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Items 1 to 100 of about 175
1. Tanvetyanon T, Elmishad AG, Carbone M: Development of malignant mesothelioma during treatment for prolymphocytic leukemia: is asbestos or simian virus 40 a link? Anticancer Res; 2005 Jan-Feb;25(1B):429-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of malignant mesothelioma during treatment for prolymphocytic leukemia: is asbestos or simian virus 40 a link?
  • A patient with a history of heavy asbestos exposure presented with B-prolymphocytic leukemia/lymphoma (B-PLL).
  • Since asbestos, simian virus 40 (SV40), or both have been associated with lymphoproliferative disease and mesothelioma, we investigated both possible links in our patient.
  • [MeSH-major] Asbestos / adverse effects. Leukemia, Prolymphocytic / pathology. Lung Neoplasms / etiology. Lung Neoplasms / secondary. Mesothelioma / etiology. Mesothelioma / secondary. Simian virus 40 / metabolism. Vidarabine / analogs & derivatives
  • [MeSH-minor] Aged. Blotting, Southern. Bone Marrow / metabolism. DNA Primers / chemistry. DNA, Viral / metabolism. Disease Progression. Humans. Immunosuppressive Agents / pharmacology. Male. Polymerase Chain Reaction. Tomography, X-Ray Computed

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  • (PMID = 15816607.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA92657
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Viral; 0 / Immunosuppressive Agents; 1332-21-4 / Asbestos; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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2. Wanko SO, de Castro C: Hairy cell leukemia: an elusive but treatable disease. Oncologist; 2006 Jul-Aug;11(7):780-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hairy cell leukemia: an elusive but treatable disease.
  • Hairy cell leukemia (HCL) is a unique chronic lymphoproliferative disorder that can mimic or coexist with other clonal hematologic disorders and has been associated with autoimmune disorders.
  • It should be entertained as an alternative diagnosis in patients with cytopenias being assigned the diagnosis of aplastic anemia, hypoplastic myelodysplastic syndrome, atypical chronic lymphocytic leukemia, B-prolymphocytic leukemia, or idiopathic myelofibrosis.
  • The typical presentation is that of a middle-aged man with an incidental finding of pancytopenia, splenomegaly, and inaspirable bone marrow.
  • Relapsed disease after a prolonged remission can often be successfully retreated with the same initial agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Hairy Cell / pathology. Leukemia, Hairy Cell / therapy

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  • (PMID = 16880237.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 395575MZO7 / Pentostatin; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab; 9008-11-1 / Interferons
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3. Chaar BT, Petruska PJ: Complete response to alemtuzumab in a patient with B prolymphocytic leukemia. Am J Hematol; 2007 May;82(5):417
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  • [Title] Complete response to alemtuzumab in a patient with B prolymphocytic leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Prolymphocytic / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. B-Lymphocytes / pathology. Combined Modality Therapy. Humans. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Remission Induction. Transplantation, Autologous

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  • (PMID = 17160995.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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4. Tarsitano M, Palmieri S, Ferrara F, Riccardi C, Cavaliere ML, Vicari L: Detection of the t(11;14)(q13;q32) without CCND1/IGH fusion in a case of acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Dec;195(2):164-7
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  • [Title] Detection of the t(11;14)(q13;q32) without CCND1/IGH fusion in a case of acute myeloid leukemia.
  • The t(11;14)(q13;q32) is a hallmark of mantle cell lymphoma.
  • It has been found less frequently in other lymphoproliferative disorders, such as B-prolymphocytic leukemia, plasma cell leukemia, chronic lymphocytic leukemia, and multiple myeloma.
  • Here, we describe a patient with acute myeloid leukemia (AML), categorized as M5b according to French-American-British classification, in which conventional cytogenetic analysis revealed a karyotype with t(11;14)(q13;q32).
  • [MeSH-major] Cyclin D1 / genetics. Immunoglobulin Heavy Chains / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 19963117.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / Immunoglobulin Heavy Chains; 136601-57-5 / Cyclin D1
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5. Cavalcanti Júnior GB, Sales VS, Cavalcanti e Silva DG, Lopes MC, Paiva Ade S, da Fonseca HE, do Nascimento Júniors FF, Fernandes MZ: Detection of CD5 in B-cell chronic lymphoproliferative diseases by flow cytometry: a strong expression in B-cell chronic lymphocytic leukemia. Acta Cir Bras; 2005;20 Suppl 1:101-7
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  • [Title] Detection of CD5 in B-cell chronic lymphoproliferative diseases by flow cytometry: a strong expression in B-cell chronic lymphocytic leukemia.
  • PURPOSE: CD5 is a T cell marker, aberrantly express in B cell chronic lymphocytic leukemia (B-CLL) and mantle cell lymphoma (MCL).
  • Other chronic B cell malignancies including hairy cell leukemia (HCL) and B cell prolymphocytic leukemia (B-PLL) are CD5 negative or express this antigen in a weak way.
  • In this study, CD5 expression was investigated in leukemic cells from 42 patients with chronic B cell lymphoproliferative disease.
  • METHODS: We studied the CD5 expression in leukemic cells from 42 patients with chronic B-cell malignancies by flow cytometry.

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  • (PMID = 16186976.001).
  • [ISSN] 0102-8650
  • [Journal-full-title] Acta cirurgica brasileira
  • [ISO-abbreviation] Acta Cir Bras
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / Biomarkers, Tumor
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6. Nguyen-Khac F, Davi F, Receveur A, Maloum K, Morel V, Le Garff-Tavernier M, Ong J, Berger R, Leblond V, Merle-Béral H: Burkitt-type acute leukemia in a patient with B-prolymphocytic leukemia: evidence for a common origin. Cancer Genet Cytogenet; 2005 May;159(1):74-8
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  • [Title] Burkitt-type acute leukemia in a patient with B-prolymphocytic leukemia: evidence for a common origin.
  • Burkitt-type acute leukemia cells were present in the bone marrow of a patient with B-prolymphocytic leukemia diagnosed from peripheral blood cell morphology.
  • These data indicated the common origin of the two coexisting leukemias and are the first example of such occurrence in a leukemic patient.
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Prolymphocytic / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic
  • [MeSH-minor] Bone Marrow / pathology. Cell Lineage. Cytogenetic Analysis. Female. Gene Rearrangement. Genes, myc. Humans. In Situ Hybridization, Fluorescence. Middle Aged

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  • (PMID = 15860362.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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7. Naseem S, Gupta R, Kashyap R, Nityanand S: T-cell prolymphocytic leukemia: a report of two cases with review of literature. Indian J Hematol Blood Transfus; 2008 Dec;24(4):178-81

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia: a report of two cases with review of literature.
  • T-cell Prolymphocytic Leukemia (T-PLL) is a mature post-thymic T-cell malignancy with aggressive clinical course.
  • The principal disease characteristics are organomegaly, skin lesions and raised lymphocyte counts.
  • T-PLL is a rare T-cell malignancy with characteristic clinical and laboratory features and a poor prognosis.
  • It needs to be differentiated from B-Cell prolymphocytic leukemia (B-PLL) and other mature T-cell lymphoproliferative disorders with predominant leukemic pattern.
  • Differentiation can be made by a comprehensive approach taking into account the clinical features, the cell morphology and the immunophenotype of leukemic cells.

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  • (PMID = 23100959.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3475431
  • [Keywords] NOTNLM ; Immunophenotyping / Prolymphocyte / T-PLL
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8. Del Giudice I, Davis Z, Matutes E, Osuji N, Parry-Jones N, Morilla A, Brito-Babapulle V, Oscier D, Catovsky D: IgVH genes mutation and usage, ZAP-70 and CD38 expression provide new insights on B-cell prolymphocytic leukemia (B-PLL). Leukemia; 2006 Jul;20(7):1231-7
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  • [Title] IgVH genes mutation and usage, ZAP-70 and CD38 expression provide new insights on B-cell prolymphocytic leukemia (B-PLL).
  • B-prolymphocytic leukemia (B-PLL) is a rare disease with poor prognosis.
  • To further characterize the biological features of this disease, we analyzed immunoglobulin heavy chain (IgVH) mutations, ZAP-70 and CD38 in 19 cases with de novo B-PLL.
  • [MeSH-major] Antigens, CD38 / genetics. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Prolymphocytic / genetics. Membrane Glycoproteins / genetics. ZAP-70 Protein-Tyrosine Kinase / genetics

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  • (PMID = 16642047.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Membrane Glycoproteins; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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9. Troussard X, Cornet E: Outline for writing an article for current treatment options in oncology: splenic lymphoma with villous lymphocytes. Curr Treat Options Oncol; 2007 Apr;8(2):97-108

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • SLVL is a rare leukemic and indolent B-cell chronic lymphoproliferative disorder (B-CLPD) that we have to differentiate from hairy cell leukemia (HCL), B prolymphocytic leukemia (B-PLL) and follicular lymphoma (FL).
  • However, the diagnosis can be difficult to make on morphological criteria, especially in patients without absolute lymphocytosis.
  • SLVL has a relatively clinical benign course but a few patients could require treatment, because of a symptomatic splenomegaly and/or a severe cytopenia.
  • [MeSH-major] B-Lymphocytes / pathology. Lymphoma, B-Cell / therapy. Splenic Neoplasms / therapy

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  • (PMID = 17634839.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 45
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10. Maljaei SH, Asvadi-E-Kermani I, Eivazi-E-Ziaei J, Nikanfar A, Vaez J: Usefulness of CD45 density in the diagnosis of B-cell chronic lymphoproliferative disorders. Indian J Med Sci; 2005 May;59(5):187-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Usefulness of CD45 density in the diagnosis of B-cell chronic lymphoproliferative disorders.
  • BACKGROUND: Although many B-cell chronic lymphoproliferative disorders (BCLPDs) including B-cell chronic lymphocytic leukemia (B-CLL) have characteristic clinical and biological features, the overlapping morphologic and immunophenotypic profiles of various BCLPDs, is still the main problem.
  • MATERIALS AND METHODS: The expression of CD45 in 37 patients with BCLPD including typical B-CLL (Group I), atypical B-CLL and CLL/PLL (II), and hairy cell leukemia (HCL), B-prolymphocytic leukemia (B-PLL), and B-non Hodgkin's lymphoma (B-NHL) as non-CLL BCLPDs (III) and in eight healthy age matched controls (IV) was quantitatively compared by flow cytometric CD45/RALS gating strategy.
  • [MeSH-major] Antigens, CD45 / immunology. Leukemia, B-Cell / diagnosis. Membrane Proteins / biosynthesis. Phosphoproteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. B-Lymphocytes / immunology. B-Lymphocytes / metabolism. Biomarkers / blood. Diagnosis, Differential. Female. Flow Cytometry. Fluorescent Antibody Technique, Direct. Follow-Up Studies. Humans. Intracellular Signaling Peptides and Proteins. Male. Middle Aged. Prospective Studies

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  • (PMID = 15985726.001).
  • [ISSN] 0019-5359
  • [Journal-full-title] Indian journal of medical sciences
  • [ISO-abbreviation] Indian J Med Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / PTPRCAP protein, human; 0 / Phosphoproteins; EC 3.1.3.48 / Antigens, CD45
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11. Inoue T, Yoshida M, Oowashi K, Yoshida T: [CD5-positive B-cell prolymphocytic leukemia]. Rinsho Ketsueki; 2010 Jan;51(1):80-2
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  • [Title] [CD5-positive B-cell prolymphocytic leukemia].
  • CD5 is a T-cell marker that is expressed in mature B cell malignancies and other B cell chronic lymphoproliferative disorders, but the biologic function of CD5 is unknown.
  • We report a 68-year-old woman with B-cell prolymphocytic leukemia (B-PLL) expressing CD5 antigen.
  • Hematological examination demonstrated a platelet count of 2.8 x 10(4)/microl and a white blood cell count of 19,900/microl with 69% PLL cells.
  • [MeSH-major] Antigens, CD5 / blood. Biomarkers, Tumor / blood. Leukemia, Prolymphocytic, B-Cell / blood. Leukemia, Prolymphocytic, B-Cell / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Fatal Outcome. Female. Humans. Leukocyte Count. Platelet Count

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  • (PMID = 20134145.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / Biomarkers, Tumor
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12. Absi A, Hsi E, Kalaycio M: Prolymphocytic leukemia. Curr Treat Options Oncol; 2005 May;6(3):197-208
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  • [Title] Prolymphocytic leukemia.
  • Prolymphocytic leukemia is a rare chronic lymphoproliferative disorder that includes two subtypes, B cell and T cell, each with its own distinct clinical, laboratory and pathological features.
  • T-cell prolymphocytic leukemia has an aggressive course with short median survival and poor response to chemotherapy.
  • We recommend alemtuzumab as initial therapy and offer stem cell transplant (SCT) to selected young, healthy patients who respond.
  • Although B-cell prolymphocytic leukemia is also a progressive disease, some patients can achieve a prolonged progression-free-survival with fludarabine.
  • Rituximab is a promising agent and further investigations are warranted to better define its role in treatment of this disorder.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, B-Cell / therapy. Leukemia, Prolymphocytic / therapy. Leukemia, T-Cell / therapy
  • [MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / administration & dosage. Female. Humans. Male. Pentostatin / administration & dosage. Rituximab. Stem Cell Transplantation

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  • (PMID = 15869731.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 54
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13. Machii T, Chou T, Suzuki M, Ohe Y, Katagiri S, Kitano K, Fujiyama Y, Izumi T, Shimazaki C, Nanba K, Ohashi Y, Kitani T, members of the Cladribine Study Group: Phase II Clinical Study of Cladribine in the Treatment of Hairy Cell Leukemia. Int J Hematol; 2005 Oct;82(3):230-235

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II Clinical Study of Cladribine in the Treatment of Hairy Cell Leukemia.
  • We conducted a phase II clinical study to evaluate the therapeutic efficacy of cladribine (2-chlorodeoxyadenosine [2-CdA]) in the treatment of Japanese patients with hairy cell leukemia (HCL).
  • Seven patients with classic HCL and 3 with a prolymphocytic HCL variant were administered 2-CdA (0.09 mg/kg per day) by continuous intravenous infusion for 7 days.

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  • (PMID = 28401520.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Keywords] NOTNLM ; 2—Chlorodeoxyadenosine / Cladribine / HCL / Hairy cell leukemia; / Phase II clinical study
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14. Nakashima H, Saito B, Ariizumi H, Matsuda I, Nakamaki T, Tomoyasu S: [Splenic irradiation as a successful treatment for an elderly patient with B-cell prolymphocytic leukemia]. Rinsho Ketsueki; 2008 Dec;49(12):1619-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Splenic irradiation as a successful treatment for an elderly patient with B-cell prolymphocytic leukemia].
  • We report a case of B-cell prolymphocytic leukemia (B-PLL) that was treated successfully with splenic irradiation (SI).
  • Peripheral blood showed hemoglobin level 9.8 g/dl and white blood cell count 38.1x10(9)/l with 91% atypical cells.
  • A diagnosis of B-PLL was made.
  • [MeSH-major] Leukemia, Prolymphocytic, B-Cell / radiotherapy. Spleen

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  • (PMID = 19110524.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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15. Telek B, Batár P, Rejto L, Udvardy M: [Successful treatment of B-cell prolymphocytic leukemia (B-PLL) with FCR-Lite (fludarabine, cyclophosphamide, rituximab) protocol]. Orv Hetil; 2010 Aug 1;151(31):1261-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful treatment of B-cell prolymphocytic leukemia (B-PLL) with FCR-Lite (fludarabine, cyclophosphamide, rituximab) protocol].
  • [Transliterated title] B-sejtes prolymphocytás leukaemia (B-PLL) sikeres kezelése FCR-Lite (fludarabin, cyclophosphamid, rituximab) protokoll alkalmazásával.
  • B-cell prolymphocytic leukemia (B-PLL) is a rare disorder characterized by marked lymphocytosis in the peripheral blood, matured lymphocytic infiltration in the bone marrow and splenomegaly.
  • The authors present a case of a patient with typical B-PLL treated with FCR-Lite (fludarabine, cyclophosphamide, rituximab) protocol achieving complete hematological (and immunophenotypic) remission.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Prolymphocytic, B-Cell / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Cyclophosphamide / administration & dosage. Diagnosis, Differential. Humans. Immunophenotyping. Male. Prognosis. Rituximab. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 20656663.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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16. Crisostomo RH, Fernandez JA, Caceres W: Complex karyotype including chromosomal translocation (8;14) (q24;q32) in one case with B-cell prolymphocytic leukemia. Leuk Res; 2007 May;31(5):699-701
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex karyotype including chromosomal translocation (8;14) (q24;q32) in one case with B-cell prolymphocytic leukemia.
  • We report a case of a 64-year-old white female patient, who presented with symptomatic anemia (Hgb: 6.8g/dl), thrombocytopenia (platelets: 94,000/mcl) and leukocytosis (WBC: 156,000/mcl).
  • Peripheral blood smear revealed markedly increased white blood cell count with predominance of atypical lymphoid cells of intermediate size, moderately dense chromatin, and prominent large single nucleoli.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 8. Leukemia, B-Cell / genetics. Leukemia, Prolymphocytic / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - B Cell Prolymphocytic Leukemia.
  • Hazardous Substances Data Bank. DOXORUBICIN .
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  • (PMID = 16997373.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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17. Dungarwalla M, Matutes E, Dearden CE: Prolymphocytic leukaemia of B- and T-cell subtype: a state-of-the-art paper. Eur J Haematol; 2008 Jun;80(6):469-76
MedlinePlus Health Information. consumer health - Chronic Lymphocytic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolymphocytic leukaemia of B- and T-cell subtype: a state-of-the-art paper.
  • Prolymphocytic leukaemias of B and T cell subtype are rare diseases.
  • Despite recent advances in immunophenotyping and molecular cytogenetics, leading to a better understanding of the underlying cell biology of the prolymphocytic leukaemias, prognosis for these patients remains poor.
  • Purine analogues and monoclonal antibodies have shown efficacy in B-cell prolymphocytic leukaemia although further studies are warranted.
  • Monoclonal antibody therapy with alemtuzumab has significantly improved outcome in T-cell prolymphocytic leukaemia (T-PLL) but responses are still transient and further disease progression is inevitable.
  • While allogeneic stem cell transplant is an attractive option, due to the older age group of T-PLL patients the morbidity and mortality associated with the procedure is significant.
  • [MeSH-major] B-Lymphocytes / immunology. Leukemia, Lymphoid / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Disease Progression. Humans

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  • (PMID = 18331594.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Number-of-references] 49
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18. Krishnan B, Matutes E, Dearden C: Prolymphocytic leukemias. Semin Oncol; 2006 Apr;33(2):257-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolymphocytic leukemias.
  • T and B subtypes of prolymphocytic leukemias (PLLs) are rare, highly aggressive lymphoid malignancies with characteristic morphologic, immunophenotypical, cytogenetic, and molecular features.
  • Recent studies have highlighted the role of specific oncogenes such as TCL1, MTCP-1, and ATM in the case of T-cell and p53 mutations in the case of B-cell PLLs.
  • [MeSH-major] Leukemia, Prolymphocytic

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  • (PMID = 16616073.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 46
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19. Dearden CE: T-cell prolymphocytic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S239-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia is a rare postthymic malignancy with distinctive clinical, morphologic, immunophenotypic, and cytogenetic features.
  • Nevertheless, responses are relatively short, and the only potential curative treatment is allogeneic stem cell transplantation.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia, Prolymphocytic, T-Cell / therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Female. Gene Expression Regulation, Leukemic. Humans. Immunophenotyping. Male. Medical Oncology / methods. Middle Aged. Pentostatin / therapeutic use. Stem Cell Transplantation / methods. Transplantation, Homologous / methods. Treatment Outcome

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  • (PMID = 19778847.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab
  • [Number-of-references] 38
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20. Dearden CE: T-cell prolymphocytic leukemia. Med Oncol; 2006;23(1):17-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive post-thymic malignancy with poor response to conventional treatment and short survival.
  • It can readily be distinguished from other T-cell leukemias on the basis of the distinctive morphology, immunophenotype, and cytogenetics.
  • Consistent chromosomal translocations involving the T-cell receptor gene and one of two protooncogenes (TCL-1 and MTCP-1) are seen in the majority of cases and are likely to be involved in the pathogenesis of the disorder.
  • However, relapse is inevitable and strategies using both autologous and allogeneic stem cell transplantation are currently being explored.
  • [MeSH-major] Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy

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  • (PMID = 16645226.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 28
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21. Khot A, Dearden C: T-cell prolymphocytic leukemia. Expert Rev Anticancer Ther; 2009 Mar;9(3):365-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia is a rare post-thymic lymphoid disorder, which has distinctive clinical, morphologic, immunophenotypic and cytogenetic features.
  • However, responses are transient and allogeneic hematopoietic progenitor-cell transplantation remains the only potential curative option.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / therapy
  • [MeSH-minor] Antibodies, Monoclonal / genetics. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / genetics. Antibodies, Neoplasm / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diagnosis, Differential. Drug Administration Schedule. Hematopoietic Stem Cell Transplantation. Humans. Prognosis. Stem Cell Transplantation. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 19275513.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Number-of-references] 46
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22. Jahanmehr SA, Rogers M, Zheng J, Lai R, Wang C: Quantitation of cytological parameters of malignant lymphocytes using computerized image analysis. Int J Lab Hematol; 2008 Aug;30(4):278-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, image analysis program was used to quantitate cytological parameters of lymphocytes in B-cell lymphoproliferative disorders.
  • Chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL) and B-cell prolymphocytic leukemia (B-PLL) were selected to represent typically small, medium, and large-sized lymphocytes, respectively.
  • A set of measurements was generated for quantitation of total cell area, cell diameter, cytoplasm area, nuclear area, nuclear/cell ratio, and nuclear density.
  • The results from image analysis may assist in defining morphological criteria and in developing quantitative cell morphology.
  • [MeSH-minor] Humans. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Prolymphocytic, B-Cell / pathology. Lymphoma, Mantle-Cell / pathology. Microscopy

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  • (PMID = 18665824.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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23. Zhang YN, Zhou XG, Zhang SH, Wang P, Zhang CH, Huang SF: [Clinicopathologic study of 369 B-cell non-Hodgkin lymphoma cases, with reference to the 2001 World Health Organization classification of lymphoid neoplasms]. Zhonghua Bing Li Xue Za Zhi; 2005 Apr;34(4):193-7
Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinicopathologic study of 369 B-cell non-Hodgkin lymphoma cases, with reference to the 2001 World Health Organization classification of lymphoid neoplasms].
  • OBJECTIVE: To describe the relative frequency, morphologic features, immunophenotype and clinical data of different types of B-cell non-Hodgkin lymphoma (B-NHL) and to evaluate the practical application of the 2001 World Health Organization (WHO) classification of lymphoid neoplasms.
  • Diffuse large B-cell lymphoma, extranodal marginal zone lymphoma and follicular lymphoma were the commonest subtypes, accounting for 51.2% (189 cases), 14.9% (55 cases) and 10.6% (39 cases) of all cases respectively.
  • B-cell prolymphocytic leukemia and hairy cell leukemia were not identified.
  • When comparing the diagnosis based on morphologic examination alone with the diagnosis based on both morphology and immunophenotype, there was a 80% concordance rate.
  • Immunohistochemical study was helpful in reaching the correct diagnosis in many cases and could improve the overall diagnostic accuracy by about 20%.
  • CONCLUSIONS: Amongst cases of B-NHL, diffuse large B-cell lymphoma is the commonest subtype, followed by MALToma and follicular lymphoma.
  • While morphologic examination forms the basis for lymphoma diagnosis, immunohistochemical study also plays an important role in further subtyping.
  • A combination of both modalities are sufficient for arriving at an accurate diagnosis in most cases of B-NHL, in keeping with the recommendation of the 2001 WHO classification of lymphoid neoplasms.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, B-Cell, Marginal Zone / pathology. Lymphoma, Follicular / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Non-Hodgkin / classification

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
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  • (PMID = 16091170.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, CD43; 0 / Antigens, CD79
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24. Valbuena JR, Herling M, Admirand JH, Padula A, Jones D, Medeiros LJ: T-cell prolymphocytic leukemia involving extramedullary sites. Am J Clin Pathol; 2005 Mar;123(3):456-64
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  • [Title] T-cell prolymphocytic leukemia involving extramedullary sites.
  • T-cell prolymphocytic leukemia (T-PLL) can involve extramedullary sites, but the diagnosis is usually established by examination of blood and bone marrow.
  • Cytologically, the T-PLL cells were round (n = 16) or Sezary cell-like (n = 3).
  • Immunostaining for T-cell leukemia-1 (TCL-1) was positive in specimens from 9 (64%) of 14 patients.
  • TCL-1 expression can aid in diagnosis at extramedullary sites.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, T-Cell / pathology. Lymphoid Tissue / pathology. Skin Neoplasms / pathology

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  • (PMID = 15716243.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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25. Le Toriellec E, Despouy G, Pierron G, Gaye N, Joiner M, Bellanger D, Vincent-Salomon A, Stern MH: Haploinsufficiency of CDKN1B contributes to leukemogenesis in T-cell prolymphocytic leukemia. Blood; 2008 Feb 15;111(4):2321-8
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  • [Title] Haploinsufficiency of CDKN1B contributes to leukemogenesis in T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia (T-PLL) is consistently associated with inactivation of the ATM gene and chromosomal re-arrangements leading to an overexpression of MTCP1/TCL1 oncoproteins.
  • The absence of biallelic inactivation of CDKN1B for most patients suggested a haploinsufficiency mechanism for tumor suppression, which was investigated in an animal model of the disease.
  • [MeSH-major] Chromosomes, Human, Pair 12. Intracellular Signaling Peptides and Proteins / deficiency. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Prolymphocytic, T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Animals. Ataxia Telangiectasia Mutated Proteins. Cell Cycle Proteins / genetics. Chromosome Mapping. Cyclin-Dependent Kinase Inhibitor p27. DNA Primers. DNA-Binding Proteins / genetics. Gene Deletion. Humans. Mice. Mice, Transgenic. Open Reading Frames. Polymerase Chain Reaction. Polymorphism, Single Nucleotide. Protein-Serine-Threonine Kinases / genetics. Tumor Cells, Cultured. Tumor Suppressor Proteins / genetics

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  • (PMID = 18073348.001).
  • [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 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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26. Zhang JF, Miao KR, Qiu HR, Yang H, Wu YJ, Qiao C, Li JY: [Acute myeloid leukemia with the morphological characteristics of prolymphocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Oct;16(5):1211-4
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  • [Title] [Acute myeloid leukemia with the morphological characteristics of prolymphocytic leukemia].
  • To investigate the clinical, cellular morphology, immunophenotype, and cytogenetic characteristics of acute myeloid leukemia (AML) which are very similar to the morphological characteristics of prolymphocytic leukemia (PLL), the morphological features of bone marrow cells from patient were observed by light microscope, the immunophenotypes were detected by flow cytometry, the karyotypes were analyzed by conventional cytogenetic method, the hybridization signals were determined by fluorescence in situ hybridization.
  • The results indicated that the clinical features were in accordance with acute leukemia and the immunophenotyping results showed malignant cells originated from myeloid lineage, while the cytomorphology analysis showed that the blastic cells were more like the lymphoid lineage.
  • In conclusion, acute leukemia has high heterogenicity, which could be defined as AML, but more like lymphocytic origination by morphological study.
  • Immunophenotyping analysis could contribute to the final diagnosis of malignant cells.

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  • (PMID = 18928630.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
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27. Kalaycio ME, Kukreja M, Woolfrey AE, Szer J, Cortes J, Maziarz RT, Bolwell BJ, Buser A, Copelan E, Gale RP, Gupta V, Maharaj D, Marks DI, Pavletic SZ, Horowitz MM, Arora M: Allogeneic hematopoietic cell transplant for prolymphocytic leukemia. Biol Blood Marrow Transplant; 2010 Apr;16(4):543-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic hematopoietic cell transplant for prolymphocytic leukemia.
  • The poor prognosis of patients with prolymphocytic leukemia (PLL) has led some clinicians to recommend allogeneic hematopoietic cell transplant (HCT).
  • Further study of a larger population of patients is needed to determine which patients are more likely to benefit.

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  • [Copyright] Copyright (c) 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 19961946.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / 5U01HL069294; United States / NCI NIH HHS / CA / U24 CA076518; United States / NCI NIH HHS / CA / U24 CA076518-12; United States / NCI NIH HHS / CA / U24 CA76518; United States / NHLBI NIH HHS / HL / U01 HL069294; United States / NCI NIH HHS / CA / CA076518-12
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS162699; NLM/ PMC2839005
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28. Nusz KJ, Pang NK, Woog JJ: Periorbital edema as the initial presentation of T-cell prolymphocytic leukemia. Ophthal Plast Reconstr Surg; 2006 May-Jun;22(3):215-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Periorbital edema as the initial presentation of T-cell prolymphocytic leukemia.
  • Laboratory tests revealed T-cell prolymphocytic leukemia.
  • This life-threatening disorder should be added to the differential diagnosis of eyelid edema.
  • [MeSH-major] Edema / etiology. Eyelid Diseases / etiology. Leukemia, Prolymphocytic / complications. Leukemia, T-Cell / complications. Orbital Diseases / etiology

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  • (PMID = 16714934.001).
  • [ISSN] 0740-9303
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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29. Foucar K: Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome. Am J Clin Pathol; 2007 Apr;127(4):496-510
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome.
  • The 2005 Society for Hematopathology/European Association for Haematopathology Workshop Session 1 was devoted to case presentations with discussions of 3 types of mature T-cell leukemias--T-cell prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome.
  • The application of clinical, morphologic, immunophenotypic, and genetic studies to the assessment and characterization of these 3 disorders is presented, along with specific diagnostic recommendations and differential diagnostic considerations.
  • [MeSH-major] Leukemia, Prolymphocytic / diagnosis. Leukemia, T-Cell / diagnosis. Sezary Syndrome / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Antigens, CD / metabolism. Chromosome Aberrations. Diagnosis, Differential. Humans. Immunophenotyping

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  • (PMID = 17369126.001).
  • [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
  • [Chemical-registry-number] 0 / Antigens, CD
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30. 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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31. Ravandi F, O'Brien S, Jones D, Lerner S, Faderl S, Ferrajoli A, Wierda W, Garcia-Manero G, Thomas D, Koller C, Verstovsek S, Giles F, Cortes J, Herling M, Kantarjian H, Keating M: T-cell prolymphocytic leukemia: a single-institution experience. Clin Lymphoma Myeloma; 2005 Nov;6(3):234-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia: a single-institution experience.
  • BACKGROUND: T-cell prolymphocytic leukemia is an uncommon, aggressive, mature T-cell leukemia characterized by proliferation of T-cell lymphocytes.
  • The recent availability of modern immunophenotypic and molecular tools has allowed a better distinction of this disorder from its B-cell counterpart and other mature T-cell leukemias.
  • PATIENTS AND METHODS: The clinical, pathologic, and cytogenetic features of 57 patients with T-PLL who were evaluated at the Department of Leukemia, M. D.
  • RESULTS: The most common cytogenetic abnormality was inv(14)(q11;q32), which was present in 7 patients.
  • In all 7 patients, this abnormality was associated with other chromosomal aberrations.
  • CONCLUSION: Treatment with alemtuzumab results in higher response rates and a better survival rate in patients with T-cell prolymphocytic leukemia.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Leukemia, Prolymphocytic / metabolism. Proto-Oncogene Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Chromosome Inversion. Disease-Free Survival. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies

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  • (PMID = 16354329.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human
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32. Röth A, Dürig J, Himmelreich H, Bug S, Siebert R, Dührsen U, Lansdorp PM, Baerlocher GM: Short telomeres and high telomerase activity in T-cell prolymphocytic leukemia. Leukemia; 2007 Dec;21(12):2456-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Short telomeres and high telomerase activity in T-cell prolymphocytic leukemia.
  • To test the role of telomere biology in T-cell prolymphocytic leukemia (T-PLL), a rare aggressive disease characterized by the expansion of a T-cell clone derived from immuno-competent post-thymic T-lymphocytes, we analyzed telomere length and telomerase activity in subsets of peripheral blood leukocytes from 11 newly diagnosed or relapsed patients with sporadic T-PLL.
  • Targeting the short telomeres and telomerase activity in T-PLL seems an attractive strategy for the future treatment of this devastating disease.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / genetics. Neoplasm Proteins / analysis. Telomerase / analysis. Telomere / ultrastructure

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  • (PMID = 17898784.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminobenzoates; 0 / BIBR 1532; 0 / Naphthalenes; 0 / Neoplasm Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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33. Magro CM, Morrison CD, Heerema N, Porcu P, Sroa N, Deng AC: T-cell prolymphocytic leukemia: an aggressive T cell malignancy with frequent cutaneous tropism. J Am Acad Dermatol; 2006 Sep;55(3):467-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia: an aggressive T cell malignancy with frequent cutaneous tropism.
  • BACKGROUND: T-cell prolymphocytic leukemia (T-PLL), formerly categorized as T-cell chronic lymphocytic leukemia, is a rare and aggressive hematologic malignancy.
  • The disease was associated in all with skin involvement with facial preference; edema, purpura, and lesional symmetry were characteristic.
  • All expressed T-cell leukemia 1 (TCL-1) and CD7; cutaneous lymphocyte antigen expression was discernible in a dot-like perinuclear array.
  • In two cases tested, T-cell receptor beta rearrangements were observed.
  • Four patients died from their disease within 18 months of diagnosis.
  • CONCLUSION: T-PLL is a distinctive post-thymic T-cell malignancy with frequent cutaneous tropism.
  • A diagnosis is possible in almost all cases based on characteristic clinical, light microscopic, phenotypic, and cytogenetic features.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, Prolymphocytic, T-Cell / pathology. Skin / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Aneuploidy. Antigens, CD / metabolism. Antigens, Neoplasm / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / pathology. Cytogenetic Analysis. Face. Female. Gene Amplification. Gene Rearrangement. Glycoproteins / metabolism. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Phenotype. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-myc / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics

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  • [CommentIn] J Am Acad Dermatol. 2007 Sep;57(3):533-4 [17707160.001]
  • (PMID = 16908353.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / TCL1A protein, human
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34. Osuji N, Matutes E, Catovsky D, Lampert I, Wotherspoon A: Histopathology of the spleen in T-cell large granular lymphocyte leukemia and T-cell prolymphocytic leukemia: a comparative review. Am J Surg Pathol; 2005 Jul;29(7):935-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histopathology of the spleen in T-cell large granular lymphocyte leukemia and T-cell prolymphocytic leukemia: a comparative review.
  • We review retrospectively the spleen histology in 8 patients with T-cell large granular lymphocyte (LGL) leukemia and 4 with T-cell prolymphocytic leukemia (T-PLL) to identify characteristic patterns of involvement and to distinguish such patterns from those described in other low grade B- and T-cell malignancies.
  • Moderate splenic enlargement with red pulp expansion due to lymphocytic infiltration was characteristic of LGL leukemia.
  • Unlike in hairy cell leukemia, the main differential diagnosis for red pulp lymphocytosis, the white pulp was not only preserved in T-cell LGL leukemia but showed germinal center hyperplasia with expansion of the mantle zones.
  • T-cell prolymphocytes did not express cytotoxic granule proteins or NK-cell markers, were CD5+, CD45RO+ like normal spleen T cells, were CD2+, CD3+, CD45+, CD43+, TCRbeta+, but CD25-, CD30-, ALK-1-, TRAP-, DBA44-, and TdT-.
  • These observations on the morphologic and immunohistochemical appearances of the spleen in T-cell LGL leukemia and T-PLL may aid diagnosis of these uncommon T-cell disorders, particularly T-cell LGL leukemia, where presentation may be cryptic and where unique pathognomonic features, are absent.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, T-Cell / pathology. Spleen / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Lymphocytes / metabolism. Lymphocytes / pathology. Male. Middle Aged. Retrospective Studies

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  • (PMID = 15958859.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 23
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35. Toyota S, Nakamura N, Dan K: Small cell variant of T-cell prolymphocytic leukemia with a gammadelta immunophenotype. Int J Hematol; 2005 Jan;81(1):66-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small cell variant of T-cell prolymphocytic leukemia with a gammadelta immunophenotype.
  • T-cell prolymphocytic leukemia (T-PLL) is a rare postthymic T-cell disorder.
  • The disease is characterized by lymphadenopathy, splenomegaly, skin lesions, a high white blood cell count, and an aggressive clinical course.
  • The small cell variant of T-PLL occurs in approximately 20% of patients.
  • Most T-PLL patients express membrane T-cell receptors (TCR) of the alphabeta phenotype.
  • The diagnosis of small cell variant T-PLL in a 56-year-old woman was based on the findings of abnormal lymphocytosis, immunophenotype, lymphadenopathy, and aggressive clinical behavior.
  • This case was typical T-PLL except for the morphologically small cell type and the lack of the typical chromosome aberration.
  • If cases accumulate in the future, the specific features of the gamma8 type of T-PLL will become clearer.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, T-Cell / pathology. Receptors, Antigen, T-Cell, gamma-delta / metabolism

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  • (PMID = 15717692.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, gamma-delta
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36. Reiniger L, Bödör C, Bognár A, Balogh Z, Csomor J, Szepesi A, Kopper L, Matolcsy A: Richter's and prolymphocytic transformation of chronic lymphocytic leukemia are associated with high mRNA expression of activation-induced cytidine deaminase and aberrant somatic hypermutation. Leukemia; 2006 Jun;20(6):1089-95
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  • [Title] Richter's and prolymphocytic transformation of chronic lymphocytic leukemia are associated with high mRNA expression of activation-induced cytidine deaminase and aberrant somatic hypermutation.
  • Chronic lymphocytic leukemia (CLL) is an indolent B-cell non-Hodgkin's lymphoma that may transform into higher-grade lymphoma.
  • The transformation involves an increased number of prolymphocytic cells, termed prolymphocytic transformation (PLT) or the development of diffuse large B-cell lymphoma (DLBL), also referred to as Richter's transformation (RT).
  • To analyze whether activation-induced cytidine deaminase (AID), which is essential for somatic hypermutation (SHM) of normal B-cells, and malfunction of SHM termed aberrant somatic hypermutation (ASHM) are associated with higher-grade transformation of CLL, AID mRNA expression and the mutation pattern of c-MYC, PAX-5 and RhoH genes were analyzed in eight cases of CLL without transformation and in 21 cases that showed RT or PLT.
  • Chronic lymphocytic leukemia cases, which showed no transformation or eventually transformed into higher-grade lymphoma, showed low levels of AID mRNA expression and low frequency of mutations of c-MYC, PAX-5 and RhoH genes.
  • In both RT and PLT, high-levels of AID mRNA expression and high-frequency mutations of c-MYC, PAX-5 and RhoH genes were detected.
  • These results indicate that AID expression and ASHM are associated with higher-grade transformation of CLL and provide further evidences that AID expression and ASHM may be activated during the clonal history of B-cell lymphomas.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Cytidine Deaminase / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. RNA, Messenger / biosynthesis. Somatic Hypermutation, Immunoglobulin / genetics
  • [MeSH-minor] B-Cell-Specific Activator Protein / genetics. Gene Expression Profiling. Humans. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Mutation. Proto-Oncogene Proteins c-myc / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription Factors / genetics. rho GTP-Binding Proteins / genetics

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  • (PMID = 16541139.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / PAX5 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / RhoH protein, human; 0 / Transcription Factors; EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase; EC 3.6.5.2 / rho GTP-Binding Proteins
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37. Lan K, Murakami M, Choudhuri T, Tsai DE, Schuster SJ, Wasik MA, Robertson ES: Detection of Epstein-Barr virus in T-cell prolymphocytic leukemia cells in vitro. J Clin Virol; 2008 Nov;43(3):260-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of Epstein-Barr virus in T-cell prolymphocytic leukemia cells in vitro.
  • BACKGROUND: Epstein-Barr virus (EBV) is closely associated with the development of a number of tumors.
  • During latent infection, EBV continuously expresses a number of viral genes which are essential for cell transformation and maintenance of the malignant phenotype of EBV-related tumors.
  • There has been no previous link between EBV and T-cell prolymphocytic leukemia (T-PLL), a distinctive form of leukemia derived from T-cells at an intermediate stage of differentiation between a cortical thymocyte and a mature peripheral blood T-cell.
  • STUDY DESIGN: T-PLL cells were isolated from the peripheral blood of a patient diagnosed with T-PLL and continuously cultured for about 1 year.

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  • (PMID = 18790666.001).
  • [ISSN] 1386-6532
  • [Journal-full-title] Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
  • [ISO-abbreviation] J. Clin. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA174439; United States / NCI NIH HHS / CA / R01 CA091792; United States / NIDCR NIH HHS / DE / R01 DE014136; United States / NIDDK NIH HHS / DK / P30 DK050306; United States / NIDCR NIH HHS / DE / DE014136-04; United States / NCI NIH HHS / CA / CA091792; United States / NCI NIH HHS / CA / R01 CA177423; United States / NCI NIH HHS / CA / R01 CA108461; United States / NCI NIH HHS / CA / CA072510
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / DNA, Viral
  • [Other-IDs] NLM/ NIHMS78635; NLM/ PMC4289600
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38. Maeda A, Iwai K, Ishibashi T: [Successful treatment of T-cell prolymphocytic leukemia (T-PLL) with fludarabine monophosphate]. Rinsho Ketsueki; 2009 Aug;50(8):658-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful treatment of T-cell prolymphocytic leukemia (T-PLL) with fludarabine monophosphate].
  • We report a 79-year-old woman with T-cell prolymphocytic leukemia (T-PLL) who was successfully treated with fludarabine monophosphate.
  • The reticulocyte count increased gradually, and she became free from red cell transfusions.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Leukemia, Prolymphocytic, T-Cell / drug therapy. Vidarabine Phosphate / analogs & derivatives

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  • (PMID = 19915381.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 106XV160TZ / Vidarabine Phosphate; 1X9VK9O1SC / fludarabine phosphate
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39. Ogasawara T, Narita C, Kawauchi K: Production of vascular endothelial growth factor in T-cell prolymphocytic leukemia. Leuk Res; 2007 Mar;31(3):403-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Production of vascular endothelial growth factor in T-cell prolymphocytic leukemia.
  • We describe a 79-year-old man who had massive pleural effusion and a proliferation of prolymphocytic leukemia cells in the peripheral blood, bone marrow, and pleural effusion fluid.
  • Immunophenotyping of leukemia cells revealed either CD3+CD4+CD8-CD25+ or CD3+CD4+CD8+CD25+.
  • The antibody against human T-cell lymphotropic virus type I was negative.
  • A diagnosis of T-PLL was made.
  • Moreover, polymerase chain reaction analysis demonstrated an expression of VEGF mRNA in the leukemia cells, indicating a production of VEGF from leukemia cells and its involvement in the pathogenesis of T-PLL.
  • [MeSH-major] Leukemia, Prolymphocytic / immunology. Leukemia, T-Cell / immunology. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 16620970.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
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40. Nowak D, Le Toriellec E, Stern MH, Kawamata N, Akagi T, Dyer MJ, Hofmann WK, Ogawa S, Koeffler HP: Molecular allelokaryotyping of T-cell prolymphocytic leukemia cells with high density single nucleotide polymorphism arrays identifies novel common genomic lesions and acquired uniparental disomy. Haematologica; 2009 Apr;94(4):518-27
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  • [Title] Molecular allelokaryotyping of T-cell prolymphocytic leukemia cells with high density single nucleotide polymorphism arrays identifies novel common genomic lesions and acquired uniparental disomy.
  • BACKGROUND: T-cell prolymphocytic leukemia is a rare aggressive lymphoproliferative disease with a mature T-cell phenotype and characteristic genomic lesions such as inv(14)(q11q34), t(14;14)(q11;q32) or t(X;14)(q28;q11), mutation of the ATM gene on chromosome 11 and secondary alterations such as deletions of chromosome 8p and duplications of 8q.
  • DESIGN AND METHODS: We analyzed malignant cells from 18 patients with T-cell prolymphocytic leukemia using high density 250K single nucleotide polymorphism arrays and molecular allelokaryotyping to refine understanding of known alterations and identify new target genes.
  • CONCLUSIONS: The first high density single nucleotide polymorphism array allelokaryotyping of T-cell prolymphocytic leukemia genomes added substantial new details about established alterations in this disease and moreover identified numerous new potential target genes in common breakpoints, deletions and regions of acquired uniparental disomy.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / genetics. Polymorphism, Single Nucleotide / genetics. Uniparental Disomy

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  • (PMID = 19278963.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2663615
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41. Bug S, Dürig J, Oyen F, Klein-Hitpass L, Martin-Subero JI, Harder L, Baudis M, Arnold N, Kordes U, Dührsen U, Schneppenheim R, Siebert R: Recurrent loss, but lack of mutations, of the SMARCB1 tumor suppressor gene in T-cell prolymphocytic leukemia with TCL1A-TCRAD juxtaposition. Cancer Genet Cytogenet; 2009 Jul;192(1):44-7
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  • [Title] Recurrent loss, but lack of mutations, of the SMARCB1 tumor suppressor gene in T-cell prolymphocytic leukemia with TCL1A-TCRAD juxtaposition.
  • In T-cell prolymphocytic leukemia (T-PLL), chromosomal imbalances affecting the long arm of chromosome 22 are regarded as typical chromosomal aberrations secondary to a TCRAD-TCL1A fusion due to inv(14) or t(14;14).
  • [MeSH-major] Chromosomal Proteins, Non-Histone / genetics. DNA-Binding Proteins / genetics. Gene Deletion. Leukemia, Prolymphocytic, T-Cell / genetics. Protein-Serine-Threonine Kinases / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 19480937.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / SMARCB1 protein, human; 0 / TCL1A protein, human; 0 / Transcription Factors; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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42. Herling M, Patel KA, Teitell MA, Konopleva M, Ravandi F, Kobayashi R, Jones D: High TCL1 expression and intact T-cell receptor signaling define a hyperproliferative subset of T-cell prolymphocytic leukemia. Blood; 2008 Jan 1;111(1):328-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High TCL1 expression and intact T-cell receptor signaling define a hyperproliferative subset of T-cell prolymphocytic leukemia.
  • The T-cell leukemia 1 (TCL1) oncoprotein is overexpressed by chromosomal rearrangement in the majority of cases of T-cell prolymphocytic leukemia (T-PLL).
  • In vitro, TCL1 can modulate the activity of the serine-threonine kinase AKT, a downstream effector of T-cell receptor (TCR) signaling.
  • High-level TCL1 in TCR-expressing T-PLL is associated with higher presenting white blood cell counts, faster tumor cell doubling, and enhanced in vitro growth response to TCR engagement.
  • In primary tumors and TCL1-transfected T-cell lines, TCR engagement leads to rapid recruitment of TCL1 and AKT to transient membrane activation complexes that include TCR-associated tyrosine kinases, including LCK.
  • Pharmacologic inhibition of AKT activation alters the localization, stability, and levels of these transient TCL1-AKT complexes and reduces tumor cell growth.

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  • (PMID = 17890451.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA90571; United States / NCI NIH HHS / CA / R01 CA107300; United States / NCI NIH HHS / CA / R01 CA090571; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA107300
  • [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 / Proto-Oncogene Proteins; 0 / Receptors, Antigen, T-Cell; 0 / TCL1A protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2200815
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43. Moid F, Day E, Schneider MA, Goldstein K, DePalma L: An indolent case of T-prolymphocytic leukemia with t(3;22)(q21;q11.2) and elevated serum beta2-microglobulin. Arch Pathol Lab Med; 2005 Sep;129(9):1164-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An indolent case of T-prolymphocytic leukemia with t(3;22)(q21;q11.2) and elevated serum beta2-microglobulin.
  • We report a novel case of T-prolymphocytic leukemia, small cell variant, associated with complex cytogenetic findings including t(3;22)(q21;11.2) and elevated serum beta2-microglobulin.
  • The diagnosis is based on morphologic, immunophenotypic, cytogenetic, and molecular analysis of peripheral blood and bone marrow.
  • In contrast to most reported cases of T-prolymphocytic leukemia, this patient did not present with lymphadenopathy or organomegaly.
  • In the absence of any specific treatment, the patient is doing well, with a stable white blood cell count 12 months following presentation.
  • [MeSH-major] Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 3 / genetics. Leukemia, Prolymphocytic. Leukemia, Prolymphocytic, T-Cell. Translocation, Genetic / genetics. beta 2-Microglobulin / blood

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  • (PMID = 16119992.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / beta 2-Microglobulin
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44. Jamet D, Quinio D, Moalic E, Ianotto JC, Dalbies F, Guillerm G, Marion V, Berthou C, Nevez G: [Systemic microsporidiosis and toxoplasmosis in a patient with T prolymphocytic leukemia]. Med Mal Infect; 2009 Jun;39(6):406-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Systemic microsporidiosis and toxoplasmosis in a patient with T prolymphocytic leukemia].
  • [Transliterated title] Microsporidiose et toxoplasmose disséminées chez une patiente présentant une leucémie prolymphocytaire T.
  • We report a case of microsporidiosis in a 72-year-old woman presenting with prolymphocytic leukemia.
  • The underlying conditions 7 months after leukemia was diagnosed were pancytopenia and immunosuppression due to alemtuzumab and pentostatin.
  • The present case in a patient with lymphoid leukemia is the first to be reported.
  • [MeSH-major] Encephalitozoonosis / complications. Leukemia, Prolymphocytic, T-Cell / complications

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  • (PMID = 19046839.001).
  • [ISSN] 0399-077X
  • [Journal-full-title] Médecine et maladies infectieuses
  • [ISO-abbreviation] Med Mal Infect
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] F4216019LN / Albendazole
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45. Madaris L: T-cell prolymphocytic leukemia: A rare disease in an elderly female. J Am Acad Nurse Pract; 2010 Dec;22(12):648-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia: A rare disease in an elderly female.
  • This report includes a review of the morphology of T-cell prolymphocytic leukemia (PLL), diagnosis, and the treatment options considered.
  • DATA SOURCES: T-cell PLL is a rare blood disorder that represents a very small number of all chronic leukemias.
  • An extensive review of scientific literature related to the cell morphology and pathology of this disease, as well as clinical trials of treatment options provided the background for this case report.
  • CONCLUSION: A diagnosis of T-cell PLL was made after a computed tomography scan of the abdomen confirmed splenomegaly and a bone marrow biopsy showed a hypercellular marrow infiltrated with numerous small lymphocytes, consistent with this disease.
  • Currently, there is no optimal treatment for T-cell PLL, but alemtuzumab has shown success with extending survival 1-3 years.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia, Prolymphocytic, T-Cell / drug therapy

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  • [Copyright] ©2010 The Author Journal compilation ©2010 American Academy of Nurse Practitioners.
  • (PMID = 21129072.001).
  • [ISSN] 1745-7599
  • [Journal-full-title] Journal of the American Academy of Nurse Practitioners
  • [ISO-abbreviation] J Am Acad Nurse Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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46. de Oliveira FM, Tone LG, Simões BP, Rego EM, Marinato AF, Jácomo RH, Falcão RP: Translocations t(X;14)(q28;q11) and t(Y;14)(q12;q11) in T-cell prolymphocytic leukemia. Int J Lab Hematol; 2009 Aug;31(4):453-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocations t(X;14)(q28;q11) and t(Y;14)(q12;q11) in T-cell prolymphocytic leukemia.
  • We report a case of T-cell prolymphocytic leukemia (T-PLL) in a 41-year-old male.
  • Classical cytogenetic, spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH) studies of a blood sample obtained at diagnosis revealed the co-existence of t(X;14)(q28;q11), t(Y;14)(q12;q11) and a ring chromosome derived from i(8)(q10).
  • Immunophenotypic studies revealed involvement of T-cell lineage, with proliferation of CD4(-) CD8+.
  • Chromosomal instability associated with the disease progression may have allowed the emergence of cell clones with translocations involving the sex chromosomes and the ring chromosome observed.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, X / genetics. Chromosomes, Human, Y / genetics. Leukemia, Prolymphocytic, T-Cell / genetics. Ring Chromosomes. Translocation, Genetic

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  • (PMID = 18294235.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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47. Dürig J, Bug S, Klein-Hitpass L, Boes T, Jöns T, Martin-Subero JI, Harder L, Baudis M, Dührsen U, Siebert R: Combined single nucleotide polymorphism-based genomic mapping and global gene expression profiling identifies novel chromosomal imbalances, mechanisms and candidate genes important in the pathogenesis of T-cell prolymphocytic leukemia with inv(14)(q11q32). Leukemia; 2007 Oct;21(10):2153-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined single nucleotide polymorphism-based genomic mapping and global gene expression profiling identifies novel chromosomal imbalances, mechanisms and candidate genes important in the pathogenesis of T-cell prolymphocytic leukemia with inv(14)(q11q32).
  • T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive lymphoma derived from mature T cells, which is, in most cases, characterized by the presence of an inv(14)(q11q32)/t(14;14)(q11;q32) and a characteristic pattern of secondary chromosomal aberrations.
  • DNA microarray technology was employed to compare the transcriptomes of eight immunomagnetically purified CD3+ normal donor-derived peripheral blood cell samples, with five highly purified inv(14)/t(14;14)-positive T-PLL blood samples.
  • Between the two experimental groups, 734 genes were identified as differentially expressed, including functionally important genes involved in lymphomagenesis, cell cycle regulation, apoptosis and DNA repair.
  • In conclusion, combined transcriptional and molecular cytogenetic profiling identified novel specific chromosomal loci and genes that are likely to be involved in disease progression and suggests a gene dosage effect as a pathogenic mechanism in T-PLL.
  • [MeSH-major] Chromosome Inversion. Chromosome Mapping / methods. Chromosomes, Human, Pair 14. Gene Expression Profiling. Leukemia, Prolymphocytic / genetics. Leukemia, T-Cell / genetics. Polymorphism, Single Nucleotide
  • [MeSH-minor] Antigens, CD3 / biosynthesis. Apoptosis. Chromosome Aberrations. DNA Repair. Disease Progression. Gene Dosage. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 17713554.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3
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48. Krejcí M, Adam Z, Pour L, Brychtová Y, Mayer J, Vorlícek J: [B-cell chronic lymphocytic leukaemia and the similar states]. Vnitr Lek; 2009 Sep;55(9):746-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [B-cell chronic lymphocytic leukaemia and the similar states].
  • [Transliterated title] Chronická B-lymfatická leukemie a jí podobné stavy.
  • B-cell chronic lymphocytic leukaemia and the similar diseases are seen predominantly in patients above the age 50 years, i.e. at the age when the patients also have other co-morbidities.
  • The aim of the present review is to provide the medical community with the main information on this disease as patients with B-cell chronic lymphocytic leukaemia and similar disease states are of older age and very often suffer from a range of co-morbidities.
  • The aim of the following text is to present a clear overview of the basic information about this group of diseases that might be useful to all physicians who provide care to patients with B-cell chronic lymphocytic leukaemia and similar conditions.
  • Since monoclonal immunoglobulin is sometimes identified in patients with these diseases, it is important to consider these conditions in the differential diagnosis of the states with the presence of monoclonal immunoglobulin.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Leukemia, Hairy Cell / diagnosis. Leukemia, Prolymphocytic / diagnosis. Multiple Myeloma / diagnosis. Paraproteinemias / diagnosis

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  • (PMID = 19785372.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 41
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49. Ghosh S, Advani SH: T- cell prolymphocytic leukemia - a rare case. Indian J Cancer; 2005 Apr-Jun;42(2):104-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T- cell prolymphocytic leukemia - a rare case.
  • T- cell Prolymhocytic leukemia (T-PLL) is a rare mature post-thymic T-cell malignancy that is usually reported in the elderly and follows an aggressive course.
  • T- PLL is a rare T cell disorder with characteristic clinical and laboratory features.
  • [MeSH-major] Leukemia, Prolymphocytic / diagnosis
  • [MeSH-minor] Aged. Bone Marrow Cells / pathology. Diagnosis, Differential. Humans. Male. Weight Loss

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  • (PMID = 16141512.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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50. Okamura K, Ikeda T, Shimakura Y, Yoshiba F, Kishi K, Ando K, Hotta T: [Allogeneic bone marrow transplantation for chemotherapy-resistant T-prolymphocytic leukemia]. Rinsho Ketsueki; 2005 Jul;46(7):527-31
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  • [Title] [Allogeneic bone marrow transplantation for chemotherapy-resistant T-prolymphocytic leukemia].
  • Leukocyte count at diagnosis was 17,900/microl with 58% atypical lymphocytes having a convoluted nucleus and prominent nucleoli.
  • The patient was treated with Ara-C and etoposide before conditioning to decrease the high leukemia burden.
  • Because 9.4% of residual recipient type T-cells was seen with STR analysis on day 22, we decreased the dose of Cs'A.
  • After the occurrence of mild acute GVHD, the residual T-cell number decreased.
  • [MeSH-major] Bone Marrow Transplantation. Graft vs Leukemia Effect. Leukemia, Prolymphocytic / therapy. Leukemia, T-Cell / therapy
  • [MeSH-minor] Adult. Combined Modality Therapy. Female. Graft vs Host Disease / prevention & control. Humans. Remission Induction. Transplantation Conditioning. Transplantation, Homologous

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  • (PMID = 16440747.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 9
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51. Curtin NJ, Schwarer AP: Nonmyeloablative peripheral blood stem cell transplant for T-cell prolymphocytic leukaemia complicated by fulminant haemolysis and acute renal failure at engraftment secondary to minor ABO incompatibility. Clin Lab Haematol; 2005 Jun;27(3):206-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonmyeloablative peripheral blood stem cell transplant for T-cell prolymphocytic leukaemia complicated by fulminant haemolysis and acute renal failure at engraftment secondary to minor ABO incompatibility.
  • We present a 54-year-old man who underwent human leucocyte antigen-identical sibling nonmyeloablative peripheral blood stem cell transplant for primary refractory T-cell prolymphocytic leukaemia (T-PLL).
  • [MeSH-major] ABO Blood-Group System / adverse effects. Acute Kidney Injury / etiology. Blood Group Incompatibility / complications. Hematopoietic Stem Cell Transplantation / adverse effects. Hemolysis. Leukemia, Prolymphocytic / complications. Leukemia, T-Cell / complications

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  • (PMID = 15938729.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABO Blood-Group System
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52. Mikaelsson E, Danesh-Manesh AH, Lüppert A, Jeddi-Tehrani M, Rezvany MR, Sharifian RA, Safaie R, Roohi A, Osterborg A, Shokri F, Mellstedt H, Rabbani H: Fibromodulin, an extracellular matrix protein: characterization of its unique gene and protein expression in B-cell chronic lymphocytic leukemia and mantle cell lymphoma. Blood; 2005 Jun 15;105(12):4828-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fibromodulin, an extracellular matrix protein: characterization of its unique gene and protein expression in B-cell chronic lymphocytic leukemia and mantle cell lymphoma.
  • Fibromodulin is an extracellular matrix protein normally produced by collagen-rich tissues; the fibromodulin gene has been found to be the most overexpressed gene in B-cell chronic lymphocytic leukemia.
  • In this study, fibromodulin was expressed at the gene level (reverse transcription-polymerase chain reaction [RT-PCR]) in all patients with B-CLL (n = 75) and in most (5 of 7) patients with mantle cell lymphoma (MCL).
  • Fibromodulin was also detected at the protein level in the cytoplasm of the B-CLL cells and in the supernatant after in vitro cultivation, but not at the cell surface.
  • Fibromodulin was not found in patients with T-cell chronic lymphocytic leukemia (T-CLL), B-cell prolymphocytic leukemia (B-PLL), T-cell prolymphocytic leukemia (T-PLL), hairy cell leukemia, follicular lymphoma, lymphoplasmacytic lymphoma, multiple myeloma, acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), or chronic myelogenous leukemia (CML) or in 36 hematologic cell lines.
  • [MeSH-major] Extracellular Matrix / metabolism. Extracellular Matrix Proteins / chemistry. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Lymphoma, Mantle-Cell / metabolism. Proteoglycans / chemistry
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / biosynthesis. Antigens, CD19 / biosynthesis. Antigens, CD5 / biosynthesis. Antigens, Differentiation, T-Lymphocyte / biosynthesis. Biomarkers, Tumor / metabolism. Blotting, Western. Cell Line, Transformed. Cell Line, Tumor. Coculture Techniques. Collagen / metabolism. Cytoplasm / metabolism. DNA Mutational Analysis. DNA, Complementary / metabolism. Female. Fibroblasts / metabolism. Flow Cytometry. Hematologic Neoplasms / metabolism. Humans. Immunoblotting. Lectins, C-Type. Leukemia, T-Cell / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Mutation. Palatine Tonsil / metabolism. RNA, Messenger / metabolism. Receptors, Interleukin-2 / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Tetradecanoylphorbol Acetate / pharmacology. Time Factors

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  • (PMID = 15741214.001).
  • [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 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD5; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / CD69 antigen; 0 / DNA, Complementary; 0 / Extracellular Matrix Proteins; 0 / Lectins, C-Type; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / Receptors, Interleukin-2; 126468-95-9 / fibromodulin; 9007-34-5 / Collagen; NI40JAQ945 / Tetradecanoylphorbol Acetate
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53. Singhal M, Raina V, Gupta R, Das P: T cell-prolymphocytic leukemia detected in a patient of breast cancer at the time of recurrence: a case report. Cases J; 2010;3:4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T cell-prolymphocytic leukemia detected in a patient of breast cancer at the time of recurrence: a case report.
  • It includes acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS); however T-cell prolymphocytic leukemia (T-PLL) has not been described earlier in relation to breast cancer and its therapy.
  • T-PLL is a rare chronic T-cell lymphoproliferative disease with a mature post-thymic T-cell immunophenotype and aggressive clinical course.
  • She was doing well on follow up until the completion of fifth year of her disease, when she presented with complaints of mild fever and weakness.
  • Peripheral blood examination revealed medium sized lymphoid cells, constituting almost 75% of total nucleated cell population.
  • Immunophenotying, established a diagnosis of post thymic T-cell prolymphocytic leukemia.
  • Unfortunately, both her malignancies progressed after an initial stable disease of two months.
  • CONCLUSION: Our case describes the potential of breast chemotherapy to cause grave second hematological malignancies of the T-cell lymphoid lineage, not described earlier.

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  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):791-8 [19124806.001]
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  • (PMID = 20076807.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2806858
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54. Jeong KH, Lew BL, Sim WY: Generalized leukaemia cutis from a small cell variant of T-cell prolymphocytic leukaemia presenting with exfoliative dermatitis. Acta Derm Venereol; 2009;89(5):509-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Generalized leukaemia cutis from a small cell variant of T-cell prolymphocytic leukaemia presenting with exfoliative dermatitis.
  • T-cell prolymphocytic leukaemia (T-PLL) is a rare, aggressive neoplasm of mature T lymphocytes.
  • The small cell variant occurs in approximately 20% of T-PLL patients.
  • The skin findings of leukaemia consist of leukaemia-specific skin lesions, which are infiltrated by leukaemia cells, and non-specific lesions.
  • The former type of lesion signifies leukaemia cutis.
  • Leukaemia cutis presents clinically as tumours, nodules, or patches on the scalp, face and trunk.
  • We suspected a hidden malignancy and diagnosed small cell variant T-PLL through blood and bone marrow examination.
  • Most of the atypical lymphocytes stained positively with CD markers such as CD2, CD3, CD4, CD5, CD7 and CD8, thereby confirming the presence of leukaemia cells.
  • To our knowledge, this is the first case of generalized leukaemia cutis from small cell variant of T-PLL presenting with exfoliative dermatitis over the whole body.
  • [MeSH-major] Dermatitis, Exfoliative / etiology. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemic Infiltration. Skin / pathology. T-Lymphocytes / pathology

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  • (PMID = 19734979.001).
  • [ISSN] 1651-2057
  • [Journal-full-title] Acta dermato-venereologica
  • [ISO-abbreviation] Acta Derm. Venereol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; VB0R961HZT / Prednisone
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55. Meeuse JJ, Sprenger HG, van Assen S, Leduc D, Daenen SM, Arends JP, van der Werf TS: Rhodococcus equi infection after alemtuzumab therapy for T-cell prolymphocytic leukemia. Emerg Infect Dis; 2007 Dec;13(12):1942-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rhodococcus equi infection after alemtuzumab therapy for T-cell prolymphocytic leukemia.
  • [MeSH-major] Actinomycetales Infections / etiology. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / adverse effects. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Leukemia, Prolymphocytic, T-Cell / drug therapy. Rhodococcus equi

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  • [Cites] Blood. 2001 Sep 15;98(6):1721-6 [11535503.001]
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  • (PMID = 18258054.001).
  • [ISSN] 1080-6040
  • [Journal-full-title] Emerging infectious diseases
  • [ISO-abbreviation] Emerging Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ PMC2876741
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56. Fidani L, Hatzitolios AI, Goulas A, Savopoulos C, Basayannis C, Kotsis A: Cholesteryl ester transfer protein TaqI B and lipoprotein lipase Ser447Ter gene polymorphisms are not associated with ischaemic stroke in Greek patients. Neurosci Lett; 2005 Aug 12-19;384(1-2):102-5
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  • Cholesteryl ester transfer protein (CETP) and lipoprotein lipase (LPL) are both key players in plasma lipoprotein homeostasis and, as such, genetically induced alterations in their respective activities may affect susceptibility to cerebrovascular diseases.
  • In this study, we examined the distribution of two common polymorphisms, namely CETP TaqI B and LPL Ser447Ter in a cohort of Greek clinically diagnosed late-onset ischaemic stroke patients (n = 98) and an ethnicity-, age- and sex-matched control group with no manifestations of vascular disease (n = 100).
  • [MeSH-minor] Aged. Aged, 80 and over. Case-Control Studies. Cholesterol Ester Transfer Proteins. Female. Gene Frequency. Genetic Predisposition to Disease. Greece / epidemiology. Humans. Male. Odds Ratio

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  • (PMID = 15896905.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CETP protein, human; 0 / Carrier Proteins; 0 / Cholesterol Ester Transfer Proteins; 0 / Glycoproteins; 452VLY9402 / Serine; EC 3.1.1.34 / Lipoprotein Lipase
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57. Klobusicka M, Kusenda J, Stevulova L, Kovarikova A, Babusikova O: Possible prognostic value of nucleolar morphology in pathologic cells of B-chronic lymphocytic leukemia. Neoplasma; 2010;57(5):429-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possible prognostic value of nucleolar morphology in pathologic cells of B-chronic lymphocytic leukemia.
  • B-cell chronic lymphocytic leukemia (B-CLL) represents a heterogeneous disease with a very variable outcome.
  • The reliable prognosis of this disease at the time of initial diagnosis is difficult to predict.
  • The purpose of this preliminary study was to utilize the nucleolar morphology and to investigate the incidence of main nucleolar types in leukemic lymphocytes in B-CLL patients to assess their possible predictive value for the disease outcome, in correlation with immunophenotype parameters.
  • The evaluation of nucleolar morphology of pathologic lymphocytes was performed at diagnosis and during the course of disease.
  • Median follow up period of patients was 16.4 months (range from 2 to 32 months) from diagnosis.
  • The presence of ring shaped and compact nucleoli in leukemic lymphocytes divided patients into two subgroups with different outcome of the disease.
  • The population of leukemic cells of a small group of B-CLL patients (Group 2, 13 patients, 15.4%) was characterized by the presence of various proportions of pathologic lymphocytes with one large compact nucleolus.Different response to the therapy discriminated the B-CLL patients whose leukemic lymphocytes revealed evident compact nucleoli at presentation, to next two subsets.
  • None of our B-CLL patients had the signs of transformation to prolymphocytic or other type of B cell neoplasms during the follow up.
  • The simplicity and utility of the nucleolar test as a possible prognostic parameter may help to identify the subset of patients with early B-CLL disease that will run a more progressive course.
  • [MeSH-major] Cell Nucleolus / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphocytes / ultrastructure

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  • (PMID = 20568897.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] EC 3.2.2.5 / Antigens, CD38
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58. Hofbauer SW, Piñón JD, Brachtl G, Haginger L, Wang W, Jöhrer K, Tinhofer I, Hartmann TN, Greil R: Modifying akt signaling in B-cell chronic lymphocytic leukemia cells. Cancer Res; 2010 Sep 15;70(18):7336-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modifying akt signaling in B-cell chronic lymphocytic leukemia cells.
  • Emerging evidence suggests that the survival of B-cell chronic lymphocytic leukemia (CLL) cells is dependent on microenvironmental influences such as antigenic stimulation and support by stromal cells.
  • We investigated the role of Akt and its modulation by the protooncogene T-cell leukemia 1a (Tcl1a) in the survival pathways of primary CLL samples and CLL-derived prolymphocytic cell lines MEC-1 and MEC-2.
  • Akt activation was increased by the protective presence of human bone marrow stromal cells and B-cell receptor mimicking signals but antagonized by direct Akt blockade with the novel specific inhibitor AiX, with preferential apoptosis induction in CLL cells with an unmutated immunoglobulin status, which predicts poor clinical outcome.
  • In contrast, decreasing Tcl1a levels by small interfering RNA reduced Akt activation in the fludarabine-insensitive CLL cell line MEC-2 and sensitized the malignant cells to fludarabine treatment.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Humans. Oxazines / pharmacology. RNA, Small Interfering / genetics. Signal Transduction. Transfection

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  • [Copyright] ©2010 AACR.
  • (PMID = 20823161.001).
  • [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 / Enzyme Inhibitors; 0 / Oxazines; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / TCL1A protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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59. Trageser D, Iacobucci I, Nahar R, Duy C, von Levetzow G, Klemm L, Park E, Schuh W, Gruber T, Herzog S, Kim YM, Hofmann WK, Li A, Storlazzi CT, Jäck HM, Groffen J, Martinelli G, Heisterkamp N, Jumaa H, Müschen M: Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function. J Exp Med; 2009 Aug 3;206(8):1739-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function.
  • B cell lineage acute lymphoblastic leukemia (ALL) arises in virtually all cases from B cell precursors that are arrested at pre-B cell receptor-dependent stages.
  • Here, we demonstrate that the pre-B cell receptor functions as a tumor suppressor upstream of IKAROS through induction of cell cycle arrest in Ph(+) ALL cells.
  • Pre-B cell receptor-mediated cell cycle arrest in Ph(+) ALL cells critically depends on IKAROS function, and is reversed by coexpression of the dominant-negative IKAROS splice variant IK6.
  • IKAROS also promotes tumor suppression through cooperation with downstream molecules of the pre-B cell receptor signaling pathway, even if expression of the pre-B cell receptor itself is compromised.
  • In this case, IKAROS redirects oncogenic BCR-ABL1 tyrosine kinase signaling from SRC kinase-activation to SLP65, which functions as a critical tumor suppressor downstream of the pre-B cell receptor.
  • These findings provide a rationale for the surprisingly high frequency of IKAROS deletions in Ph(+) ALL and identify IKAROS-mediated cell cycle exit as the endpoint of an emerging pathway of pre-B cell receptor-mediated tumor suppression.

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  • (PMID = 19620627.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009659-16; None / None / / R01 CA137060-01A1; United States / NCI NIH HHS / CA / T32 CA009659; United States / NCI NIH HHS / CA / R01 CA090321; United States / NCI NIH HHS / CA / R01CA090321; United States / NCI NIH HHS / CA / R21 CA152497; None / None / / R01 CA137060-02; None / None / / R01 CA139032-01; United States / NCI NIH HHS / CA / R01CA137060; United States / NCI NIH HHS / CA / R01 CA139032-02; None / None / / R01 CA139032-02; United States / NCI NIH HHS / CA / R01 CA139032-01; United States / NCI NIH HHS / CA / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA137060-02; United States / NCI NIH HHS / CA / R01 CA137060-01A1; None / None / / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA139032; United States / NCI NIH HHS / CA / R01CA139032; United States / NCI NIH HHS / CA / R01 CA137060
  • [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 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / IKZF1 protein, human; 0 / Pre-B Cell Receptors; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC2722172
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60. Dixit M, Choudhuri G, Mittal B: Association of lipoprotein receptor, receptor-associated protein, and metabolizing enzyme gene polymorphisms with gallstone disease: A case-control study. Hepatol Res; 2006 Sep;36(1):61-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of lipoprotein receptor, receptor-associated protein, and metabolizing enzyme gene polymorphisms with gallstone disease: A case-control study.
  • INTRODUCTION: To identify high risk alleles for gallstone disease, we analyzed association of LDLRAvaII, LRPAP1 insertion/deletion, CETPTaqI B, and LPLHindIII polymorphisms with gallstone disease.
  • RESULTS: LRPAP1 gene insertion/deletion polymorphism was found to be significantly associated with gallstone disease.
  • Genotype II was conferring significant risk for gallstone disease in females only (P=0.019; OR 2.577, 95% CI 1.144-5.806).
  • LDLRAvaII, CETPTaqI B, and LPLHindIII polymorphisms were not found to be associated with gallstone disease either at genotype or allele level.
  • CONCLUSIONS: LRPAP1, II genotype carrier females may have increased risk for gallstone disease.
  • On the other hand, LDLR AvaII, CETP TaqI B, and LPL HindIII polymorphisms may not be associated with gallstone disease.

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  • (PMID = 16837242.001).
  • [ISSN] 1386-6346
  • [Journal-full-title] Hepatology research : the official journal of the Japan Society of Hepatology
  • [ISO-abbreviation] Hepatol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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61. Lundin J, Karlsson C, Celsing F: Alemtuzumab therapy for severe autoimmune hemolysis in a patient with B-cell chronic lymphocytic leukemia. Med Oncol; 2006;23(1):137-9
Genetic Alliance. consumer health - Leukemia, B-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab therapy for severe autoimmune hemolysis in a patient with B-cell chronic lymphocytic leukemia.
  • B-cell chronic lymphocytic leukemia (B-CLL) is the most common cause of autoimmune hemolytic anemia (AIHA), and a subgroup of these patients who develop both these conditions fail to respond to corticosteroids, cytotoxic drugs, splenectomy, and iv immunoglobulins.
  • Alemtuzumab is a humanized anti-CD52 monoclonal antibody that is an effective therapy for B-CLL, mycosis fungoides, and T-cell prolymphocytic leukemia.
  • Here we present a case report of a 78-yr-old woman with B-CLL and progressive life-threatening AIHA with hemoglobin count 5.5 g/dL following fludarabine treatment, who was treated successfully with alemtuzumab.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / complications

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  • (PMID = 16645240.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
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62. Dong HY, Weisberger J, Liu Z, Tugulea S: Immunophenotypic analysis of CD103+ B-lymphoproliferative disorders: hairy cell leukemia and its mimics. Am J Clin Pathol; 2009 Apr;131(4):586-95
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotypic analysis of CD103+ B-lymphoproliferative disorders: hairy cell leukemia and its mimics.
  • CD103 is characteristically expressed in hairy cell leukemia (HCL), a B-lymphoproliferative disorder highly responsive to treatment with purine analogs.
  • Other CD103+ diseases are rare and do not respond well to the same therapy, including HCL variant (HCLv) and splenic marginal zone B-cell lymphoma (SMZL) variants.
  • The CD25- cases had variable morphologic features ranging from HCLv and SMZL to prolymphocytic leukemia and diffuse large B-cell lymphoma.
  • Clinically, patients with CD25- disease tended to be older (P= .001), typically had leukocytosis (P= .014), and did not respond well to cladribine or pentostatin.
  • While HCL coexpresses CD25 and annexin-A1, diseases lacking CD25 and annexin-A1 behave clinically differently and can be separated from HCL on diagnosis.
  • [MeSH-major] Antigens, CD / biosynthesis. Integrin alpha Chains / biosynthesis. Interleukin-2 Receptor alpha Subunit / biosynthesis. Leukemia, Hairy Cell / classification. Receptors, Peptide / biosynthesis
  • [MeSH-minor] Diagnosis, Differential. Flow Cytometry. Humans. Immunohistochemistry. Immunophenotyping. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology

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  • (PMID = 19289595.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Integrin alpha Chains; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Peptide; 0 / alpha E integrins; 0 / annexin-A1 receptor, human
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63. Watanabe N, Takahashi T, Sugimoto N, Tanaka Y, Kurata M, Matsushita A, Maeda A, Nagai K, Nasu K: Excellent response of chemotherapy-resistant B-cell-type chronic lymphocytic leukemia with meningeal involvement to rituximab. Int J Clin Oncol; 2005 Oct;10(5):357-61
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Excellent response of chemotherapy-resistant B-cell-type chronic lymphocytic leukemia with meningeal involvement to rituximab.
  • A 70-year-old woman was diagnosed with B-cell-type chronic lymphocytic leukemia (B-CLL) in May 2001.
  • Initial white blood cell (WBC) count was 37 x 10(9)/l and most of the cells were mature small lymphocytes.
  • The surface phenotype of these cells was identical to that of circulating lymphocytes, indicating meningeal involvement of leukemia, a rare complication in B-CLL.
  • At the time of this WBC elevation, 24% of circulating lymphocytes had prominent nucleoli, indicating progression of the disease to CLL/prolymphocytic leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Meningeal Neoplasms / therapy

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  • (PMID = 16247665.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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64. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Nair R, Sengar M, Nair C: Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia. Indian J Cancer; 2010 Apr-Jun;47(2):189-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia.
  • INTRODUCTION: Mature T/NK cell lymphomas (MTNKL) presenting as leukemia are rare and show considerable overlapping of clinical, morphological and immunophenotypic features.
  • MATERIALS AND METHODS: We reviewed 380 consecutive cases of mature lymphoid neoplasm that presented as leukemia and were diagnosed on morphology and immunophenotyping of bone marrow and/or peripheral blood samples.
  • MTNKL constituted 4% (nine cases) of all mature lymphoid neoplasms presenting as leukemia.
  • It included four cases of T-large granular leukemia (T-LGL), two of T-cell prolymphocytic leukemia small cell variant (T-PLL), two of adult T-cell leukemia/lymphoma (ATLL) and one of primary cutaneous gamma delta T-cell lymphoma (PCGDTCL).
  • One case of T- PLL small cell variant showed CD4+/CD8- phenotype, while the other revealed CD4-/CD8+ phenotype.
  • CONCLUSION: Mature nodal T/NK cell neoplasms are rare and MTNKL presenting as leukemia are even rarer.
  • There is an overlap between the immunophenotypic profiles of different MTNKL subtypes and elaborate T/NK cell panels are required for their evaluation.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, T-Cell / diagnosis
  • [MeSH-minor] Adult. Aged. Bone Marrow / immunology. Bone Marrow / pathology. Diagnosis, Differential. Female. Flow Cytometry. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 20448385.001).
  • [ISSN] 1998-4774
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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65. Duek A, Shvidel L, Braester A, Berrebi A: Clinical and immunologic aspects of B chronic lymphocytic leukemia associated with autoimmune disorders. Isr Med Assoc J; 2006 Dec;8(12):828-31
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  • [Title] Clinical and immunologic aspects of B chronic lymphocytic leukemia associated with autoimmune disorders.
  • BACKGROUND: Autoimmune disorders often develop during the course of B chronic lymphocytic leukemia.
  • We evaluated the lymphocyte morphology, immunoglobulin G and beta-2-microglobulin serum levels and positivity of the CD38 and FMC7 markers, and compared these values with those of a matched CLL population without autoimmune disorder.
  • We found atypical prolymphocytic morphology in 22%, high expression of the activation antigens CD38 and/or FMC7 in 30%, and high level of immunoglobulin G (> 1000 mg/dl) and beta-2-microglobulin in 57% and 78% respectively.
  • When compared with a matched CLL population without an autoimmune disorder, these values were statistically significant.
  • CONCLUSIONS: Our data, which show activated lymphocyte morphology, high levels of IgG and beta-2-microglobulin, and increased expression of CD38 and/or FMC7 in a significant number of cases, suggest that some degree of activation of B cells may lead to the occurrence of an autoimmune disorder in CLL.
  • [MeSH-major] Autoimmune Diseases / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

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  • [CommentIn] Isr Med Assoc J. 2006 Dec;8(12):864 [17214107.001]
  • (PMID = 17214095.001).
  • [ISSN] 1565-1088
  • [Journal-full-title] The Israel Medical Association journal : IMAJ
  • [ISO-abbreviation] Isr. Med. Assoc. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Biomarkers; 0 / Immunoglobulin G; 0 / beta 2-Microglobulin; EC 3.2.2.5 / Antigens, CD38
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66. Meyerson HJ, MacLennan G, Husel W, Cocco A, Tse W, Lazarus HM, Kaplan D: D cyclins in CD5+ B-cell lymphoproliferative disorders: cyclin D1 and cyclin D2 identify diagnostic groups and cyclin D1 correlates with ZAP-70 expression in chronic lymphocytic leukemia. Am J Clin Pathol; 2006 Feb;125(2):241-50
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  • [Title] D cyclins in CD5+ B-cell lymphoproliferative disorders: cyclin D1 and cyclin D2 identify diagnostic groups and cyclin D1 correlates with ZAP-70 expression in chronic lymphocytic leukemia.
  • We analyzed protein expression of cyclin D1, cyclin D2, and cyclin D3 using high-resolution enzymatic amplification staining and flow cytometry in the neoplastic cells from 80 patients with CD5+ B-cell lymphoproliferative disorders.
  • The D cyclins were expressed differentially in chronic lymphocytic leukemia (CLL), prolymphocytic leukemia (PLL), and mantle cell lymphoma (MCL) with strong staining of cyclin D1 and D2 in MCL, strong staining of cyclin D1 but weak staining of cyclin D2 in 4 of 5 PLLs, and low-level staining for both cyclins in most CLLs.
  • The results indicate that flow cytometric analysis of D cyclins may help in classification of CD5+ B-cell lymphoproliferative disorders.
  • [MeSH-major] Antigens, CD5 / analysis. Cyclin D1 / analysis. Cyclins / analysis. Leukemia, Lymphocytic, Chronic, B-Cell / classification. Leukemia, Prolymphocytic / classification. Lymphoma, Mantle-Cell / classification. ZAP-70 Protein-Tyrosine Kinase / analysis
  • [MeSH-minor] Antigens, CD38 / analysis. Cell Proliferation. Cyclin D2. Flow Cytometry. Humans. Phosphatidylinositol 3-Kinases / physiology

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  • [ErratumIn] Am J Clin Pathol. 2006 May;125(5):796. Cocco, Amy [added]
  • (PMID = 16393687.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA77428
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 136601-57-5 / Cyclin D1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38
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67. Osuji N, Del Giudice I, Matutes E, Morilla A, Owusu-Ankomah K, Morilla R, Dunlop A, Catovksy D: CD52 expression in T-cell large granular lymphocyte leukemia--implications for treatment with alemtuzumab. Leuk Lymphoma; 2005 May;46(5):723-7
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  • [Title] CD52 expression in T-cell large granular lymphocyte leukemia--implications for treatment with alemtuzumab.
  • Few reports on the successful treatment of T-cell large granular lymphocyte (LGL) leukemia with the humanized anti-CD52 monoclonal antibody alemtuzumab are emerging in the literature.
  • Using semi-quantitative 2- and 3-color flow cytometry, we documented the expression of CD52 in 100% of abnormal cells in T-cell LGL leukemia (n = 11) and natural killer (NK) cell LGL leukemia (n = 2), and showed no significant difference in CD52 expression between T-cell prolymphocytic leukemia (PLL) and T-cell LGL leukemia.
  • Higher CD52 expression has been noted in responders to alemtuzumab in T-cell PLL and in chronic lymphocytic leukemia (CLL), a B-cell disorder.
  • The strong and consistent expression of CD52 shown here highlights the potential role of alemtuzumab in the treatment of refractory T-cell LGL leukemia and possibly aggressive NK cell leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / biosynthesis. Antigens, Neoplasm / biosynthesis. Antineoplastic Agents / therapeutic use. Glycoproteins / biosynthesis. Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / immunology. Leukemia, T-Cell / drug therapy

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  • (PMID = 16019510.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
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68. Dai HP, Xue YQ, Zhang J, Wu YF, Pan JL, Wang Y, Shen J: Translocation t(2;8)(p12;q24) in two patients with B Cell chronic lymphocytic leukemia. Acta Haematol; 2008;120(4):232-6
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  • [Title] Translocation t(2;8)(p12;q24) in two patients with B Cell chronic lymphocytic leukemia.
  • In this study, we report for the first time on 2 cases of chronic lymphocytic leukemia (CLL) with t(2;8).
  • They were diagnosed as having typical CLL (case 1) and CLL/prolymphocytic leukemia (case 2), respectively, based on morphology and immunophenotyping.
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 8. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Translocation, Genetic

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19246886.001).
  • [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 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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69. Kurihara K, Harashima N, Hanabuchi S, Masuda M, Utsunomiya A, Tanosaki R, Tomonaga M, Ohashi T, Hasegawa A, Masuda T, Okamura J, Tanaka Y, Kannagi M: Potential immunogenicity of adult T cell leukemia cells in vivo. Int J Cancer; 2005 Mar 20;114(2):257-67
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  • [Title] Potential immunogenicity of adult T cell leukemia cells in vivo.
  • Experimental vaccines targeting human T cell leukemia virus type-I (HTLV-I) Tax have been demonstrated in a rat model of HTLV-I-induced lymphomas.
  • However, the scarcity of HTLV-I-expression and the presence of defective HTLV-I-proviruses in adult T cell leukemia (ATL) cells have raised controversy about the therapeutic potential of HTLV-I-targeted immunotherapy in humans.
  • In flow cytometric analysis, we found that 3 of 5 acute-type and six of fifteen chronic-type ATL patients tested showed significant induction of HTLV-I Tax and Gag in their ATL cells in a 1-day culture.
  • Representative CTL epitopes restricted by HLA-A2 or A24 were conserved in 4 of 5 acute-type ATL patients tested.
  • Furthermore, spleen T cells from rats, which had been subcutaneously inoculated with formalin-fixed uncultured ATL cells, exhibited a strong interferon gamma-producing helper T cell responses specific for HTLV-I Tax-expressing cells.
  • Our study indicated that ATL cells from about half the patients tested readily express HTLV-I antigens including Tax in vitro, and that ATL cells express sufficient amounts of Tax or Tax-induced antigens to evoke specific T cell responses in vivo.
  • [MeSH-minor] Adult. Aged. Animals. Base Sequence. DNA Primers. Female. Humans. Japan. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemia, Prolymphocytic, T-Cell / virology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology. Male. Middle Aged. Polymerase Chain Reaction. Rats. Rats, Inbred F344. Reference Values. Transplantation, Heterologous / pathology

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551352.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers
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70. 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.
  • He remains alive and well seven months after initial diagnosis.
  • [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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71. Mahshid Y, Lisy MR, Wang X, Spanbroek R, Flygare J, Christensson B, Björkholm M, Sander B, Habenicht AJ, Claesson HE: High expression of 5-lipoxygenase in normal and malignant mantle zone B lymphocytes. BMC Immunol; 2009;10:2
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  • In order to better understand and define the role of 5-LO in B cells, we investigated the expression of 5-LO mRNA and protein in subsets of B cells from human tonsils and different types of B cell lymphoma.
  • This pattern of 5-LO expression was preserved in malignant lymphoma with high expression in mantle B cell lymphoma (MCL) and weak or no expression in follicular lymphoma.
  • Primary leukemized MCL, so called B-prolymphocytic leukaemia cells, and MCL cell lines also expressed 5-LO and readily produced LTB4 after activation.
  • [MeSH-major] Arachidonate 5-Lipoxygenase / biosynthesis. B-Lymphocyte Subsets / enzymology. B-Lymphocytes / enzymology. Leukemia, Prolymphocytic, B-Cell / enzymology. Lymphoma, Follicular / enzymology. Lymphoma, Mantle-Cell / enzymology
  • [MeSH-minor] Blotting, Western. Cell Differentiation. Cell Line. Cell Transformation, Neoplastic. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Leukemic. Humans. Immunity, Cellular. Immunologic Memory. Immunophenotyping. Leukotriene B4 / secretion. Lymphocyte Activation. Microscopy, Fluorescence. Palatine Tonsil / cytology. Palatine Tonsil / immunology. Polymerase Chain Reaction. Signal Transduction

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  • (PMID = 19134178.001).
  • [ISSN] 1471-2172
  • [Journal-full-title] BMC immunology
  • [ISO-abbreviation] BMC Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 1HGW4DR56D / Leukotriene B4; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase
  • [Other-IDs] NLM/ PMC2631017
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72. Wang ZY, Chen QS: [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Apr;13(2):169-73
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  • [Title] [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial].
  • One of the important approaches for further prolonging remission duration and eradicating minimal residual disease in acute leukemia is immunotherapy.
  • Four kinds of immunotherapy for acute leukemia are under investigation:.
  • (1) monoclonal antibodies, among them, Mylotarg (cytotoxic antibiotic calicheamicin linked to CD33 Mab) is given for the treatment of refractory or relapsed acute myeloid leukemia and molecular relapse in acute promyelocytic leukemia with good results, Campath-1H (antiCD52 Mab) is administered in the treatment of prolymphocytic leukemia and Rituximab (anti-CD20 Mab) in B-PLL with high complete remission rates.
  • Other Mabs under preclinical and clinical trials include anti-IL-2 receptor Mab for the treatment of acute T lymphocytic leukemia, anti-220 kD Mab-6G7 for acute leukemias, recombinant immune toxin BL22 (anti-CD22) for hairy cell leukemia and Mabs labeled with radio-isotopes for different types of acute leukemias;.
  • (2) adoptive cellular immunotherapy using cytokine-induced killer cell, alloreactive NK cells, allogeneic or autologous leukemic-specific CD8(+) cytotoxic T lymphocytes, and other immune effector cells;.
  • (4) leukemia vaccines of several different formulations including antigen-specific, leukemia cell-based, leukemia antigen-pulsed dendritic cell (DC) and leukemia-derived DC vaccines, the latter two formulations are more attractive.
  • In conclusion, up to now, the most effective example of immunotherapy in acute leukemia is provided by the administration of Mabs, and the majority of other approaches in immunotherapy for acute leukemia although promising, need further studies.

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  • (PMID = 15854271.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Editorial; English Abstract
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines
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73. Machii T, Chou T, Suzuki M, Ohe Y, Katagiri S, Kitano EK, Kitano K, Fujiyama Y, Izumi T, Shimazaki C, Nanba K, Ohashi Y, Kitani T, Cladribine Study Group: Phase II clinical study of cladribine in the treatment of hairy cell leukemia. Int J Hematol; 2005 Oct;82(3):230-5
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  • [Title] Phase II clinical study of cladribine in the treatment of hairy cell leukemia.
  • We conducted a phase II clinical study to evaluate the therapeutic efficacy of cladribine (2-chlorodeoxyadenosine [2-CdA]) in the treatment of Japanese patients with hairy cell leukemia (HCL).
  • Seven patients with classic HCL and 3 with a prolymphocytic HCL variant were administered 2-CdA (0.09 mg/kg per day) by continuous intravenous infusion for 7 days.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Cladribine / administration & dosage. Leukemia, Hairy Cell / drug therapy

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  • (PMID = 16207596.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 47M74X9YT5 / Cladribine
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74. Wang J, Hasui K, Utsunomiya A, Jia X, Matsuyama T, Murata F: Association of high proliferation in adult T-cell leukemia cells with apoptosis, and expression of p53 protein in acute type ATL. J Clin Exp Hematop; 2008 Apr;48(1):1-10
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  • [Title] Association of high proliferation in adult T-cell leukemia cells with apoptosis, and expression of p53 protein in acute type ATL.
  • Proliferation, apoptosis and p53 protein expression in adult T-cell leukemia (ATL) cells were investigated.
  • Twenty peripheral blood tissue specimens (PBTS) comprising 7 cases of acute type ATL, 7 cases of chronic type ATL and 6 other leukemias were examined by means of antigen retrieval and the polymer method employing anti-Ki67 antigen (MIB-1), anti-cleaved caspase-3, anti-single stranded DNA and three kinds of anti-p53 protein antibodies including DO7.
  • Most acute and chronic cases of ATL included more than 10% MIB-1-positive proliferating leukemia cells and more than 1% cleaved caspase-3-positive apoptotic cells.
  • Some cells which were positive for both MIB-1 and anti-cleaved caspase-3 antibody were observed in acute type ATL.
  • Nuclear deposition of p53 protein labeled by DO7 was often found in acute type (p < 0.05).
  • Within the medium-sized population of ATL cell nuclei, DO7-positive ATL cells had a smaller nuclear area factor (long axis x short axis) than DO7-negative ATL cells.
  • A few proliferating ATL cells entered apoptosis, and the appearance of a subclone of ATL cells with nuclear deposition of p53 protein labeled by DO7 characterized acute type.
  • [MeSH-major] Apoptosis / physiology. Cell Proliferation. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 18434687.001).
  • [ISSN] 1346-4280
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 3.4.22.- / Caspase 3
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75. Stano-Kozubik K, Malcikova J, Tichy B, Kotaskova J, Borsky M, Hrabcakova V, Francova H, Valaskova I, Bourkova L, Smardova J, Doubek M, Brychtova Y, Pospisilova S, Mayer J, Trbusek M: Inactivation of p53 and amplification of MYCN gene in a terminal lymphoblastic relapse in a chronic lymphocytic leukemia patient. Cancer Genet Cytogenet; 2009 Feb;189(1):53-8
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  • [Title] Inactivation of p53 and amplification of MYCN gene in a terminal lymphoblastic relapse in a chronic lymphocytic leukemia patient.
  • B-cell chronic lymphocytic leukemia (CLL) is an incurable disease with a highly variable clinical course.
  • A recent association has been observed between the presence of aberrant somatic hypermutations in leukemic cells (hypermutations occurring outside of the immunoglobulin locus) and the transformation to a diffuse large B-cell lymphoma or prolymphocytic leukemia.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Nuclear Proteins / genetics. Oncogene Proteins / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 19167613.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MYCN protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins; 0 / Tumor Suppressor Protein p53
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76. Takizawa M, Matsushima T, Yokohama A, Handa H, Tsukamoto N, Karasawa M, Murakami H, Nojima Y: [Unclassified mature T cell leukemia with cerebriform nuclei]. Rinsho Ketsueki; 2005 Jul;46(7):486-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Unclassified mature T cell leukemia with cerebriform nuclei].
  • Adult T cell leukemia (ATL) and Sézary syndrome (SS) were ruled out because of the negative HTLV-1 test and the absence of skin lesions, respectively.
  • T-prolymphocytic leukemia (T-PLL), which is characterized by a marked increase in leukocytes having a CD7-phenotype and a progressive fatal course, was also excluded.
  • Recently, the TCL1 onco-protein has been shown to be overexpressed in progressive T-PLL but not in other mature T cell leukemias including Sézary syndrome.
  • In its morphology and phenotypes, our case resembled 'Sézary cell leukemia (SCL)' but the clinical course was much more indolent.
  • This case did not match any of the mature T cell leukemias defined in the WHO classification.
  • [MeSH-major] Cell Nucleus / ultrastructure. Leukemia, T-Cell / diagnosis

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  • (PMID = 16440739.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human
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77. Narat S, Gandla J, Dogan A, Mehta A: Successful treatment of hairy cell leukemia variant with rituximab. Leuk Lymphoma; 2005 Aug;46(8):1229-32
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  • [Title] Successful treatment of hairy cell leukemia variant with rituximab.
  • Hairy cell leukemia (HCL) variant is a rare low-grade B-cell disorder affecting the elderly or middle-aged population with features intermediate between those of HCL and prolymphocytic leukemia.
  • We report a case of a 53-year-old man who had refractory thrombocytopenia and lymphocytosis for 8 years.
  • Investigations and analysis of spleen and bone marrow revealed a diagnosis of HCL variant.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Hairy Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Cell Count. Humans. Male. Middle Aged. Remission Induction / methods. Rituximab. Treatment Outcome

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  • (PMID = 16085567.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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78. Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M: Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma. Int J Hematol; 2007 Apr;85(3):212-8
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  • [Title] Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
  • We analyzed NOTCH1 gene mutation in 53 adults with mature T-cell leukemia/lymphoma: 21 patients with adult T-cell leukemia (ATL), 25 with T-cell non-Hodgkin's lymphoma (T-NHL), and 7 with T-cell prolymphocytic leukemia.
  • We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an ATL patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-cell lymphoma-unspecified (PTCL-u).
  • These findings suggest that nonsense mutation in the PEST domain in the ATL case was associated with NOTCH1 signaling through a pathway different from that for T-cell acute lymphoblastic leukemia (T-ALL).
  • Although NOTCH1 mutation occurs infrequently in mature T-cell leukemia/lymphoma, NOTCH1 may be involved in leukemogenesis associated with various forms of T-cell leukemia/lymphoma rather than only with T-ALL.
  • [MeSH-major] Codon, Nonsense. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Receptor, Notch1 / genetics

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  • (PMID = 17483057.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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79. Reindl L, Bacher U, Dicker F, Alpermann T, Kern W, Schnittger S, Haferlach T, Haferlach C: Biological and clinical characterization of recurrent 14q deletions in CLL and other mature B-cell neoplasms. Br J Haematol; 2010 Oct;151(1):25-36

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  • [Title] Biological and clinical characterization of recurrent 14q deletions in CLL and other mature B-cell neoplasms.
  • 14q-deletions have been repeatedly described in mature B-cell neoplasms, but not yet characterized in a larger cohort.
  • Based on chromosome banding analysis, the present study identified 47 del(14q) cases in 3054 mature B-cell neoplasms (1·5%) (chronic lymphocytic leukaemia [CLL]: 1·9%; CLL/prolymphocytic leukaemia [PL]: 9·0%; others: 0·2%).
  • In conclusion, the del(14q) is a rare recurrent alteration in diverse mature B-cell neoplasms, shows variable size but distinct clustering of breakpoints, and is associated with short time to treatment.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 14 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Prolymphocytic / genetics

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20649559.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region
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80. Ishigaki T, Sasaki K, Watanabe K, Nakamura N, Toyota S, Kobayashi H, Tohda S: Amplification of IGH/CCND1 fusion gene in a primary plasma cell leukemia case. Cancer Genet Cytogenet; 2010 Aug;201(1):62-5
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  • [Title] Amplification of IGH/CCND1 fusion gene in a primary plasma cell leukemia case.
  • The IGH/CCND1 fusion gene has been reported in many hematologic tumors such as mantle cell lymphoma, chronic lymphocytic leukemia, prolymphocytic leukemia, multiple myeloma, and plasma cell leukemia.
  • We report a case of plasma cell leukemia showing five IGH/CCND1 fusion signals by interphase fluorescence in situ hybridization (FISH).
  • The amplification of the IGH/CCND1 fusion gene may contribute to the aggressive course of the disease.
  • To our knowledge, this is the first case showing amplification of the IGH/CCND1 gene in plasma cell neoplasms.
  • [MeSH-major] Cyclin D1 / genetics. Immunoglobulin Heavy Chains / genetics. Leukemia, Plasma Cell / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20633772.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / Immunoglobulin Heavy Chains; 136601-57-5 / Cyclin D1
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81. Calfa CJ, Lossos IS, Ruiz P, Davis JL: Ocular involvement as the initial manifestation of T-cell chronic lymphocytic leukemia. Am J Ophthalmol; 2007 Aug;144(2):326-9
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  • [Title] Ocular involvement as the initial manifestation of T-cell chronic lymphocytic leukemia.
  • PURPOSE: To present a case of T-cell chronic lymphocytic leukemia (T-CLL) manifesting as an intraocular lymphoma.
  • Morphologic, immunohistochemical, flow cytometry, and molecular analysis by polymerase chain reaction of vitreous fluid, peripheral blood, bone marrow aspirate, and biopsy were performed.
  • RESULTS: Cytofluorographic and molecular analysis of vitreous cells demonstrated a monoclonal T-cell population consistent with a T-cell intraocular lymphoma.
  • Systemic evaluation established diagnosis of T-cell CLL.
  • CONCLUSION: T-CLL is a rare disease with an aggressive clinical course.
  • We present a case of T-cell intraocular lymphoma as the initial manifestation of an otherwise asymptomatic T-CLL.
  • [MeSH-major] Eye Neoplasms / diagnosis. Leukemia, Prolymphocytic, T-Cell / diagnosis. Lymphoma, T-Cell, Peripheral / diagnosis. Vitreous Body / pathology
  • [MeSH-minor] Aged. Antibiotics, Antineoplastic / therapeutic use. Biomarkers, Tumor / genetics. Biopsy. Bone Marrow Cells / pathology. DNA, Neoplasm / analysis. Diagnosis, Differential. Female. Flow Cytometry. Fluorescein Angiography. Follow-Up Studies. Fundus Oculi. Humans. Immunohistochemistry. Pentostatin / therapeutic use. Polymerase Chain Reaction. Tomography, Optical Coherence. Vitrectomy

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  • (PMID = 17659976.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109335
  • [Publication-type] Case Reports; 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 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 395575MZO7 / Pentostatin
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82. Marx A, Müller-Hermelink HK, Hartmann M, Geissinger E, Zettl A, Adam P, Rüdiger T: [Lymphomas of the spleen]. Pathologe; 2008 Mar;29(2):136-42
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  • Exceptions include splenic marginal zone lymphomas and hepatosplenic T-cell lymphomas that are typically diagnosed from histological findings.
  • In addition, hairy-cell leukemia, LGL leukemia and T-cell prolymphocytic leukemia typically show characteristic patterns of infiltration in the spleen which may be diagnostically useful.
  • [MeSH-minor] Antigens, CD / analysis. Diagnosis, Differential. Humans. Leukemia, Hairy Cell / pathology. Leukemia, Prolymphocytic, T-Cell / pathology. Lymphoma, T-Cell / pathology. Splenectomy

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  • (PMID = 18214484.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
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83. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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84. Diop S, Letestu R, Orsolani D, Leboeuf Y, Le Tutour P, Thiam D, Diakhate L, Valensi F: [Expression of proliferation marker Ki 67 in chronic lymphocytic leukemia]. Dakar Med; 2005;50(2):65-8
Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.

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  • [Title] [Expression of proliferation marker Ki 67 in chronic lymphocytic leukemia].
  • [Transliterated title] Expression du marqueur de proliferation Ki 67 dans les leucemies lymphoides chroniques.
  • Chronic lymphocytic leukemia (CLL) is characterized by a clonal expansion of low proliferating mature B and T lymphocytes in the bone marrow and peripheral blood.
  • The nuclear antigen Ki 67 is a protein detected in G1, S, G2 and M phases of the cell cycle, but not in G0, and thus, is a widely accepted proliferation marker of Human tumors.
  • Our results allows to characterize between CLL: one group which proliferation rate (percentage of Ki 67 positive cells) was equal or less than 2%, represented by 14 cases (29,2%) with morphological aspect of typical CLL, one group which proliferation rate was between 3% and 9% represented by 32 cases (66,6%) with morphological aspect of polymorph CLL or prolymphocytic leukemia, and a last group with proliferation rate equal or up to 10% and corresponding to two cases (4,2%) of transformation of CLL to high grade Non Hodgkin lymphoma.
  • These data reinforce the notion that CLL is a disease with heterogeneity in clinical behavior, immunophenotype, cytogenetic, molecular aspects, and thus, prognostic.
  • [MeSH-major] Ki-67 Antigen / blood. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / blood. B-Lymphocytes / immunology. Biomarkers. Cell Division. Female. Flow Cytometry. Humans. Lymphocyte Activation. Male. Middle Aged. Retrospective Studies. T-Lymphocytes / immunology

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  • (PMID = 16295759.001).
  • [ISSN] 0049-1101
  • [Journal-full-title] Dakar médical
  • [ISO-abbreviation] Dakar Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Senegal
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / Ki-67 Antigen
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85. Mahmoud IS, Sughayer MA, Mohammad HA, Awidi AS, EL-Khateeb MS, Ismail SI: The transforming mutation E17K/AKT1 is not a major event in B-cell-derived lymphoid leukaemias. Br J Cancer; 2008 Aug 5;99(3):488-90
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] The transforming mutation E17K/AKT1 is not a major event in B-cell-derived lymphoid leukaemias.
  • Despite the major role of the AKT/PKB family of proteins in the regulation of many growth and survival mechanisms in the cell, and the increasing evidence suggesting that AKT disruption could play a key role in many human malignancies, no major mutations of AKT genes had been reported, until very recently when Carpten et al reported a novel transforming mutation (E17K) in the pleckstrin homology domain of the AKT1 gene in solid tumours.
  • Considering the importance of the PI3K/AKT pathway in mediating survival and antiapoptotic signals in the B-cell types of chronic lymphocytic leukaemia (CLL) and acute lymphoblastic leukaemia (ALL), we sequenced the AKT1 exon 3 for the above mentioned mutation in 87 specimens, representing 45 CLLs, 38 ALLs and 4 prolymphocytic leukaemia (PLL) cases, which are all of B-cell origin.
  • We conclude that this mutation is not a major event in B-cell-derived lymphoid leukaemias.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Transformation, Neoplastic / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Promyelocytic, Acute / genetics. Point Mutation. Proto-Oncogene Proteins c-akt / genetics

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  • (PMID = 18665177.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2527790
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86. Bacher U, Haferlach T, Schnittger S, Weiss T, Burkhard O, Bechtel B, Kern W, Haferlach C: Detection of a t(4;14)(p16;q32) in two cases of lymphoma showing both the immunophenotype of chronic lymphocytic leukemia. Cancer Genet Cytogenet; 2010 Jul 15;200(2):170-4
Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of a t(4;14)(p16;q32) in two cases of lymphoma showing both the immunophenotype of chronic lymphocytic leukemia.
  • Reciprocal IGH/14q32 translocations are detectable in 55-70% of patients with plasma cell myeloma; e.g., the adverse t(4;14)(p16;q32) fusing the IGH and FGFR3 genes (immunoglobulin heavy chain/fibroblast growth factor receptor 3).
  • In a minority of patients with B-lineage chronic lymphocytic leukemia (CLL), reciprocal IGH/14q32 translocations have been reported as well.
  • We describe the occurrence of a t(4;14)(p16;q32) in two lymphoma patients showing the immunophenotype of B-CLL, which, to our knowledge, is the first report on such an association.
  • Immunophenotyping revealed the phenotype of CLL/PLL (chronic lymphocytic leukemia/prolymphocytic leukemia).
  • These two cases with an t(4;14), but the immunophenotype of B-CLL, demonstrate the genetic variability of B-cell lymphomas and the potential of specific metaphase cultivation techniques using oligonucleotides to increase our insights in the genetic pathways of these heterogeneous disorders.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 4. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, B-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Female. Humans. Immunoglobulin Heavy Chains / genetics. Immunophenotyping. Male. Receptor, Fibroblast Growth Factor, Type 3 / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20620602.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; EC 2.7.10.1 / FGFR3 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 3
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87. Gandhi V, Tam C, O'Brien S, Jewell RC, Rodriguez CO Jr, Lerner S, Plunkett W, Keating MJ: Phase I trial of nelarabine in indolent leukemias. J Clin Oncol; 2008 Mar 1;26(7):1098-105
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of nelarabine in indolent leukemias.
  • PURPOSE: To test whether nelarabine is an effective agent for indolent leukemias and to evaluate whether there is a relationship between cellular pharmacokinetics of the analog triphosphate and clinical responses.
  • PATIENTS AND METHODS: Thirty-five patients with relapsed/refractory leukemias (n = 24, B-cell chronic lymphocytic leukemia and n = 11, T-cell prolymphocytic leukemia) were entered onto three different protocols.
  • Pharmacokinetics of plasma nelarabine and arabinosylguanine (ara-G) and of cellular ara-G triphosphate (ara-GTP) were similar in the two groups of diagnoses, and the elimination of ara-GTP from leukemia cells was slow (median, > 24 hours).
  • CONCLUSION: Nelarabine is an effective regimen against indolent leukemias, and combining it with fludarabine was most promising.
  • Determination of tumor cell ara-GTP levels may provide a predictive test for response to nelarabine.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Prolymphocytic, T-Cell / drug therapy

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  • (PMID = 18309944.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA57629; United States / NCI NIH HHS / CA / CA81534
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 0 / Arabinonucleotides; 60158CV180 / nelarabine; 72490-81-4 / 9-beta-D-arabinofuranosylguanosine 5'-triphosphate; 86-01-1 / Guanosine Triphosphate; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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88. Li ZQ, Chen HS, Liu EB, Sun Q, Fang LH, Sun FJ, Zhang PH, Yang QY, Qiu LG: [Clinicopathologic study of 15 splenectomy specimens of patients with hairy cell leukemia]. Zhonghua Bing Li Xue Za Zhi; 2009 Nov;38(11):769-73
Genetic Alliance. consumer health - Hairy Cell Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinicopathologic study of 15 splenectomy specimens of patients with hairy cell leukemia].
  • OBJECTIVE: To investigate the clinicopathologic features, diagnosis, differential diagnosis and the prognosis of hairy cell leukemia (HCL).
  • The abundant cytoplasm and prominent cell border resulted in a "fried egg" appearance.
  • Definite diagnosis of HCL requires a combined histological and immunohistochemical assessment of the splenectomy specimen, bone marrow biopsy and aspirate.
  • [MeSH-major] Leukemia, Hairy Cell / metabolism. Leukemia, Hairy Cell / pathology. Lymphoma, B-Cell, Marginal Zone / pathology. Spleen / pathology. Splenectomy
  • [MeSH-minor] Adult. Aged. Annexin A1 / metabolism. Antigens, CD11c / metabolism. Antigens, CD20 / metabolism. Antigens, CD45 / metabolism. Antigens, CD79 / metabolism. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Ki-67 Antigen / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Prolymphocytic / metabolism. Leukemia, Prolymphocytic / pathology. Lymphoma, Follicular / metabolism. Lymphoma, Follicular / pathology. Lymphoma, Mantle-Cell / metabolism. Lymphoma, Mantle-Cell / pathology. Male. Middle Aged. Retrospective Studies. Survival Rate

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  • (PMID = 20079018.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Annexin A1; 0 / Antigens, CD11c; 0 / Antigens, CD20; 0 / Antigens, CD79; 0 / Ki-67 Antigen; EC 3.1.3.48 / Antigens, CD45
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89. Umehara F, Hagiwara T, Yoshimura M, Higashi K, Arimura K: Enlarged, multifocal upper limb neuropathy with HTLV-I associated myelopathy in a patient with chronic adult T-cell leukemia. J Neurol Sci; 2008 Mar 15;266(1-2):167-70
Hazardous Substances Data Bank. GADOLINIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enlarged, multifocal upper limb neuropathy with HTLV-I associated myelopathy in a patient with chronic adult T-cell leukemia.
  • The authors herein describe a case of multifocal peripheral neuropathy with HTLV-I-associated myelopathy (HAM) in a patient with chronic adult T-cell leukemia (ATL).
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / complications. Paraparesis, Tropical Spastic / complications. Peripheral Nervous System Diseases / etiology. Peripheral Nervous System Diseases / pathology. Upper Extremity / pathology
  • [MeSH-minor] Blood Cell Count. Contrast Media. Female. Fluorodeoxyglucose F18. Gadolinium. Humans. Magnetic Resonance Imaging. Middle Aged. Neural Conduction / physiology. Neurologic Examination. Peripheral Nerves / pathology. Peripheral Nerves / physiopathology. Positron-Emission Tomography

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  • (PMID = 18096188.001).
  • [ISSN] 0022-510X
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Contrast Media; 0Z5B2CJX4D / Fluorodeoxyglucose F18; AU0V1LM3JT / Gadolinium
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90. Chen J, Petrus M, Bryant BR, Nguyen VP, Goldman CK, Bamford R, Morris JC, Janik JE, Waldmann TA: Autocrine/paracrine cytokine stimulation of leukemic cell proliferation in smoldering and chronic adult T-cell leukemia. Blood; 2010 Dec 23;116(26):5948-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autocrine/paracrine cytokine stimulation of leukemic cell proliferation in smoldering and chronic adult T-cell leukemia.
  • Adult T-cell leukemia (ATL), a heterogeneous disease, can be divided into smoldering, chronic, lymphoma, and acute types clinically.
  • Here, we demonstrated that smoldering/chronic ATL peripheral blood mononuclear cells spontaneously proliferated ex vivo in a cytokine (interleukin-12 [IL-12]/IL-9/IL-15)-dependent manner, while acute-type ATL peripheral blood mononuclear cells did not proliferate or proliferated independent of cytokines.
  • In conclusion, our data provide evidence that there is autocrine/paracrine cytokine stimulation of leukemic cell proliferation in patients with smoldering/chronic ATL that could be targeted for treatment.

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  • [Cites] J Immunol. 2001 Feb 15;166(4):2602-9 [11160322.001]
  • (PMID = 20858854.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cytokines
  • [Other-IDs] NLM/ PMC3031384
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91. Schweighofer CD, Fätkenheuer G, Staib P, Hallek M, Reiser M: Lyme disease in a patient with chronic lymphocytic leukemia mimics leukemic meningeosis. Onkologie; 2007 Nov;30(11):564-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lyme disease in a patient with chronic lymphocytic leukemia mimics leukemic meningeosis.
  • BACKGROUND: Involvement of the central nervous system (CNS) is a rare complication of chronic lymphocytic leukemia (CLL) and seems to be more frequent in patients with Richter's syndrome or prolymphocytic transformation.
  • PATIENT AND METHODS: We present the case of a 75-year-old male patient who was admitted to a rural hospital with ataxia, disorientation, and signs of progressive CLL disease.
  • RESULTS: When referred to our center, careful immunophenotyping of the CNS lymphocytes as well as assessment for infectious causes of lymphocytic meningitis led to the diagnosis of Lyme disease/neuroborreliosis.
  • CONCLUSION: In conclusion, this case report should alert clinicians that lymphocytic meningeal involvement in CLL patients accounts for the rare leukemic meningeosis only if cerebrospinal fluid cells show a predominating immunophenotype of typical BCLL cells, i.e. by flow cytometry, and if any infectious cause including Lyme disease has been ruled out.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Lyme Disease / complications. Lyme Disease / diagnosis. Meningitis / complications. Meningitis / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged


92. Zanesi N, Aqeilan R, Drusco A, Kaou M, Sevignani C, Costinean S, Bortesi L, La Rocca G, Koldovsky P, Volinia S, Mancini R, Calin G, Scott CP, Pekarsky Y, Croce CM: Effect of rapamycin on mouse chronic lymphocytic leukemia and the development of nonhematopoietic malignancies in Emu-TCL1 transgenic mice. Cancer Res; 2006 Jan 15;66(2):915-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of rapamycin on mouse chronic lymphocytic leukemia and the development of nonhematopoietic malignancies in Emu-TCL1 transgenic mice.
  • Chronic lymphocytic leukemia (CLL) is the most common leukemia in the world.
  • The TCL1 gene, responsible for prolymphocytic T cell leukemia, is also overexpressed in human B cell malignancies and overexpression of the Tcl1 protein occurs frequently in CLL.
  • Aging transgenic mice that overexpress TCL1 under control of the mu immunoglobulin gene enhancer, develop a CD5+ B cell lymphoproliferative disorder mimicking human CLL and implicating TCL1 in the pathogenesis of CLL.
  • This approach allowed us to verify the involvement of the Tcl1/Akt/mTOR biochemical pathway in the disease by testing the ability of a specific pharmacologic agent, rapamycin, to slow CLL.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Sirolimus / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Humans. Immunohistochemistry. Mice. Mice, Transgenic


93. Marie I, Robaday S, Kerleau JM, Jardin F, Levesque H: Typhlitis as a complication of alemtuzumab therapy. Haematologica; 2007 May;92(5):e62-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It is an effective immunotherapeutic agent in patients with malignancies such as non-Hodgkin lymphoma, B cell chronic lymphocytic leukemia and T cell pro- lymphocytic leukemia.
  • We recently observed a case of particular interest as the patient with T cell prolymphocytic leukaemia treated with alemtuzumab, exhibited symptomatic reactivation of CMV infection and developed subsequently typhlitis.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antibodies, Neoplasm / adverse effects. Antineoplastic Agents / adverse effects. Typhlitis / diagnosis. Typhlitis / etiology
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Female. Humans. Leukemia, Prolymphocytic / immunology. Leukemia, Prolymphocytic / therapy. Leukemia, T-Cell / immunology. Leukemia, T-Cell / therapy. Middle Aged

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  • (PMID = 17562596.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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94. Robak T: Novel drugs for chronic lymphoid leukemias: mechanism of action and therapeutic activity. Curr Med Chem; 2009;16(18):2212-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel drugs for chronic lymphoid leukemias: mechanism of action and therapeutic activity.
  • Chronic lymphoid leukemias include well defined mature B-cell and T-cell neoplasms with diverse natural history and specific morphological, immunophenotypic and molecular characteristics.
  • The most common adult leukemia in the Western world is chronic lymphocytic leukemia (CLL).
  • Rarer indolent lymphoid leukemias include prolymphocytic leukemia, hairy cell leukemia, large granular lymphocyte leukemia and T-cell leukemia/lymphoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Design. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

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  • (PMID = 19519388.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 230
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95. Geyeregger R, Shehata M, Zeyda M, Kiefer FW, Stuhlmeier KM, Porpaczy E, Zlabinger GJ, Jäger U, Stulnig TM: Liver X receptors interfere with cytokine-induced proliferation and cell survival in normal and leukemic lymphocytes. J Leukoc Biol; 2009 Nov;86(5):1039-48
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Liver X receptors interfere with cytokine-induced proliferation and cell survival in normal and leukemic lymphocytes.
  • Recent data indicate an additional role of LXR in immunity by controlling dendritic cell and T-cell function and in breast and prostate cancer cells.
  • Here, we show that LXR activation interferes with IL-2 and IL-7-induced proliferation and cell cycle progression of human T-cell blasts mainly through inhibited phosphorylation of the retinoblastoma protein and decreased expression of the cell cycle protein cyclin B.
  • Comparable results were obtained with IL-2-dependent chronic lymphoblastic leukemia (CLL) T cells.
  • Furthermore, we show for B-CLL cells that LXR are functionally active and inhibit expression of survival genes bcl-2 and MMP-9, and significantly reduce cell viability, suggesting an interference of LXR with cytokine-dependent CLL cell survival.
  • [MeSH-major] Cytokines / pharmacology. Leukemia / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Lymphocytes / immunology. Lymphocytes / pathology. Orphan Nuclear Receptors / physiology
  • [MeSH-minor] Antigens, CD / immunology. Cell Division / drug effects. Cell Survival / drug effects. Cholesterol / metabolism. Humans. Leukemia, Prolymphocytic, T-Cell / immunology. Leukemia, Prolymphocytic, T-Cell / pathology. Lipids / physiology. Methylphenazonium Methosulfate / pharmacology. T-Lymphocytes / immunology

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  • [CommentIn] J Leukoc Biol. 2009 Nov;86(5):1019-21 [19875628.001]
  • (PMID = 19671841.001).
  • [ISSN] 1938-3673
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cytokines; 0 / Lipids; 0 / Orphan Nuclear Receptors; 0 / liver X receptor; 299-11-6 / Methylphenazonium Methosulfate; 97C5T2UQ7J / Cholesterol
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96. Ravandi F, Kantarjian H, Jones D, Dearden C, Keating M, O'Brien S: Mature T-cell leukemias. Cancer; 2005 Nov 1;104(9):1808-18
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mature T-cell leukemias.
  • Mature T-cell and NK-cell leukemias are a group of relatively uncommon neoplasms derived from mature or postthymic T-cells accounting for a relatively small percentage of lymphoid malignancies.
  • The recent availability of modern immunophenotypic and molecular tools has allowed a better distinction of these disorders from their B-cell counterparts.
  • Herein, we review the clinical and pathological features of mature T-cell leukemias.
  • [MeSH-major] Leukemia, T-Cell / diagnosis
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Human T-lymphotropic virus 1. Humans. Immunophenotyping. Leukemia, Lymphoid. Leukemia, Prolymphocytic / diagnosis. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / genetics. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / virology. Middle Aged. Tumor Virus Infections

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 16136598.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 143
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97. Kardum-Skelin I, Planinc-Peraica A, Ostojić Kolonić S, Radić-Kristo D, Milas M, Vrhovac R, Sustercić D, Minigo H, Jaksić B: [Clinical and laboratory prognostic parameters for leukemic types of chronic lymphoproliferative diseases]. Acta Med Croatica; 2008 Oct;62(4):351-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Analysis was performed in the overall CLLPD population and separately in a subgroup of patients with B chronic lymphocytic leukemia with variants (B-CLL+V) including typical B chronic lymphocytic leukemia (B-CLL), mixed chronic lymphocytic leukemia and prolymphocytic leukemia (CLL/PLL), and a variant of chronic lymphocytic leukemia with lymphoplasmocytoid differentiation (CLL/IMC).
  • Poorer disease outcome was associated with interstitial and nodular infiltration found on bone biopsy.
  • Poorer prognosis was associated with red blood cell count <2.5 x 10(12)/L, leukocyte count >100 x 10(9)/L, reticulocyte count >5/10(3) E, hemoglobin <100 g/L and iron <15 mol/L.
  • CONCLUSION: Careful clinical examination is an important step on assessing the extent and progression of the disease, and a major chain on tailoring individualized therapeutic approach, along with clinical stages according to Rai and Binet, CLLPD subtype and progression factors (DTM and DTL).
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Prolymphocytic / pathology. Lymphoproliferative Disorders / pathology

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  • (PMID = 19205412.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
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98. Brüggemann M, White H, Gaulard P, Garcia-Sanz R, Gameiro P, Oeschger S, Jasani B, Ott M, Delsol G, Orfao A, Tiemann M, Herbst H, Langerak AW, Spaargaren M, Moreau E, Groenen PJ, Sambade C, Foroni L, Carter GI, Hummel M, Bastard C, Davi F, Delfau-Larue MH, Kneba M, van Dongen JJ, Beldjord K, Molina TJ: Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936. Leukemia; 2007 Feb;21(2):215-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936.
  • Polymerase chain reaction (PCR) assessment of clonal T-cell receptor (TCR) and immunoglobulin (Ig) gene rearrangements is an important diagnostic tool in mature T-cell neoplasms.
  • To obtain reference values for Ig/TCR rearrangement patterns, 19 European laboratories investigated 188 T-cell malignancies belonging to five World Health Organization-defined entities.
  • TCR clonality was detected in 99% (143/145) of all definite cases of T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia, peripheral T-cell lymphoma (unspecified) and angioimmunoblastic T-cell lymphoma (AILT), whereas nine of 43 anaplastic large cell lymphomas did not show clonal TCR rearrangements.
  • Our study indicates that the BIOMED-2 multiplex PCR tubes provide a powerful strategy for clonality assessment in T-cell malignancies assisting the firm diagnosis of T-cell neoplasms.
  • The detected TCR gene rearrangements can also be used as PCR targets for monitoring of minimal residual disease.
  • [MeSH-major] Genes, Immunoglobulin. Leukemia, T-Cell / genetics. Lymphoma, T-Cell / genetics. Polymerase Chain Reaction / methods. Receptors, Antigen, T-Cell / genetics
  • [MeSH-minor] Gene Amplification. Gene Rearrangement. Genotype. Humans. Immunohistochemistry. Leukemia, Prolymphocytic / genetics. Leukemia, Prolymphocytic / immunology. Leukemia, Prolymphocytic / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Large B-Cell, Diffuse / pathology. T-Lymphocytes / immunology

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  • (PMID = 17170730.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
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99. Lau SK, Weiss LM, Zhang Y, Huang Q: Prolymphocytoid transformation of follicular lymphoma with coexpression of CD5 and CD10. Leuk Lymphoma; 2006 Mar;47(3):541-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Histologic transformation of follicular lymphoma is usually to a diffuse large B-cell lymphoma.
  • We present a rare example of a histologic transformation of follicular lymphoma manifested by prolymphocytoid morphology and an unusual immunophenotype characterized by coexpression of CD5 and CD10.
  • Prolymphocytoid transformation, similar to other histologic forms of transformation of follicular lymphoma, appears to accompany clinical progression of disease.
  • [MeSH-major] Antigens, CD5 / biosynthesis. Cell Transformation, Neoplastic / pathology. Leukemia, Prolymphocytic / pathology. Lymphoma, Follicular / pathology. Neoplasms, Second Primary / pathology. Neprilysin / biosynthesis
  • [MeSH-minor] Adult. Disease Progression. Fatal Outcome. Female. Humans. Immunophenotyping. Remission Induction. Treatment Failure

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  • (PMID = 16396778.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD5; EC 3.4.24.11 / Neprilysin
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100. Weston VJ, Oldreive CE, Skowronska A, Oscier DG, Pratt G, Dyer MJ, Smith G, Powell JE, Rudzki Z, Kearns P, Moss PA, Taylor AM, Stankovic T: The PARP inhibitor olaparib induces significant killing of ATM-deficient lymphoid tumor cells in vitro and in vivo. Blood; 2010 Nov 25;116(22):4578-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Ataxia Telangiectasia Mutated (ATM) gene is frequently inactivated in lymphoid malignancies such as chronic lymphocytic leukemia (CLL), T-prolymphocytic leukemia (T-PLL), and mantle cell lymphoma (MCL) and is associated with defective apoptosis in response to alkylating agents and purine analogues.
  • We investigated in vitro sensitivity to the poly (ADP-ribose) polymerase inhibitor olaparib (AZD2281) of 5 ATM mutant lymphoblastoid cell lines (LCL), an ATM mutant MCL cell line, an ATM knockdown PGA CLL cell line, and 9 ATM-deficient primary CLLs induced to cycle and observed differential killing compared with ATM wildtype counterparts.
  • A nonobese diabetic/severe combined immunodeficient (NOD/SCID) murine xenograft model of an ATM mutant MCL cell line demonstrated significantly reduced tumor load and an increased survival of animals after olaparib treatment in vivo.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Phthalazines / therapeutic use. Piperazines / therapeutic use. Poly(ADP-ribose) Polymerase Inhibitors. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Ataxia Telangiectasia Mutated Proteins. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. DNA Damage / drug effects. Gene Knockdown Techniques. Humans. Mice. Mice, SCID. Mutation

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  • (PMID = 20739657.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G9901249; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Phthalazines; 0 / Piperazines; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; WOH1JD9AR8 / olaparib
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