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1. Patel AP, Ghatak SB, Patel JA: Long term survival in aggressive NK cell leukemia. Indian Pediatr; 2010 Sep;47(9):807-8
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  • [Title] Long term survival in aggressive NK cell leukemia.
  • Aggressive natural killer cell leukemia (ANKL) is a rare type of leukemia.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / drug therapy. Leukemia, Large Granular Lymphocytic / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Humans. Male. Prognosis. Remission Induction

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  • [CommentIn] Indian Pediatr. 2011 Jan;48(1):79-80 [21317480.001]
  • (PMID = 21048272.001).
  • [ISSN] 0974-7559
  • [Journal-full-title] Indian pediatrics
  • [ISO-abbreviation] Indian Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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2. Ichikawa S, Fukuhara N, Yamamoto J, Suzuki M, Nakajima S, Okitsu Y, Kohata K, Onishi Y, Ishizawa K, Kameoka J, Harigae H: Successful allogeneic hematopoietic stem cell transplantation for aggressive NK cell leukemia. Intern Med; 2010;49(17):1907-10
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  • [Title] Successful allogeneic hematopoietic stem cell transplantation for aggressive NK cell leukemia.
  • Aggressive natural killer cell leukemia (ANKL) is a highly aggressive lymphoproliferative disease.
  • An appropriate therapeutic strategy for ANKL remains to be established, but a few case reports have suggested that allogeneic hematopoietic stem cell transplantation (allo-HCT) can be curative.
  • Intensive remission induction chemotherapy followed by conventional myeloablative allo-HCT is a promising approach for long-term remission in cases of this aggressive malignancy.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / surgery. Peripheral Blood Stem Cell Transplantation

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  • (PMID = 20823655.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Myeloablative Agonists; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 3.5.1.1 / Asparaginase; UM20QQM95Y / Ifosfamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; CHOP protocol
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3. Skorupa A, Chaudhary UB, Lazarchick J: Cold agglutinin induced autoimmune hemolytic anemia and NK-cell leukemia: a new association. Am J Hematol; 2007 Jul;82(7):668-71
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  • [Title] Cold agglutinin induced autoimmune hemolytic anemia and NK-cell leukemia: a new association.
  • Cold agglutinin induced autoimmune hemolytic anemia is uncommonly associated with leukemia and lymphomas.
  • We present a case of a young Mexican female presenting with a cold agglutinin hemolytic anemia with expression of a rare Pr antigen specificity and an aggressive NK-cell leukemia.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / metabolism. Anemia, Hemolytic, Autoimmune / pathology. Killer Cells, Natural / metabolism. Killer Cells, Natural / pathology. Leukemia / metabolism. Leukemia / pathology


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4. Alekshun TJ, Sokol L: Diseases of large granular lymphocytes. Cancer Control; 2007 Apr;14(2):141-50
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  • [Title] Diseases of large granular lymphocytes.
  • BACKGROUND: Clonal diseases of large granular lymphocytes (LGLs) are rare lymphoproliferative malignancies that arise from either mature T-cell (CD3+) or natural killer (NK)-cell (CD3-) lineages.
  • They manifest a distinct biologic behavior that ranges from indolent to very aggressive.
  • METHODS: We discuss four distinct diseases involving LGLs: indolent T-cell LGL leukemia, aggressive T-cell LGL leukemia, chronic NK-cell leukemia, and aggressive NK-cell leukemia.
  • RESULTS: Sustained LGLs, characteristic immunophenotype, clonal origin of leukemic cells, and clinical presentation are the most important features that distinguish indolent from aggressive subtypes of LGL leukemia and guide the selection of therapy.
  • Patients with symptomatic indolent T-cell or NK-cell LGL leukemia are usually treated with immunosuppressive therapies in contrast to aggressive T-cell and NK-cell LGL leukemia, which require intensive chemotherapy induction regimens.
  • CONCLUSIONS: Future scientific advances focusing on the delineation of molecular pathogenic mechanisms and the development of new targeted therapies for each distinct LGL leukemia entity should lead to improved outcomes of patients with these disorders.
  • [MeSH-major] Antigens, CD3. Killer Cells, Natural / pathology. Leukemia, Lymphoid / pathology. Leukemia, T-Cell / pathology. Lymphocytes / pathology

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  • (PMID = 17387299.001).
  • [ISSN] 1073-2748
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3
  • [Number-of-references] 71
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5. Sawada A, Sato E, Koyama M, Higuchi B, Kusuki S, Kim JY, Takeshita Y, Sakata A, Sakata N, Okamura T, Yasui M, Inoue M, Kawa K: NK-cell repertoire is feasible for diagnosing Epstein-Barr virus-infected NK-cell lymphoproliferative disease and evaluating the treatment effect. Am J Hematol; 2006 Aug;81(8):576-81

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  • [Title] NK-cell repertoire is feasible for diagnosing Epstein-Barr virus-infected NK-cell lymphoproliferative disease and evaluating the treatment effect.
  • Epstein-Barr virus (EBV) occasionally infects T and NK cells and causes EBV-infected T/NK-cell lymphoproliferative disease (LPD), which comprises chronic active EBV infection, EBV-associated hemophagocytic syndrome, mosquito allergy, hydroa vacciniforme, aggressive NK-cell leukemia, and NK/T-cell lymphoma.
  • The diagnosis is proven by the monoclonal proliferation of EBV-infected T or NK cells, which is a time-consuming and complicated method.
  • T-cell monoclonality is helpful for the screening of EBV-infected T-cell LPD in patients with EBV-genome burden and is easily shown with T-cell-receptor rearrangement or the T-cell repertoire, whereas NK-cell monoclonality is difficult to prove due to its lacking such rearranged receptors.
  • We investigated a set of killer immunoglobulin-like receptors (KIRs) and also CD94-NKG2 heterodimers on NK cells, namely the NK-cell repertoire.
  • Skewed repertoires were seen in all patients with EBV-infected NK-cell LPD, but not in any patients with EBV-infected T-cell LPD and were restored only after successful treatment.
  • The normal KIR repertoire is variable for each individual and it seems difficult to detect minimal residual EBV-infected lymphocytes.
  • However, the NK-cell repertoire is feasible for identifying EBV-infected NK-cell LPD and evaluating the treatment effect.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Epstein-Barr Virus Infections / immunology. Killer Cells, Natural / immunology. Killer Cells, Natural / virology. Lymphoproliferative Disorders / immunology. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Biomarkers / analysis. Biomarkers / metabolism. Child. Child, Preschool. Disease Progression. Drug Evaluation. Female. Humans. Infant. Male. Recurrence. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 16823820.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
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6. Ino K, Masuya M, Nakamori Y, Suzuki K, Mizutani M, Sekine T, Yamaguchi M, Nakase K, Kaida K, Ogawa H, Katayama N: [Aggressive NK-cell leukemia with sustained relapse-free survival after allogeneic peripheral blood stem cell transplantation]. Rinsho Ketsueki; 2010 Apr;51(4):258-63
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  • [Title] [Aggressive NK-cell leukemia with sustained relapse-free survival after allogeneic peripheral blood stem cell transplantation].
  • A bone marrow examination showed several hemophagocytic macrophages, and a diagnosis of hemophagocytic syndrome was made.
  • A repeat bone marrow examination demonstrated that 28.4% of marrow nucleated cells were atypical lymphocytes, which were positive for CD2, CD7, CD16, CD56, and HLA-DR.
  • Clonality of these proliferating NK cells was confirmed by an analysis of EB virus terminal repeat sequence and cytogenetic analysis, and final diagnosis of aggressive NK-cell leukemia was made.
  • He received allogeneic peripheral blood stem cell transplantation from his one locus mismatched son, and is alive with no evidence of disease 20 months after transplantation.
  • [MeSH-major] Killer Cells, Natural. Leukemia, Lymphoid / therapy. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Antigens, CD. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Herpesvirus 4, Human / genetics. Humans. Male. Middle Aged. Remission Induction. Terminal Repeat Sequences. Transplantation, Homologous


7. Suzuki R, Suzumiya J, Yamaguchi M, Nakamura S, Kameoka J, Kojima H, Abe M, Kinoshita T, Yoshino T, Iwatsuki K, Kagami Y, Tsuzuki T, Kurokawa M, Ito K, Kawa K, Oshimi K, NK-cell Tumor Study Group: Prognostic factors for mature natural killer (NK) cell neoplasms: aggressive NK cell leukemia and extranodal NK cell lymphoma, nasal type. Ann Oncol; 2010 May;21(5):1032-40
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  • [Title] Prognostic factors for mature natural killer (NK) cell neoplasms: aggressive NK cell leukemia and extranodal NK cell lymphoma, nasal type.
  • BACKGROUND: Patients with natural killer (NK) cell neoplasms, aggressive NK cell leukemia (ANKL) and extranodal NK cell lymphoma, nasal type (ENKL), have poor outcome.
  • The purpose of this study is to draw a prognostic model of total NK cell neoplasms.
  • Using these four variables, an NK prognostic index was successfully constructed.
  • CONCLUSION: The current prognostic model successfully stratified patients with NK cell neoplasms with different outcomes.


8. Makishima H, Ito T, Momose K, Nakazawa H, Shimodaira S, Kamijo Y, Nakazawa Y, Ichikawa N, Ueno M, Kobayashi H, Kitano K, Saito H, Kiyosawa K, Ishida F: Chemokine system and tissue infiltration in aggressive NK-cell leukemia. Leuk Res; 2007 Sep;31(9):1237-45
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  • [Title] Chemokine system and tissue infiltration in aggressive NK-cell leukemia.
  • NK cell-type lymphoproliferative disease of granular lymphocytes can be subdivided into aggressive NK-cell leukemia (ANKL) and chronic NK-cell lymphocytosis (CNKL).
  • [MeSH-major] Chemokines / blood. Fas Ligand Protein / metabolism. Killer Cells, Natural / pathology. Leukemia, Lymphoid / blood. Lymphocytosis / blood

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  • (PMID = 17123604.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines; 0 / Fas Ligand Protein; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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9. Makishima H, Ito T, Asano N, Nakazawa H, Shimodaira S, Kamijo Y, Nakazawa Y, Suzuki T, Kobayashi H, Kiyosawa K, Ishida F: Significance of chemokine receptor expression in aggressive NK cell leukemia. Leukemia; 2005 Jul;19(7):1169-74
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  • [Title] Significance of chemokine receptor expression in aggressive NK cell leukemia.
  • Natural killer (NK) cell-type lymphoproliferative diseases of granular lymphocytes can be subdivided into aggressive NK cell leukemia (ANKL) and chronic NK cell lymphocytosis (CNKL).
  • The mechanisms of cell trafficking associated with the chemokine system have been investigated in NK cells.
  • To clarify the mechanism of systemic migration of leukemic NK cells, we enrolled nine ANKL and six CNKL cases, and analyzed the expression profiles and functions of chemokine receptors by flowcytometry and chemotaxis assay.
  • CXCR1 was detected on NK cells in all groups, and CCR5 was positive in all ANKL cells.
  • Proliferating NK cells were simultaneously positive for CXCR1 and CCR5 in all ANKL patients examined, and NK cells with this phenotype did not expand in CNKL patients or healthy donors.
  • These results indicated that the chemokine system might play an important role in the pathophysiology of ANKL and that chemokine receptor profiling might be a novel tool for discriminating ANKL cells from benign NK cells.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Lymphoid / genetics. Lymphocytosis / genetics. Receptors, Chemokine / genetics
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / physiology. Cell Movement / drug effects. Cell Movement / physiology. Chemokines / pharmacology. Child. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Phenotype. Receptors, CCR5 / genetics. Receptors, CCR5 / physiology. Receptors, Interleukin-8A / genetics. Receptors, Interleukin-8A / physiology

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  • (PMID = 15902300.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chemokines; 0 / Receptors, CCR5; 0 / Receptors, Chemokine; 0 / Receptors, Interleukin-8A
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10. Sino-US Shanghai Leukemia Cooperative Group: [Aggressive NK-cell leukemia: report of nine cases and review of literature]. Zhonghua Xue Ye Xue Za Zhi; 2006 Feb;27(2):116-9
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  • [Title] [Aggressive NK-cell leukemia: report of nine cases and review of literature].
  • OBJECTIVE: To improve the diagnostic accuracy of aggressive NK-cell leukemia (ANKL).
  • The disease had an aggressive clinical course.
  • (2) Neutropenia, anemia and thrombocytopenia with high number of circulating large granular lymphocytes;.
  • (3) large granular lymphocytes infiltrated in bone marrow aspirate and core biopsy;.
  • No T-cell receptor (TCR) genes rearrangement;.
  • (6) No unique karyotypic abnormality, sometimes del (6) (q21q25);.
  • (7) Exclusion of other diseases with large granular lymphocytosis.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / diagnosis

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  • (PMID = 16732967.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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11. Makishima H: [Analysis of chemokine receptor expression in aggressive NK-cell leukemia and chronic NK-cell lymphocytosis]. Rinsho Ketsueki; 2008 Jan;49(1):3-9
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  • [Title] [Analysis of chemokine receptor expression in aggressive NK-cell leukemia and chronic NK-cell lymphocytosis].
  • [MeSH-major] Chemokines / genetics. Chemokines / physiology. Killer Cells, Natural. Leukemia, Lymphoid / genetics. Leukemia, Lymphoid / pathology. Lymphocytosis / genetics. Lymphocytosis / pathology. Receptors, Chemokine / genetics. Receptors, Chemokine / physiology

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  • (PMID = 18277590.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Chemokines; 0 / Receptors, CCR5; 0 / Receptors, Chemokine; 0 / Receptors, Interleukin-8A
  • [Number-of-references] 20
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12. Nakashima Y, Tagawa H, Suzuki R, Karnan S, Karube K, Ohshima K, Muta K, Nawata H, Morishima Y, Nakamura S, Seto M: Genome-wide array-based comparative genomic hybridization of natural killer cell lymphoma/leukemia: different genomic alteration patterns of aggressive NK-cell leukemia and extranodal Nk/T-cell lymphoma, nasal type. Genes Chromosomes Cancer; 2005 Nov;44(3):247-55
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  • [Title] Genome-wide array-based comparative genomic hybridization of natural killer cell lymphoma/leukemia: different genomic alteration patterns of aggressive NK-cell leukemia and extranodal Nk/T-cell lymphoma, nasal type.
  • Natural killer (NK) cell lymphomas/leukemias are highly aggressive lymphoid malignancies, but little is known about their genomic alterations, and thus there is an urgent need for identification and analysis of NK cell lymphomas/leukemias.
  • We performed an array CGH analysis for 27 NK-cell lymphoma/leukemia cases that were classified into two disease groups based on the World Health Organization Classification (10 aggressive NK-cell leukemia cases and 17 extranodal NK/T-cell [NK/T] lymphomas, nasal type).
  • The recurrent regions characteristic of the aggressive NK-cell leukemia group compared with those of the extranodal NK/T lymphoma, nasal-type group, were gain of 1q and loss of 7p15.1-p22.3 and 17p13.1.
  • Recurrent regions characteristic of the extranodal NK/T lymphoma, nasal-type group, compared with those of the other group were gain of 2q, and loss of 6q16.1-q27, 11q22.3-q23.3, 5p14.1-p14.3, 5q34-q35.3, 1p36.23-p36.33, 2p16.1-p16.3, 4q12, and 4q31.3-q32.1.
  • Our results can be expected to provide further insights into the genetic basis of lymphomagenesis and the clinicopathologic features of NK-cell lymphomas/leukemias.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Genome, Human. Killer Cells, Natural / pathology. Leukemia, T-Cell / genetics. Lymphoma, T-Cell / genetics. Nose Neoplasms / genetics

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16049916.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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13. Suzuki R: Treatment of advanced extranodal NK/T cell lymphoma, nasal-type and aggressive NK-cell leukemia. Int J Hematol; 2010 Dec;92(5):697-701
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  • [Title] Treatment of advanced extranodal NK/T cell lymphoma, nasal-type and aggressive NK-cell leukemia.
  • Extranodal NK/T cell lymphoma, nasal type (ENKL) with advanced stage and aggressive NK-cell leukemia (ANKL) are highly aggressive neoplasms with a dismal clinical outcome.
  • This is a major reason for the refractoriness to conventional chemotherapeutic regimens for malignant lymphoma containing anthracycline.
  • ANKL needs another treatment strategy because of a systemic disease progression and extensive organ insufficiency.
  • Optimal treatment scheme using such effective agents for these unfavorable NK-cell tumors should further be explored.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Killer Cells, Natural / pathology. Leukemia, T-Cell / therapy. Lymphoma, Extranodal NK-T-Cell / drug therapy

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  • (PMID = 21116747.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.1 / Asparaginase; UM20QQM95Y / Ifosfamide; YL5FZ2Y5U1 / Methotrexate
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14. Sasaki M, Sugimoto K, Kawahara S, Yasuda H, Suto H, Oshimi K: Rapid elimination of circulating leukemia cells with a small dose of alemtuzumab in refractory aggressive NK-cell leukemia. Eur J Haematol; 2007 Jun;78(6):545
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  • [Title] Rapid elimination of circulating leukemia cells with a small dose of alemtuzumab in refractory aggressive NK-cell leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphoid / drug therapy. Neoplastic Cells, Circulating

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  • (PMID = 17419749.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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15. Jaccard A, Petit B, Girault S, Suarez F, Gressin R, Zini JM, Coiteux V, Larroche C, Devidas A, Thiéblemont C, Gaulard P, Marin B, Gachard N, Bordessoule D, Hermine O: L-asparaginase-based treatment of 15 western patients with extranodal NK/T-cell lymphoma and leukemia and a review of the literature. Ann Oncol; 2009 Jan;20(1):110-6
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  • [Title] L-asparaginase-based treatment of 15 western patients with extranodal NK/T-cell lymphoma and leukemia and a review of the literature.
  • BACKGROUND: Extranodal natural killer (NK)/T-cell lymphoma, nasal type, and aggressive NK-cell leukemia are highly aggressive diseases with a poor outcome.
  • PATIENTS AND METHODS: We report a multicentric French retrospective study of 15 patients with relapsed, refractory, or disseminated disease, treated with L-asparaginase-containing regimens in seven French centers.
  • CONCLUSION: These data, although retrospective, confirm the excellent activity of L-asparaginase-containing regimens in refractory extranodal NK/T-cell lymphoma and aggressive NK-cell leukemia.
  • Therefore, L-asparaginase-based regimen should be considered as a salvage treatment, especially for patients with disseminated disease.
  • First-line L-asparaginase combination therapy for extranodal NK/T-cell lymphoma and aggressive NK-cell leukemia should be tested in prospective trials.

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  • (PMID = 18701429.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.5.1.1 / Asparaginase
  • [Number-of-references] 26
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16. Oshimi K, Kawa K, Nakamura S, Suzuki R, Suzumiya J, Yamaguchi M, Kameoka J, Tagawa S, Imamura N, Ohshima K, Kojya S, Iwatsuki K, Tokura Y, Sato E, Sugimori H, NK-cell Tumor Study Group: NK-cell neoplasms in Japan. Hematology; 2005 Jun;10(3):237-45
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  • [Title] NK-cell neoplasms in Japan.
  • Neoplasms putatively originating from precursor and mature natural killer (NK) cells are rare, and their clinical features are unclear.
  • A nationwide survey was performed in Japan to clarify the clinical features of these neoplasms diagnosed between 1994 and 1998, and data for 237 patients who met the criteria for putative NK cell-lineage neoplasms were analyzed.
  • Among them, 11 had myeloid/NK-cell precursor acute leukemia, 15 blastic NK-cell lymphoma, 21 precursor NK-cell acute lymphoblastic leukemia, 22 aggressive NK-cell leukemia/lymphoma, 149 nasal-type NK-cell lymphoma (123 nasal and 26 extranasal) and 19 chronic NK lymphocytosis.
  • The median overall survival time of patients with aggressive NK-cell leukemia/lymphoma was 2 months, which for chronic NK lymphocytosis was more than 8 years, and that for the other types of NK-cell neoplasms was between 6 and 22 months.
  • Nasal NK-cell lymphoma and extranasal NK-cell lymphoma share the same histology.
  • The age of affliction was the same, but the sex was different with males predominantly having nasal NK-cell lymphoma and females extranasal NK-cell lymphoma.
  • Patients with extranasal NK-cell lymphoma had the tendency to exhibit a more advanced state of disease, with significantly higher International Prognostic Index and LDH levels, and significantly lower hemoglobin and platelet levels.
  • Precursor NK-cell acute lymphoblastic leukemia and blastic NK-cell lymphoma were arbitrarily defined by the presence or absence of 30% or more of blastic cells in the bone marrow or peripheral blood, but there were no significant differences for affected age, gender, involved sites or prognosis.
  • Aggressive NK-cell leukemia/lymphoma and extranasal NK-cell lymphoma were arbitrarily defined by the presence or absence of 30% or more of large granular lymphocytes in the bone marrow or peripheral blood and it is possible that aggressive NK-cell leukemia/lymphoma is a leukemic phase of extranasal NK-cell lymphoma.
  • The incidence of skin involvement, however, was significantly higher for extranasal NK-cell lymphoma, suggesting that the two diseases are different.
  • In nasal NK-cell lymphoma, Epstein-Barr virus in tumor cells was detected in all patients tested, suggesting its causative role.
  • [MeSH-major] Killer Cells, Natural. Leukemia, Myeloid, Acute / mortality. Lymphoma / mortality. Nasopharyngeal Neoplasms / mortality
  • [MeSH-minor] Disease-Free Survival. Epstein-Barr Virus Infections / mortality. Epstein-Barr Virus Infections / pathology. Female. Herpesvirus 4, Human. Humans. Japan. Male. Survival Analysis

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  • (PMID = 16019472.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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17. Greer JP, Mosse CA: Natural killer-cell neoplasms. Curr Hematol Malig Rep; 2009 Oct;4(4):245-52
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  • [Title] Natural killer-cell neoplasms.
  • The natural killer (NK)-cell neoplasms are rare, representing less than 1% of non-Hodgkin lymphoma, except in Asia and Latin America, where they represent 3% to 6%.
  • NK-cell neoplasms include immature acute leukemias; a blastic NK-cell lymphoma, which is obsolete because of its plasmacytoid dendritic-cell origin; and mature NK neoplasms, comprising extranodal NK/T-cell lymphoma (ENKL), nasal-type; aggressive NK-cell leukemia; and chronic NK-cell lymphoproliferative disorders, which are often reactive.
  • Epstein-Barr virus is usually detected in tumor cells of ENKL and aggressive NK-cell leukemia.
  • The latter two mature NK neoplasms are relatively chemoresistant because of the frequent expression of P-glycoprotein.
  • Stem cell transplantation is recommended for advanced disease, owing to a poor prognosis.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia / pathology. Lymphoma / pathology. Lymphoproliferative Disorders / pathology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cell Lineage. Cell Transformation, Neoplastic. Humans. Stem Cell Transplantation

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  • (PMID = 20425414.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 42
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18. Ham MF, Ko YH: Natural killer cell neoplasm: biology and pathology. Int J Hematol; 2010 Dec;92(5):681-9

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  • [Title] Natural killer cell neoplasm: biology and pathology.
  • Natural killer (NK) cell neoplasm is a heterogeneous disease group.
  • In the latest World Health Organization (WHO) classification of tumours of hematopoietic and lymphoid tissues (2008), disease entities considered as NK-cell derivation include NK-lymphoblastic leukemia/lymphoma, chronic lymphoproliferative disorders of NK cells, aggressive NK-cell leukemia, and extranodal NK-cell lymphoma, nasal-type.
  • Despite recent advances in NK-cell research, which have expanded our understanding of the biology of NK-cell neoplasm, it cannot yet be sharply delineated from myeloid neoplasms and T-cell neoplasms even in some "well-known" entity, such as extranodal NK/T-cell lymphoma.
  • This review describes current knowledge of the biology of NK cells and pathology of NK neoplasms as classified in the 2008 WHO classification of tumours of hematopoietic and lymphoid tissues.
  • [MeSH-major] Killer Cells, Natural / pathology. Neoplasms / pathology
  • [MeSH-minor] Humans. Lymphoma, Extranodal NK-T-Cell / pathology. Lymphoproliferative Disorders / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 21132576.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
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19. Kawamata N, Inagaki N, Mizumura S, Sugimoto KJ, Sakajiri S, Ohyanagi-Hara M, Oshimi K: Methylation status analysis of cell cycle regulatory genes (p16INK4A, p15INK4B, p21Waf1/Cip1, p27Kip1 and p73) in natural killer cell disorders. Eur J Haematol; 2005 May;74(5):424-9
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  • [Title] Methylation status analysis of cell cycle regulatory genes (p16INK4A, p15INK4B, p21Waf1/Cip1, p27Kip1 and p73) in natural killer cell disorders.
  • Natural killer (NK) cell disorders are rare diseases.
  • In this study we analyze the methylation status of the genes associated with cell cycle regulation, including p16INK4A, p15INK4B, p21/Waf1/Cip1, p27/Kip1, p73, and p14ARF, by methylation specific (MS) PCR and/or bisulfite sequencing.
  • We examined 29 cases of NK cell disorders (five aggressive NK cell leukemia/lymphoma, three blastic NK cell lymphoma/leukemia, five nasal NK cell lymphoma, three myeloid/NK cell precursor acute leukemia, 13 chronic NK lymphocytosis).
  • We found methylation of the first exon of the p16INK4A gene in two cases (one aggressive, one blastic), and methylation of the p14ARF gene in one aggressive NK cell leukemia.
  • MS-PCR suggested that the p73 and p21 genes were methylated in seven cases, respectively (p73: one blastic, one nasal, five chronic; p21: one myeloid/NK, one aggressive, one nasal, and four chronic); bisulfite sequencing confirmed that methylated alleles of these genes were dominant in the samples except three cases (one myeloid/NK, one aggressive, and one chronic) in which methylated alleles of the p21 genes were less than 34% of all alleles.
  • These results suggested that inactivation of the cell cycle regulatory genes by DNA methylation could be associated with tumorigenesis in NK cell disorders, not only aggressive subtypes but also chronic subtype.
  • [MeSH-major] Cell Cycle / genetics. Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA Methylation. DNA-Binding Proteins / genetics. Killer Cells, Natural / physiology. Leukemia / genetics. Lymphoma / genetics. Nuclear Proteins / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Base Sequence. Chronic Disease. Cyclin-Dependent Kinase Inhibitor p15. Cyclin-Dependent Kinase Inhibitor p21. DNA Primers. Genes, Tumor Suppressor. Humans

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  • (PMID = 15813917.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
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20. 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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21. Gross SA, Zhu X, Bao L, Ryder J, Le A, Chen Y, Wang XQ, Irons RD: A prospective study of 728 cases of non-Hodgkin lymphoma from a single laboratory in Shanghai, China. Int J Hematol; 2008 Sep;88(2):165-73
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  • [Title] A prospective study of 728 cases of non-Hodgkin lymphoma from a single laboratory in Shanghai, China.
  • Diagnosis and classification was established in a single laboratory according to the 2001 WHO classification system.
  • The frequency of non-Hodgkin lymphoma was 87.6% (n = 728) and Hodgkin lymphoma was 12.4% (n = 103).
  • The most prevalent NHL subtypes diagnosed using WHO criteria were diffuse large B cell lymphoma (DLBCL), precursor B lymphoblastic leukemia/lymphoma and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL).
  • Although a low incidence has been reported in some Asian populations, CLL/SLL was commonly encountered, indicating that chronic lymphoid neoplasms are not rare in Shanghai.
  • Consistent with previous reports, our findings indicate a decrease in the frequency of follicular lymphoma and an increase in T cell neoplasms compared to the West.
  • Precursor T lymphoblastic leukemia/lymphoma, anaplastic large T cell lymphoma, aggressive NK cell leukemia, angioimmunoblastic T cell lymphoma and peripheral T cell lymphoma were prominent subtypes of T cell NHL.
  • [MeSH-major] Asian Continental Ancestry Group / statistics & numerical data. Lymphoma, Non-Hodgkin / classification. Lymphoma, Non-Hodgkin / ethnology

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  • (PMID = 18648906.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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22. Kim D, Ko Y, Suh Y, Koo H, Huh J, Lee W: Characteristics of Epstein-Barr virus associated childhood non-Hodgkin's lymphoma in the Republic of Korea. Virchows Arch; 2005 Sep;447(3):593-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characteristics of Epstein-Barr virus associated childhood non-Hodgkin's lymphoma in the Republic of Korea.
  • To analyze the clinicopathologic characteristics of childhood non-Hodgkin's lymphoma (NHL) associated with Epstein-Barr virus (EBV), EBER in situ hybridization was performed in 80 cases of NHLs.
  • EBER-positive lymphomas account for 25% (20/80) and include NK/T-cell lymphoma (6/6), aggressive NK-cell leukemia (1/1), peripheral T cell lymphoma (5/11), diffuse large B-cell lymphoma (5/14), hydroa-like T-cell lymphoma (1/1), marginal zone B-cell lymphoma (1/2), and post-transplantation lymphoproliferative disorder (1/1).
  • Other types including 19 cases of Burkitt's lymphoma were negative.
  • Clinically, patients with EBV-positive B-cell lymphomas were cured with chemotherapy, whereas EBV-associated NK- and T cell lymphomas pursued fatal clinical course.
  • In conclusion, EBVs infected in childhood NHLs are frequently associated not only with NK- and T- cell lymphomas but also large B-cell lymphomas.
  • [MeSH-major] Epstein-Barr Virus Infections / epidemiology. Lymphoma, Non-Hodgkin / virology. Tumor Virus Infections / epidemiology

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  • [Cites] Jpn J Cancer Res. 2000 Dec;91(12):1233-40 [11123421.001]
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  • (PMID = 15991005.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / EBNA-2 protein, Human herpesvirus 4; 0 / EBV-associated membrane antigen, Epstein-Barr virus; 0 / Epstein-Barr Virus Nuclear Antigens; 0 / RNA-Binding Proteins; 0 / Ribosomal Proteins; 0 / Viral Matrix Proteins; 0 / Viral Proteins; 135844-68-7 / RPL22 protein, human
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23. Kwong YL: Natural killer-cell malignancies: diagnosis and treatment. Leukemia; 2005 Dec;19(12):2186-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natural killer-cell malignancies: diagnosis and treatment.
  • Natural killer (NK)-cell malignancies are uncommon diseases.
  • Previously known as polymorphic reticulosis or angiocentric T-cell lymphomas, they are classified by the World Health Organization as NK/T-cell lymphoma, nasal type and aggressive NK-cell leukemia.
  • Pathologically, NK-cell lymphomas show a polymorphic neoplastic infiltrate with an angioinvasive and angiodestructive pattern.
  • Lymphoma cells are characteristically CD2+, CD56+ and cytoplasmic CD3epsilon+.
  • T-cell receptor gene is germline, and clonal Epstein-Barr virus (EBV) infection is almost invariably.
  • Clinically, they can be divided into nasal, non-nasal, and aggressive lymphoma/leukemia subtypes.
  • Most nasal NK-cell lymphomas present with stage I/II disease, and frontline radiotherapy is the most important key to successful treatment.
  • Chemotherapy is indicated for advanced nasal NK-cell lymphoma, and the non-nasal and aggressive subtypes.
  • High-dose chemotherapy with hematopoietic stem cell transplantation may be beneficial to selected patients.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia. Lymphoma

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  • (PMID = 16179910.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 83
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24. Ishida F, Kwong YL: Diagnosis and management of natural killer-cell malignancies. Expert Rev Hematol; 2010 Oct;3(5):593-602
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and management of natural killer-cell malignancies.
  • Natural killer (NK)-cell malignancies are uncommon neoplasms, which have been referred to as polymorphic reticulosis or angiocentric T-cell lymphomas in the past.
  • In the current WHO classification, they are categorized as extranodal NK/T-cell lymphoma, nasal type and aggressive NK-cell leukemia.
  • NK-cell malignancies show a geographical predilection for Asian and South American populations and are rare in the west.
  • Pathologically, NK-cell lymphomas show a polymorphic neoplastic infiltrate with angioinvasion and angiodestruction.
  • The lymphoma cells are CD2(+), cytoplasmic CD3ε(+) and CD56(+), with germline T-cell receptor gene.
  • Clinically, NK-cell lymphomas can be classified into nasal, non-nasal and aggressive lymphoma/leukemia subtypes.
  • Most nasal NK-cell lymphomas present with stage I/II disease.
  • Chemotherapy is indicated for stage III/IV nasal NK-cell lymphoma, and the non-nasal and aggressive subtypes.
  • High-dose chemotherapy and hematopoietic stem-cell transplantation with autologous or allogeneic hematopoietic stem cells may be beneficial to selected patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Asparaginase / administration & dosage. Killer Cells, Natural / drug effects. Leukemia / diagnosis. Leukemia / therapy. Lymphoma, Extranodal NK-T-Cell / diagnosis. Lymphoma, Extranodal NK-T-Cell / therapy
  • [MeSH-minor] Antigens, CD. Asia / epidemiology. Female. Hematopoietic Stem Cell Transplantation. Herpesvirus 4, Human. Humans. Male. Middle Aged. Prognosis. Recurrence. Severity of Illness Index. South America / epidemiology. Transplantation, Autologous

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  • (PMID = 21083476.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; EC 3.5.1.1 / Asparaginase
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25. Huang Q, Chang KL, Gaal KK, Weiss LM: An aggressive extranodal NK-cell lymphoma arising from indolent NK-cell lymphoproliferative disorder. Am J Surg Pathol; 2005 Nov;29(11):1540-3
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  • [Title] An aggressive extranodal NK-cell lymphoma arising from indolent NK-cell lymphoproliferative disorder.
  • Indolent NK-cell lymphoproliferative disorder, also known as chronic natural killer (NK) cell large granular lymphocytosis (leukemia), is a very rare entity in the World Health Organization (WHO) Classification of Tumors of Hematopoietic & Lymphoid Tissues.
  • Unlike aggressive NK-cell leukemia, which is malignant, the WHO does not specify whether indolent NK-cell lymphoproliferative disorder is reactive or neoplastic.
  • Patients with indolent NK-cell lymphoproliferative disorder are usually asymptomatic older adults who have a nonprogressive, very stable clinical course.
  • We report an unusual case of an aggressive extranodal NK-cell lymphoma, non-nasal type, which presented as a subcutaneous tissue mass, which apparently transformed from a preexisting, untreated indolent NK-cell lymphoproliferative disorder in an 65-year-old otherwise healthy white man.
  • The extranodal NK-cell lymphoma and the NK-cell lymphoproliferative disorder in the blood and bone marrow share a distinctive and identical NK-cell immunophenotype and genotype: CD56/CD8/TIA-1-positive and surface CD3-negative, negative for Epstein-Barr virus infection, and no evidence of T-cell and B-cell receptor gene rearrangements.
  • To the best of our knowledge, such aggressive lymphomatous transformation in an indolent NK-cell lymphoproliferative disorder has not been previously reported.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoproliferative Disorders / complications
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Disease Progression. Doxorubicin / therapeutic use. Fatal Outcome. Guillain-Barre Syndrome / etiology. Humans. Male. Prednisone / therapeutic use. Respiratory Insufficiency / etiology. Vincristine / therapeutic use

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  • (PMID = 16224224.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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26. Liang X, Graham DK: Natural killer cell neoplasms. Cancer; 2008 Apr 1;112(7):1425-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natural killer cell neoplasms.
  • Natural killer (NK) cell tumors are an uncommon and heterogeneous group of disorders.
  • The World Health Organization (WHO) classified mature NK cell neoplasms into 2 types:.
  • 1) extranodal NK cell lymphoma, nasal type and 2) aggressive NK cell leukemia.
  • The mature NK cell tumors are prevalent in Asia and Central and South America.
  • Although blastic NK cell lymphoma, currently referred to as CD4+/CD56+ hematodermic neoplasm, also was included in the NK cell lymphoma category in the WHO classification scheme, existing evidence indicates a plasmacytoid dendritic cell derivation as opposed to an NK cell origin.
  • These tumors are characterized by blastic appearance, CD3-/CD4-/CD56+/CD13-/CD33- phenotype, T-cell receptor and immunoglobulin genes in germline configuration, and no evidence of EBV, suggesting a true immature NK cell derivation.
  • For this article, the authors reviewed the recent concepts and progress in clinicopathologic features, pathogenesis, genetic characteristics, diagnosis, differential diagnosis, treatment approaches, and outcomes of all subtypes of NK cell neoplasms.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia / pathology. Lymphoma / pathology

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  • (PMID = 18286525.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 103
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27. Kawahara S, Sasaki M, Isobe Y, Ando J, Noguchi M, Koike M, Hirano T, Oshimi K, Sugimoto K: Clinical analysis of 52 patients with granular lymphocyte proliferative disorder (GLPD) showed frequent anemia in indolent T-cell GLPD in Japan. Eur J Haematol; 2009 Apr;82(4):308-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical analysis of 52 patients with granular lymphocyte proliferative disorder (GLPD) showed frequent anemia in indolent T-cell GLPD in Japan.
  • We present here clinical and hematological findings of 52 cases of granular lymphocyte-proliferative disorder (GLPD), which contained 35 indolent T-cell lineage granular lymphocyte-proliferative disorder (T-GLPD), two atypical T-GLPD, 12 chronic NK-cell lymphocytosis (CNKL), and three aggressive NK-cell leukemia (ANKL).
  • Hemoglobin level <8.0 g/dL was recognized in 21 cases of indolent T-GLPD (60%), among which 15 patients met the criteria of pure red cell aplasia.
  • Neutrophil counts <500/microL occurred only in two cases of T-GLPD (6%).
  • Therefore, although two atypical T-GLPD cases were CD56-positive, CD56 should not be a specific marker for aggressive T-GLPD.
  • All CNKL patients had a chronic course with a stable granular lymphocyte count.
  • [MeSH-major] Anemia / epidemiology. Lymphoproliferative Disorders / blood. Lymphoproliferative Disorders / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / blood. Female. Humans. Immunosuppressive Agents / therapeutic use. Japan. Karyotyping. Leukemia / epidemiology. Leukocyte Count. Male. Middle Aged. Prognosis. Young Adult

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  • (PMID = 19220421.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Immunosuppressive Agents
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28. Suzuki R, Suzumiya J, Nakamura S, Kagami Y, Kameoka JI, Sakai C, Mukai H, Takenaka K, Yoshino T, Tsuzuki T, Sugimori H, Kawa K, Kodera Y, Oshimi K, NK-cell Tumor Study Group: Hematopoietic stem cell transplantation for natural killer-cell lineage neoplasms. Bone Marrow Transplant; 2006 Feb;37(4):425-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematopoietic stem cell transplantation for natural killer-cell lineage neoplasms.
  • Neoplasms of natural killer (NK)-lineage are rare.
  • Their prognosis is generally poor except for cases of solitary nasal NK-cell lymphoma.
  • The NK-cell Tumor Study Group performed a survey in Japan on patients diagnosed between 1994 and 1998.
  • The underlying diseases were myeloid/NK cell precursor acute leukemia (n = 4), blastic NK-cell lymphoma (n = 11), aggressive NK-cell leukemia (n = 3), and nasal-type extranodal NK-cell lymphoma (n = 22).
  • Sixteen died of disease progression, and six of treatment-related causes.
  • These findings suggest that the HSCT is a promising treatment strategy for NK-cell lineage.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / pathology. Leukemia / therapy. Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Disease Progression. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Japan. Male. Middle Aged. Prognosis. Survival Rate. Transplantation Conditioning. Transplantation, Autologous. Transplantation, Homologous

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  • (PMID = 16400344.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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29. Yamaguchi M, Suzuki R, Kwong YL, Kim WS, Hasegawa Y, Izutsu K, Suzumiya J, Okamura T, Nakamura S, Kawa K, Oshimi K: Phase I study of dexamethasone, methotrexate, ifosfamide, L-asparaginase, and etoposide (SMILE) chemotherapy for advanced-stage, relapsed or refractory extranodal natural killer (NK)/T-cell lymphoma and leukemia. Cancer Sci; 2008 May;99(5):1016-20
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  • [Title] Phase I study of dexamethasone, methotrexate, ifosfamide, L-asparaginase, and etoposide (SMILE) chemotherapy for advanced-stage, relapsed or refractory extranodal natural killer (NK)/T-cell lymphoma and leukemia.
  • Extranodal natural killer (NK)/T-cell lymphoma, nasal type, and aggressive NK-cell leukemia are rare, and their standard therapy has not been established.
  • They are Epstein-Barr virus-associated lymphoid malignancies, and tumor cells express P-glycoprotein leading to multidrug resistance of the disease.
  • To develop an efficacious chemotherapeutic regimen, we conducted a dose-escalation feasibility study of a new chemotherapeutic regimen, SMILE, comprising the steroid dexamethasone, methotrexate, ifosfamide, L-asparaginase, and etoposide.
  • Etoposide shows both in vitro and in vivo efficacy for Epstein-Barr virus-associated lymphoproliferative disorders.
  • At level 1, six patients with extranodal NK/T-cell lymphoma, nasal type, were enrolled.
  • Their disease status was newly diagnosed stage IV (n = 3), first relapse (n = 2), and primary refractory (n = 1).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Lymphoid / drug therapy. Lymphoma, Extranodal NK-T-Cell / drug therapy

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  • (PMID = 18294294.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.1 / Asparaginase; UM20QQM95Y / Ifosfamide; YL5FZ2Y5U1 / Methotrexate
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30. Franco G, Palazzolo R, Liardo E, Tripodo C, Mancuso S: T cell large granular lymphocytic leukemia in association with Sjögren's syndrome. Acta Haematol; 2010;124(1):5-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T cell large granular lymphocytic leukemia in association with Sjögren's syndrome.
  • T cell large granular lymphocytic (LGL) leukemia is a rare condition accounting for 2-3% of all mature lymphoid leukemias.
  • Here, we present the case of a 73-year-old woman presenting with neutropenia and anemia (hemoglobin 9.9 g/dl).
  • Hematological assessment revealed the presence of a T cell LGL leukemia.
  • At the time of T cell LGL leukemia diagnosis, the patient developed xerophthalmia and xerostomia, and a diagnosis of Sjögren's syndrome was made following salivary gland biopsy.
  • The finding of large granular lymphocytes in the context of autoimmune disorders is well-known, though it often occurs with rheumatoid arthritis or in association with a positive autoantibody titer in the absence of an overt clinical picture.
  • The concomitant presentation of T cell LGL leukemia with Sjögren's syndrome is a rare event which is worth reporting.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / complications. Sjogren's Syndrome / complications

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20501987.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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31. Kothapalli R, Nyland SB, Kusmartseva I, Bailey RD, McKeown TM, Loughran TP Jr: Constitutive production of proinflammatory cytokines RANTES, MIP-1beta and IL-18 characterizes LGL leukemia. Int J Oncol; 2005 Feb;26(2):529-35
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  • [Title] Constitutive production of proinflammatory cytokines RANTES, MIP-1beta and IL-18 characterizes LGL leukemia.
  • Large granular lymphocyte (LGL) leukemia is a lymphoproliferative disease often associated with autoimmune disorders such as rheumatoid arthritis.
  • High levels of soluble Fas ligand have been implicated in development of chronic neutropenia.
  • However, a comprehensive analysis of constitutive chemokine and lymphokine production in LGL leukemia has not previously been reported.
  • RANTES, IL-8, MIP-1alpha, MIP-1beta, IL-1beta, IL-10, IL-12 p35, IL-18, IFN-gamma and IL-1Ra were the cytokine transcripts expressed in elevated levels from RNA of peripheral blood mononuclear cells of LGL leukemia patients.
  • Confirmatory ELISAs indicated that sera from LGL leukemia patients have elevated levels of RANTES, MIP-1beta, IL-18, and to a lesser extent IL-8 and IL-1Ra.
  • This pattern of cytokine upregulation is similar to that seen in some chronic infections or in autoimmune diseases, thus characterizing LGL leukemia as a proinflammatory disorder.

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  • (PMID = 15645140.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098472; United States / NCI NIH HHS / CA / CA83947; United States / NCI NIH HHS / CA / CA90633; United States / NCI NIH HHS / CA / CA98472
  • [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] Greece
  • [Chemical-registry-number] 0 / Chemokine CCL3; 0 / Chemokine CCL4; 0 / Chemokine CCL5; 0 / Chemokines; 0 / Cytokines; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / IL1RN protein, human; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-18; 0 / Macrophage Inflammatory Proteins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / Sialoglycoproteins; 63231-63-0 / RNA
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32. Hofmann A, Zaharatos G, Miller M: Case report and review of the literature: Toxoplasma gondii encephalitis in a 40-year-old woman with common variable immunodeficiency and a new diagnosis of large granular lymphocytic leukemia. Can J Infect Dis Med Microbiol; 2008 Jul;19(4):309-10

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case report and review of the literature: Toxoplasma gondii encephalitis in a 40-year-old woman with common variable immunodeficiency and a new diagnosis of large granular lymphocytic leukemia.
  • The present study describes a case of central nervous system toxoplasmosis in a patient with common variable immunodeficiency and newly diagnosed large granular lymphocytic leukemia, with a review of the literature for this association.

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  • [Cites] Infect Immun. 2005 Aug;73(8):4913-21 [16041005.001]
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  • (PMID = 19436513.001).
  • [ISSN] 1712-9532
  • [Journal-full-title] The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale
  • [ISO-abbreviation] Can J Infect Dis Med Microbiol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2604779
  • [Keywords] NOTNLM ; Cerebral toxoplasmosis / Common variable immunodeficiency / Large granular lymphocytic leukemia / Toxoplasma gondii
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33. Sprague WS, TerWee JA, VandeWoude S: Temporal association of large granular lymphocytosis, neutropenia, proviral load, and FasL mRNA in cats with acute feline immunodeficiency virus infection. Vet Immunol Immunopathol; 2010 Mar 15;134(1-2):115-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temporal association of large granular lymphocytosis, neutropenia, proviral load, and FasL mRNA in cats with acute feline immunodeficiency virus infection.
  • During acute feline immunodeficiency virus-C(PGammar) (FIV-C-PG) infection, we observed that cats develop large granular lymphocyte (LGL) lymphocytosis concurrent with a marked neutropenia that is temporally associated with the rise and fall of FIV-C-PG proviral loads.
  • LGLs, generally considered to be analogous to natural killer (NK) cells, can also be highly cytolytic CD8/CD57 T cells.
  • During HIV-1 infection, LGLs have been shown to be both CD16(+) NK cells and CD8(+)/CD57(+) T cells, but an association with neutropenia has not been described.
  • However, neutropenia with concurrent LGL lymphocytosis has been demonstrated in both LGL leukemia and common variable immunodeficiency syndrome in people, and in both syndromes, an increase in soluble Fas ligand (FasL) has been associated with neutrophil apoptosis leading to neutropenia.
  • Flow cytometric analysis demonstrated increases in CD56 and CD8 peripheral blood cell surface expression during acute FIV-C-PG infection.
  • We describe an interesting temporal association between innate immune responses and viral load during acute FIV-C-PG infection, which has similarities to HIV-1 infection and other immune dyscrasias of people, and which may contribute to the neutropenia and LGL lymphocytosis during FIV-C-PG infection.

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  • [Copyright] Copyright 2009 Elsevier B.V. All rights reserved.
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  • (PMID = 19896217.001).
  • [ISSN] 1873-2534
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL092791-07; United States / NHLBI NIH HHS / HL / R01 HL092791; United States / PHS HHS / / 5 R01 AL-52055; United States / NHLBI NIH HHS / HL / HL092791-07; United States / NHLBI NIH HHS / HL / 5R0HL092791
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, CD8; 0 / CD8 antigen, alpha chain; 0 / Fas Ligand Protein; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS152697; NLM/ PMC2821998
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34. Petterson TE, Bosco AA, Cohn RJ: Aggressive natural killer cell leukemia presenting with hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer; 2008 Mar;50(3):654-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive natural killer cell leukemia presenting with hemophagocytic lymphohistiocytosis.
  • Aggressive natural killer cell leukemia (ANKL) is a very rare condition and when reported occurs almost exclusively in adults.
  • We report a pediatric case of ANKL that presented with hemophagocytic syndrome, preceding the onset of leukemia by 12 weeks.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / complications. Lymphohistiocytosis, Hemophagocytic / etiology
  • [MeSH-minor] Aneuploidy. Antigens, CD8 / analysis. Child, Preschool. Chromosome Aberrations. Chromosomes, Human, Pair 6 / ultrastructure. Chromosomes, Human, Pair 7 / ultrastructure. Disease Progression. Epstein-Barr Virus Infections / complications. Fatal Outcome. Humans. Male. Multiple Organ Failure / etiology. Opportunistic Infections / etiology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17853464.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD8
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35. Duong YT, Jia H, Lust JA, Garcia AD, Tiffany AJ, Heneine W, Switzer WM: Short communication: Absence of evidence of HTLV-3 and HTLV-4 in patients with large granular lymphocyte (LGL) leukemia. AIDS Res Hum Retroviruses; 2008 Dec;24(12):1503-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Short communication: Absence of evidence of HTLV-3 and HTLV-4 in patients with large granular lymphocyte (LGL) leukemia.
  • Clonal disorders of large granular lymphocytes (LGL) result in leukemia due to the expansion of a discrete subset of either CD3(+) T cells or natural killer (NK) cells.
  • The possible involvement of human T cell lymphotropic virus types 1 and 2 (HTLV-1 and HTLV-2) in this disease has been studied but no conclusive evidence has linked either virus with LGL leukemia.
  • In this study, we examined whether HTLV-3 or HTLV-4, two newly identified HTLV groups discovered in Central Africa in primate hunters, is involved in LGL leukemia.
  • We developed two specific real-time PCR quantitative assays that are highly sensitive, capable of detecting 10 copies of HTLV-3 or HTLV-4 pol sequences in a background of 1 microg of DNA from human peripheral blood lymphocytes (PBL).
  • We tested PBL DNA samples from 40 LGL leukemia patients in the United States and found that all samples were negative for HTLV-3 or HTLV-4 infection.
  • These results suggest that HTLV-3 and HTLV-4 are not the causative agent of LGL leukemia.
  • [MeSH-major] HIV / isolation & purification. HIV-2 / isolation & purification. Leukemia, Large Granular Lymphocytic / virology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Lymphocytes / virology. Male. Middle Aged. Polymerase Chain Reaction / methods. United States

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  • (PMID = 19102684.001).
  • [ISSN] 1931-8405
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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36. Shah MV, Zhang R, Irby R, Kothapalli R, Liu X, Arrington T, Frank B, Lee NH, Loughran TP Jr: Molecular profiling of LGL leukemia reveals role of sphingolipid signaling in survival of cytotoxic lymphocytes. Blood; 2008 Aug 1;112(3):770-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular profiling of LGL leukemia reveals role of sphingolipid signaling in survival of cytotoxic lymphocytes.
  • T-cell large granular lymphocyte (LGL) leukemia is characterized by clonal expansion of CD3(+)CD8(+) cells.
  • Leukemic LGLs correspond to terminally differentiated effector-memory cytotoxic T lymphocytes (CTLs) that escape Fas-mediated activation-induced cell death (AICD) in vivo.
  • The gene expression signature of peripheral blood mononuclear cells from 30 LGL leukemia patients showed profound dysregulation of expression of apoptotic genes and suggested uncoupling of activation and apoptotic pathways as a mechanism for failure of AICD in leukemic LGLs.
  • Collectively, these results show a role for sphingolipid-mediated signaling as a mechanism for long-term survival of CTLs.
  • Therapeutic targeting of this pathway, such as use of FTY720, may have efficacy in LGL leukemia.

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  • (PMID = 18477771.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090633; United States / NCI NIH HHS / CA / R01 CA098472; United States / NCI NIH HHS / CA / CA90633; United States / NCI NIH HHS / CA / CA94872
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Lysosphingolipid; 0 / Sphingolipids; EC 3.2.1.47 / Galactosylgalactosylglucosylceramidase
  • [Other-IDs] NLM/ PMC2481553
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37. Bourgault-Rouxel AS, Loughran TP Jr, Zambello R, Epling-Burnette PK, Semenzato G, Donadieu J, Amiot L, Fest T, Lamy T: Clinical spectrum of gammadelta+ T cell LGL leukemia: analysis of 20 cases. Leuk Res; 2008 Jan;32(1):45-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical spectrum of gammadelta+ T cell LGL leukemia: analysis of 20 cases.
  • We report on the clinico-biological characteristics of 20 cases of gammadelta T cell large granular lymphocyte (LGL) leukemia.
  • All the data were compared to that of 196 cases with alphabeta T cell subtype, which represents the majority of T cell LGL leukemias.
  • Gammadelta LGL predominantly expressed a CD3+/CD4-/CD8+/CD16+/CD57+ phenotype, in 50% of cases.
  • gammadelta and alphabeta T cell LGL leukemia harbor a very similar clinico-biological behavior and represent part of an antigen-driven T cell lymphoproliferation.
  • [MeSH-major] Leukemia, T-Cell / diagnosis. Receptors, Antigen, T-Cell, gamma-delta
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Autoimmune Diseases / complications. Clone Cells. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Humans. Immunophenotyping. Leukopenia / diagnosis. Male. Middle Aged. Receptors, Antigen, T-Cell, alpha-beta. Splenomegaly / diagnosis

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  • (PMID = 17544120.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta
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38. Nagata Y, Ohashi K, Fukuda S, Kamata N, Akiyama H, Sakamaki H: Clinical features of dasatinib-induced large granular lymphocytosis and pleural effusion. Int J Hematol; 2010 Jun;91(5):799-807
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical features of dasatinib-induced large granular lymphocytosis and pleural effusion.
  • During follow-up of leukocyte counts in 20 consecutive patients (age range 29-81 years) treated with dasatinib, 9 patients (7 chronic myeloid leukemia in chronic phase, 2 Philadelphia chromosome-positive acute lymphoid leukemia in complete remission) developed lymphocytosis (>3,000/microl).
  • Peripheral blood smears revealed a population of large granular lymphocytes.
  • Large granular lymphocytosis (LGL) was first noted between 1 and 8 months after initiation of dasatinib, and it has persisted up to 33 months from the onset of LGL in one patient.
  • Peak numbers of large granular lymphocytes ranged from 2,915 to 17,425/microl.
  • The occurrence of LGL might interfere with achieving molecular response (MR, real-time quantification of major BCR-ABL1 mRNA less than 50 copies/microg RNA) in our small cohort; 8 (89%) of 9 patients with LGL attained MR, while only 6 (55%) of 11 patients without LGL eventually achieved MR.
  • With respect to the relationship between LGL and pleural effusion (PE), 3 (27%) of 11 patients without LGL developed PE, while 5 (56%) of 9 patients with LGL developed PE.
  • Moreover, the mean peak number of LGL was 9,215/microl, which was much higher than the mean peak number (4,635/microl) of LGL in patients without PE.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / chemically induced. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pleural Effusion / chemically induced. Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects. Thiazoles / adverse effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cohort Studies. Dasatinib. Female. Humans. Lymphocytes / pathology. Lymphocytosis / chemically induced. Male. Middle Aged

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  • (PMID = 20405252.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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39. Ryder J, Wang X, Bao L, Gross SA, Hua F, Irons RD: Aggressive natural killer cell leukemia: report of a Chinese series and review of the literature. Int J Hematol; 2007 Jan;85(1):18-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive natural killer cell leukemia: report of a Chinese series and review of the literature.
  • Aggressive natural killer cell leukemia (ANKL) is a rare Epstein-Barr virus (EBV)-associated fulminating disease that is widely disseminated at diagnosis.
  • Because of its typically extranodal presentation, differing degrees of NK cell involvement, and varying bone marrow pathology, ANKL can be confused with a reactive process.
  • Constant features at presentation included disseminated disease, high fever, bone marrow involvement, and a high lactate dehydrogenase index.
  • All cases were positive for EBV early region protein and negative for latent membrane protein 1, and all had a germline T-cell receptor gene configuration.
  • Peripheral blood counts were variable, with severe thrombocytopenia being the most frequently encountered abnormality (7 of 9 cases).
  • Because of its aggressive course, rapid and accurate diagnosis of ANKL is essential for a better understanding of the etiology, pathogenesis, and treatment of the disease.
  • [MeSH-major] Killer Cells, Natural / virology. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / epidemiology
  • [MeSH-minor] Adult. Aged. Blood Cell Count. Bone Marrow Diseases / pathology. China. Cytogenetic Analysis. Female. Herpesvirus 4, Human. Humans. Immunophenotyping. Male. Middle Aged. Thrombocytopenia

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  • (PMID = 17261497.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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40. Thomas A, Perzova R, Abbott L, Benz P, Poiesz MJ, Dube S, Loughran T, Ferrer J, Sheremata W, Glaser J, Leon-Ponte M, Poiesz BJ: LGL leukemia and HTLV. AIDS Res Hum Retroviruses; 2010 Jan;26(1):33-40
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  • [Title] LGL leukemia and HTLV.
  • Samples were obtained from 53 large granular lymphocytic leukemia (LGLL) patients and 10,000 volunteer blood donors (VBD).
  • Forty four percent of LGLL patients vs. 0.12 % of VBD had anti-HTLV antibodies via EIA (p < 0.001).
  • WB and PCR revealed that four LGLL patients (7.5%) vs. one VBD patient (0.01%) were infected with HTLV-2 (p < 0.001), suggesting an HTLV-2 etiology in a minority of cases.
  • No LGLL patient was positive for HTLV-1, -3, or -4, whereas only one EIA-positive VBD was positive for HTLV-1 and none for HTLV-3 or -4.
  • The HTLV EIA-positive, PCR-negative LGLL patients' sera reacted to epitopes within HTLV p24 gag and gp21 env.
  • Although three LGLL patients (5.7%) vs. none of 110 VBD patients tested positive for antibodies to the homologous HERV K10 peptide (p = 0.03), the significance of the anti-HTLV seroreactivity observed in many LGLL patients remains unclear.
  • [MeSH-major] HIV-2 / isolation & purification. Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 2 / isolation & purification. Human T-lymphotropic virus 3 / isolation & purification. Leukemia, Large Granular Lymphocytic / virology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Animals. Antibodies, Viral / blood. Blotting, Western / methods. Cross Reactions. Endogenous Retroviruses / immunology. Enzyme-Linked Immunosorbent Assay / methods. Female. Humans. Leukemia Virus, Bovine / immunology. Male. Middle Aged. Polymerase Chain Reaction / methods. Seroepidemiologic Studies. Young Adult

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  • (PMID = 20047475.001).
  • [ISSN] 1931-8405
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral
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41. Oka K, Nagayama R, Mori N: Epstein-Barr virus-associated proliferative disorder presenting as Hodgkin's lymphoma and developing as aggressive natural killer-cell leukemia 19 years later: a case report of composite lymphoma. Pathol Res Pract; 2009;205(10):730-4
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  • [Title] Epstein-Barr virus-associated proliferative disorder presenting as Hodgkin's lymphoma and developing as aggressive natural killer-cell leukemia 19 years later: a case report of composite lymphoma.
  • We describe a patient who was diagnosed as having classic Hodgkin's lymphoma at 29 years of age, and aggressive natural killer-cell leukemia at 48 years.
  • Hodgkin and Reed-Sternberg cells in the lymph node expressed CD30, CD15, T-cell intracellular antigen-1 (TIA-1), perforin, granzyme B, and Epstein-Barr virus-encoded RNA (EBER).
  • Natural killer-cell leukemia cells in the bone marrow expressed cytoplasmic CD3epsilon, TIA-1, perforin, granzyme B, and EBER, and some neoplastic cells expressed CD56 (123C3).
  • Fluorescence-activated cell sorter (FACS) analysis showed that neoplastic cells expressed CD56.
  • Neither a rearrangement band of the T-cell receptor gene nor that of the immunoglobulin heavy chain gene was detected.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Hodgkin Disease / pathology. Leukemia, Large Granular Lymphocytic / pathology. Neoplasms, Second Primary / pathology

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  • (PMID = 19269751.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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42. Chang H, Kamel-Reid S, Hussain N, Lipton J, Messner HA: T-cell large granular lymphocytic leukemia of donor origin occurring after allogeneic bone marrow transplantation for B-cell lymphoproliferative disorders. Am J Clin Pathol; 2005 Feb;123(2):196-9
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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 large granular lymphocytic leukemia of donor origin occurring after allogeneic bone marrow transplantation for B-cell lymphoproliferative disorders.
  • T-cell lymphoproliferative disorders are uncommon occurrences after bone marrow transplantation (BMT).
  • We describe 2 patients in whom a monoclonal T-cell large granular lymphocytosis (T-LGL) developed after allogeneic BMT for B-cell lymphoproliferative disorders.
  • Both patients showed a persistent expansion of CD3+, CD8+, and CD57+ large granular lymphocytes of donor origin with clonally rearranged T-cell receptor gamma genes and no evidence of Epstein-Barr virus-related infection.
  • The manifestations were consistent with T-LGL leukemia as defined by the World Health Organization criteria.
  • In both patients, graft-vs-host disease developed, and 1 had recurrent episodes of cytomegalovirus viremia.
  • Both patients remain in complete remission from their B-cell lymphoproliferative disorders and do not have symptoms related to T-LGL leukemia.
  • These data show that T-LGL leukemia should be included as one of the types of posttransplantation lymphoproliferative disorders that can occur after allogeneic BMT for B-cell neoplasms.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, T-Cell / pathology. Tissue Donors. Waldenstrom Macroglobulinemia / therapy
  • [MeSH-minor] Clone Cells. DNA, Neoplasm / analysis. Humans. Male. Middle Aged. Polymerase Chain Reaction. Receptors, Antigen, T-Cell, gamma-delta / genetics. Remission Induction. Transplantation, Homologous

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  • (PMID = 15842042.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Receptors, Antigen, T-Cell, gamma-delta
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43. Gaur S, Mansoor S, Aish L: T-cell large granular lymphocytic leukemia and hereditary hemochromatosis: a fortuitous association? Am J Hematol; 2005 Apr;78(4):299-301
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  • [Title] T-cell large granular lymphocytic leukemia and hereditary hemochromatosis: a fortuitous association?
  • We describe a patient with hereditary hemochromatosis (homozygous for C282Y mutation) and neutropenia who was found to have underlying T-cell large granular lymphocytic (T-LGL) leukemia.
  • The diagnosis was confirmed by demonstrating T-cell receptor (TCR) gene rearrangement by polymerase chain reaction (PCR).
  • [MeSH-major] Hemochromatosis / complications. Hemochromatosis / genetics. Leukemia, T-Cell / complications
  • [MeSH-minor] Female. Ferritins / blood. Gene Rearrangement, T-Lymphocyte. Humans. Middle Aged. Phlebotomy. Treatment Outcome

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  • (PMID = 15795911.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-73-2 / Ferritins
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44. Shah MV, Zhang R, Loughran TP Jr: Never say die: survival signaling in large granular lymphocyte leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S244-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Never say die: survival signaling in large granular lymphocyte leukemia.
  • Large granular lymphocyte (LGL) leukemia is a rare disorder of mature cytotoxic T or natural killer cells.
  • Large granular lymphocyte leukemia is characterized by the accumulation of cytotoxic cells in blood and infiltration in the bone marrow, liver, and spleen.
  • Herein, we review clinical features of LGL leukemia.
  • We focus our discussion on known survival signals believed to play a role in the pathogenesis of LGL leukemia and their potential therapeutic implications.

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  • (PMID = 19778848.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098472; United States / NCI NIH HHS / CA / CA94872
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fas Ligand Protein; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Number-of-references] 88
  • [Other-IDs] NLM/ NIHMS671956; NLM/ PMC4377229
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45. Thomas J, Haseman JK, Goodman JI, Ward JM, Loughran TP Jr, Spencer PJ: A review of large granular lymphocytic leukemia in Fischer 344 rats as an initial step toward evaluating the implication of the endpoint to human cancer risk assessment. Toxicol Sci; 2007 Sep;99(1):3-19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A review of large granular lymphocytic leukemia in Fischer 344 rats as an initial step toward evaluating the implication of the endpoint to human cancer risk assessment.
  • Large granular lymphocyte leukemia (LGLL) is a common fatal disease in aging F344 rats.
  • The current understanding of rat LGLL and a search for mechanistic data/correlations to human leukemia were examined with the goal of improving evaluation of the LGLL endpoint in cancer bioassays as it relates to human cancer risk assessments.
  • The exact cell of origin of the F344 rat LGLL is not fully resolved, although natural killer (NK) cell characteristics were demonstrated in most, if not all cases.
  • Similarities between rat LGLL and a rare human NK-LGLL exist, invalidating claims of no human counterpart, although the underlying etiopathogenesis may be different.
  • There is insufficient data to establish a mode of action of chemical-induced rat LGLL.
  • Evaluation of the National Toxicology Program database revealed only 34 substances (out of over 500 studied) that were possibly associated with increased incidences of LGLL.
  • Of these, only five produced definitive LGLL effects in both sexes; the remaining 29 produced single sex responses and/or only "equivocal" associations with LGLL.
  • Trends of increasing background/variability in LGLL incidence and its modulation by extraneous factors (e.g., corn oil gavage) are key confounders in interpretation.
  • Given that LGLL is a common tumor in control F344 rats, interpretations of bioassays can be improved by increasing the statistical stringency (e.g., p<0.01 over traditional p<0.05), as an indicator of possible carcinogenic effects, but that alone would be insufficient evidence for declaring treatment-related increases.
  • Thus, it was concluded that the evaluation of possible chemically related increases in rat LGLL utilize a "weight-of-evidence" approach.
  • [MeSH-major] Carcinogenicity Tests / methods. Disease Models, Animal. Leukemia, Lymphoid / pathology

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  • (PMID = 17522071.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 84
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46. Xu X, Broome EH, Rashidi HH, South ST, Dell'aquila ML, Wang HY: CD20dim-positive T-cell large granular lymphocytic leukemia in a patient with concurrent hairy cell leukemia and plasma cell myeloma. Int J Clin Exp Pathol; 2010;3(8):798-807
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD20dim-positive T-cell large granular lymphocytic leukemia in a patient with concurrent hairy cell leukemia and plasma cell myeloma.
  • We report a CD20dim- positive T-cell large granular lymphocytic (T-LGL) leukemia in a patient with concurrent hairy cell leukemia and plasma cell myeloma.
  • This patient was first diagnosed with T-LGL leukemia with dim CD20 expression, which by itself was a rare entity.
  • He received no treatment for T-LGL leukemia.
  • The patient later developed a hairy cell leukemia, which went into complete clinical remission after one cycle of 2-CdA.
  • Five years later, he was diagnosed with a third malignancy, plasma cell myeloma.
  • Complex cytogenetic aberrancies were present at the time when plasma cell myeloma was diagnosed.
  • [MeSH-major] Antigens, CD20 / metabolism. Leukemia, Hairy Cell / pathology. Leukemia, Large Granular Lymphocytic / metabolism. Leukemia, Large Granular Lymphocytic / pathology. Multiple Myeloma / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 21151394.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Other-IDs] NLM/ PMC2993231
  • [Keywords] NOTNLM ; CD20 / T-cell large granular lymphocytic leukemia / hairy cell leukemia / plasma cell myeloma
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47. Delia M, Liso V, Capalbo S, Napoli A, Ricco R, Semenzato G, Liso A: Common variable immunodeficiency patient with large granular lymphocytosis developing extranodal diffuse large B-cell lymphoma: a case report. Haematologica; 2006 Dec;91(12 Suppl):ECR61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Common variable immunodeficiency patient with large granular lymphocytosis developing extranodal diffuse large B-cell lymphoma: a case report.
  • Here we describe a Common Variable Immunodeficiency (CVI) patient with large granular (LG) lymphocytosis and systemic non-malignant lymphadenopathy who developed diffuse large B-cell lymphoma of the stomach.
  • This is the first report of gastric high-grade lymphoma with widespread lymphadenopathy in a patient with LG lymphocytosis associated with CVI.
  • [MeSH-major] Common Variable Immunodeficiency / complications. Lymphocytosis / etiology. Lymphoma, Large B-Cell, Diffuse / etiology. Stomach Neoplasms / etiology
  • [MeSH-minor] Adult. B-Lymphocytes / pathology. Humans. Immunophenotyping. Lymph Nodes / pathology. Lymphoma, Non-Hodgkin / etiology. Lymphoma, Non-Hodgkin / pathology. Male. Postoperative Complications / etiology. Postoperative Complications / pathology. Splenectomy. T-Lymphocytes / pathology


48. Osuji N, Matutes E, Morilla A, Del Giudice I, Wotherspoon A, Catovsky D: Prolonged treatment response in aggressive natural killer cell leukemia. Leuk Lymphoma; 2005 May;46(5):757-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolonged treatment response in aggressive natural killer cell leukemia.
  • We describe a case of natural killer (NK) cell leukemia with acute presentation, systemic symptoms and hepatosplenomegaly.
  • The uniform and aberrant phenotype of NK cells with infiltration of bone marrow and spleen was in keeping with a malignant diagnosis.
  • Aggressive presentation was demonstrated by marked constitutional symptoms and significant tumor burden (liver, spleen, blood, bone marrow).
  • We discuss the difficulties in the diagnosis of this condition, explore possible causes of cytopenia(s), and highlight the role of immunosuppression in controlling disease manifestations in large granular lymphocyte proliferative disorders.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Killer Cells, Natural / pathology. Leukemia / therapy

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  • (PMID = 16019515.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 395575MZO7 / Pentostatin; 83HN0GTJ6D / Cyclosporine
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49. Kitchen BJ, Boxer LA: Large granular lymphocyte leukemia (LGL) in a child with hyper IgM syndrome and autoimmune hemolytic anemia. Pediatr Blood Cancer; 2008 Jan;50(1):142-5
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  • [Title] Large granular lymphocyte leukemia (LGL) in a child with hyper IgM syndrome and autoimmune hemolytic anemia.
  • Flow cytometry of the peripheral blood revealed the presence of a marked predominance of cytotoxic T lymphocytes, shown to be clonal, with concomitant natural killer (NK) antigen expression.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / complications. Hyper-IgM Immunodeficiency Syndrome / complications. Leukemia, Large Granular Lymphocytic / complications


50. Yoo EH, Kim HJ, Lee ST, Kim WS, Kim SH: Frequent CD7 antigen loss in aggressive natural killer-cell leukemia: a useful diagnostic marker. Korean J Lab Med; 2009 Dec;29(6):491-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent CD7 antigen loss in aggressive natural killer-cell leukemia: a useful diagnostic marker.
  • BACKGROUND: Aggressive natural killer-cell leukemia (ANKL) is a rare neoplasm characterized by systemic proliferation of NK cells.
  • However, the differential diagnosis of NK lymphoproliferative disorders is difficult because of the absence of a distinct diagnostic hallmark.
  • The immunophenotype of the leukemic NK-cells was cytoplasmic CD3(+), surface CD3(-), CD16/56(+), CD2(+), and CD5(-).
  • In conjunction with the cytogenetic findings, this characteristic immunophenotypic finding can serve as a reliable marker for the timely diagnosis of ANKL.
  • Therefore, immunophenotypic analysis of CD7 expression should be included in the diagnosis of NK cell neoplasms.
  • [MeSH-major] Antigens, CD7 / analysis. Biomarkers, Tumor / analysis. Leukemia, Large Granular Lymphocytic / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Blood Cell Count. Child. Child, Preschool. Cytogenetics. Female. Herpesvirus 4, Human / isolation & purification. Humans. Immunophenotyping. Karyotyping. Male. Middle Aged. Retrospective Studies

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  • (PMID = 20046078.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Biomarkers, Tumor
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51. Yu J, Ershler M, Yu L, Wei M, Hackanson B, Yokohama A, Mitsui T, Liu C, Mao H, Liu S, Liu Z, Trotta R, Liu CG, Liu X, Huang K, Visser J, Marcucci G, Plass C, Belyavsky AV, Caligiuri MA: TSC-22 contributes to hematopoietic precursor cell proliferation and repopulation and is epigenetically silenced in large granular lymphocyte leukemia. Blood; 2009 May 28;113(22):5558-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TSC-22 contributes to hematopoietic precursor cell proliferation and repopulation and is epigenetically silenced in large granular lymphocyte leukemia.
  • Here we demonstrate that the TSC-22 promoter is methylated in primary mouse T or natural killer (NK) large granular lymphocyte (LGL) leukemia and this is associated with down-regulation or silencing of TSC-22 expression.
  • The TSC-22 deregulation was reversed in vivo by a 5-aza-2'-deoxycytidine therapy of T or NK LGL leukemia, which significantly increased survival of the mice bearing this disease.
  • Ectopic expression of TSC-22 in mouse leukemia or lymphoma cell lines resulted in delayed in vivo tumor formation.
  • Collectively, our data suggest that TSC-22 normally contributes to the regulation of HPC function and is a putative tumor suppressor gene that is hypermethylated and silenced in T or NK LGL leukemia.

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  • (PMID = 19329776.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101956; United States / NCI NIH HHS / CA / CA93548; United States / NCI NIH HHS / CA / P01 CA101956; United States / NCI NIH HHS / CA / R01 CA093548; United States / NCI NIH HHS / CA / CA68458; United States / NCI NIH HHS / CA / R01 CA068458; United States / NCI NIH HHS / CA / P01 CA095426; United States / NCI NIH HHS / CA / CA95426; United States / NCI NIH HHS / CA / R37 CA068458
  • [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 / Repressor Proteins; 0 / Tgfb1i4 protein, mouse
  • [Other-IDs] NLM/ PMC2689053
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52. Zambello R, Berno T, Cannas G, Baesso I, Binotto G, Bonoldi E, Bevilacqua P, Miorin M, Facco M, Trentin L, Agostini C, Semenzato G: Phenotypic and functional analyses of dendritic cells in patients with lymphoproliferative disease of granular lymphocytes (LDGL). Blood; 2005 Dec 1;106(12):3926-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phenotypic and functional analyses of dendritic cells in patients with lymphoproliferative disease of granular lymphocytes (LDGL).
  • We investigated whether dendritic cells (DCs) play a role in favoring granular lymphocyte (GL) proliferation in patients with lymphoproliferative disease of granular lymphocytes (LDGL).
  • Autologous immature (iDCs) and mature (mDCs) DCs generated in vitro were studied for stimulatory activity on cell proliferation of CD3+ and CD3- GLs.
  • Analysis of BM biopsies demonstrated a topographic distribution of DCs and GLs that indicates contact between the 2 cell types.
  • The putative contact between DCs and GLs in the BM and, more crucial, the proliferative response of discrete GL populations to DC stimulation suggest the presence of a specific antigen within BM DCs, providing evidence for a role of DCs in the pathogenesis of LDGL.
  • [MeSH-major] Cell Communication / immunology. Dendritic Cells / metabolism. Granulocytes / metabolism. Lymphoproliferative Disorders / metabolism
  • [MeSH-minor] Antigens, CD3 / metabolism. Cell Proliferation. Flow Cytometry. Humans. Immunohistochemistry. Immunophenotyping. Killer Cells, Natural / immunology. Killer Cells, Natural / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / metabolism

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  • (PMID = 16091452.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3
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53. Ko YH, Park S, Kim K, Kim SJ, Kim WS: Aggressive natural killer cell leukemia: is Epstein-Barr virus negativity an indicator of a favorable prognosis? Acta Haematol; 2008;120(4):199-206

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive natural killer cell leukemia: is Epstein-Barr virus negativity an indicator of a favorable prognosis?
  • Aggressive natural killer (NK) cell leukemia (ANKL) is a prototype of an Epstein-Barr virus (EBV)-associated lymphoid malignancy, which is characterized by a fulminant clinical course and a median survival interval <2 months.
  • In conclusion, EBV-negative ANKL is an uncommon malignancy that pursues a less aggressive clinical course than EBV-positive ANKL.
  • [MeSH-major] Epstein-Barr Virus Infections / virology. Leukemia, T-Cell / virology
  • [MeSH-minor] Adolescent. Adult. Aged. Fatal Outcome. Female. Humans. Kaplan-Meier Estimate. Killer Cells, Natural / immunology. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Recurrence. Young Adult

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19153474.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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54. Mohan SR, Clemente MJ, Afable M, Cazzolli HN, Bejanyan N, Wlodarski MW, Lichtin AE, Maciejewski JP: Therapeutic implications of variable expression of CD52 on clonal cytotoxic T cells in CD8+ large granular lymphocyte leukemia. Haematologica; 2009 Oct;94(10):1407-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic implications of variable expression of CD52 on clonal cytotoxic T cells in CD8+ large granular lymphocyte leukemia.
  • BACKGROUND: T-cell large granular lymphocytic leukemia is a clonal proliferation of cytotoxic T-lymphocytes which often results in severe cytopenia.
  • Current treatment options favor chronic immunosuppression.
  • DESIGN AND METHODS: We retrospectively examined treatment outcomes in 59 patients with CD8+ T-cell large granular lymphocytic leukemia, 41 of whom required therapy.
  • Flow cytometry was used to monitor expression of glycophosphatidylinositol-anchored CD52, CD55, and CD59 as well as to characterize T-cell clonal expansions by T-cell receptor variable beta-chain (Vbeta) repertoire.
  • RESULTS: Analysis of the effects of alemtuzumab revealed remissions with restoration of platelets in one of one patient, red blood cell transfusion independence in three of five patients and improvement of neutropenia in one of three, resulting in an overall response rate of 50% (4/8 patients).
  • Clonal large granular lymphocytes exhibited decreased CD52 expression post-therapy in patients refractory to treatment.
  • Samples of large granular lymphocytes collected prior to therapy also unexpectedly had a significant proportion of CD52-negative cells while a healthy control population had no such CD52 deficiency (p=0.026).
  • CONCLUSIONS: While alemtuzumab may be highly effective in large granular lymphocytic leukemia, prospective serial monitoring for the presence of CD52-deficient clonal cytotoxic T-lymphocytes should be a component of clinical trials investigating the efficacy of this drug.
  • CD52 deficiency may explain lack of response to alemtuzumab, and such therapy may confer a survival advantage to glycophosphatidylinositol-negative clonal cytotoxic T-lymphocytes.

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  • (PMID = 19794084.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA113972; United States / NCRR NIH HHS / RR / U54 RR019397; United States / NCRR NIH HHS / RR / U54 RR 019397
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ PMC2754957
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55. Shah A, Diehl LF, St Clair EW: T cell large granular lymphocyte leukemia associated with rheumatoid arthritis and neutropenia. Clin Immunol; 2009 Aug;132(2):145-52
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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 large granular lymphocyte leukemia associated with rheumatoid arthritis and neutropenia.
  • T cell large granular lymphocyte leukemia (T-LGL) is a disease characterized by clonal expansion of cytotoxic T cells (CTLs).
  • It generally follows an indolent course and is notable for an association with chronic inflammation, neutropenia and rheumatoid arthritis (RA).
  • We present herein a case of a patient with rheumatoid arthritis (RA), neutropenia, large granular lymphocytosis, and an expanded clonal population of peripheral blood CD3(+)CD8(+)TCRalphabeta CTLs, consistent with the diagnosis of T-LGL.
  • T-LGL is part of a spectrum of large granular lymphocytic (LGL) disorders, which includes the more common indolent variety of this disease (as illustrated by the case herein), an aggressive but rare form of this leukemia, natural killer (NK) cell LGL leukemia, Felty's syndrome (FS), and chronic large granular lymphocytosis.
  • T-LGL appears to be a relatively rare disease, but the true prevalence is not known.
  • Thus, T-LGL leukemia and FS with LGL expansion in the setting of RA is classically distinguished by the clonality of the CTL population, with monoclonality in T-LGL and polyclonality in FS.
  • Despite this difference, T-LGL and FS are often similar in their clinical and biological behavior.
  • Both may respond to immunosuppressive therapy, and pursue a smoldering course typical of a chronic inflammatory disease.
  • [MeSH-major] Arthritis, Rheumatoid / complications. Leukemia, Large Granular Lymphocytic / diagnosis. Neutropenia / complications
  • [MeSH-minor] Flow Cytometry. Humans. Lymphocytosis / complications. Male. Middle Aged. Review Literature as Topic. T-Lymphocytes, Cytotoxic / immunology


56. Tanaka Y, Matsui K, Yamashita K, Matsuda K, Shinohara K, Matsutani A: T-gamma delta large granular lymphocyte leukemia preceded by pure red cell aplasia and complicated with hemophagocytic syndrome caused by Epstein-Barr virus infection. Intern Med; 2006;45(9):631-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-gamma delta large granular lymphocyte leukemia preceded by pure red cell aplasia and complicated with hemophagocytic syndrome caused by Epstein-Barr virus infection.
  • A 51-year-old man developed anemia, and was diagnosed with pure red cell aplasia through the absence of erythroid progenitors.
  • Large granular lymphocyte (LGL) leukemia with the T-cell gamma delta phenotype evolved after 6 months showing CD2+, CD3+, CD8- and CD56- with the T-cell receptor beta gene rearrangement, clonalities of gamma and delta genes and complex chromosome abnormality simultaneously with hemophagocytic syndrome (HPS).
  • In the present patient, it seemed that lymphoproliferative disease of large granular lymphocytes (LDGL) manifested initially as PRCA, gammadelta LGL leukemia evolved, and finally fatal HPS become complicated, presumably caused by the EBV reactivation in the immunodeficiency state with the administration of immunosuppressants.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Leukemia, Lymphoid / complications. Lymphocytes / metabolism. Lymphohistiocytosis, Hemophagocytic / complications. Lymphohistiocytosis, Hemophagocytic / virology. Receptors, Antigen, T-Cell, gamma-delta / metabolism. Red-Cell Aplasia, Pure / complications


57. Momose K, Makishima H, Ito T, Nakazawa H, Shimodaira S, Kiyosawa K, Ishida F: Close resemblance between chemokine receptor expression profiles of lymphoproliferative disease of granular lymphocytes and their normal counterparts in association with elevated serum concentrations of IP-10 and MIG. Int J Hematol; 2007 Aug;86(2):174-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Close resemblance between chemokine receptor expression profiles of lymphoproliferative disease of granular lymphocytes and their normal counterparts in association with elevated serum concentrations of IP-10 and MIG.
  • T-cell large granular lymphocyte (T-LGL) leukemia and chronic natural killer (NK) cell lymphocytosis (CNKL) are major subtypes of lymphoproliferative disease of granular lymphocytes (LDGL).
  • To clarify the mechanism of LGL proliferation and the relationship with the chemokine system in LDGL, we enrolled 22 T-LGL leukemia patients and 8 CNKL cases, analyzed the expression profiles of chemokine receptors, and measured the serum concentrations of the corresponding chemokines.
  • There were no significant differences in chemokine receptor expression profiles between T-LGL leukemia patients and healthy donors.
  • An association of CCR5 and CXCR3 expression levels on LGLs was recognized in T-LGL leukemia patients (r = 0.84; P < .001).
  • The chemokine receptor phenotypes of LDGL cells are essentially similar to those of normal T-cells and NK cells.
  • [MeSH-major] Chemokine CXCL10 / blood. Chemokine CXCL9 / blood. Gene Expression Profiling. Lymphoproliferative Disorders / genetics. Receptors, Chemokine / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Humans. Killer Cells, Natural / pathology. Leukemia / pathology. Lymphocytosis / pathology. Male. Middle Aged. T-Lymphocytes / pathology

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  • (PMID = 17875534.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CXCL10 protein, human; 0 / CXCL9 protein, human; 0 / Chemokine CXCL10; 0 / Chemokine CXCL9; 0 / Receptors, Chemokine
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58. 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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  • [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.
  • Abnormal lymphocytes expressed cytotoxic granule proteins and were consistently CD45RO and CD5 negative in contrast to normal red pulp T cells.
  • 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-PLL lymphocytes, unlike LGLs, were more invasive, infiltrating the spleen capsule as well as white pulp areas.
  • 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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59. Alekshun TJ, Tao J, Sokol L: Aggressive T-cell large granular lymphocyte leukemia: a case report and review of the literature. Am J Hematol; 2007 Jun;82(6):481-5
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  • [Title] Aggressive T-cell large granular lymphocyte leukemia: a case report and review of the literature.
  • The majority of patients with T-cell large granular lymphocyte (LGL) leukemia will have an indolent clinical course.
  • Herein, we report a case of an aggressive T-cell LGL leukemia in a previously healthy 42-year-old Caucasian male who presented with acute onset of B-symptoms, hepatosplenomegaly, lymphocytosis, moderate anemia, and thrombocytopenia.
  • Immunophenotypically, the malignant cells co-expressed CD3(+)CD8(+)CD56(+) markers and the T-cell receptor beta (TCR beta) gene demonstrated clonal rearrangement.
  • A systematic review of all available English literature revealed 12 well-described cases of aggressive T-cell LGL leukemia suggesting that this variant is a new and distinct entity in the spectrum of LGL disorders.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Progression. Follow-Up Studies. Humans. Immunophenotyping. Karyotyping. Male. Remission Induction. Treatment Outcome

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17205534.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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60. Sano T, Ozaki K, Kodama Y, Matsuura T, Narama I: Malignant Lymphoma with Severe Infiltrative Growth into Skeletal Muscles in WBN/Kob Rats. J Toxicol Pathol; 2009 Sep;22(3):173-8
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  • [Title] Malignant Lymphoma with Severe Infiltrative Growth into Skeletal Muscles in WBN/Kob Rats.
  • Although spontaneously occurring neoplasms have been reported repeatedly in F344, SD and Wistar rats, which are commonly used strains for routine toxicologic and carcinogenicity studies, there are only a few reports of malignant lymphoma or lymphatic leukemia except for large granular lymphocytic leukemia (LGL) in F344 rats.
  • Malignant lymphoma (lymphosarcoma) is thought to be uncommon in F344 rats.
  • The authors encountered malignant lymphomas of the non-LGL leukemia type with characteristic pathologic features in WBN/Kob rats.
  • The mean age at onset of the disease in all 13 affected rats (8 males and 5 females) was about 60 weeks.
  • Immunohistochemically, all tumor cells were positive for B-cell markers (PAX-5, CD79a and CD45) and negative for CD3.
  • From the results of immunohistochemistry and morphological examination, these tumors were diagnosed as malignant B-cell lymphomas.

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  • (PMID = 22271991.001).
  • [ISSN] 0914-9198
  • [Journal-full-title] Journal of toxicologic pathology
  • [ISO-abbreviation] J Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Other-IDs] NLM/ PMC3251631
  • [Keywords] NOTNLM ; B cell / WBN/Kob rat / malignant lymphoma
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61. Duarte AF, Nogueira A, Mota A, Baudrier T, Canelhas A, Cancela J, Lima M, Azevedo F: Leg ulcer and thigh telangiectasia associated with natural killer cell CD56(-) large granular lymphocyte leukemia in a patient with pseudo-Felty syndrome. J Am Acad Dermatol; 2010 Mar;62(3):496-501
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leg ulcer and thigh telangiectasia associated with natural killer cell CD56(-) large granular lymphocyte leukemia in a patient with pseudo-Felty syndrome.
  • Clonal disorders of large granular lymphocytes (LGL) represent a rare spectrum of biologically distinct lymphoproliferative diseases originating either from mature T cells or natural killer cells.
  • Both subtypes can manifest as indolent or aggressive disorders.
  • Because of the association of rheumatoid arthritis, splenomegaly, and nonspecific neutropenia, the diagnosis of Felty syndrome was initially made.
  • Further investigation allowed the diagnosis of a CD56(-) natural killer-cell LGL leukemia and documented skin infiltration by natural killer cells.
  • Cutaneous manifestations of LGL leukemia have been rarely reported.
  • This report of pseudo-Felty syndrome with CD56(-) LGL leukemia, presenting with a leg ulcer and telangiectasia, enhances the role of dermatology in the diagnosis of hematologic neoplasia.
  • [MeSH-major] Leg Ulcer / pathology. Leukemia, Large Granular Lymphocytic / pathology. Telangiectasis / pathology
  • [MeSH-minor] Aged. Antigens, CD56 / analysis. Arthritis, Rheumatoid / complications. Felty Syndrome / diagnosis. Felty Syndrome / pathology. Female. Humans. Killer Cells, Natural / pathology. Neutropenia / pathology

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  • [Copyright] Copyright 2009 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.
  • (PMID = 19962215.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56
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62. Chen X, Bai F, Sokol L, Zhou J, Ren A, Painter JS, Liu J, Sallman DA, Chen YA, Yoder JA, Djeu JY, Loughran TP, Epling-Burnette PK, Wei S: A critical role for DAP10 and DAP12 in CD8+ T cell-mediated tissue damage in large granular lymphocyte leukemia. Blood; 2009 Apr 2;113(14):3226-34
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  • [Title] A critical role for DAP10 and DAP12 in CD8+ T cell-mediated tissue damage in large granular lymphocyte leukemia.
  • Large granular lymphocyte (LGL) leukemia, or LGLL, is characterized by increased numbers of circulating clonal LGL cells in association with neutropenia, anemia, rheumatoid arthritis, and pulmonary artery hypertension (PAH).
  • Emerging evidence suggests that LGLL cells with a CD8(+)CD28(null) phenotype induce these clinical manifestations through direct destruction of normal tissue.
  • Compared with CD8(+)CD28(null) T cells from healthy controls, CD8(+)CD28(null) T cells from LGLL patients have acquired the ability to directly lyse pulmonary artery endothelial cells and human synovial cells.
  • Here, we show that LGLL cells from patients possess enhanced cytotoxic characteristics and express elevated levels of activating natural killer receptors as well as their signaling partners, DAP10 and DAP12.
  • Moreover, downstream targets of DAP10 and DAP12 are constitutively activated in LGLL cells, and expression of dominant-negative DAP10 and DAP12 dramatically reduces their lytic capacity.
  • These are the first results to show that activating NKR-ligand interactions play a critical role in initiating the DAP10 and DAP12 signaling events that lead to enhanced lytic potential of LGLL cells.
  • Results shown suggest that inhibitors of DAP10 and DAP12 or other proteins involved in this signaling pathway will be attractive therapeutic targets for the treatment of LGLL and other autoimmune diseases and syndromes.

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  • (PMID = 19075187.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098472; United States / NCI NIH HHS / CA / R01 CA11211201; United States / NCI NIH HHS / CA / R01 CA94872; United States / NIAID NIH HHS / AI / AI056213; United States / NCI NIH HHS / CA / R01 CA098080; United States / NIAID NIH HHS / AI / R01 AI056213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD28; 0 / HCST protein, human; 0 / Membrane Proteins; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell; 0 / TYROBP protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ PMC2665892
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63. Epling-Burnette PK, Sokol L, Chen X, Bai F, Zhou J, Blaskovich MA, Zou J, Painter JS, Edwards TD, Moscinski L, Yoder JA, Djeu JY, Sebti S, Loughran TP Jr, Wei S: Clinical improvement by farnesyltransferase inhibition in NK large granular lymphocyte leukemia associated with imbalanced NK receptor signaling. Blood; 2008 Dec 1;112(12):4694-8
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  • [Title] Clinical improvement by farnesyltransferase inhibition in NK large granular lymphocyte leukemia associated with imbalanced NK receptor signaling.
  • Large granular lymphocyte (LGL) leukemia is commonly associated with poor hematopoiesis.
  • The first case of pulmonary artery hypertension (PAH) was observed in a 57-year-old woman with natural killer (NK)-LGL leukemia and transfusion-dependent anemia.
  • Using a genetic approach, we demonstrated that killing of pulmonary endothelial cells by patient NK cells was mediated by dysregulated balance in activating and inhibitory NK-receptor signaling.
  • Elevated pulmonary artery pressure and erythroid differentiation improved after disrupting the NK-receptor signaling pathway with 4 courses of a farnesyltransferase inhibitor, tipifarnib.
  • Coincidental association between PAH and LGL leukemia suggest a causal relationship between the expanded lymphocyte population and these clinical manifestations.

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  • (PMID = 18791165.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098472; United States / NCRR NIH HHS / RR / U54 RR019397; United States / NIAID NIH HHS / AI / AI056213; United States / NCI NIH HHS / CA / CA94872; United States / NCRR NIH HHS / RR / U54RR019397-05; United States / NCI NIH HHS / CA / CA11211201; United States / NIAID NIH HHS / AI / R01 AI056213
  • [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 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Quinolones; 0 / Receptors, Natural Killer Cell; 192185-72-1 / tipifarnib; EC 2.5.1.29 / Farnesyltranstransferase
  • [Other-IDs] NLM/ PMC2597136
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64. Yang J, Liu X, Nyland SB, Zhang R, Ryland LK, Broeg K, Baab KT, Jarbadan NR, Irby R, Loughran TP Jr: Platelet-derived growth factor mediates survival of leukemic large granular lymphocytes via an autocrine regulatory pathway. Blood; 2010 Jan 7;115(1):51-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Platelet-derived growth factor mediates survival of leukemic large granular lymphocytes via an autocrine regulatory pathway.
  • Large granular lymphocyte (LGL) leukemia results from chronic expansion of cytotoxic T cells or natural killer (NK) cells.
  • Recent network modeling analyses identified platelet-derived growth factor (PDGF) as a key master switch in controlling these survival pathways in T-cell LGL leukemia.
  • Here we show that an autocrine PDGF regulatory loop mediates survival of leukemic LGLs of both T- and NK-cell origin.
  • We found high levels of circulating PDGF-BB in platelet-poor plasma samples from LGL leukemia patients.
  • Leukemic cells expressed much higher levels of PDGFR-beta transcripts than purified normal CD8(+) T cells or NK cells.
  • We observed that phosphatidylinositol-3-kinase (PI3 kinase), Src family kinase (SFK), and downstream protein kinase B (PKB)/AKT pathways were constitutively activated in both T- and NK-LGL leukemia.
  • Neutralizing antibody to PDGF-BB inhibited PKB/AKT phosphorylation induced by LGL leukemia sera.
  • These results suggest that targeting of PDGF-BB, a pivotal regulator for the long-term survival of leukemic LGLs, may be an important therapeutic strategy.
  • [MeSH-major] Autocrine Communication. Leukemia, Large Granular Lymphocytic / pathology. Platelet-Derived Growth Factor / metabolism. Signal Transduction
  • [MeSH-minor] Antibodies, Neutralizing / pharmacology. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Enzyme-Linked Immunosorbent Assay. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation, Leukemic / drug effects. Humans. Immunohistochemistry. Lymphocytes / drug effects. Lymphocytes / enzymology. Lymphocytes / pathology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-sis. Receptor, Platelet-Derived Growth Factor beta / genetics. Receptor, Platelet-Derived Growth Factor beta / metabolism. Staining and Labeling. src-Family Kinases / antagonists & inhibitors

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  • (PMID = 19880494.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA112112
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neutralizing; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / platelet-derived growth factor BB; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ PMC2803691
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65. Crompton L, Khan N, Khanna R, Nayak L, Moss PA: CD4+ T cells specific for glycoprotein B from cytomegalovirus exhibit extreme conservation of T-cell receptor usage between different individuals. Blood; 2008 Feb 15;111(4):2053-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD4+ T cells specific for glycoprotein B from cytomegalovirus exhibit extreme conservation of T-cell receptor usage between different individuals.
  • Antigen-specific CD8(+) cytotoxic T cells often demonstrate extreme conservation of T-cell receptor (TCR) usage between different individuals, but similar characteristics have not been documented for CD4(+) T cells.
  • CD4(+) T cells predominantly have a helper immune role, but a cytotoxic CD4(+) T-cell subset has been characterized, and we have studied the cytotoxic CD4(+) T-cell response to a peptide from human cytomegalovirus glycoprotein B presented through HLA-DRB*0701.
  • We show that this peptide elicits a cytotoxic CD4(+) T-cell response that averages 3.6% of the total CD4(+) T-cell repertoire of cytomegalovirus-seropositive donors.
  • Moreover, CD4(+) cytotoxic T-cell clones isolated from different individuals exhibit extensive conservation of TCR usage, which indicates strong T-cell clonal selection for peptide recognition.
  • Remarkably, this TCR sequence was recently reported in more than 50% of cases of CD4(+) T-cell large granular lymphocytosis.
  • Immunodominance of cytotoxic CD4(+) T cells thus parallels that of CD8(+) subsets and suggests that cytotoxic effector function is critical to the development of T-cell clonal selection, possibly from immune competition secondary to lysis of antigen-presenting cells.
  • In addition, these TCR sequences are highly homologous to those observed in HLA-DR7(+) patients with CD4(+) T-cell large granular lymphocytosis and implicate cytomegalovirus as a likely antigenic stimulus for this disorder.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / virology. Cytomegalovirus Infections / immunology. Receptors, Antigen, T-Cell / immunology. Viral Envelope Proteins / immunology
  • [MeSH-minor] Cell Culture Techniques. Clone Cells. Dendritic Cells / immunology. Enzyme-Linked Immunosorbent Assay. Fetus. Fibroblasts / immunology. HLA-DR7 Antigen / immunology. Humans. RNA / genetics. RNA / isolation & purification. Skin / cytology. Skin / immunology

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  • (PMID = 17986665.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G9818340; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA-DR7 Antigen; 0 / Receptors, Antigen, T-Cell; 0 / Viral Envelope Proteins; 0 / glycoprotein B, Simplexvirus; 63231-63-0 / RNA
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66. Osuji N, Matutes E, Wotherspoon A, Catovsky D: Lessons from a case of T-cell large granular lymphocytic leukaemia suggesting that immunomodulatory therapy is more effective than intensive treatment. Leuk Res; 2005 Feb;29(2):225-8
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lessons from a case of T-cell large granular lymphocytic leukaemia suggesting that immunomodulatory therapy is more effective than intensive treatment.
  • Leukemia treatment strives to eradicate the malignant clone.
  • With T-cell large granular lymphocytic (LGL) leukemia, the onus of treatment appears to be modification of the disease rather than eradication of the clone.
  • We describe a case of T-cell LGL leukemia where aggressive, eradicative type therapy proved ineffective.
  • The patient achieved hematological response to low dose oral methotrexate after failing to respond to and/or tolerate eight previous treatments including CAMPATH-1H and peripheral blood stem cell transplantation.
  • We highlight the resistant nature of the LGL clone and discuss the relative merits of immunomodulatory type therapy in this disease.
  • [MeSH-major] Immunosuppressive Agents / pharmacology. Leukemia, T-Cell / drug therapy. Methotrexate / pharmacology. T-Lymphocytes / drug effects
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Humans. Immunotherapy / methods. Male. Peripheral Blood Stem Cell Transplantation / methods

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  • [CommentIn] Leuk Res. 2005 Feb;29(2):123-5 [15607357.001]
  • (PMID = 15607372.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Immunosuppressive Agents; 3A189DH42V / alemtuzumab; YL5FZ2Y5U1 / Methotrexate
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67. Sokol L, Loughran TP Jr: Large granular lymphocyte leukemia. Curr Hematol Malig Rep; 2007 Oct;2(4):278-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large granular lymphocyte leukemia.
  • Clonal diseases of large granular lymphocytes (LGLs) represent a spectrum of clinically rare lymphoproliferative malignancies arising from either mature T-cell (CD3(+)) or natural killer (NK)-cell (CD3(-)) lineages.
  • The clinical behavior of these disorders ranges from indolent to very aggressive.
  • Patients with symptomatic indolent T-cell or NK-cell LGL leukemia are usually treated with immunosuppressive therapies; in contrast, aggressive T-cell or NK-cell LGL leukemias require intensive chemotherapy regimens.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Clinical Trials as Topic. Combined Modality Therapy. Disease Progression. Female. Humans. Immunophenotyping. Killer Cells, Natural / pathology. Leukemia, T-Cell / complications. Leukemia, T-Cell / epidemiology. Leukemia, T-Cell / immunology. Leukemia, T-Cell / pathology. Leukemia, T-Cell / therapy. Male. Middle Aged. Myelodysplastic Syndromes / pathology. Neutropenia / etiology. Opportunistic Infections / etiology. Stem Cell Transplantation

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  • (PMID = 20425381.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Number-of-references] 39
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68. Friedman J, Schattner A, Shvidel L, Berrebi A: Characterization of T-cell large granular lymphocyte leukemia associated with Sjogren's syndrome-an important but under-recognized association. Semin Arthritis Rheum; 2006 Apr;35(5):306-11
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of T-cell large granular lymphocyte leukemia associated with Sjogren's syndrome-an important but under-recognized association.
  • OBJECTIVE: Patients with T-cell (CD3+) large granular lymphocyte (LGL) leukemia have a high prevalence of autoantibodies and associated autoimmune diseases.
  • We set to determine the prevalence of Sjogren's syndrome in LGL leukemia and its cytokine profile.
  • METHODS: Every patient with a confirmed diagnosis of LGL leukemia diagnosed at a single academic medical center over the last 15 years was evaluated for Sjogren's syndrome by questioning about sicca symptoms.
  • Supernatants obtained from T-LGL leukemic cells following phytohemagglutinin (PHA) activation were analyzed for cytokine production by enzyme-linked immunosorbent assay and patients with or without Sjogren's syndrome were compared with controls.
  • Supernatants of T-LGL leukemia cells incubated with PHA revealed markedly increased levels of multiple cytokines (especially soluble interleukin 2 receptor, tumor necrosis factor alpha, IL-6, IL-8) compared with healthy controls.
  • However, this increase was common to LGL leukemia patients with or without Sjogren's syndrome.
  • CONCLUSIONS: Sjogren's syndrome was commonly identified in the patients with T-cell LGL leukemia in this study.
  • [MeSH-major] Leukemia, T-Cell / epidemiology. Sjogren's Syndrome / epidemiology
  • [MeSH-minor] Adult. Aged. Autoantibodies / immunology. Cytokines / immunology. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Humans. Male. Middle Aged. Prevalence

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  • (PMID = 16616153.001).
  • [ISSN] 0049-0172
  • [Journal-full-title] Seminars in arthritis and rheumatism
  • [ISO-abbreviation] Semin. Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Cytokines
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69. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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70. Sokol L, Loughran TP Jr: Large granular lymphocyte leukemia. Oncologist; 2006 Mar;11(3):263-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large granular lymphocyte leukemia.
  • Clonal disorders of large granular lymphocytes (LGLs) represent a spectrum of biologically distinct lymphoproliferative diseases originating either from mature T cells (CD3+) or natural killer (NK) cells (CD3-).
  • Both subtypes, T-cell and NK-cell LGL leukemia, can manifest as indolent or aggressive disorders.
  • The majority of patients with T-cell LGL leukemia have a clinically indolent course with a median survival time >10 years.
  • Several cases of an aggressive variant (CD3+ CD56+) of T-cell LGL leukemia with a poor prognosis have also been reported.
  • Aggressive NK-cell LGL leukemia is usually a rapidly progressive disorder associated with Epstein-Barr virus (EBV), with a higher prevalence in Asia and South America.
  • This disease is usually refractory to conventional chemotherapy, with a median survival time of 2 months.
  • Chronic NK-cell leukemia/lymphocytosis is a rare EBV-negative disorder with an indolent clinical course.
  • The malignant origin of this subtype is uncertain because clonality is difficult to determine in LGLs of NK-cell origin.
  • [MeSH-major] Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / therapy
  • [MeSH-minor] Algorithms. Autoimmune Diseases / etiology. Cytogenetic Analysis. Diagnosis, Differential. Hematologic Diseases / etiology. Humans. Phenotype

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  • (PMID = 16549811.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 76
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71. Moura J, Rodrigues J, Santos AH, Teixeira Mdos A, Queirós ML, Santos M, Gonçalves M, Fonseca S, Laranjeira C, Rodrigues AS, Correia Júnior E, Ribeiro F, Acosta MJ, Lima M: Chemokine receptor repertoire reflects mature T-cell lymphoproliferative disorder clinical presentation. Blood Cells Mol Dis; 2009 Jan-Feb;42(1):57-63

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemokine receptor repertoire reflects mature T-cell lymphoproliferative disorder clinical presentation.
  • The World Health Organization classification of mature T-cell lymphoproliferative disorders, combines clinical, morphological and immunophenotypic data.
  • The latter is a major contributor to the classification, as well as to the understanding of the malignant T-cell behavior.
  • The fact that T-cell migration is regulated by chemokines should, in theory, enable us to identify tissue tropism and organ involvement by neoplastic T-cells by monitoring chemokine receptor surface expression.
  • To address this issue we compared the expression of several early and late inflammatory, homeostatic, and organ specific chemokine receptors on blood T-cells from normal individuals and patients with T-cell large granular lymphocytic leukemia and peripheral T-cell lymphoma.
  • T-cell large granular lymphocytic leukemia cells mainly express late inflammatory chemokine receptors (CXCR1 and CXCR2), whereas peripheral T-cell lymphoma cells usually express one or more organ homing receptors (CCR4, CCR6 and CCR7).
  • Compared to their normal counterparts, lymphoma T-cells displayed an exaggerated CCR4 expression, whereas leukemic T-cells had abnormally high CXCR1 and CXCR2 expression.
  • Further analysis revealed that, in leukemia patients, the percentage of neoplastic cells expressing CCR5 correlates directly with lymphocytosis.
  • In addition, in the case of CD8 T-cell leukemia patients, an inverse correlation with neutropenia was found.
  • In lymphoma patients, higher CCR4 and CCR7 expression is accompanied by lower to absent CCR5 expression.
  • [MeSH-major] Leukemia, T-Cell / classification. Leukemia, T-Cell / diagnosis. Lymphoma, T-Cell / classification. Lymphoma, T-Cell / diagnosis. Receptors, Chemokine / immunology. T-Lymphocyte Subsets / immunology

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  • (PMID = 18842429.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Receptors, Chemokine
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72. 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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  • The spleen is commonly affected by malignant lymphomas and the macroscopic findings of the spleen correlate with different lymphoma entities.
  • 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-major] Lymphoma / pathology. Splenic Neoplasms / pathology
  • [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
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD
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73. Yang J, Epling-Burnette PK, Painter JS, Zou J, Bai F, Wei S, Loughran TP Jr: Antigen activation and impaired Fas-induced death-inducing signaling complex formation in T-large-granular lymphocyte leukemia. Blood; 2008 Feb 1;111(3):1610-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antigen activation and impaired Fas-induced death-inducing signaling complex formation in T-large-granular lymphocyte leukemia.
  • Clonal T-cell expansion in patients with T-large-granular lymphocyte (LGL) leukemia occurs by an undefined mechanism that may be related to Fas apoptosis resistance.
  • We show that cells from LGL leukemia patients express increased levels of c-FLIP and display resistance to Fas-mediated apoptosis and abridged recruitment of proteins that comprise the death-inducing signaling complex (DISC), including the Fas-associated protein with death-domain (FADD) and caspase-8.
  • Exposure to interleukin-2 (IL-2) for only 24 hours sensitized leukemic LGL to Fas-mediated apoptosis with enhanced formation of the DISC, and increased caspase-8 and caspase-3 activities.
  • We observed dysregulation of c-FLIP by IL-2 in leukemic LGL, suggesting a role in Fas resistance.
  • Our results demonstrate that expanded T cells in patients with LGL leukemia display both functional and phenotypic characteristics of prior antigen activation in vivo and display reduced capacity for Fas-mediated DISC formation.

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  • (PMID = 17993614.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098472; United States / NCI NIH HHS / CA / R01 CA112112; United States / NIAID NIH HHS / AI / R01-AI056213; United States / NCI NIH HHS / CA / R01-CA94872; United States / NCI NIH HHS / CA / R01-CA112112; United States / CSRD VA / CX / I01 CX000114; United States / NIAID NIH HHS / AI / R01 AI056213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD8; 0 / Antigens, CD95; 0 / Interleukin-2; 0 / Receptors, Antigen, T-Cell
  • [Other-IDs] NLM/ PMC2214759
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74. Ishmael J, Dugard PH: A review of perchloroethylene and rat mononuclear cell leukemia. Regul Toxicol Pharmacol; 2006 Jul;45(2):178-84
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  • [Title] A review of perchloroethylene and rat mononuclear cell leukemia.
  • Mononuclear cell leukemia (MNCL) is an extremely common spontaneous disease of ageing F344 rats accompanied by splenomegaly, anemia, thrombocytopenia, and leukemic infiltration (initially of the spleen, liver, and lung).
  • MNCL cells possess natural killer (NK) cell characteristics and apparently, the neoplastic cells derive from large granular lymphocytes (LGL), hence the alternative name of LGL leukemia.
  • LGL leukemia is uncommon in man and occurs in two forms: T-LGL leukemia which has a chronic course, and the much rarer NK-LGL leukemia.
  • In addition to cell type, the latter resembles F344 LGL leukemia being acute in course and involving more pronounced splenomegaly and thrombocytopenia.
  • Chemically related increases in MNCL in F344 rats have not been associated with induction of human LGL leukemia.
  • [MeSH-major] Carcinogens, Environmental / toxicity. Leukemia, Lymphoid / chemically induced. Tetrachloroethylene / toxicity

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  • (PMID = 16684583.001).
  • [ISSN] 0273-2300
  • [Journal-full-title] Regulatory toxicology and pharmacology : RTP
  • [ISO-abbreviation] Regul. Toxicol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens, Environmental; TJ904HH8SN / Tetrachloroethylene
  • [Number-of-references] 53
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75. Reddy LH, Ferreira H, Dubernet C, Mouelhi SL, Desmaele D, Rousseau B, Couvreur P: Squalenoyl nanomedicine of gemcitabine is more potent after oral administration in leukemia-bearing rats: study of mechanisms. Anticancer Drugs; 2008 Nov;19(10):999-1006
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  • [Title] Squalenoyl nanomedicine of gemcitabine is more potent after oral administration in leukemia-bearing rats: study of mechanisms.
  • In an earlier report, we demonstrated the superior anticancer efficacy of orally administered squalenoyl gemcitabine (SQdFdC) nanomedicine over its parent drug gemcitabine on rats bearing RNK-16 large granular lymphocytic (LGL) leukemia.
  • In the present communication, we investigated the mechanisms behind this observation both at the cell and tissue level.
  • The mechanisms were investigated by performing cytotoxicity, cell uptake, and biodistribution experiments.
  • In the presence of cytidine deaminase, SQdFdC nanoassemblies resisted deamination and exerted significant anticancer activity in vitro against RNK-16 LGL leukemia cells, whereas the cytotoxicity of free gemcitabine decreased by approximately 83-fold, indicating its degradation due to deamination.
  • The resistance to deamination, followed by the improved pharmacokinetic and tissue distribution, and greater accumulation and retention at the level of cancer cells, are the key factors for the superiority of SQdFdC nanoassemblies over free gemcitabine against RNK-16 LGL leukemia in rats.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Deoxycytidine / analogs & derivatives. Leukemia, Experimental / drug therapy. Nanomedicine. Squalene / analogs & derivatives
  • [MeSH-minor] Administration, Oral. Animals. Cell Line, Tumor. Rats. Rats, Inbred F344

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  • (PMID = 18827565.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-(N)-tris-nor-qualenoyl-gemcitabine; 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 7QWM220FJH / Squalene; B76N6SBZ8R / gemcitabine
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76. Hodge DL, Yang J, Buschman MD, Schaughency PM, Dang H, Bere W, Yang Y, Savan R, Subleski JJ, Yin XM, Loughran TP Jr, Young HA: Interleukin-15 enhances proteasomal degradation of bid in normal lymphocytes: implications for large granular lymphocyte leukemias. Cancer Res; 2009 May 1;69(9):3986-94
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  • [Title] Interleukin-15 enhances proteasomal degradation of bid in normal lymphocytes: implications for large granular lymphocyte leukemias.
  • Large granular lymphocyte (LGL) leukemia is a clonal proliferative disease of T and natural killer (NK) cells.
  • Interleukin (IL)-15 is important for the development and progression of LGL leukemia and is a survival factor for normal NK and T memory cells.
  • Using an adoptive transfer model, we show that NK cells from Bid-deficient mice survive longer than cells from wild-type control mice when transferred into IL-15-null mice.
  • In normal human NK cells, IL-15 significantly reduces Bid accumulation.
  • In primary leukemic LGLs, Bid levels are low but are reversed with bortezomib treatment with subsequent increases in LGL apoptosis.
  • Overall, these data provide a novel molecular mechanism for IL-15 control of Bid that potentially links this cytokine to leukemogenesis through targeted proteasome degradation of Bid and offers the possibility that proteasome inhibitors may aid in the treatment of LGL leukemia.

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  • (PMID = 19366803.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / Intramural NIH HHS / / ZIA BC009283-25
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / Bid protein, mouse; 0 / Interleukin-15; 0 / Interleukin-2; 0 / Proteasome Inhibitors; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ NIHMS161038; NLM/ PMC2786937
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77. Sokol L, Agrawal D, Loughran TP Jr: Characterization of HTLV envelope seroreactivity in large granular lymphocyte leukemia. Leuk Res; 2005 Apr;29(4):381-7
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  • [Title] Characterization of HTLV envelope seroreactivity in large granular lymphocyte leukemia.
  • T-cell large granular lymphocyte (T-LGL) leukemia is a rare chronic lymphoproliferative disorder of unknown etiology.
  • We have previously reported that patients with T-LGL leukemia were seroreactive against BA21, a 34 amino acid peptide derived from HTLV-I envelope protein p21.
  • We tested sera from 70 patients with T-LGL leukemia and found that 21/70 (30%) of them were seroreactive against fusion peptide GST-BA21.
  • Competitive Western blot assay with use of fusion peptides revealed that the minimal HTLV-I epitope responsible for seroreactivity found in patients with T-LGL leukemia is a decapeptide PP10 (p21 env 417-426).
  • These results further define the epitope responsible for HTLV env seroreactivity observed in LGL leukemia.
  • [MeSH-major] Deltaretrovirus Antigens / blood. Leukemia, Lymphoid / virology. Viral Envelope Proteins / blood

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  • (PMID = 15725471.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Deltaretrovirus Antigens; 0 / Peptide Fragments; 0 / Recombinant Fusion Proteins; 0 / Viral Envelope Proteins
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78. Manucha V, Zhao F, Rodgers W: Atypical lymphoid cells in cerebrospinal fluid in acute Epstein Barr virus infection: a case report demonstrating a pitfall in cerebrospinal fluid cytology. Acta Cytol; 2008 May-Jun;52(3):334-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Cytologic examination of cerebrospinal fluid (CSF) continues to be important in the diagnosis of malignancies involving the leptomeninges.
  • A well-recognized pitfall is overinterpretation of the presence of atypical lymphocytes that resemble malignant lymphoid cells in the CSF.
  • A definite diagnosis is often difficult because of limited viability of cells and small sample size of CSF.
  • CASE: A 25-year-old patient with a past history of treated large granular lymphocytic leukemia and presence of a predominant population of large, atypical lymphoid cells in the CSF, giving us the impression of involvement with large cell lymphoma.
  • CONCLUSION: The presence of atypical cells in the CSF certainly warrants a detailed look at the patient's laboratory investigations and communication with the hematologist, because it may be the only specimen available for diagnosis on which therapy and prognosis is based.
  • [MeSH-major] Cerebrospinal Fluid / cytology. Cytological Techniques / methods. Epstein-Barr Virus Infections / cerebrospinal fluid. Epstein-Barr Virus Infections / pathology. Lymphocytes / pathology
  • [MeSH-minor] Adult. DNA, Viral / analysis. DNA, Viral / blood. Hepatomegaly / ultrasonography. Humans. Leukemia, Large Granular Lymphocytic / drug therapy. Lymph Nodes / pathology. Lymph Nodes / radiography. Lymphatic Diseases / pathology. Lymphatic Diseases / radiography. Male. Pleural Effusion / radiography. Splenectomy

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  • (PMID = 18540300.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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79. Dearden C: The role of alemtuzumab in the management of T-cell malignancies. Semin Oncol; 2006 Apr;33(2 Suppl 5):S44-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of alemtuzumab in the management of T-cell malignancies.
  • T-cell malignancies are rare, making up 10% to 15% of all lymphoid neoplasms in adults.
  • They include many different types of disorders such as T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia, adult T-cell leukemia/lymphoma, cutaneous T-cell lymphoma, and peripheral T-cell lymphoma, which are themselves divided into multiple subcategories.
  • Most T-cell malignancies arise as a result of chromosomal abnormalities, including T-cell receptor rearrangement anomalies.
  • Viral infections are implicated in the development of adult T-cell leukemia/lymphoma and some cases of peripheral T-cell lymphoma have been linked to Epstein-Barr virus or human immunodeficiency virus infection.
  • With the possible exception of T-cell large granular lymphocytic leukemia, which often has an indolent course, T-cell malignancies have not responded well to conventional chemotherapeutic treatment.
  • The introduction of monoclonal antibodies for the treatment of cancer has changed the outlook for patients with T-cell malignancies.
  • Recent studies with single-agent alemtuzumab, an anti-CD52 monoclonal antibody, have shown improved response rates and survival in patients with T-cell prolymphocytic leukemia and cutaneous T-cell lymphoma.
  • Preliminary data also suggest that alemtuzumab may have activity in patients with heavily pretreated peripheral T-cell lymphoma who are refractory to conventional chemotherapy.
  • Preclinical studies with mice bearing human adult T-cell leukemia/lymphoma cells suggest that alemtuzumab may have a potential therapeutic role in this setting.
  • Treatment of T-cell hematologic malignancies with alemtuzumab appears promising.
  • Earlier treatment and combination with chemotherapeutic agents may improve treatment outcome for patients with these malignancies and allow for consolidation with stem cell transplant strategies in selected patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Neoadjuvant Therapy. Remission Induction. Stem Cell Transplantation. Survival Rate

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  • (PMID = 16720203.001).
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 103
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80. Wada T, Yokoyama T, Nakagawa H, Asai E, Toga A, Sakakibara Y, Shibata F, Tone Y, Shimizu M, Toma T, Yachie A: Flow cytometric analysis of skin blister fluid induced by mosquito bites in a patient with chronic active Epstein-Barr virus infection. Int J Hematol; 2009 Dec;90(5):611-5
MedlinePlus Health Information. consumer health - Insect Bites and Stings.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flow cytometric analysis of skin blister fluid induced by mosquito bites in a patient with chronic active Epstein-Barr virus infection.
  • In chronic active Epstein-Barr virus (EBV) infection (CAEBV), ectopic EBV infection has been described in T or natural killer (NK) cells.
  • NK cell-type infection (NK-CAEBV) is characterized by large granular lymphocytosis, high IgE levels and unusual reactions to mosquito bites, including severe local skin reactions, fever and liver dysfunction.
  • Herein, we describe a patient with NK-CAEBV whose blister fluid after mosquito bites was analyzed.
  • The patient exhibited significant increases in the percentage of CD56(+) NK cells in the fluid compared with a simple mosquito allergy, in which the majority of infiltrated cells were CD203c(+) cells, indicating basophils and/or mast cells.
  • These results suggest that CD203c(+) cells as well as NK cells may play pathogenic roles in the severe skin reactions to mosquito bites in NK-CAEBV.
  • [MeSH-minor] Animals. Body Fluids. Child. Chronic Disease. Culicidae. Flow Cytometry / methods. Humans. Killer Cells, Natural / pathology. Male. Phosphoric Diester Hydrolases / analysis. Pyrophosphatases / analysis

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  • [Cites] Curr Opin Allergy Clin Immunol. 2007 Aug;7(4):350-4 [17620829.001]
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  • (PMID = 19915947.001).
  • [ISSN] 1865-3774
  • [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 / ENPP3 protein, human; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.6.1.- / Pyrophosphatases
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81. Rauch D, Gross S, Harding J, Bokhari S, Niewiesk S, Lairmore M, Piwnica-Worms D, Ratner L: T-cell activation promotes tumorigenesis in inflammation-associated cancer. Retrovirology; 2009 Dec 17;6:116
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  • [Title] T-cell activation promotes tumorigenesis in inflammation-associated cancer.
  • Chronic inflammation has long been associated with a wide range of malignancies, is now widely accepted as a risk factor for development of cancer, and has been implicated as a promoter of a variety of cancers including hematopoietic malignancies.
  • We have described a mouse model uniquely suited to examine the link between inflammation and lymphoma in which the Tax oncogene, expressed in activated T and NK cells, perpetuates chronic inflammation that begins as microscopic intraepithelial lesions and develops into inflammatory nodules, subcutaneous tumors, and large granular lymphocytic leukemia.
  • Here we demonstrate that bioluminescence induction in these mice correlated with inflammation resulting from wounding, T cell activation, and exposure to chemical agents.
  • In experiments in which long-term effects of inflammation on disease outcome were monitored, the development of lymphoma was promoted by an inflammatory stimulus.
  • Finally we demonstrated that activation of T-cells in T-cell receptor (TCR) transgenic TAX-LUC animals dramatically exacerbated the development of subcutaneous TCR- CD16+ LGL tumors.

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  • (PMID = 20017942.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100730-07; United States / NCI NIH HHS / CA / CA63417; United States / NCI NIH HHS / CA / CA10073; United States / NCI NIH HHS / CA / CA10521; United States / NCI NIH HHS / CA / CA94056; United States / NCI NIH HHS / CA / CA100730-07; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / NF-kappa B; 0 / Receptors, Antigen, T-Cell
  • [Other-IDs] NLM/ PMC2806367
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82. Osuji N, Matutes E, Tjonnfjord G, Grech H, Del Giudice I, Wotherspoon A, Swansbury JG, Catovsky D: T-cell large granular lymphocyte leukemia: A report on the treatment of 29 patients and a review of the literature. Cancer; 2006 Aug 1;107(3):570-8
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  • [Title] T-cell large granular lymphocyte leukemia: A report on the treatment of 29 patients and a review of the literature.
  • BACKGROUND: To the authors' knowledge, there is no standard treatment for patients with T-cell large granular lymphocyte (LGL) leukemia.
  • METHODS: The authors report on the use of immunosuppressants (cyclosporin A [CSA] and low-dose oral methotrexate [MTX] given continuously) and cytotoxic agents in the treatment of 29 patients with T-cell LGL leukemia age over the past 20 years.
  • Alemtuzumab induced a PR in 1 patient who had refractory disease.
  • CONCLUSIONS: Both MTX and CSA were efficacious in the treatment of T-cell LGL leukemia but generally required long-term maintenance therapy.
  • The authors highlight the risks of second malignancies and persistence of bone marrow disease.
  • Although MTX and CSA were effective as first-line therapy, alemtuzumab and pentostatin merit further investigation, particularly for refractory disease.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Leukemia, Lymphoid / drug therapy. Leukemia, T-Cell / drug therapy

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  • [Copyright] Copyright 2006 American Cancer Society.
  • [ErratumIn] Cancer. 2006 Dec 1;107(11):2744
  • (PMID = 16795070.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 395575MZO7 / Pentostatin; 83HN0GTJ6D / Cyclosporine; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 41
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83. Ahmad E, Kingma DW, Jaffe ES, Schrager JA, Janik J, Wilson W, Stetler-Stevenson M: Flow cytometric immunophenotypic profiles of mature gamma delta T-cell malignancies involving peripheral blood and bone marrow. Cytometry B Clin Cytom; 2005 Sep;67(1):6-12
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  • [Title] Flow cytometric immunophenotypic profiles of mature gamma delta T-cell malignancies involving peripheral blood and bone marrow.
  • BACKGROUND: In this study we compared clinical findings with flow cytometric immunophenotypic results in a series of patients with aggressive and indolent gamma delta T-cell malignancies with peripheral blood and/or bone marrow involvement.
  • METHODS: Gamma delta T-cell malignancies were detected based on flow cytometric demonstration of an abnormal T-cell population staining positive with T-cell receptor gamma delta and confirmed by morphologic and clinical reviews.
  • Hepatosplenic and cutaneous gamma delta T-cell lymphomas had an aggressive clinical course, whereas the gamma delta T-cell large granular lymphocyte (LGL) leukemias had an indolent course.
  • Expressions of CD5, CD8, CD16, and CD57 differed in gamma delta T-cell LGL leukemia compared with hepatosplenic and cutaneous gamma delta T-cell lymphomas.
  • CONCLUSIONS: Gamma delta T-cell malignancies have a poor prognosis with the exception of gamma delta T-cell LGL leukemia (indolent process).
  • Because CD57 expression is specific for gamma delta T-cell LGL leukemias, expression of this antigen may be associated with a more indolent clinical course.
  • Because cutaneous gamma delta T-cell lymphoma can present with peripheral blood involvement, flow cytometric evaluation of peripheral blood is important in staging these patients.
  • [MeSH-major] Bone Marrow / immunology. Flow Cytometry. Immunophenotyping. Leukemia, T-Cell / immunology. Lymphoma, T-Cell / immunology. Receptors, Antigen, T-Cell, gamma-delta / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Separation. Female. Humans. Male. Neoplasms / diagnosis. Neoplasms / immunology. Prognosis

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15973700.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, gamma-delta
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84. Choi YL, Moriuchi R, Osawa M, Iwama A, Makishima H, Wada T, Kisanuki H, Kaneda R, Ota J, Koinuma K, Ishikawa M, Takada S, Yamashita Y, Oshimi K, Mano H: Retroviral expression screening of oncogenes in natural killer cell leukemia. Leuk Res; 2005 Aug;29(8):943-9
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  • [Title] Retroviral expression screening of oncogenes in natural killer cell leukemia.
  • Aggressive natural killer cell leukemia (ANKL) is an intractable malignancy that is characterized by the outgrowth of NK cells.
  • To identify transforming genes in ANKL, we constructed a retroviral cDNA expression library from an ANKL cell line KHYG-1.
  • Mutation-specific PCR analysis indicated that the KRAS mutation was present only in KHYG-1 cells, not in another ANKL cell line or in clinical specimens (n=8).
  • [MeSH-major] Gene Expression Regulation, Leukemic. Genetic Testing / methods. Killer Cells, Natural / metabolism. Leukemia / genetics. Oncogenes. Proto-Oncogene Proteins / genetics. Retroviridae / genetics
  • [MeSH-minor] 3T3 Cells. Animals. Cell Line. DNA, Complementary / genetics. Gene Library. Humans. Mice. Mutation. Transfection. ras Proteins

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  • (PMID = 15978945.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
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85. Lazaro E, Caubet O, Menard F, Pellegrin JL, Viallard JF: [Large granular lymphocyte leukemia]. Presse Med; 2007 Nov;36(11 Pt 2):1694-700
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  • [Title] [Large granular lymphocyte leukemia].
  • [Transliterated title] Leucémies à grands lymphocytes granuleux.
  • Large granular lymphocyte (LGL) leukemia is a clonal proliferation of cytotoxic cells, either CD3(+) (T-cell) or CD3(-) (natural killer, or NK).
  • Both subtypes can manifest as indolent or aggressive disorders.
  • T-LGL leukemia is associated with cytopenias and autoimmune diseases and most often has an indolent course and good prognosis.
  • NK-LGL leukemias can be more aggressive.
  • LGL expansion is currently hypothesized to be a virus (Ebstein Barr or human T-cell leukemia viruses) antigen-driven T-cell response that involves disruption of apoptosis.
  • The diagnosis of T-LGL is suggested by flow cytometry and confirmed by T-cell receptor gene rearrangement studies.
  • Clonality is difficult to determine in NK-LGL but use of monoclonal antibodies specific for killer cell immunoglobulin-like receptor (KIR) has improved this process.
  • Treatment is required when T-LGL leukemia is associated with recurrent infections secondary to chronic neutropenia.
  • NK-LGL leukemias may be more aggressive and refractory to conventional therapy.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic

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  • (PMID = 17596907.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 35
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86. Rossi D, Franceschetti S, Capello D, De Paoli L, Lunghi M, Conconi A, Gaidano G: Transient monoclonal expansion of CD8+/CD57+ T-cell large granular lymphocytes after primary cytomegalovirus infection. Am J Hematol; 2007 Dec;82(12):1103-5
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  • [Title] Transient monoclonal expansion of CD8+/CD57+ T-cell large granular lymphocytes after primary cytomegalovirus infection.
  • Lymphocytosis associated with viral infection is generally polyclonal or oligoclonal.
  • In this article, we describe a case of transient monoclonal CD8+/CD57+ T-cell lymphocytosis with large granular lymphocyte (LGL) morphology occurring after primary CMV infection and review cases of virus-associated monoclonal CD8+ T-cell expansions reported in the literature.
  • Several clinical features shared by virus-associated monoclonal CD8+ T-cell expansions suggest the reactive nature of the lymphocytosis.
  • Based on this, our case report and those reported in the literature support the notion that T-cell receptor clonality per se is not necessarily indicative of malignancy.
  • These observations further corroborate the need for a close follow-up before assigning the diagnosis of LGL leukemia to individuals developing monoclonal CD8+ T-cell expansions.
  • [MeSH-major] Antigens, CD57 / immunology. Antigens, CD8 / immunology. Cytomegalovirus Infections / immunology. Lymphocytosis / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Antigens, CD / immunology. DNA Repeat Expansion. Humans. Lymphocyte Activation. Male. Middle Aged

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  • (PMID = 17626255.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD57; 0 / Antigens, CD8
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87. Risitano AM, Maciejewski JP, Muranski P, Wlodarski M, O'Keefe C, Sloand EM, Young NS: Large granular lymphocyte (LGL)-like clonal expansions in paroxysmal nocturnal hemoglobinuria (PNH) patients. Leukemia; 2005 Feb;19(2):217-22
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  • [Title] Large granular lymphocyte (LGL)-like clonal expansions in paroxysmal nocturnal hemoglobinuria (PNH) patients.
  • In vivo expansion of dominant T-cell clones can reflect an antigen-driven immune response but may also represent autonomous proliferation, such as in large granular lymphocytic (LGL)-leukemia.
  • T-cell clonality can be assessed by a combination of T-cell receptor (TCR) flow cytometry and complementarity-determining-region-3 (CDR3) molecular analysis.
  • We studied 24 PNH patients for evidence of in vivo dominant T-cell responses by flow cytometry; TCR-Vbeta-specific expansions were identified in all patients.
  • In four cases, extreme expansions of one Vbeta-subset of CD8+/CD28-/CD56+ (effector) phenotype mimicked subclinical LGL-disease.
  • We conclude that the molecular analysis of TCR-beta chain may demonstrate clonal LGL-like expansions at unexpected frequency in PNH patients.
  • Our observations blur the classical boundaries between different bone marrow failure syndromes such as AA, PNH, and LGL, and support the hypothesis that in PNH, the mutant clone may expand as a result of an immune-escape from antigen-driven lymphocyte attack on hematopoietic progenitors.
  • [MeSH-major] Leukemia, Lymphoid / etiology. Membrane Proteins / blood

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  • (PMID = 15668701.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / Glycosylphosphatidylinositols; 0 / Membrane Proteins; 0 / Peptide Fragments; 0 / phosphatidylinositol glycan-class A protein
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88. Olteanu H, Karandikar NJ, Eshoa C, Kroft SH: Laboratory findings in CD4(+) large granular lymphocytoses. Int J Lab Hematol; 2010 Feb;32(1 Pt 1):e9-16
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  • [Title] Laboratory findings in CD4(+) large granular lymphocytoses.
  • Large granular lymphocytic (LGL) leukemia is an uncommon disorder of mature T or natural killer (NK) cells.
  • Most T-LGL proliferations are CD3(+)/CD8(+), although rare CD4(+) clonal T-LGL expansions have been reported.
  • We report the clinicopathologic features of eight patients with aberrant CD4(+), cytotoxic T-cell lymphocytoses.
  • Morphologic expansions of granulated lymphocytes were evident in 6/8.
  • Abnormal levels of expression of two or more T-cell antigens were seen in all cases.
  • Our results support that CD4(+) T-LGL lymphocytosis is a clonal disorder with clinicopathologic characteristics distinct from the more common CD8(+) variant.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. Leukemia, Large Granular Lymphocytic / immunology

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  • (PMID = 20089001.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, CD57
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89. Liu X, Ryland L, Yang J, Liao A, Aliaga C, Watts R, Tan SF, Kaiser J, Shanmugavelandy SS, Rogers A, Loughran K, Petersen B, Yuen J, Meng F, Baab KT, Jarbadan NR, Broeg K, Zhang R, Liao J, Sayers TJ, Kester M, Loughran TP Jr: Targeting of survivin by nanoliposomal ceramide induces complete remission in a rat model of NK-LGL leukemia. Blood; 2010 Nov 18;116(20):4192-201
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  • [Title] Targeting of survivin by nanoliposomal ceramide induces complete remission in a rat model of NK-LGL leukemia.
  • The natural killer (NK) type of aggressive large granular lymphocytic (LGL) leukemia is a fatal illness that pursues a rapid clinical course.
  • Here we report that the survivin was highly expressed in both aggressive and chronic leukemic NK cells but not in normal NK cells.
  • In vitro treatment of human and rat NK-LGL leukemia cells with cell-permeable, short-chain C₆-ceramide (C₆) in nanoliposomal formulation led to caspase-dependent apoptosis and diminished survivin protein expression, in a time- and dose-dependent manner.
  • Importantly, systemic intravenous delivery of nanoliposomal ceramide induced complete remission in the syngeneic Fischer F344 rat model of aggressive NK-LGL leukemia.
  • These data suggest that in vivo targeting of survivin through delivery of nanoliposomal C₆-ceramide may be a promising therapeutic approach for a fatal leukemia.

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  • (PMID = 20671121.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA133525; United States / NCI NIH HHS / CA / R01 CA098472; United States / NCI NIH HHS / CA / CA133525; United States / NCI NIH HHS / CA / CA098472; United States / NCI NIH HHS / CA / N01CO12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Birc5 protein, rat; 0 / Ceramides; 0 / Liposomes; 0 / Microtubule-Associated Proteins; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC2993625
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90. Isoda A, Tsukamoto N, Mitsui T, Yamane A, Hatsumi N, Matsushima T, Murakami H, Nojima Y, Karasawa M: Expression of CD55 and CD59 on peripheral blood cells in patients with lymphoproliferative disease of granular lymphocytes. Int J Lab Hematol; 2007 Feb;29(1):52-7
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  • [Title] Expression of CD55 and CD59 on peripheral blood cells in patients with lymphoproliferative disease of granular lymphocytes.
  • Lymphoproliferative disease of granular lymphocytes (LDGL) is a disorder characterized by the clonal expansion of granular lymphocytes.
  • It has recently been shown that the clonal expansion of granular lymphocytes occurs in patients with paroxysmal nocturnal hemoglobinuria (PNH) in a subclinical fashion.
  • An unexpected finding was the significantly lower CD55/59 expression on granular lymphocytes from patients with CD16(+)CD56(-) phenotype LDGL than from patients with CD16(+)CD56(+) phenotype LDGL, or natural killer (NK) and NK/T lymphocytes from healthy individuals.
  • The positive correlation between the expression of CD56 and CD55/59 might have some relevance to the functional properties of the CD56(+) subset of large granular lymphocytes.
  • [MeSH-major] Antigens, CD55 / biosynthesis. Antigens, CD59 / biosynthesis. Gene Expression Regulation. Killer Cells, Natural / metabolism. Lymphoproliferative Disorders / metabolism. T-Lymphocytes / metabolism

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  • (PMID = 17224008.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD55; 0 / Antigens, CD59; 101754-01-2 / CD59 protein, human
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91. Viny AD, Lichtin A, Pohlman B, Loughran T, Maciejewski J: Chronic B-cell dyscrasias are an important clinical feature of T-LGL leukemia. Leuk Lymphoma; 2008 May;49(5):932-8
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] Chronic B-cell dyscrasias are an important clinical feature of T-LGL leukemia.
  • T cell large granular lymphocyte leukemia (T-LGL) is characterised by semiautonomous proliferation of monoclonal cytotoxic T lymphocytes, which can result in neutropenia, splenomegaly, and is associated with various autoimmune disorders, particularly rheumatoid arthritis.
  • The coexistence of T-LGL leukemia with B cell abnormalities has previously been identified in case reports.
  • Analysis of 63 T-LGL patients revealed a frequent association with humoral immune system abnormalities.
  • We identified coexisting B cell dyscrasias in 17 T-LGL patients (27% of total), of whom 12 had monoclonal gammopathy of unknown significance (MGUS) (19%), and 5 had chronic lymphocytic leukemia (CLL) (8%).
  • The presence of both MGUS and CLL was found in 2 patients (3%) and follicular lymphoma was identified with MGUS in another T-LGL patient (2%).
  • Additionally, polyclonal hypergammaglobulinemia or hypogammaglobulinemia was found in 10 additional LGL leukemia patients bringing the total frequency of B cell abnormalities in T-LGL leukemia to 43% in our cohort.
  • The co-association of B cell pathology with T-LGL suggests that either a common antigen drives clonal B and T cells, or that humoral malignancy could serve as the stimulus for lymphocyte expansion representing an overactive anti-tumour surveillance.
  • [MeSH-major] B-Lymphocytes / pathology. Leukemia, Large Granular Lymphocytic / etiology. Lymphoproliferative Disorders / complications
  • [MeSH-minor] Agammaglobulinemia / complications. Comorbidity. Humans. Hypergammaglobulinemia / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Lymphoma, Follicular / complications. Monoclonal Gammopathy of Undetermined Significance / complications

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  • [CommentIn] Leuk Lymphoma. 2008 May;49(5):845-6 [18464104.001]
  • (PMID = 18452068.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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92. Sabnani I, Zucker MJ, Tsang P, Palekar S: Clonal T-large granular lymphocyte proliferation in solid organ transplant recipients. Transplant Proc; 2006 Dec;38(10):3437-40
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  • [Title] Clonal T-large granular lymphocyte proliferation in solid organ transplant recipients.
  • Large granular lymphocytic (LGL) leukemia is a rare disorder, usually caused by clonal proliferation of CD3+ CD57+ T-LGL cells.
  • T-cell clonality is confirmed by rearrangements of the T-cell receptor (TCR) gene.
  • Characteristic features of T-LGL leukemia include neutropenia, anemia, and constitutional symptoms such as fatigue.
  • The purpose of this study was to determine the prevalence of T-LGL proliferation in solid organ transplant recipients and demonstrate its association with leukopenia and anemia.
  • Ten of 14 (71%) cardiac transplant patients and 4 of 9 (44%) renal transplant patients, without evidence of either allograft rejection or a viral syndrome, were found to have clonal expansion of T-LGL cells.
  • Although TCR gene rearrangement is considered a hallmark of T-LGL leukemia, we believe that this monoclonality is not a true form of posttransplant lymphoproliferative disorder.
  • [MeSH-major] Heart Transplantation / immunology. Kidney Transplantation / immunology. Lymphocyte Activation. T-Lymphocytes / immunology
  • [MeSH-minor] Anemia / immunology. Antigens, CD3 / immunology. Cell Division. Gene Rearrangement, T-Lymphocyte. Humans. Leukopenia / immunology. Postoperative Complications / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 17175296.001).
  • [ISSN] 0041-1345
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3
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93. Wlodarski MW, Nearman Z, Jiang Y, Lichtin A, Maciejewski JP: Clonal predominance of CD8(+) T cells in patients with unexplained neutropenia. Exp Hematol; 2008 Mar;36(3):293-300

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: T-cell-mediated autoimmunity may be involved in some cases of idiopathic neutropenia.
  • We hypothesized that a precise T-cell receptor repertoire analysis may uncover cytotoxic T-cell (CTL) expansions that are less pronounced than those seen in T large granular lymphocyte leukemia (T-LGL), but are pathophysiologically analogous and thus can serve as markers of a T-cell-mediated process.
  • MATERIALS AND METHODS: Using rational algorithms for T-cell receptor analysis and in vivo tracking of CTL responses previously established in our laboratory, we studied patients with unexplained chronic neutropenia (n = 20), T-LGL (n = 15), and healthy controls (n = 12).
  • In comparison to LGL leukemia, these clones were less immunodominant, but clearly discernible from subclinical lymphoproliferations in controls.
  • Oligogoclonal CTL expansions in chronic neutropenia may indicate an ongoing autoimmune process, while highly polarized monoclonalities in a subset of neutropenic LGL patients may represent the "extreme" end of the clonal continuum.

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  • (PMID = 18279717.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA113972-04; United States / NCRR NIH HHS / RR / U54 RR 019391; United States / NCRR NIH HHS / RR / U54 RR019397-05S16959; United States / NCI NIH HHS / CA / CA 113972-01; United States / NHLBI NIH HHS / HL / R01 HL 73429; United States / NCI NIH HHS / CA / R01 CA113972; United States / NCRR NIH HHS / RR / RR019397-05S16959; United States / NHLBI NIH HHS / HL / R01 HL073429-04; United States / NCI NIH HHS / CA / R01 CA113972-04; United States / NHLBI NIH HHS / HL / HL073429-04; United States / NCRR NIH HHS / RR / U54 RR019397; United States / NHLBI NIH HHS / HL / R01 HL073429; United States / NCRR NIH HHS / RR / S10 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ NIHMS83525; NLM/ PMC2643087
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94. Howe EC, Wlodarski M, Ball EJ, Rybicki L, Maciejewski JP: Killer immunoglobulin-like receptor genotype in immune-mediated bone marrow failure syndromes. Exp Hematol; 2005 Nov;33(11):1357-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Killer immunoglobulin-like receptor genotype in immune-mediated bone marrow failure syndromes.
  • OBJECTIVE: Recent reports have shown that killer immunoglobulin-like receptors (KIR) and KIR ligand (KIR-L) genotype play a role in the pathophysiology of autoimmune disorders.
  • The objective of this study is to establish the frequency of specific KIR genes and KIR-L alleles in aplastic anemia (AA), paroxysmal nocturnal hemoglobinuria (PNH), myelodysplasia (MDS), and large granular lymphocyte leukemia (LGL), as compared with healthy control patients.
  • METHODS: KIR genotyping was performed on DNA from 113 patients with AA, PNH, MDS, and LGL using sequence specific primer amplification.
  • [MeSH-minor] Anemia, Aplastic / genetics. Anemia, Aplastic / immunology. Case-Control Studies. Gene Frequency. Genotype. Hemoglobinuria, Paroxysmal / genetics. Hemoglobinuria, Paroxysmal / immunology. Histocompatibility Antigens Class I / genetics. Humans. Immunity. Leukemia, Lymphoid / genetics. Leukemia, Lymphoid / immunology. Ligands. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / immunology. Receptors, KIR. Syndrome

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  • (PMID = 16263420.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I; 0 / Ligands; 0 / Receptors, Immunologic; 0 / Receptors, KIR
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95. Mohan SR, Maciejewski JP: Diagnosis and therapy of neutropenia in large granular lymphocyte leukemia. Curr Opin Hematol; 2009 Jan;16(1):27-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and therapy of neutropenia in large granular lymphocyte leukemia.
  • PURPOSE OF REVIEW: T-cell large granular lymphocyte leukemia is a chronic clonal lymphoproliferation of cytotoxic T cells often associated with immune-mediated cytopenias.
  • This review will address the diagnostic challenges of and therapeutic options for T-cell large granular lymphocyte leukemia.
  • SUMMARY: T-cell large granular lymphocyte leukemia may assume an indolent course but sometimes manifests with significant cytopenias.
  • In these cases, a variety of agents maybe used successfully though chronic therapy is often necessary.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / complications. Leukemia, Large Granular Lymphocytic / therapy. Neutropenia / therapy

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  • (PMID = 19057202.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 89
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96. van Steensel MA, van Gelder M, van Marion AM, Kremer B, Frank J: T-cell large granular lymphocytic leukaemia with an uncommon clinical and immunological phenotype. Acta Derm Venereol; 2009;89(2):172-4
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  • [Title] T-cell large granular lymphocytic leukaemia with an uncommon clinical and immunological phenotype.
  • Histopathological examination and peripheral blood analysis both showed a population of T-cell large granular lymphocytes, which were CD1+, CD2+, CD5+, CD7+ and CD16+, with expression of cutaneous lymphocyte-associated antigen.
  • Further laboratory examination revealed severe neutropaenia, relative lymphocytosis and a clonally rearranged T-cell receptor.
  • The cutaneous manifestation of T-cell large granular lymphocytic leukaemia is very rare.
  • In this particular patient, however, it was instrumental in establishing the diagnosis and may have been enabled by the expression of cutaneous lymphocyte-associated antigen on the cell surface.
  • [MeSH-major] Leukemia, Large Granular Lymphocytic / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Antigens, Differentiation, T-Lymphocyte. Antigens, Neoplasm / analysis. Cheek. Humans. Lymphocyte Subsets. Male. Membrane Glycoproteins / analysis. Skin / immunology

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  • (PMID = 19326004.001).
  • [ISSN] 0001-5555
  • [Journal-full-title] Acta dermato-venereologica
  • [ISO-abbreviation] Acta Derm. Venereol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / CTAGE1 protein, human; 0 / Membrane Glycoproteins
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97. Kim DH, Kamel-Reid S, Chang H, Sutherland R, Jung CW, Kim HJ, Lee JJ, Lipton JH: Natural killer or natural killer/T cell lineage large granular lymphocytosis associated with dasatinib therapy for Philadelphia chromosome positive leukemia. Haematologica; 2009 Jan;94(1):135-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natural killer or natural killer/T cell lineage large granular lymphocytosis associated with dasatinib therapy for Philadelphia chromosome positive leukemia.
  • Dasatinib, a dual tyrosine kinase inhibitor, is known to modulate or suppress T-cell activation and proliferation.
  • We report a series of 8 patients who developed chronic peripheral lymphocytosis, identified as natural killer cells or natural killer/T-cells based on their large granular lymphocyte morphologies and CD16(+), CD56(+), CD3(-) or CD3(+) immunophenotypic profiles, out of 18 patients receiving dasatinib therapy.
  • All cases that developed large granular lymphocyte lymphocytosis achieved optimal molecular response (8/8 in large granular lymphocyte(+) patients vs. 3/10 in large granular lymphocyte(-) patients, p=0.002).
  • A (51)Cr release assay demonstrated that natural killer cell cytotoxicity has been enhanced in a case of large granular lymphocyte lymphocytosis compared to normal healthy donors, and that natural killer cell cytotoxicity in dasatinib-responders was superior to that in non-responders.
  • In summary, the present study suggests that natural killer or natural killer/T cell lineage large granular lymphocyte lymphocytosis develops in association with dasatinib therapy and that large granular lymphocyte might have a therapeutic effect on Ph(+) leukemic cells.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cell Lineage / drug effects. Killer Cells, Natural / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lymphocytosis / chemically induced. Natural Killer T-Cells / drug effects. Pyrimidines / adverse effects. Thiazoles / adverse effects

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  • (PMID = 19066329.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC2625403
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98. Kusumoto S, Mori S, Nosaka K, Morita-Hoshi Y, Onishi Y, Kim SW, Watanabe T, Heike Y, Tanosaki R, Takaue Y, Tobinai K: T-cell large granular lymphocyte leukemia of donor origin after cord blood transplantation. Clin Lymphoma Myeloma; 2007 Jul;7(7):475-9
MedlinePlus Health Information. consumer health - Blood Transfusion and Donation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell large granular lymphocyte leukemia of donor origin after cord blood transplantation.
  • We report the first case of T-cell large granular lymphocyte leukemia of donor origin after a second cord blood transplantation for acute myeloid leukemia, and review the literature regarding rare cases of T-cell-origin posttransplantation lymphoproliferative disorders.
  • [MeSH-major] Blood Donors. Cord Blood Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Leukemia, T-Cell / etiology. Neoplasms, Second Primary / etiology


99. Bareau B, Rey J, Hamidou M, Donadieu J, Morcet J, Reman O, Schleinitz N, Tournilhac O, Roussel M, Fest T, Lamy T: Analysis of a French cohort of patients with large granular lymphocyte leukemia: a report on 229 cases. Haematologica; 2010 Sep;95(9):1534-41
Genetic Alliance. consumer health - Large granular lymphocyte leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of a French cohort of patients with large granular lymphocyte leukemia: a report on 229 cases.
  • BACKGROUND: Large granular lymphocyte leukemia is a rare lymphoproliferative disorder associated with autoimmune diseases and impaired hematopoiesis.
  • This study describes the clinical and biological characteristics of 229 patients with T-cell or NK-cell large granular lymphocyte leukemia.
  • DESIGN AND METHODS: The diagnosis was based on a large granular lymphocyte expansion (> 0.5x10(9)/L) lasting more than 6 months.
  • Monoclonal T-cell receptor gamma gene rearrangement was detected in all the cases of T-cell large granular lymphocyte leukemia.
  • Patients with chronic NK-cell lymphocytosis had an indolent disease, while those with multiorgan large granular lymphocyte infiltration and an aggressive clinical disease were considered to have NK-cell large granular lymphocyte leukemia.
  • RESULTS: The diagnosis of T-cell large granular lymphocyte leukemia was confirmed in 201 cases, chronic NK-cell lymphocytosis in 27 cases and NK-cell large granular lymphocyte leukemia in one case.
  • There were 15 large granular lymphocyte leukemia-related deaths.
  • CONCLUSIONS: Patients with T-cell large granular lymphocyte leukemia and chronic NK-cell lymphocytosis have similar clinical and biological features and responses to treatment.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Large Granular Lymphocytic / diagnosis. Leukemia, Large Granular Lymphocytic / epidemiology. T-Lymphocytes / pathology
  • [MeSH-minor] Adult. Aged. Cohort Studies. Female. France / epidemiology. Humans. Lymphocytosis / diagnosis. Male. Middle Aged. Registries. Treatment Outcome

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  • (PMID = 20378561.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2930955
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100. Gattazzo C, Teramo A, Miorin M, Scquizzato E, Cabrelle A, Balsamo M, Agostini C, Vendrame E, Facco M, Albergoni MP, Trentin L, Vitale M, Semenzato G, Zambello R: Lack of expression of inhibitory KIR3DL1 receptor in patients with natural killer cell-type lymphoproliferative disease of granular lymphocytes. Haematologica; 2010 Oct;95(10):1722-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of expression of inhibitory KIR3DL1 receptor in patients with natural killer cell-type lymphoproliferative disease of granular lymphocytes.
  • BACKGROUND: Natural killer cell-type lymphoproliferative disease of granular lymphocytes is a disorder characterized by chronic proliferation of CD3(-)CD16(+) granular lymphocytes.
  • By flow cytometry analysis, we previously demonstrated a dysregulation in killer immunoglobulin-like receptor (KIR) expression in natural killer cells from patients with this lymphoproliferative disease, the activating KIR receptors being mostly expressed.
  • We also found that patients with natural killer cell-type lymphoproliferative disease of granular lymphocytes usually had KIR genotypes characterized by multiple activating KIR genes.
  • DESIGN AND METHODS: We investigated the mRNA levels of the KIR3DL1 inhibitory and the related KIR3DS1 activating receptors in 15 patients with natural killer cell-type lymphoproliferative disease of granular lymphocytes and in ten controls.
  • CONCLUSIONS: In this study we showed, for the first time, a consistent down-regulation of the inhibitory KIR3DL1 signal due to marked methylation of its promoter, thus suggesting that together with the increased expression of activating receptors, the lack of the inhibitory signal could also play a role in the pathogenesis of natural killer cell-type lymphoproliferative disease of granular lymphocytes.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Large Granular Lymphocytic / pathology. Receptors, KIR3DL1 / deficiency

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  • (PMID = 20410181.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, KIR3DL1; 0 / Receptors, KIR3DS1
  • [Other-IDs] NLM/ PMC2948098
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