependent B-cell receptor (BCR) signaling is considered a promising therapeutic approach in chronic lymphocytic leukemia (CLL), but experimental in vivo evidence to support this view is still lacking.
  • We have now investigated whether inhibition of BCR signaling with the selective Syk inhibitor fostamatinib disodium (R788) will affect the growth of the leukemias that develop in the Eμ-TCL1 transgenic mouse model of CLL.
  • Similarly to human CLL, these leukemias express stereotyped BCRs that react with autoantigens exposed on the surface of senescent or apoptotic cells, suggesting that they are antigen driven.
  • Importantly, the effect of R788 was found to be selective for the malignant clones, as no disturbance in the production of normal B lymphocytes was observed.
  • Collectively, these data provide further rationale for clinical trials with R788 in CLL and establish the BCR-signaling pathway as an important therapeutic target in this disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Oxazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyridines / pharmacology
  • [MeSH-minor] Adoptive Transfer. Animals. Blotting, Western. Cell Separation. Disease Models, Animal. Flow Cytometry. Immunophenotyping. In Situ Nick-End Labeling. Mice. Mice, Transgenic. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins / genetics. Receptors, Antigen, B-Cell / drug effects. Signal Transduction / drug effects

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  • (PMID = 20716772.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Intracellular Signaling Peptides and Proteins; 0 / Oxazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 0 / Receptors, Antigen, B-Cell; 0 / Tcl1 protein, mouse; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; SQ8A3S5101 / fostamatinib
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11. 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
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  • [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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12. Wu HY, Chang AC, Wang CC, Kuo FH, Lee CY, Liu DZ, Jan TR: Cannabidiol induced a contrasting pro-apoptotic effect between freshly isolated and precultured human monocytes. Toxicol Appl Pharmacol; 2010 Aug 1;246(3):141-7
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  • It has been documented that cannabidiol (CBD) induced apoptosis in a variety of transformed cells, including lymphocytic and monocytic leukemias.
  • In contrast, a differential sensitivity between normal lymphocytes and monocytes to CBD-mediated apoptosis has been reported.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20471992.001).
  • [ISSN] 1096-0333
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Protoporphyrins; 0 / Sulfhydryl Compounds; 15442-64-5 / zinc protoporphyrin; 19GBJ60SN5 / Cannabidiol; 80168379AG / Doxorubicin; EC 1.14.99.3 / HMOX1 protein, human; EC 1.14.99.3 / Heme Oxygenase-1; GAN16C9B8O / Glutathione; WYQ7N0BPYC / Acetylcysteine
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13. Howard RA, Gilbert ES, Chen BE, Hall P, Storm H, Pukkala E, Langmark F, Kaijser M, Andersson M, Joensuu H, Fossa SD, Travis LB: Leukemia following breast cancer: an international population-based study of 376,825 women. Breast Cancer Res Treat; 2007 Nov;105(3):359-68
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  • [Title] Leukemia following breast cancer: an international population-based study of 376,825 women.
  • PURPOSE: To quantify long-term temporal trends in the excess absolute risk (EAR) of secondary leukemia among breast cancer (BC) survivors, using multivariate analyses to evaluate the effects of subtype, age at BC diagnosis, attained age, and calendar year.
  • RESULTS: A total of 687 non-chronic lymphocytic leukemias (EAR = 9.05; 95% confidence interval (CI) = 7.5-10.7) was reported.
  • Significantly elevated risks were observed for the first time for chronic myeloid leukemia (CML) (EAR = 2.06; 95% CI = 1.3-2.9) and acute lymphoblastic leukemia (ALL) (EAR = 0.62; 95% CI = 0.2-1.1), in addition to acute myeloid leukemia (AML) (EAR = 5.00; 95% CI = 3.9-6.2).
  • Excesses of CML, ALL, AML and all leukemias combined persisted over 25 years after BC diagnosis.
  • For all leukemias, EAR decreased with increasing calendar year (P = 0.04) of BC diagnosis.
  • Risk for all leukemia and AML by calendar year of BC diagnosis depended on age at diagnosis.
  • For women diagnosed with BC after 1985, the 10-year cumulative risk of leukemia for those diagnosed before and after age 50 was small, 0.10% and 0.14%, respectively.
  • CONCLUSIONS: Although secondary leukemia is a rare event, BC survivors experience statistically significant excesses for at least 25 years after diagnosis, including CML and ALL.
  • Decreasing leukemia risks in recent calendar years likely reflect changes in treatment.
  • [MeSH-major] Breast Neoplasms / complications. Breast Neoplasms / epidemiology. Leukemia / complications. Leukemia / epidemiology. Neoplasms, Second Primary / complications. Neoplasms, Second Primary / epidemiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Leukemia, Radiation-Induced / complications. Leukemia, Radiation-Induced / diagnosis. Leukemia, Radiation-Induced / epidemiology. Middle Aged. Risk Factors

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  • (PMID = 17221155.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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14. Lazaro E, Caubet O, Menard F, Pellegrin JL, Viallard JF: [Large granular lymphocyte leukemia]. Presse Med; 2007 Nov;36(11 Pt 2):1694-700
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  • [Title] [Large granular lymphocyte leukemia].
  • [Transliterated title] Leucémies à grands lymphocytes granuleux.
  • Large granular lymphocyte (LGL) leukemia is a clonal proliferation of cytotoxic cells, either CD3(+) (T-cell) or CD3(-) (natural killer, or NK).
  • T-LGL leukemia is associated with cytopenias and autoimmune diseases and most often has an indolent course and good prognosis.
  • NK-LGL leukemias can be more aggressive.
  • LGL expansion is currently hypothesized to be a virus (Ebstein Barr or human T-cell leukemia viruses) antigen-driven T-cell response that involves disruption of apoptosis.
  • The diagnosis of T-LGL is suggested by flow cytometry and confirmed by T-cell receptor gene rearrangement studies.
  • Clonality is difficult to determine in NK-LGL but use of monoclonal antibodies specific for killer cell immunoglobulin-like receptor (KIR) has improved this process.
  • Treatment is required when T-LGL leukemia is associated with recurrent infections secondary to chronic neutropenia.
  • NK-LGL leukemias may be more aggressive and refractory to conventional therapy.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic

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  • (PMID = 17596907.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 35
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15. Xu W, Li JY, Wu YJ, Cao X, Fan L, Qiao C, Liu Q, Yao L, Miao KR: Clinical features and outcome of Chinese patients with monoclonal B-cell lymphocytosis. Leuk Res; 2009 Dec;33(12):1619-22
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  • [Title] Clinical features and outcome of Chinese patients with monoclonal B-cell lymphocytosis.
  • B-cell chronic lymphocytic leukemia (CLL) is the most common type of adult leukemias in the Western countries, however, infrequent in the Eastern.
  • A diagnosis of CLL requires a count of B-lymphocytes >/=5.0x10(9)/L.
  • Asymptomatic person with <5.0x10(9)/L B-lymphocytes is defined as monoclonal B-cell lymphocytosis (MBL).
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / physiopathology. Lymphocytosis / physiopathology

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  • (PMID = 19250675.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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16. Chiron D, Bekeredjian-Ding I, Pellat-Deceunynck C, Bataille R, Jego G: Toll-like receptors: lessons to learn from normal and malignant human B cells. Blood; 2008 Sep 15;112(6):2205-13
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  • These encounters promote plasma cell differentiation and antibody production.
  • In hematologic malignancies, cells often retain B cell-specific receptors and associated functions.
  • Among these, TLRs are currently exploited to target different subclasses of B-cell leukemia, and TLR agonists are currently being evaluated in clinical trials.
  • However, accumulating evidence suggests that endogenous TLR ligands or chronic infections promote tumor growth, thus providing a need for further investigations to decipher the exact function of TLRs in the B-cell lineage and in neoplastic B cells.
  • [MeSH-major] B-Lymphocytes / immunology. Toll-Like Receptors / immunology
  • [MeSH-minor] Antibody Formation. Humans. Leukemia, B-Cell / pathology. Ligands. Lymphoma, B-Cell / pathology

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  • (PMID = 18591383.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Toll-Like Receptors
  • [Number-of-references] 80
  • [Other-IDs] NLM/ PMC2532798
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17. Goldstein BD: Benzene as a cause of lymphoproliferative disorders. Chem Biol Interact; 2010 Mar 19;184(1-2):147-50
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  • There is a long standing issue concerning the strength of evidence relating benzene to lymphocytic neoplasms.
  • Because benzene is a known cause of human acute myelogenous leukemia there has been little reason for organizations such as the International Agency for Research on Cancer (IARC) or the US National Toxicology Program (NTP) to perform standard hazard identification reviews of benzene as a possible cause of other cancers such as lymphomas.
  • A broad range of genotoxic effects in the lymphocytes of benzene-exposed workers has been well documented, as has the role of chromosomal effects in carcinogenesis.
  • This includes the not infrequent finding of biphenotypic lineage as well as the formation of lymphoid as well as myeloid leukemias following chemotherapy.
  • Studies of the mechanism of benzene toxicity are consistent with a relatively non-specific mechanism capable of producing multiple chromosomal changes, and there is evidence that the early hematopoietic stem cell, which is believed to be targeted by benzene in causing myeloid cancers, is also the progenitor of lymphocytic cell types.
  • Furthermore, the classification of lymphomas has evolved so that non-Hodgkin lymphoma now includes such formerly distinct disorders as chronic lymphocytic leukemia and multiple myeloma, and there is less of a distinction between leukemia and non-leukemia forms of lymphoma.

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  • [Copyright] Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20035727.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] J64922108F / Benzene
  • [Number-of-references] 54
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18. Long H, Tang SQ, Zhang XF: [Preliminary study on graft versus leukemia effect of camouflage of mice bone marrow transplantation with methoxy polyethylene glycol modification]. Zhonghua Er Ke Za Zhi; 2005 May;43(5):377-80
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  • [Title] [Preliminary study on graft versus leukemia effect of camouflage of mice bone marrow transplantation with methoxy polyethylene glycol modification].
  • OBJECTIVE: To study if methoxy polyethylene glycol modification (mPEG) affects grafts versus leukemia (GVL) when donor bone marrow mononuclear cells are camouflaged with mPEG in murine bone marrow transplantation (BMT).
  • The bone marrow cells (1 x 10(7)) were mixed with the spleen cells (1 x 10(7)), which were camouflaged or not camouflaged with mPEG, were transplanted into irradiated leukemia mice in C and D groups.
  • The mice in irradiated group (group B) with leukemia cell died of leukemia.
  • The average survival time of group D (with mPEG modification) was 24.2 days, which was longer than that of the other groups (P < 0.05), and the survival rate of group D (27%) was significantly higher than that of the others (P < 0.05), 11 mice (11/15) died of leukemia and the others were still alive.
  • [MeSH-major] Bone Marrow Transplantation. Graft vs Leukemia Effect. Polyethylene Glycols / pharmacology
  • [MeSH-minor] Animals. Female. Graft vs Host Disease / prevention & control. Male. Mice. Mice, Inbred BALB C

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  • (PMID = 15924758.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 30IQX730WE / Polyethylene Glycols; 9004-74-4 / monomethoxypolyethylene glycol
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19. de Totero D, Meazza R, Zupo S, Cutrona G, Matis S, Colombo M, Balleari E, Pierri I, Fabbi M, Capaia M, Azzarone B, Gobbi M, Ferrarini M, Ferrini S: Interleukin-21 receptor (IL-21R) is up-regulated by CD40 triggering and mediates proapoptotic signals in chronic lymphocytic leukemia B cells. Blood; 2006 May 1;107(9):3708-15
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  • [Title] Interleukin-21 receptor (IL-21R) is up-regulated by CD40 triggering and mediates proapoptotic signals in chronic lymphocytic leukemia B cells.
  • Here we demonstrate that surface IL-21 receptor (R) is expressed at variable levels by chronic lymphocytic leukemia (CLL) B cells freshly isolated from 33 different patients.
  • IL-21R expression was up-regulated following cell stimulation via surface CD40.
  • IL-21 signaling failed to stimulate CLL B-cell proliferation, but induced their apoptosis.
  • The present findings thus provide a set of new mechanisms involved in the balance between cell-survival and apoptotic signals in CLL B cells.
  • [MeSH-major] Antigens, CD40 / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Receptors, Interleukin / genetics

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  • (PMID = 16391014.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / DNA, Neoplasm; 0 / IL21R protein, human; 0 / Il21r protein, mouse; 0 / Interleukin-21 Receptor alpha Subunit; 0 / JAK3 protein, human; 0 / Jak1 protein, mouse; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-21; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Jak3 protein, mouse; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3
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20. Nurzyńska-Flak J, Kowalczyk JR: [Incidence of childhood leukemia in the Lublin region of Poland in 1988-2000]. Wiad Lek; 2005;58(5-6):284-6
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  • [Title] [Incidence of childhood leukemia in the Lublin region of Poland in 1988-2000].
  • Purpose of the work was the analysis of the number and structure of leukemia in children living in the Lublin Region of Poland.
  • Among leukemias, according to the International Classification of Childhood Cancers, were counted: lymphoid leukemia, acute non-lymphocytic leukemia, chronic myeloid leukemia, other specified and unspecified leukemias.
  • Number of cases and incidence for the whole group as well as sex, age and descending (rural and urban) distribution of leukemias were calculated.
  • RESULTS: 244 cases of leukemia were reported (152 boys--62.3% and 92 girls--37.7%).
  • CONCLUSIONS: In the Lublin Region lower percentage of leukemia was observed compared to the values determined for the country.
  • Incidence of leukemia was falling, but the analysis in age-groups proved, that it was caused by the decreasing incidence in children under 5 year.
  • [MeSH-major] Leukemia / epidemiology

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  • (PMID = 16238118.001).
  • [ISSN] 0043-5147
  • [Journal-full-title] Wiadomości lekarskie (Warsaw, Poland : 1960)
  • [ISO-abbreviation] Wiad. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
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21. 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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22. Chai YH, Lü H, Li JQ, Lu J, Xiao PF, He YX, Shao XJ: [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2007 Sep;45(9):684-6
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  • [Title] [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia].
  • OBJECTIVE: In childhood acute lymphoblastic leukemia (ALL), cytogenetics plays an important role in diagnosis, allocation of treatment and prognosis.
  • Multiplex polymerase chain reaction (Multiplex PCR) analysis was performed to detect the 29 most common leukemia translocations for routine molecular diagnostic hematopathology practice, and complement the information gained from conventional cytogenetic analysis.
  • Thirteen cases of TEL-AML1, 10 cases of rearrangement in the MLL gene, 4 cases of E2A-PBX1, 4 cases of E2A-HLF, 3 cases of BCR-ABL, 2 cases of TLS-ERG, 32 cases of HOX11 were detected by Multiplex PCR in B-lineage leukemias.
  • SIL-TAL1 had been found in 4 of 7 of T-lineage leukemias.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Cytogenetic Analysis. Karyotyping. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Basic Helix-Loop-Helix Transcription Factors / genetics. Child. Child, Preschool. DNA-Binding Proteins / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Fusion / genetics. Homeodomain Proteins. Humans. Immunophenotyping / methods. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18021563.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / TEL-AML1 fusion protein; 0 / pbx1 protein, human; 135471-20-4 / TAL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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23. 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


24. Romano S, Mallardo M, Chiurazzi F, Bisogni R, D'Angelillo A, Liuzzi R, Compare G, Romano MF: The effect of FK506 on transforming growth factor beta signaling and apoptosis in chronic lymphocytic leukemia B cells. Haematologica; 2008 Jul;93(7):1039-48
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  • [Title] The effect of FK506 on transforming growth factor beta signaling and apoptosis in chronic lymphocytic leukemia B cells.
  • BACKGROUND: Loss of response to transforming growth factor-beta (TGF-beta ) is thought to contribute to the progression of chronic lymphocytic leukemia.
  • Recent findings of over-activation of the TGF-beta signal in FKBP12-knockout mouse prompted us to investigate whether FK506, the canonical ligand of FKBP, can activate the TGF-beta signal in chronic lymphocytic leukemia.
  • DESIGN AND METHODS: We studied 62 chronic lymphocytic leukemia samples from patients with Rai/Binet stage 0 to 4 disease.
  • RESULTS: Twenty-two out of 62 chronic lymphocytic leukemia samples were sensitive to TGF-beta-induced apoptosis.
  • A loss of mitochondrial membrane potential preceded caspase activation and cell death.
  • CONCLUSIONS: Our study shows that most chronic lymphocytic leukemia cells escape the homeostatic control of TGF-beta and that FK506 restores the TGF-beta signal in a proportion of non-responsive samples.
  • We demonstrated that FK506 activates TGF-beta receptor I kinase activity in chronic lymphocytic leukemia, which transduces apoptosis by a mitochondrial-dependent pathway.
  • [MeSH-major] Apoptosis. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Tacrolimus / pharmacology. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Disease Progression. Humans. Immunosuppressive Agents / pharmacology. Kinetics. Ligands. Mitochondria / metabolism. Mutation. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction. Smad Proteins / metabolism. Tacrolimus Binding Proteins / metabolism. bcl-X Protein / metabolism

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  • (PMID = 18492692.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Ligands; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Smad Proteins; 0 / Transforming Growth Factor beta; 0 / bcl-X Protein; EC 5.2.1.- / Tacrolimus Binding Proteins; WM0HAQ4WNM / Tacrolimus
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25. Chen YH, Tang YM, Shen HQ, Song H, Yang SL, Shi SW, Qian BQ, Xu WQ, Ning BT: [Targeted killing of the Nalm-6 cells with 2E8-Genistein immunotoxin and its mechanism]. Zhonghua Er Ke Za Zhi; 2009 Jan;47(1):57-61
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  • OBJECTIVE: Leukemia is the most common hematopoietic malignancies in children.
  • Chemotherapy is currently the primary modality of treatment for this fatal disease.
  • Although chemotherapy is very effective in terms of cell killing, severe side effects such as severe infections, intracranial hemorrhage etc. are frequently encountered due to its poor selective damage between normal and malignant cells or tissues.
  • The aim of this study was to investigate the targeting efficacy in vitro with a new clone of anti-human CD19 antibody immunotoxin 2E8-Genistein on B lineage leukemia cell line Nalm-6 cells and its mechanisms in order to provide the evidence of target therapy on B lineage leukemia and lymphoma.
  • Nalm-6, a CD19+ B cell leukemia cell line, was used as target cells, while Molt-3, a CD19-T cell leukemia cell line, was taken as the negative control.
  • Two-color flow cytometry was applied to study the mechanism of cell killing.
  • RESULTS: After 24 hours of culture, 2E8-Genistein showed marked target killing on Nalm-6 cells at nine different concentrations from 20 nmol/L through 100 nmol/L with cell survival rates from (71.8 +/- 7.9)% down to (16.6 +/- 12.9)%, respectively (n = 3), which were all significantly lower than that of control group (100 +/- 13.9)% (P < 0.05).
  • Significant difference was observed between the cell growth curve of Nalm-6 cultured with 100 nmol/L of 2E8-Gen and those of Nalm-6 cultured with medium (blank), PBS (negative control) or the same concentration of pure 2E8 antibody (negative control) groups (F = 152.15, P = 2.15 x 10(-7)), but there was no significant difference among the three control groups (F = 1.51, P = 0.29).
  • When Molt-3 cells were used as target cells, the cell growth curves of Molt-3 cultured with 2E8-Gen (100 nmol/L) and with negative control of blank did not show any significant difference (F = 0.34, P = 0.59).
  • [MeSH-minor] Antigens, CD19. Apoptosis / drug effects. Cell Line, Tumor. Flow Cytometry. Humans. Leukemia, B-Cell / immunology

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  • (PMID = 19573385.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / Immunotoxins; DH2M523P0H / Genistein
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26. 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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27. Klinger MB, Guilbault B, Goulding RE, Kay RJ: Deregulated expression of RasGRP1 initiates thymic lymphomagenesis independently of T-cell receptors. Oncogene; 2005 Apr 14;24(16):2695-704
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  • [Title] Deregulated expression of RasGRP1 initiates thymic lymphomagenesis independently of T-cell receptors.
  • RasGRP1 is a Ras-specific exchange factor, which is activated by T-cell receptor (TCR) and promotes TCR-dependent positive selection of thymocytes.
  • RasGRP1 is highly expressed on most T lymphocytic leukemias and is a common site of proviral insertion in retrovirus-induced murine T-cell lymphomas.
  • We used RasGRP1 transgenic mice to determine if deregulated expression of RasGRP1 has a causative role in the development of T-cell malignancies.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Guanine Nucleotide Exchange Factors / metabolism. Lymphoma, T-Cell / genetics. Receptors, Antigen, T-Cell / genetics
  • [MeSH-minor] Animals. Female. Flow Cytometry. Humans. Leukemia / genetics. Male. Mice. Mice, Transgenic. Phenotype. Transgenes

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  • (PMID = 15829980.001).
  • [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 / Guanine Nucleotide Exchange Factors; 0 / Rasgrp1 protein, mouse; 0 / Receptors, Antigen, T-Cell
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28. Vallera DA, Brechbiel MW, Burns LJ, Panoskaltsis-Mortari A, Dusenbery KE, Clohisy DR, Vitetta ES: Radioimmunotherapy of CD22-expressing Daudi tumors in nude mice with a 90Y-labeled anti-CD22 monoclonal antibody. Clin Cancer Res; 2005 Nov 1;11(21):7920-8
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  • Labeled RFB4 selectively bound to the CD22(+) Burkitt's lymphoma cell line Daudi, but not to CD22(-) control cells in vitro as compared with a control antibody, and was more significantly bound (P = 0.03) to Daudi solid tumors growing in athymic nude mice.
  • These findings indicate that anti-CD22 radioimmunotherapy with Y22 is highly effective in vivo against CD22-expressing malignancies and may be a useful therapy for drug-refractory B cell leukemia patients.
  • [MeSH-minor] Animals. Antigens, CD19 / biosynthesis. Antigens, CD45 / biosynthesis. Antigens, Differentiation, B-Lymphocyte / chemistry. Bone Marrow / metabolism. Bone Marrow / pathology. Bone Marrow Cells / cytology. Cell Line, Tumor. Female. Flow Cytometry. Humans. Hybridomas / pathology. Mice. Mice, Nude. Protein Binding. Time Factors. Tissue Distribution

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  • (PMID = 16278417.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01-CA36725
  • [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, Monoclonal; 0 / Antigens, CD19; 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / Yttrium Radioisotopes; EC 3.1.3.48 / Antigens, CD45
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29. Migkou M, Dimopoulos MA, Gavriatopoulou M, Terpos E: Applications of monoclonal antibodies for the treatment of hematological malignancies. Expert Opin Biol Ther; 2009 Feb;9(2):207-20
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  • BACKGROUND: The introduction of mAbs has changed the clinical approach to patients with lymphoma and leukemia.
  • RESULTS: Rituximab (anti-CD20) was the first mAb developed for the treatment of B-cell lymphomas.
  • Several randomized studies have demonstrated its efficacy in lymphomas and low toxicity profile; rituximab also has significant activity in chronic lymphocytic leukemia (CLL).
  • Alemtuzumab (anti-CD52) has shown efficacy in previously untreated or refractory CLL patients, while gemtuzumab ozogamicin (anti-CD33) appears to have significant activity in acute myeloid leukemias and myelodysplastic syndromes.
  • CONCLUSIONS: In the next few years, investigations will be concentrated on the improvement of the older mAbs, and the development of new mAbs, targeting molecules important for malignant cell cycle and survival in an attempt to further improve patient survival.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy

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  • (PMID = 19236251.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
  • [Number-of-references] 107
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30. Gorini G, Stagnaro E, Fontana V, Miligi L, Ramazzotti V, Nanni O, Rodella S, Tumino R, Crosignani P, Vindigni C, Fontana A, Vineis P, Costantini AS: Alcohol consumption and risk of leukemia: A multicenter case-control study. Leuk Res; 2007 Mar;31(3):379-86
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  • [Title] Alcohol consumption and risk of leukemia: A multicenter case-control study.
  • A population-based case-control study of 649 leukemia cases and 1771 controls carried out in 11 Italian areas, offered the opportunity to evaluate the relationship between alcohol consumption and leukemia risk.
  • For all leukemias, acute lymphocytic leukemia (ALL), acute myeloid leukemia (AML), and chronic lymphocytic leukemia (CLL), we found a non-significantly inverse association for moderate levels of total alcohol and wine intake, but increased risks at high levels, with, in most cases, significant trend effects (odd ratios (OR) for all leukemias in the lowest quartile of total alcohol consumption [0.1-9.0 g/day of ethanol] versus never-drinker = 0.73; 95% confidence intervals (95% CI) = 0.51-1.03; OR in the highest quartile [> 31.7 g/day] = 1.15; 95% CI = 0.82-1.63; p of the linear trend test = 0.007).
  • For chronic myeloid leukemia (CML), we found a non-significantly positive association for all levels of total alcohol and wine intake, and a significant positive linear trend effect (p = 0.03) for wine intake (OR for 0.1-9.0 g/day of ethanol intake from wine = 1.34; 95% CI = 0.61-2.94; OR in the highest quartile of wine intake [> 27.7 g/day] = 2.13; 95% CI = 1.01-4.50).
  • No consistent dose-response was detected analysing duration of alcohol consumption for any leukemia subtypes.
  • In conclusion, even though our study did not show a clear association between alcohol intake and leukemia risk, some of the patterns of the risk estimates (a possible J-shaped dose-response curve between alcohol intake and ALL, AML, and CLL risks, and the positive association between alcohol and CML), may be suggestive.
  • [MeSH-major] Alcohol Drinking / adverse effects. Leukemia / etiology

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  • (PMID = 16919329.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA51086
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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31. 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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32. Drakos E, Rassidakis GZ, Tsioli P, Lai R, Jones D, Medeiros LJ: Differential expression of WT1 gene product in non-Hodgkin lymphomas. Appl Immunohistochem Mol Morphol; 2005 Jun;13(2):132-7
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  • The tumor suppressor gene wt1 (Wilms tumor 1) encodes a zinc finger transcription factor reported to be expressed in many tumors, including mesotheliomas, carcinomas, and acute leukemias.
  • The authors assessed for WT1 expression in six lymphoma/leukemia cell lines using Western blot methods after subcellular fractionation.
  • The B-cell NHLs analyzed were 18 diffuse large B-cell lymphomas, 13 marginal zone B-cell lymphomas, 9 small lymphocytic lymphomas, (DLBCLs), 8 follicular lymphomas, 6 mantle cell lymphomas, 5 Burkitt lymphomas, 3 lymphoplasmacytic lymphomas, and 2 B-cell lymphoblastic lymphomas.
  • The T-cell NHLs analyzed were 43 anaplastic large cell lymphomas (ALCLs), 26 peripheral T-cell lymphomas unspecified, 13 angioimmunoblastic T-cell lymphomas, 6 cutaneous ALCLs, 6 cases of mycosis fungoides, 5 extranodal NK/T-cell lymphomas of nasal type, and 4 T-cell lymphoblastic lymphomas.
  • WT1 levels were higher in cytoplasmic extracts than in nuclear extracts of the Karpas 299 and SU-DHL-1 lymphoma cell lines but were higher in nuclear extracts than in the cytoplasmic extracts of the Jurkat, HH, U-937, and K562 leukemia cell lines.
  • In NHLs, WT1 was positive in 4 of 5 (80%) Burkitt lymphomas, 9 of 12 (75%) ALK-positive ALCLs, 3 of 6 (50%) lymphoblastic lymphomas (2 of 4 T-cell, 1 of 2 B-cell), 14 of 31 (45%) ALK-negative ALCLs, 6 of 18 (33%) DLBCLs, and 1 of 6 (17%) cutaneous ALCLs.
  • WT1 immunoreactivity was primarily cytoplasmic in all positive NHLs except T-cell lymphoblastic lymphoma.

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  • (PMID = 15894924.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / WT1 Proteins
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33. Shi Y, White D, He L, Miller RL, Spaner DE: Toll-like receptor-7 tolerizes malignant B cells and enhances killing by cytotoxic agents. Cancer Res; 2007 Feb 15;67(4):1823-31
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  • Using chronic lymphocytic leukemia B cells as a model to facilitate biochemical analysis, the tolerized state was found to be associated with altered receptor components, including down-regulated expression of TLR7 mRNA and decreased levels of interleukin-1 receptor-associated kinase 1.
  • Tolerized chronic lymphocytic leukemia cells were found to be more sensitive to cytotoxic chemotherapeutic agents, in part through altered stress-activated protein kinase signaling pathways.
  • This property of the TLR7-tolerized state may potentially be exploited in the treatment of B cell cancers.
  • [MeSH-major] B-Lymphocytes / drug effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Toll-Like Receptor 7 / physiology

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  • (PMID = 17308125.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Imidazoles; 0 / Quinolines; 0 / RNA, Messenger; 0 / S 28690; 0 / TLR7 protein, human; 0 / Toll-Like Receptor 7; 0 / Tumor Necrosis Factor-alpha; 5J49Q6B70F / Vincristine; EC 2.7.11.1 / IRAK1 protein, human; EC 2.7.11.1 / IRAK4 protein, human; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
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34. 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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  • 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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35. StatBite: Estimated new cases for the four major leukemias, 2008. J Natl Cancer Inst; 2009 Mar 18;101(6):371
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  • [Title] StatBite: Estimated new cases for the four major leukemias, 2008.
  • [MeSH-major] Leukemia / epidemiology
  • [MeSH-minor] Humans. Incidence. Leukemia, Lymphocytic, Chronic, B-Cell / epidemiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Research Support as Topic / trends. United States / epidemiology

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  • (PMID = 19276455.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Hodge DL, Yang J, Buschman MD, Schaughency PM, Dang H, Bere W, Yang Y, Savan R, Subleski JJ, Yin XM, Loughran TP Jr, Young HA: Interleukin-15 enhances proteasomal degradation of bid in normal lymphocytes: implications for large granular lymphocyte leukemias. Cancer Res; 2009 May 1;69(9):3986-94
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  • [Title] Interleukin-15 enhances proteasomal degradation of bid in normal lymphocytes: implications for large granular lymphocyte leukemias.
  • Large granular lymphocyte (LGL) leukemia is a clonal proliferative disease of T and natural killer (NK) cells.
  • Interleukin (IL)-15 is important for the development and progression of LGL leukemia and is a survival factor for normal NK and T memory cells.
  • Overall, these data provide a novel molecular mechanism for IL-15 control of Bid that potentially links this cytokine to leukemogenesis through targeted proteasome degradation of Bid and offers the possibility that proteasome inhibitors may aid in the treatment of LGL leukemia.

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  • (PMID = 19366803.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / Intramural NIH HHS / / ZIA BC009283-25
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / Bid protein, mouse; 0 / Interleukin-15; 0 / Interleukin-2; 0 / Proteasome Inhibitors; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ NIHMS161038; NLM/ PMC2786937
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37. 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.
  • This combination of HU and ara-C is tolerable and has efficacy in refractory leukemias.
  • [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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38. Gupta P, Goldenberg DM, Rossi EA, Chang CH: Multiple signaling pathways induced by hexavalent, monospecific, anti-CD20 and hexavalent, bispecific, anti-CD20/CD22 humanized antibodies correlate with enhanced toxicity to B-cell lymphomas and leukemias. Blood; 2010 Oct 28;116(17):3258-67
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  • [Title] Multiple signaling pathways induced by hexavalent, monospecific, anti-CD20 and hexavalent, bispecific, anti-CD20/CD22 humanized antibodies correlate with enhanced toxicity to B-cell lymphomas and leukemias.
  • Three such constructs, 20-20, a monospecific HexAb comprising 6 Fabs of veltuzumab (humanized anti-CD20 immunoglobulin G1κ [IgG1κ]), 20-22, a bispecific HexAb comprising veltuzumab and 4 Fabs of epratuzumab (humanized anti-CD22 IgG1κ), and 22-20, a bispecific HexAb comprising epratuzumab and 4 Fabs of veltuzumab, were previously shown to inhibit pro-liferation of several lymphoma cell lines at nanomolar concentrations in the absence of a crosslinking antibody.
  • We now report an in-depth analysis of the apoptotic and survival signals induced by the 3 HexAbs in Burkitt lymphomas and provide in vitro cytotoxicity data for additional lymphoma cell lines and also chronic lymphocytic leukemia patient specimens.
  • Thus, the greatly enhanced direct toxicity of these HexAbs correlates with their ability to alter the basal expression of various intracellular proteins involved in regulating cell growth, survival, and apoptosis, with the net outcome leading to cell death.

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  • (PMID = 20628151.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA103985; United States / NCI NIH HHS / CA / P01-CA103985
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / epratuzumab; 0 / veltuzumab; 4F4X42SYQ6 / Rituximab; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2995355
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39. Ashok L, Sujatha GP, Hema G: Estimation of salivary amylase and total proteins in leukemia patients and its correlation with clinical feature and radiographic finding. Indian J Dent Res; 2010 Oct-Dec;21(4):486-90
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  • [Title] Estimation of salivary amylase and total proteins in leukemia patients and its correlation with clinical feature and radiographic finding.
  • BACKGROUND: Leukemia is a fatal disease.
  • The oral manifestations of the leukemias occur early in the course of the disease and these oral features can at times act as a diagnostic indicator.
  • MATERIALS AND METHODS: In our study, samples of unstimulated saliva of 30 leukemia patients who were not on chemotherapy were collected and analyzed for salivary amylase and total protein.
  • [MeSH-major] Amylases / analysis. Jaw Diseases / radiography. Leukemia / metabolism. Saliva / enzymology. Salivary Proteins and Peptides / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Alveolar Bone Loss / etiology. Alveolar Bone Loss / radiography. Case-Control Studies. Child. Child, Preschool. Ecchymosis / etiology. Female. Gingival Hypertrophy / etiology. Gingivitis / etiology. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / metabolism. Male. Middle Aged. Mouth Diseases / etiology. Periapical Abscess / etiology. Periapical Abscess / radiography. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Purpura / etiology. Radiography, Panoramic. Young Adult

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  • (PMID = 21187610.001).
  • [ISSN] 1998-3603
  • [Journal-full-title] Indian journal of dental research : official publication of Indian Society for Dental Research
  • [ISO-abbreviation] Indian J Dent Res
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Salivary Proteins and Peptides; EC 3.2.1.- / Amylases
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40. Chen WC, Completo GC, Sigal DS, Crocker PR, Saven A, Paulson JC: In vivo targeting of B-cell lymphoma with glycan ligands of CD22. Blood; 2010 Jun 10;115(23):4778-86
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  • [Title] In vivo targeting of B-cell lymphoma with glycan ligands of CD22.
  • Antibody-mediated cell depletion therapy has proven to provide significant clinical benefit in treatment of lymphomas and leukemias, driving the development of improved therapies with novel mechanisms of cell killing.
  • A current clinical target for B-cell lymphoma is CD22, a B-cell-specific member of the sialic acid binding Ig-like lectin (siglec) family that recognizes alpha2-6-linked sialylated glycans as ligands.
  • The targeted liposomes are actively bound and endocytosed by CD22 on B cells, and significantly extend life in a xenograft model of human B-cell lymphoma.
  • Moreover, they bind and kill malignant B cells from peripheral blood samples obtained from patients with hairy cell leukemia, marginal zone lymphoma, and chronic lymphocytic leukemia.
  • The results demonstrate the potential for using a carbohydrate recognition-based approach for efficiently targeting B cells in vivo that can offer improved treatment options for patients with B-cell malignancies.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Doxorubicin / pharmacokinetics. Drug Delivery Systems / methods. Lymphoma, B-Cell / drug therapy. Polysaccharides / agonists. Sialic Acid Binding Ig-like Lectin 2

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  • (PMID = 20181615.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA138891; United Kingdom / Wellcome Trust / / 081882; United States / NIAID NIH HHS / AI / R01 AI050143; United States / NIAID NIH HHS / AI / R01-AI050143; United States / NIGMS NIH HHS / GM / R01 GM060938; United States / NIGMS NIH HHS / GM / R01-GM060938
  • [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 / Antibiotics, Antineoplastic; 0 / CD22 protein, human; 0 / Ligands; 0 / Liposomes; 0 / Polysaccharides; 0 / Sialic Acid Binding Ig-like Lectin 2; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC2890185
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41. Robak T, Robak P: Current treatment options in prolymphocytic leukemia. Med Sci Monit; 2007 Apr;13(4):RA69-80
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  • [Title] Current treatment options in prolymphocytic leukemia.
  • Prolymphocytic leukemia (PLL) is a rare lymphoproliferative disorder characterized by marked leukocytosis and splenomegaly.
  • PLL accounts for approximately 2% of chronic lymphoid leukemias.
  • The clinical course is progressive in the majority of cases due to the resistance of the disease to conventional chemotherapy.
  • The disease is divided according to the cell of origin into the B- (B-PLL) and T-cell (T-PLL) types.
  • Approximately 80% of cases are of B-cell phenotype.
  • PLL has poorer prognosis than chronic lymphocytic leukemia (CLL), and the patients with static disease for a longer period of time are rare.
  • PLL is still considered an incurable disease.
  • Finally, high-dose chemotherapy followed by allogenic or autologous stem cell transplantation seems to be an effective, probably curative, strategy for the treatment of selected patients with PLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, Prolymphocytic / diagnosis. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / genetics. Purine Nucleosides / therapeutic use
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / therapeutic use. Cladribine / therapeutic use. Drug Therapy / methods. Humans. Pentostatin / therapeutic use. Rituximab. Splenectomy / methods. Stem Cell Transplantation / methods. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

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  • (PMID = 17392661.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Purine Nucleosides; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 118
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42. Dictor M, Ek S, Sundberg M, Warenholt J, György C, Sernbo S, Gustavsson E, Abu-Alsoud W, Wadström T, Borrebaeck C: Strong lymphoid nuclear expression of SOX11 transcription factor defines lymphoblastic neoplasms, mantle cell lymphoma and Burkitt's lymphoma. Haematologica; 2009 Nov;94(11):1563-8
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  • [Title] Strong lymphoid nuclear expression of SOX11 transcription factor defines lymphoblastic neoplasms, mantle cell lymphoma and Burkitt's lymphoma.
  • BACKGROUND: We surveyed lymphomas to determine the range of expression of the mantle cell lymphoma-associated SOX11 transcription factor and its relation to cyclin D1.
  • RESULTS: Nuclear SOX11 was strongly expressed in most B and T-lymphoblastic leukemia/lymphomas and half of childhood Burkitt's lymphomas, but only weakly expressed in some hairy cell leukemias.
  • Chronic lymphocytic leukemia/lymphoma, marginal zone, follicular and diffuse large B-cell lymphomas were negative for SOX11, as were all cases of intermediate Burkitt's lymphomas/diffuse large B-cell lymphoma, myeloma, Hodgkin's lymphomas and mature T-cell and NK/T-cell lymphomas.
  • CONCLUSIONS: In addition to mantle cell lymphoma, SOX11 is strongly expressed only in lymphoblastic malignancies and Burkitt's lymphomas.
  • Its expression is independent of cyclin D1 (except for weak expression in hairy cell leukemias) and unlikely to be due to translocations in lymphoid neoplasia.
  • [MeSH-major] Burkitt Lymphoma / chemistry. Lymphoma, Mantle-Cell / chemistry. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. SOXC Transcription Factors / analysis


43. Meyers JA, Su DW, Lerner A: Chronic lymphocytic leukemia and B and T cells differ in their response to cyclic nucleotide phosphodiesterase inhibitors. J Immunol; 2009 May 1;182(9):5400-11
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  • [Title] Chronic lymphocytic leukemia and B and T cells differ in their response to cyclic nucleotide phosphodiesterase inhibitors.
  • Phosphodiesterase (PDE)4 inhibitors, which activate cAMP signaling by reducing cAMP catabolism, are known to induce apoptosis in B lineage chronic lymphocytic leukemia (CLL) cells but not normal human T cells.
  • Affymetrix gene chip analysis in the three cell populations following treatment with the PDE4 inhibitor rolipram identified a set of up-regulated transcripts with unusually high fold changes in the CLL samples, several of which are likely part of compensatory negative feedback loops.
  • The high fold changes were due to low basal transcript levels in CLL cells, suggesting that cAMP-mediated signaling may be unusually tightly regulated in this cell type.
  • Rolipram treatment augmented cAMP levels and induced ATF-1/CREB serine 63/133 phosphorylation in both B lineage cell types but not T cells.
  • As treatment with the broad-spectrum PDE inhibitor 3-isobutyl-1-methylxanthine induced T cell CREB phosphorylation, we tested a series of family-specific PDE inhibitors for their ability to mimic 3-isobutyl-1-methylxanthine-induced ATF-1/CREB phosphorylation.
  • Combined PDE3/4 inhibition did not induce T cell apoptosis, suggesting that cAMP-mediated signal transduction that leads to robust ATF-1/CREB serine 63/133 phosphorylation is not sufficient to induce apoptosis in this lymphoid lineage.

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  • (PMID = 19380787.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106705-04; United States / NCI NIH HHS / CA / R01 CA106705; United States / NCI NIH HHS / CA / CA106705; United States / NCI NIH HHS / CA / CA106705-04; United States / NHLBI NIH HHS / HL / T32 HL007501-27; United States / NHLBI NIH HHS / HL / HL007501-27; United States / NHLBI NIH HHS / HL / T32 HL007501; United States / NHLBI NIH HHS / HL / HL007501
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phosphodiesterase 3 Inhibitors; 0 / Phosphodiesterase 4 Inhibitors; E0399OZS9N / Cyclic AMP
  • [Other-IDs] NLM/ NIHMS108934; NLM/ PMC2676892
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44. 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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  • [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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45. Karapidaki I, Bakopoulou A, Papageorgiou A, Iakovidou Z, Mioglou E, Nikolaropoulos S, Mourelatos D, Lialiaris T: Genotoxic, cytostatic, antineoplastic and apoptotic effects of newly synthesized antitumour steroidal esters. Mutat Res; 2009 Apr 30;675(1-2):51-9
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  • The genotoxic and cytotoxic effects of the compounds were investigated both in vitro, in lymphocyte cultures obtained from blood samples of healthy donors and in vivo, in ascites cells of P388 leukemia obtained from the peritoneal cavity of DBA/2 mice.
  • The newly synthesized compounds were also studied for antineoplastic activity against lymphocytic P388 and lymphoid L1210 leukemias in mice, by calculating the mean of the median survival of the drug-treated animals (T) versus the untreated control (C) (T/C%).
  • The activity of caspase-2 and caspase-3, indicators of apoptosis, was assessed biochemically in primary cultures of human lymphocytes.
  • Our results show that the newly synthesized compounds caused severe genotoxic effects by significantly increasing the frequency of SCE and decreasing the PRI values in cultures of peripheral lymphocytes in vitro and in ascites cells of lymphocytic P388 leukemia in vivo.
  • [MeSH-minor] Animals. Ascites / genetics. Ascites / metabolism. Ascites / pathology. Caspase 2 / metabolism. Caspase 3 / metabolism. Cell Proliferation / drug effects. Cells, Cultured. Drug Screening Assays, Antitumor. Esters. Female. Humans. Leukemia L1210 / pathology. Leukemia L1210 / prevention & control. Leukemia P388 / pathology. Leukemia P388 / prevention & control. Lymphocytes / cytology. Lymphocytes / drug effects. Lymphocytes / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Molecular Structure. Mutagenicity Tests. Sister Chromatid Exchange / drug effects. Survival Analysis

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  • (PMID = 19386248.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 3-hydroxy-17-acetamidoandrostan-7-one-4-N,N-bis(2-chloroethyl)aminophenyl acetate; 0 / 3-hydroxy-17a-azahomoandrostan-7-one-4-N,N-bis(2-chloroethyl)aminophenyl acetate; 0 / 3-hydroxyandrostan-7,17-dione-4-N,N-bis(2-chloroethyl)aminophenyl butyrate; 0 / Antineoplastic Agents; 0 / Azasteroids; 0 / Cytostatic Agents; 0 / Esters; 0 / Nitrogen Mustard Compounds; 0 / Steroids; C24W7J5D5R / Androsterone; EC 3.4.22.- / Caspase 2; EC 3.4.22.- / Caspase 3
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46. Manola KN, Sambani C, Karakasis D, Kalliakosta G, Harhalakis N, Papaioannou M: Leukemias associated with Turner syndrome: report of three cases and review of the literature. Leuk Res; 2008 Mar;32(3):481-6
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  • [Title] Leukemias associated with Turner syndrome: report of three cases and review of the literature.
  • Cases of leukemia associated with Turner syndrome (TS) are rare.
  • Here we report three TS patients with leukemia including one case of T-large granular lymphocyte leukemia (T-LGL), one rare case of coexistence of chronic lymphocytic leukemia (CLL) and idiopathic myelofibrosis (IMF) and one case of a patient with AML-M2 who received autologous stem cell transplantation (SCT).
  • T-LGL and coexistence of CLL and IMF associated with TS are reported for the first time while the last case represents the first report of SCT in a leukemia patient with TS.
  • Our cases and the limited data of previously reported leukemia patients with TS suggest that TS is not associated with a specific type of leukemia and that presentation, clinical course and response to treatment are similar to that of the non-TS leukemia patients.
  • Interestingly, in the mosaic TS patients, the abnormal clones were restricted to the monosomic 45,X cells, indicating that the leukemic clones possibly originate from the monosomic cell line.
  • Even in cases with no additional chromosome abnormalities, the ratio of X/XX cells in bone marrow cells was significantly increased compared to that in constitutional karyotype, indicating that monosomic cells possibly provide a survival advantage for leukemia cells or that reduced programmed cell death may be responsible for the expansion of the monosomic cells.
  • [MeSH-major] Leukemia / complications. Turner Syndrome / complications
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Large Granular Lymphocytic / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Myeloid, Acute / complications. Middle Aged. Monosomy. Treatment Outcome

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  • (PMID = 17669490.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 42
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47. Winrow CJ, Pankratz DG, Vibat CR, Bowen TJ, Callahan MA, Warren AJ, Hilbush BS, Wynshaw-Boris A, Hasel KW, Weaver Z, Lockhart DJ, Barlow C: Aberrant recombination involving the granzyme locus occurs in Atm-/- T-cell lymphomas. Hum Mol Genet; 2005 Sep 15;14(18):2671-84
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  • [Title] Aberrant recombination involving the granzyme locus occurs in Atm-/- T-cell lymphomas.
  • Ataxia telangiectasia (A-T) is an autosomal recessive disease caused by loss of function of the serine/threonine protein kinase ATM (ataxia telangiectasia mutated).
  • A-T patients have a 250-700-fold increased risk of developing lymphomas and leukemias which are typically highly invasive and proliferative.
  • In addition, a subset of adult acute lymphoblastic leukemias and aggressive B-cell chronic lymphocytic leukemias that occur in the general population show loss of heterozygosity for ATM.
  • To define the specific role of ATM in lymphomagenesis, we studied T-cell lymphomas isolated from mice with mutations in ATM and/or p53 using cytogenetic analysis and mRNA transcriptional profiling.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Lymphoma, T-Cell / genetics. Models, Biological. Protein-Serine-Threonine Kinases / genetics. Recombination, Genetic / genetics. Serine Endopeptidases / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Ataxia Telangiectasia Mutated Proteins. Blotting, Northern. Cell Line, Tumor. Computational Biology. Cytogenetic Analysis. DNA Primers. Gene Expression Profiling. Granzymes. In Situ Hybridization, Fluorescence. Mice. Mice, Knockout. Microarray Analysis. Mutation / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16087685.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS039601-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Gzmb protein, mouse; EC 3.4.21.- / Gzmc protein, mouse; EC 3.4.21.- / Serine Endopeptidases
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48. 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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  • 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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49. Casnici C, Volpe G, Lattuada D, Crotta K, Kuka M, Panuzzo C, Mastrotto C, Tonon G, Fazio VM, Saglio G, Marelli O: Out of frame peptides from BCR/ABL alternative splicing are immunogenic in HLA A2.1 transgenic mice. Cancer Lett; 2009 Apr 8;276(1):61-7
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  • New, potentially tumor-specific antigens have been described in Bcr/Abl positive leukemias.
  • These variants are expressed in chronic myelogenous leukemia and acute lymphocytic leukemia patients.
  • Peptides A and B, but not C, induced the production of specific antisera, while A and C induced the generation of specific cytotoxic T lymphocytes.
  • [MeSH-major] Alternative Splicing. Cancer Vaccines / immunology. Frameshift Mutation / immunology. Fusion Proteins, bcr-abl / immunology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Antigens, Neoplasm / genetics. Antigens, Neoplasm / immunology. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. HLA-A2 Antigen / genetics. Humans. Interferon-gamma / biosynthesis. Interferon-gamma / immunology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Molecular Sequence Data. Peptides / genetics. Peptides / immunology. Proto-Oncogene Proteins c-bcr / genetics. Proto-Oncogene Proteins c-bcr / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 19062160.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / HLA-A2 Antigen; 0 / Peptides; 82115-62-6 / Interferon-gamma; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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50. Yang I, Weiss L, Abdul-Hai A, Kasir J, Reich S, Slavin S: Induction of early post-transplant graft-versus-leukemia effects using intentionally mismatched donor lymphocytes and elimination of alloantigen-primed donor lymphocytes for prevention of graft-versus-host disease. Cancer Res; 2005 Nov 1;65(21):9735-40
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  • [Title] Induction of early post-transplant graft-versus-leukemia effects using intentionally mismatched donor lymphocytes and elimination of alloantigen-primed donor lymphocytes for prevention of graft-versus-host disease.
  • Graft-versus-leukemia (GVL) effects can be induced in tolerant mixed chimeras prepared with nonmyeloablative conditioning.
  • Unfortunately, DLI is frequently associated with graft-versus-host disease (GVHD).
  • We investigated the feasibility of induction of potent GVL effects by DLI using intentionally mismatched lymphocytes followed by elimination of alloreactive donor T cells by cyclophosphamide for prevention of lethal GVHD following induction of very short yet most potent GVL effects.
  • Mice inoculated with B-cell leukemia (BCL1) and mismatched donor lymphocytes were treated 2 weeks later with low-dose or high-dose cyclophosphamide.
  • All mice receiving cyclophosphamide 2 weeks after DLI survived GVHD, and no residual disease was detected by PCR; all control mice receiving DLI alone died of GVHD.
  • Our working hypothesis suggests that short-term yet effective and safe adoptive immunotherapy of leukemia may be accomplished early post-transplantation using alloreactive donor lymphocytes, with prevention of GVHD by elimination of GVL effector cells.
  • [MeSH-major] Graft vs Host Disease / prevention & control. Isoantigens / immunology. Leukemia, B-Cell / immunology. Leukemia, B-Cell / therapy. Lymphocytes / immunology
  • [MeSH-minor] Animals. Bone Marrow Transplantation / immunology. Cyclophosphamide / pharmacology. Graft vs Leukemia Effect. Immunosuppressive Agents / pharmacology. Lymphocyte Transfusion. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasm, Residual. Transplantation Chimera

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  • [ErratumIn] Cancer Res. 2006 Jul 1;66(13):6894. Yung, Iris [corrected to Yang, Iris]
  • (PMID = 16266994.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Isoantigens; 8N3DW7272P / Cyclophosphamide
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51. 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
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  • [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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52. Bokelmann I, Mahlknecht U: Valproic acid sensitizes chronic lymphocytic leukemia cells to apoptosis and restores the balance between pro- and antiapoptotic proteins. Mol Med; 2008 Jan-Feb;14(1-2):20-7
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  • [Title] Valproic acid sensitizes chronic lymphocytic leukemia cells to apoptosis and restores the balance between pro- and antiapoptotic proteins.
  • Chronic lymphocytic leukemia (CLL) is one of the most common leukemias in adults in the developed world.
  • The main feature of the disease is the generation of circulating B-cells with prolonged survival caused by aberrant apoptosis.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / metabolism. B-Lymphocytes / metabolism. Enzyme Inhibitors / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Valproic Acid / pharmacology

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  • (PMID = 17973028.001).
  • [ISSN] 1076-1551
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; 614OI1Z5WI / Valproic Acid; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9
  • [Other-IDs] NLM/ PMC2047630
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53. 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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  • [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


54. Liang X, Moseman EA, Farrar MA, Bachanova V, Weisdorf DJ, Blazar BR, Chen W: Toll-like receptor 9 signaling by CpG-B oligodeoxynucleotides induces an apoptotic pathway in human chronic lymphocytic leukemia B cells. Blood; 2010 Jun 17;115(24):5041-52
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  • [Title] Toll-like receptor 9 signaling by CpG-B oligodeoxynucleotides induces an apoptotic pathway in human chronic lymphocytic leukemia B cells.
  • Chronic lymphocytic leukemia (CLL) is the most prevalent human leukemia and is characterized by the progressive accumulation of long-lived malignant B cells.
  • TLR9-CpG ODN ligation-induced apoptosis of B-CLL cells is confirmed by viable cell counts, annexin V/propidium iodide and tetramethyl-rhodamine ethylester staining, Western blots of the activation, and cleaved caspases and poly (ADP-ribose) polymerase.
  • Treating B-CLL cells in vitro or in vivo with CpG-B ODN reduces the number of leukemia cells that engraft in NOD-scid mice.

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  • (PMID = 20339095.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R21 AI050737; United States / NIAID NIH HHS / AI / R01 AI050737; United States / NIAID NIH HHS / AI / AI050737; United States / NCI NIH HHS / CA / R01 CA72669; United States / NCI NIH HHS / CA / R01 CA072669
  • [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 / Adjuvants, Immunologic; 0 / CPG-oligonucleotide; 0 / IL10 protein, human; 0 / NF-kappa B; 0 / Oligodeoxyribonucleotides; 0 / Receptors, Interleukin-2; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / TLR9 protein, human; 0 / Toll-Like Receptor 9; 130068-27-8 / Interleukin-10; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2890142
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55. Terzakis JA, Santagada E, Hernandez A, Taskin M: Scanning electron microscopy of peripheral blood smears: comparison of normal blood with some common leukemias. Ultrastruct Pathol; 2005 Jan-Feb;29(1):19-28
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  • [Title] Scanning electron microscopy of peripheral blood smears: comparison of normal blood with some common leukemias.
  • Peripheral blood smears prepared routinely from nonneoplastic and leukemia cases were studied using the scanning electron microscope (SEM).
  • Certain cell features are measured as well with the use of the measuring software resident in the SEM.
  • The problem of cell constituent loss and overall shrinkage in the routinely processed and sectioned material is noted.
  • The monoblast resembles the normal monocyte but both cell size and nuclear size are greater; the moderately reticulated nuclear chromatin distinguishes the monoblast.
  • The neoplastic lymphoid cell shows coarse clumping of nuclear chromatin and in some instances coarse chromatin anastomoses to distinguish it from the normal lymphocyte.
  • Lymphoid cells of acute lymphoblastic leukemia are 33% larger than those of chronic lymphocytic leukemia and normal lymphocytes.
  • A candidate for such a cell is recognized morphologically as well.
  • [MeSH-major] Blood Cells / pathology. Blood Cells / ultrastructure. Cytodiagnosis. Leukemia / diagnosis. Microscopy, Electron, Scanning
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Size. Female. Flow Cytometry. Humans. Male. Middle Aged. Reproducibility of Results

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  • (PMID = 15931777.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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56. Gertz MA, Geyer SM, Badros A, Kahl BS, Erlichman C: Early results of a phase I trial of oblimersen sodium for relapsed or refractory Waldenstrom's macroglobulinemia. Clin Lymphoma; 2005 Mar;5(4):282-4
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  • Oblimersen sodium is an antisense oligonucleotide to the first 6 codons of the B-cell leukemia gene 2 (bcl-2) open reading frame.
  • It prevents the expression of the bcl-2 gene product and leads to apoptosis in cells that express Bcl-2. bcl-2 is one of the major apoptosis regulatory gene families and is found in a variety of low-grade B-cell non-Hodgkin's lymphomas.
  • The in vitro use of oblimersen in Waldenstrom's macroglobulinemia (WM) cell line results in enhanced toxicity when exposed to fludarabine, dexamethasone, or rituximab.

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  • (PMID = 15794866.001).
  • [ISSN] 1526-9655
  • [Journal-full-title] Clinical lymphoma
  • [ISO-abbreviation] Clin Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01 CM 17104
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Thionucleotides; 85J5ZP6YSL / oblimersen
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57. 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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58. Ren SY, Xue F, Feng J, Skorski T: Intrinsic regulation of the interactions between the SH3 domain of p85 subunit of phosphatidylinositol-3 kinase and the protein network of BCR/ABL oncogenic tyrosine kinase. Exp Hematol; 2005 Oct;33(10):1222-8
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  • OBJECTIVE: BCR/ABL fusion tyrosine kinase is responsible for the initiation and maintenance of the Philadelphia chromosome-positive chronic myelogenous leukemia (CML) and a cohort of acute lymphocytic leukemias.
  • RESULTS: We show here that the SH3 domain of p85alpha (p85alpha-SH3) pulls down the p210BCR/ABL kinase from hematopoietic cell lysates.
  • [MeSH-minor] Amino Acid Substitution. Animals. Cell Line, Tumor. Fusion Proteins, bcr-abl. Hematopoietic Stem Cells / metabolism. Humans. Immunoprecipitation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Mice. Mutagenesis, Site-Directed. Point Mutation / genetics. Protein Binding

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  • (PMID = 16219545.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA83700
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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59. Sintes J, Romero X, Marin P, Terhorst C, Engel P: Differential expression of CD150 (SLAM) family receptors by human hematopoietic stem and progenitor cells. Exp Hematol; 2008 Sep;36(9):1199-204
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  • OBJECTIVES: Human hematopoietic stem cell (HSC)-containing grafts are most commonly used to treat various blood diseases, including leukemias and autoimmune disorders.
  • [MeSH-major] Antigens, CD / biosynthesis. Gene Expression Regulation. Hematopoietic Stem Cells / metabolism. Multigene Family / genetics. Receptors, Cell Surface / biosynthesis

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  • (PMID = 18495325.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / P01 AI035714; United States / NIAID NIH HHS / AI / P01 AI065687
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD244 protein, human; 0 / CD48 antigen; 0 / CD84 protein, human; 0 / LY9 protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Immunologic; 169535-43-7 / CD150 antigen
  • [Other-IDs] NLM/ NIHMS696612; NLM/ PMC4480417
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60. Gebhart E: Genomic imbalances in human leukemia and lymphoma detected by comparative genomic hybridization (Review). Int J Oncol; 2005 Sep;27(3):593-606
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  • [Title] Genomic imbalances in human leukemia and lymphoma detected by comparative genomic hybridization (Review).
  • Some of these alterations seem to play an important role in disease progression and specificity of the disease.
  • The patterns of genomic alterations found by CGH can characterize certain disease entities and differentiate them from others.
  • If the chromosomal segments affected in > 10% of the cases of each basic disease entity [acute myeloblastic leukemia (AML), acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL) and multiple myeloma (MM)] are compared, most of the frequently involved chromosomal regions differ from entity to entity in the leukemias.
  • With respect to their clinical significance, the presence of genomic imbalances is associated with disease progression and, therefore, poorer prognosis.
  • [MeSH-major] Chromosome Aberrations. Leukemia / genetics. Lymphoma / genetics. Nucleic Acid Hybridization / methods

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  • (PMID = 16077907.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Greece
  • [Number-of-references] 148
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61. Merimi M, Ozkan Y, Cleuter Y, Griebel P, Burny A, Martiat P, Van den Broeke A: Epigenetics and leukemia: unraveling oncogenic processes in the BLV ovine model. Front Biosci (Schol Ed); 2009;1:154-63
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  • [Title] Epigenetics and leukemia: unraveling oncogenic processes in the BLV ovine model.
  • Bovine Leukemia Virus (BLV)-induced B-cell leukemia in sheep is a valuable large animal model for investigating oncogenic mechanisms, particularly those associated with human T-cell leukemia virus 1 (HTLV-1).
  • Multiple factors including viral genes, genetic and epigenetic alterations, and the host immune system are likely to contribute and cooperate in the leukemogenesis of adult T-cell leukemia (ATL) in human and B-cell leukemia in sheep.
  • Future studies in sheep will increase the number of genes identified that are aberrantly regulated by epigenetic processes and identify potential biomarkers which may be used as therapeutic targets in leukemia.
  • [MeSH-major] Epigenesis, Genetic. Leukemia / virology. Leukemia Virus, Bovine / pathogenicity. Oncogenes

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  • (PMID = 19482691.001).
  • [ISSN] 1945-0524
  • [Journal-full-title] Frontiers in bioscience (Scholar edition)
  • [ISO-abbreviation] Front Biosci (Schol Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 93
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62. 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%).
  • 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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63. 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.
  • [MeSH-major] Birth Order. Hodgkin Disease / etiology. Leukemia / etiology. Multiple Myeloma / etiology. Siblings

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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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64. Sagaert X, Sprangers B, De Wolf-Peeters C: The dynamics of the B follicle: understanding the normal counterpart of B-cell-derived malignancies. Leukemia; 2007 Jul;21(7):1378-86
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  • [Title] The dynamics of the B follicle: understanding the normal counterpart of B-cell-derived malignancies.
  • The repertoire of B cells secreting antibodies with unique antigen-binding specificities is produced at two stages: a primary B-cell repertoire is formed in the bone marrow through immunoglobulin gene rearrangements, whereas a secondary B-cell repertoire is generated in the peripheral lymphoid organs (spleen, lymph nodes and mucosa-associated lymphoid tissue) through somatic hypermutation and class-switch recombination upon antigen encounter.
  • The latter events take place within highly specialized histological structures, designated B follicles, which are composed of distinct microanatomical compartments namely the follicle centre, lymphocytic corona and marginal zone.
  • This review incorporates up-to-date information on peripheral B-cell differentiation into a challenging working model, thereby pointing to the structural and functional imprint of both the T-cell-dependent and T-cell-independent immune response on the B follicle.
  • As such, this article aims to form an excellent base for a better understanding of the normal counterpart of B-cell-derived haematological malignancies (leukemias and lymphomas).
  • [MeSH-major] B-Lymphocytes / cytology
  • [MeSH-minor] B-Lymphocyte Subsets. Humans. Lymphoid Tissue. T-Lymphocytes / immunology

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  • (PMID = 17495967.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 68
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65. Foss F: Clinical experience with denileukin diftitox (ONTAK). Semin Oncol; 2006 Feb;33(1 Suppl 3):S11-6
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  • The high-affinity form of this receptor is expressed on activated T lymphocytes, activated B lymphocytes, and activated macrophages.
  • A number of leukemias and lymphomas, including cutaneous T-cell lymphoma, chronic lymphocytic leukemia, and B-cell non-Hodgkin's lymphoma, express a component of the receptor.
  • Ex vivo studies have shown that denileukin diftitox interacts with the high- and intermediate-affinity IL-2 receptor on the cell surface and undergoes internalization.
  • Subsequent cleavage in the endosome releases the diphtheria toxin into the cytosol, which then inhibits cellular protein synthesis, resulting in rapid cell death.
  • This article examines the clinical profile and potential benefits of denileukin diftitox in the treatment of cutaneous T-cell lymphoma and other hematologic disorders.
  • [MeSH-minor] Graft vs Host Disease / drug therapy. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, T-Cell, Cutaneous / drug therapy. Receptors, Interleukin-2 / metabolism. Recombinant Fusion Proteins / therapeutic use

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  • (PMID = 16516670.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Receptors, Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 15
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66. 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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  • [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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67. 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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68. 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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69. 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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70. Burger M, Hartmann T, Krome M, Rawluk J, Tamamura H, Fujii N, Kipps TJ, Burger JA: Small peptide inhibitors of the CXCR4 chemokine receptor (CD184) antagonize the activation, migration, and antiapoptotic responses of CXCL12 in chronic lymphocytic leukemia B cells. Blood; 2005 Sep 1;106(5):1824-30
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  • [Title] Small peptide inhibitors of the CXCR4 chemokine receptor (CD184) antagonize the activation, migration, and antiapoptotic responses of CXCL12 in chronic lymphocytic leukemia B cells.
  • Growth and survival of chronic lymphocytic leukemia (CLL) B cells are favored by interactions between CLL and nontumoral accessory cells.
  • CLL cells express CXCR4 chemokine receptors that direct leukemia cell chemotaxis.
  • TC14012 and TN14003 antagonized the antiapoptotic effect of synthetic CXCL12 and stromal cell-mediated protection of CLL cells from spontaneous apoptosis.
  • As such, small molecular CXCR4 antagonists may have activity in the treatment of patients with this disease.
  • [MeSH-major] Apoptosis / drug effects. Chemokines, CXC / antagonists & inhibitors. Chemokines, CXC / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Oligopeptides / pharmacology. Receptors, CXCR4 / antagonists & inhibitors
  • [MeSH-minor] Actins / drug effects. Actins / metabolism. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / physiology. Chemokine CXCL12. Chemotaxis / drug effects. Dose-Response Relationship, Drug. Humans. Mitogen-Activated Protein Kinases / drug effects. Mitogen-Activated Protein Kinases / metabolism. Molecular Weight. Peptides / pharmacology. Stromal Cells / drug effects. Stromal Cells / physiology. Structure-Activity Relationship. Time Factors. Vidarabine / analogs & derivatives. Vidarabine / pharmacology

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  • (PMID = 15905192.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Oligopeptides; 0 / Peptides; 0 / Receptors, CXCR4; 0 / T140 peptide; 0 / TC14012; 0 / TN14003; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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71. Ohnishi N, Yuasa H, Tanaka S, Sawa H, Miura M, Matsui A, Higashi H, Musashi M, Iwabuchi K, Suzuki M, Yamada G, Azuma T, Hatakeyama M: Transgenic expression of Helicobacter pylori CagA induces gastrointestinal and hematopoietic neoplasms in mouse. Proc Natl Acad Sci U S A; 2008 Jan 22;105(3):1003-8
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  • Infection with cagA-positive Helicobacter pylori is associated with gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma of B cell origin.
  • Systemic expression of wild-type CagA further induced leukocytosis with IL-3/GM-CSF hypersensitivity and some mice developed myeloid leukemias and B cell lymphomas, the hematological malignancies also caused by gain-of-function SHP-2 mutations.
  • [MeSH-major] Antigens, Bacterial / metabolism. Bacterial Proteins / metabolism. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Gastrointestinal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Helicobacter pylori / metabolism. Hematologic Neoplasms / metabolism

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  • (PMID = 18192401.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / cagA protein, Helicobacter pylori; 21820-51-9 / Phosphotyrosine
  • [Other-IDs] NLM/ PMC2242726
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72. Erlacher M, Michalak EM, Kelly PN, Labi V, Niederegger H, Coultas L, Adams JM, Strasser A, Villunger A: BH3-only proteins Puma and Bim are rate-limiting for gamma-radiation- and glucocorticoid-induced apoptosis of lymphoid cells in vivo. Blood; 2005 Dec 15;106(13):4131-8
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  • Numerous p53 target genes have been implicated in DNA damage-induced apoptosis signaling, but proapoptotic Bcl-2 (B-cell leukemia 2) family members of the BH3 (Bcl-2 homolog region [BH] 3)-only subgroup appear to play the critical initiating role.
  • In various types of cultured cells, 3 BH3-only proteins, namely Puma (p53 up-regulated modulator of apoptosis), Noxa, and Bim (Bcl-2 interacting mediator of cell death), have been shown to initiate p53-dependent as well as p53-independent apoptosis in response to DNA damage and treatment with anticancer drugs or glucocorticoids.
  • In particular, the absence of Puma or Bim renders thymocytes and mature lymphocytes refractory to varying degrees to death induced in vitro by growth factor withdrawal, DNA damage, or glucocorticoids.
  • Absence of Puma or Bcl-2 overexpression efficiently protected diverse types of lymphocytes from the effects of gamma-radiation in vivo, and loss of Bim provided lower but significant protection in most lymphocytes, whereas Noxa deficiency had no impact.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis / radiation effects. Apoptosis Regulatory Proteins / metabolism. Glucocorticoids / pharmacology. Lymphocytes / drug effects. Lymphocytes / radiation effects. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Dexamethasone / pharmacology. Gamma Rays. Mice. Mice, Knockout. Spleen / cytology. Spleen / drug effects. Spleen / metabolism. Spleen / radiation effects. Thymus Gland / cytology. Thymus Gland / drug effects. Thymus Gland / metabolism. Thymus Gland / radiation effects

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  • (PMID = 16118324.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [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 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Glucocorticoids; 0 / Membrane Proteins; 0 / PUMA protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 7S5I7G3JQL / Dexamethasone
  • [Other-IDs] NLM/ PMC1895232
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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. Chen CZ, Lodish HF: MicroRNAs as regulators of mammalian hematopoiesis. Semin Immunol; 2005 Apr;17(2):155-65
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  • Many miRNAs cloned from mouse bone marrow cells are differentially regulated in various hematopoietic lineages, suggesting that they might influence hematopoietic lineage differentiation. miR-181, a miRNA specifically expressed in B cells within mouse bone marrow, promotes B-cell differentiation when expressed in hematopoietic stem/progenitor cells.
  • Some human miRNAs are linked to leukemias: the miR-15a/miR-16 locus is frequently deleted or down-regulated in patients with B-cell chronic lymphocytic leukemia and miR-142 is at a translocation site found in a case of aggressive B-cell leukemia.

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  • (PMID = 15737576.001).
  • [ISSN] 1044-5323
  • [Journal-full-title] Seminars in immunology
  • [ISO-abbreviation] Semin. Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL081612; United States / NHLBI NIH HHS / HL / R01 HL081612-01; United States / NHLBI NIH HHS / HL / R01 HL081612-02; 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; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Number-of-references] 114
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75. Laurencet F, Ballabeni P, Rufener B, Hess U, Cerny T, Fey M, Luthi JM, Plancherel C, Zulian GB, Swiss Group for Clinical Research (SAKK): The multicenter trial SAKK 37/95 of cladribine, cyclophosphamide and prednisone in the treatment of chronic lymphocytic leukemias and low-grade non-Hodgkin's lymphomas. Acta Haematol; 2007;117(1):40-7
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  • [Title] The multicenter trial SAKK 37/95 of cladribine, cyclophosphamide and prednisone in the treatment of chronic lymphocytic leukemias and low-grade non-Hodgkin's lymphomas.
  • A multicenter trial was performed to confirm the therapeutic efficacy and the toxicity profile of the combination of cladribine, cyclophosphamide and prednisone in low-grade non-Hodgkin's lymphoma (NHL) and chronic lymphocytic leukemia (CLL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Aged. Cladribine / administration & dosage. Cladribine / adverse effects. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Disease-Free Survival. Female. Hematologic Diseases / chemically induced. Humans. Immunocompromised Host. Infection / etiology. Infection / mortality. Male. Middle Aged. Neoplasms, Second Primary / epidemiology. Prednisone / administration & dosage. Prednisone / adverse effects. Prospective Studies. Remission Induction. Salvage Therapy. Survival Analysis. Treatment Outcome

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  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17095858.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone
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76. 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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77. Hernández Sánchez MC, García Quiroga H, Ulibarrena Redondo C, Méndez Sánchez JA: [Concurrent lymphoproliferative and myeloproliferative disorders in three patients]. An Med Interna; 2008 Feb;25(2):78-80
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  • [Transliterated title] Coexistencia de Síndrome Lifoproliferativo Crónico y Síndrome Mieloproliferativo Crónico en tres pacientes.
  • We present two patients with a diagnosis of chronic lymphoproliferative syndrome, chronic lymphocytic leukemia B (CLL B) and lymphoplasmacytic non-Hodgkin's lymphoma (NHL), who developed chronic myeloproliferative syndrome: polycythemia vera (PV) and Philadelphia-positive chronic myeloid leukemia (CML) respectively, and a third patient with chronic myeloproliferative syndrome, polycythemia vera (PV), who developed an undefined immunophenotype cyclin D1-positive chronic lymphoproliferative syndrome.

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  • (PMID = 18432364.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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78. Mankaï A, Bordron A, Renaudineau Y, Martins-Carvalho C, Takahashi S, Ghedira I, Berthou C, Youinou P: Purine-rich box-1-mediated reduced expression of CD20 alters rituximab-induced lysis of chronic lymphocytic leukemia B cells. Cancer Res; 2008 Sep 15;68(18):7512-9
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  • [Title] Purine-rich box-1-mediated reduced expression of CD20 alters rituximab-induced lysis of chronic lymphocytic leukemia B cells.
  • The anti-CD20 monoclonal antibody rituximab has been less successful in treating chronic lymphocytic leukemia (CLL) than lymphoma, possibly due to the lower density of CD20 on B lymphocytes from CLL patients than on those from lymphoma patients.
  • This abnormality is consistent with our finding of elevated levels of Flt3 ligand (FL) in 20 of 23 CLL sera tested.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD20 / biosynthesis. Antineoplastic Agents / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Proto-Oncogene Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Monoclonal, Murine-Derived. B-Lymphocytes / immunology. DNA Methylation. Female. Genetic Therapy / methods. Humans. Male. Middle Aged. Organic Cation Transport Proteins / biosynthesis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rituximab. Transfection. fms-Like Tyrosine Kinase 3 / biosynthesis. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 18794139.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 0 / Organic Cation Transport Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / SLC22A2 protein, human; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 4F4X42SYQ6 / Rituximab; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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79. 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.
  • 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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80. Volinia S, Galasso M, Costinean S, Tagliavini L, Gamberoni G, Drusco A, Marchesini J, Mascellani N, Sana ME, Abu Jarour R, Desponts C, Teitell M, Baffa R, Aqeilan R, Iorio MV, Taccioli C, Garzon R, Di Leva G, Fabbri M, Catozzi M, Previati M, Ambs S, Palumbo T, Garofalo M, Veronese A, Bottoni A, Gasparini P, Harris CC, Visone R, Pekarsky Y, de la Chapelle A, Bloomston M, Dillhoff M, Rassenti LZ, Kipps TJ, Huebner K, Pichiorri F, Lenze D, Cairo S, Buendia MA, Pineau P, Dejean A, Zanesi N, Rossi S, Calin GA, Liu CG, Palatini J, Negrini M, Vecchione A, Rosenberg A, Croce CM: Reprogramming of miRNA networks in cancer and leukemia. Genome Res; 2010 May;20(5):589-99
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  • [Title] Reprogramming of miRNA networks in cancer and leukemia.
  • We also built, for the first time, specialized miRNA networks for solid tumors and leukemias.
  • Finally, we experimentally validated the miRNA network with acute lymphocytic leukemia originated in Mir155 transgenic mice.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia. MicroRNAs / genetics. Neoplasms
  • [MeSH-minor] Adenocarcinoma / metabolism. Animals. Cell Line, Tumor. Gene Dosage. Humans. Lung / metabolism. Lung Neoplasms / metabolism. Mice. Oligonucleotide Array Sequence Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


81. 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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82. 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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  • [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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83. 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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84. Franco G, Palazzolo R, Liardo E, Tripodo C, Mancuso S: T cell large granular lymphocytic leukemia in association with Sjögren's syndrome. Acta Haematol; 2010;124(1):5-8
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  • [Title] T cell large granular lymphocytic leukemia in association with Sjögren's syndrome.
  • T cell large granular lymphocytic (LGL) leukemia is a rare condition accounting for 2-3% of all mature lymphoid leukemias.
  • Hematological assessment revealed the presence of a T cell LGL leukemia.
  • At the time of T cell LGL leukemia diagnosis, the patient developed xerophthalmia and xerostomia, and a diagnosis of Sjögren's syndrome was made following salivary gland biopsy.
  • The finding of large granular lymphocytes in the context of autoimmune disorders is well-known, though it often occurs with rheumatoid arthritis or in association with a positive autoantibody titer in the absence of an overt clinical picture.
  • The concomitant presentation of T cell LGL leukemia with Sjögren's syndrome is a rare event which is worth reporting.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / complications. Sjogren's Syndrome / complications

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20501987.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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85. 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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86. 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
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  • [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.
  • 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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87. Klener P, Szynal M, Cleuter Y, Merimi M, Duvillier H, Lallemand F, Bagnis C, Griebel P, Sotiriou C, Burny A, Martiat P, Van den Broeke A: Insights into gene expression changes impacting B-cell transformation: cross-species microarray analysis of bovine leukemia virus tax-responsive genes in ovine B cells. J Virol; 2006 Feb;80(4):1922-38
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  • [Title] Insights into gene expression changes impacting B-cell transformation: cross-species microarray analysis of bovine leukemia virus tax-responsive genes in ovine B cells.
  • Large-animal models for leukemia have the potential to aid in the understanding of networks that contribute to oncogenesis.
  • Infection of cattle and sheep with bovine leukemia virus (BLV), a complex retrovirus related to human T-cell leukemia virus type 1 (HTLV-1), is associated with the development of B-cell leukemia.
  • Whereas the natural disease in cattle is characterized by a low tumor incidence, experimental infection of sheep leads to overt leukemia in the majority of infected animals, providing a model for studying the pathogenesis associated with BLV and HTLV-1.
  • Using cDNA-spotted microarrays comprising 10,336 human genes/expressed sequence tags, we identified a cohort of differentially expressed genes, including genes related to apoptosis, DNA transcription, and repair; proto-oncogenes; cell cycle regulators; transcription factors; small Rho GTPases/GTPase-binding proteins; and previously reported Tax(HTLV-1)-responsive genes.
  • Interestingly, genes known to be associated with human neoplasia, especially B-cell malignancies, were extensively represented.
  • Although cross-species approaches do not permit a comprehensive analysis of gene expression patterns, they can provide initial clues for the functional roles of genes that participate in B-cell transformation and pinpoint molecular targets not identified using other methods in animal models.
  • [MeSH-major] B-Lymphocytes / physiology. B-Lymphocytes / virology. Cell Transformation, Viral / genetics. Gene Expression Profiling. Gene Expression Regulation. Gene Products, tax / physiology. Leukemia Virus, Bovine / physiology

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  • (PMID = 16439548.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax
  • [Other-IDs] NLM/ PMC1367148
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88. 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.
  • [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


89. Tomomatsu J, Isobe Y, Oshimi K, Tabe Y, Ishii K, Noguchi M, Hirano T, Komatsu N, Sugimoto K: Chronic lymphocytic leukemia in a Japanese population: varied immunophenotypic profile, distinctive usage of frequently mutated IGH gene, and indolent clinical behavior. Leuk Lymphoma; 2010 Dec;51(12):2230-9
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  • [Title] Chronic lymphocytic leukemia in a Japanese population: varied immunophenotypic profile, distinctive usage of frequently mutated IGH gene, and indolent clinical behavior.
  • Chronic lymphocytic leukemia (CLL) is relatively rare in Japan.
  • Among 46 cases of mature B-cell leukemia, we identified 28 Japanese patients with CLL, including prolymphocytoid and lymphoplasmacytoid morphological variants.
  • [MeSH-major] Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Asian Continental Ancestry Group. Disease Progression. Female. Gene Frequency. Genes, Immunoglobulin Heavy Chain / genetics. Genes, bcl-2 / genetics. Humans. Immunoglobulin Variable Region / genetics. Male. Middle Aged. Mutation. Population. Prognosis