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1. Lan K, Murakami M, Choudhuri T, Tsai DE, Schuster SJ, Wasik MA, Robertson ES: Detection of Epstein-Barr virus in T-cell prolymphocytic leukemia cells in vitro. J Clin Virol; 2008 Nov;43(3):260-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of Epstein-Barr virus in T-cell prolymphocytic leukemia cells in vitro.
  • BACKGROUND: Epstein-Barr virus (EBV) is closely associated with the development of a number of tumors.
  • During latent infection, EBV continuously expresses a number of viral genes which are essential for cell transformation and maintenance of the malignant phenotype of EBV-related tumors.
  • There has been no previous link between EBV and T-cell prolymphocytic leukemia (T-PLL), a distinctive form of leukemia derived from T-cells at an intermediate stage of differentiation between a cortical thymocyte and a mature peripheral blood T-cell.
  • STUDY DESIGN: T-PLL cells were isolated from the peripheral blood of a patient diagnosed with T-PLL and continuously cultured for about 1 year.

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  • (PMID = 18790666.001).
  • [ISSN] 1386-6532
  • [Journal-full-title] Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
  • [ISO-abbreviation] J. Clin. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA174439; United States / NCI NIH HHS / CA / R01 CA091792; United States / NIDCR NIH HHS / DE / R01 DE014136; United States / NIDDK NIH HHS / DK / P30 DK050306; United States / NIDCR NIH HHS / DE / DE014136-04; United States / NCI NIH HHS / CA / CA091792; United States / NCI NIH HHS / CA / R01 CA177423; United States / NCI NIH HHS / CA / R01 CA108461; United States / NCI NIH HHS / CA / CA072510
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / DNA, Viral
  • [Other-IDs] NLM/ NIHMS78635; NLM/ PMC4289600
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2. Zhang Y, Lan Q, Rothman N, Zhu Y, Zahm SH, Wang SS, Holford TR, Leaderer B, Boyle P, Zhang B, Zou K, Chanock S, Zheng T: A putative exonic splicing polymorphism in the BCL6 gene and the risk of non-Hodgkin lymphoma. J Natl Cancer Inst; 2005 Nov 2;97(21):1616-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have shown that the B-cell lymphoma 6 gene (BCL6) is an oncogene that contributes to lymphomagenesis.
  • Higher risks were observed for two NHL subtypes, namely B-cell chronic lymphatic leukemia/prolymphocytic leukemia/small lymphocytic lymphoma (OR = 3.5, 95% CI = 1.6 to 7.8) and T-cell lymphoma (OR = 5.2, 95% CI = 2.0 to 13.3).

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  • (PMID = 16264183.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / DNA-Binding Proteins
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3. Zanesi N, Aqeilan R, Drusco A, Kaou M, Sevignani C, Costinean S, Bortesi L, La Rocca G, Koldovsky P, Volinia S, Mancini R, Calin G, Scott CP, Pekarsky Y, Croce CM: Effect of rapamycin on mouse chronic lymphocytic leukemia and the development of nonhematopoietic malignancies in Emu-TCL1 transgenic mice. Cancer Res; 2006 Jan 15;66(2):915-20
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  • [Title] Effect of rapamycin on mouse chronic lymphocytic leukemia and the development of nonhematopoietic malignancies in Emu-TCL1 transgenic mice.
  • Chronic lymphocytic leukemia (CLL) is the most common leukemia in the world.
  • The TCL1 gene, responsible for prolymphocytic T cell leukemia, is also overexpressed in human B cell malignancies and overexpression of the Tcl1 protein occurs frequently in CLL.
  • Aging transgenic mice that overexpress TCL1 under control of the mu immunoglobulin gene enhancer, develop a CD5+ B cell lymphoproliferative disorder mimicking human CLL and implicating TCL1 in the pathogenesis of CLL.
  • This approach allowed us to verify the involvement of the Tcl1/Akt/mTOR biochemical pathway in the disease by testing the ability of a specific pharmacologic agent, rapamycin, to slow CLL.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Sirolimus / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Humans. Immunohistochemistry. Mice. Mice, Transgenic


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4. Röth A, Dürig J, Himmelreich H, Bug S, Siebert R, Dührsen U, Lansdorp PM, Baerlocher GM: Short telomeres and high telomerase activity in T-cell prolymphocytic leukemia. Leukemia; 2007 Dec;21(12):2456-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Short telomeres and high telomerase activity in T-cell prolymphocytic leukemia.
  • To test the role of telomere biology in T-cell prolymphocytic leukemia (T-PLL), a rare aggressive disease characterized by the expansion of a T-cell clone derived from immuno-competent post-thymic T-lymphocytes, we analyzed telomere length and telomerase activity in subsets of peripheral blood leukocytes from 11 newly diagnosed or relapsed patients with sporadic T-PLL.
  • Targeting the short telomeres and telomerase activity in T-PLL seems an attractive strategy for the future treatment of this devastating disease.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / genetics. Neoplasm Proteins / analysis. Telomerase / analysis. Telomere / ultrastructure

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  • (PMID = 17898784.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminobenzoates; 0 / BIBR 1532; 0 / Naphthalenes; 0 / Neoplasm Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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5. 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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6. Robak T, Robak P: Current treatment options in prolymphocytic leukemia. Med Sci Monit; 2007 Apr;13(4):RA69-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current treatment options in prolymphocytic leukemia.
  • Prolymphocytic leukemia (PLL) is a rare lymphoproliferative disorder characterized by marked leukocytosis and splenomegaly.
  • PLL accounts for approximately 2% of chronic lymphoid leukemias.
  • The clinical course is progressive in the majority of cases due to the resistance of the disease to conventional chemotherapy.
  • The disease is divided according to the cell of origin into the B- (B-PLL) and T-cell (T-PLL) types.
  • Approximately 80% of cases are of B-cell phenotype.
  • PLL has poorer prognosis than chronic lymphocytic leukemia (CLL), and the patients with static disease for a longer period of time are rare.
  • PLL is still considered an incurable disease.
  • Finally, high-dose chemotherapy followed by allogenic or autologous stem cell transplantation seems to be an effective, probably curative, strategy for the treatment of selected patients with PLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, Prolymphocytic / diagnosis. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / genetics. Purine Nucleosides / therapeutic use
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / therapeutic use. Cladribine / therapeutic use. Drug Therapy / methods. Humans. Pentostatin / therapeutic use. Rituximab. Splenectomy / methods. Stem Cell Transplantation / methods. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

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  • (PMID = 17392661.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Purine Nucleosides; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 118
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7. Kikuchi T, Katayama Y, Kubonishi S, Watanabe T, Watanabe Y, Matsuoka K, Maeda Y, Namba N, Masunari T, Nasu R, Ikeda K, Tanimoto M: Chronic lymphoproliferative disorder with regulatory T-cell phenotype. Am J Hematol; 2006 Sep;81(9):713-6
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  • [Title] Chronic lymphoproliferative disorder with regulatory T-cell phenotype.
  • We report a case of T-cell chronic lymphoproliferative disorder (CLPD) that shows neither features of T-cell prolymphocytic leukemia nor disease progression for more than 34 months.
  • [MeSH-minor] Aged. Antigens, CD / biosynthesis. Biomarkers / blood. Cell Differentiation. Chronic Disease. Female. Forkhead Transcription Factors / biosynthesis. Humans. Microscopy, Electron, Transmission. Phenotype. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16838340.001).
  • [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] 0 / Antigens, CD; 0 / Biomarkers; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
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8. Mikaelsson E, Danesh-Manesh AH, Lüppert A, Jeddi-Tehrani M, Rezvany MR, Sharifian RA, Safaie R, Roohi A, Osterborg A, Shokri F, Mellstedt H, Rabbani H: Fibromodulin, an extracellular matrix protein: characterization of its unique gene and protein expression in B-cell chronic lymphocytic leukemia and mantle cell lymphoma. Blood; 2005 Jun 15;105(12):4828-35
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  • [Title] Fibromodulin, an extracellular matrix protein: characterization of its unique gene and protein expression in B-cell chronic lymphocytic leukemia and mantle cell lymphoma.
  • Fibromodulin is an extracellular matrix protein normally produced by collagen-rich tissues; the fibromodulin gene has been found to be the most overexpressed gene in B-cell chronic lymphocytic leukemia.
  • In this study, fibromodulin was expressed at the gene level (reverse transcription-polymerase chain reaction [RT-PCR]) in all patients with B-CLL (n = 75) and in most (5 of 7) patients with mantle cell lymphoma (MCL).
  • Fibromodulin was also detected at the protein level in the cytoplasm of the B-CLL cells and in the supernatant after in vitro cultivation, but not at the cell surface.
  • Fibromodulin was not found in patients with T-cell chronic lymphocytic leukemia (T-CLL), B-cell prolymphocytic leukemia (B-PLL), T-cell prolymphocytic leukemia (T-PLL), hairy cell leukemia, follicular lymphoma, lymphoplasmacytic lymphoma, multiple myeloma, acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), or chronic myelogenous leukemia (CML) or in 36 hematologic cell lines.
  • [MeSH-major] Extracellular Matrix / metabolism. Extracellular Matrix Proteins / chemistry. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Lymphoma, Mantle-Cell / metabolism. Proteoglycans / chemistry
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / biosynthesis. Antigens, CD19 / biosynthesis. Antigens, CD5 / biosynthesis. Antigens, Differentiation, T-Lymphocyte / biosynthesis. Biomarkers, Tumor / metabolism. Blotting, Western. Cell Line, Transformed. Cell Line, Tumor. Coculture Techniques. Collagen / metabolism. Cytoplasm / metabolism. DNA Mutational Analysis. DNA, Complementary / metabolism. Female. Fibroblasts / metabolism. Flow Cytometry. Hematologic Neoplasms / metabolism. Humans. Immunoblotting. Lectins, C-Type. Leukemia, T-Cell / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Mutation. Palatine Tonsil / metabolism. RNA, Messenger / metabolism. Receptors, Interleukin-2 / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Tetradecanoylphorbol Acetate / pharmacology. Time Factors

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  • (PMID = 15741214.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD5; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / CD69 antigen; 0 / DNA, Complementary; 0 / Extracellular Matrix Proteins; 0 / Lectins, C-Type; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / Receptors, Interleukin-2; 126468-95-9 / fibromodulin; 9007-34-5 / Collagen; NI40JAQ945 / Tetradecanoylphorbol Acetate
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9. Reiniger L, Bödör C, Bognár A, Balogh Z, Csomor J, Szepesi A, Kopper L, Matolcsy A: Richter's and prolymphocytic transformation of chronic lymphocytic leukemia are associated with high mRNA expression of activation-induced cytidine deaminase and aberrant somatic hypermutation. Leukemia; 2006 Jun;20(6):1089-95
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  • [Title] Richter's and prolymphocytic transformation of chronic lymphocytic leukemia are associated with high mRNA expression of activation-induced cytidine deaminase and aberrant somatic hypermutation.
  • Chronic lymphocytic leukemia (CLL) is an indolent B-cell non-Hodgkin's lymphoma that may transform into higher-grade lymphoma.
  • The transformation involves an increased number of prolymphocytic cells, termed prolymphocytic transformation (PLT) or the development of diffuse large B-cell lymphoma (DLBL), also referred to as Richter's transformation (RT).
  • To analyze whether activation-induced cytidine deaminase (AID), which is essential for somatic hypermutation (SHM) of normal B-cells, and malfunction of SHM termed aberrant somatic hypermutation (ASHM) are associated with higher-grade transformation of CLL, AID mRNA expression and the mutation pattern of c-MYC, PAX-5 and RhoH genes were analyzed in eight cases of CLL without transformation and in 21 cases that showed RT or PLT.
  • Chronic lymphocytic leukemia cases, which showed no transformation or eventually transformed into higher-grade lymphoma, showed low levels of AID mRNA expression and low frequency of mutations of c-MYC, PAX-5 and RhoH genes.
  • In both RT and PLT, high-levels of AID mRNA expression and high-frequency mutations of c-MYC, PAX-5 and RhoH genes were detected.
  • These results indicate that AID expression and ASHM are associated with higher-grade transformation of CLL and provide further evidences that AID expression and ASHM may be activated during the clonal history of B-cell lymphomas.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Cytidine Deaminase / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. RNA, Messenger / biosynthesis. Somatic Hypermutation, Immunoglobulin / genetics
  • [MeSH-minor] B-Cell-Specific Activator Protein / genetics. Gene Expression Profiling. Humans. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Mutation. Proto-Oncogene Proteins c-myc / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription Factors / genetics. rho GTP-Binding Proteins / genetics

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  • (PMID = 16541139.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / PAX5 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / RhoH protein, human; 0 / Transcription Factors; EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase; EC 3.6.5.2 / rho GTP-Binding Proteins
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10. Valbuena JR, Herling M, Admirand JH, Padula A, Jones D, Medeiros LJ: T-cell prolymphocytic leukemia involving extramedullary sites. Am J Clin Pathol; 2005 Mar;123(3):456-64
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  • [Title] T-cell prolymphocytic leukemia involving extramedullary sites.
  • T-cell prolymphocytic leukemia (T-PLL) can involve extramedullary sites, but the diagnosis is usually established by examination of blood and bone marrow.
  • Cytologically, the T-PLL cells were round (n = 16) or Sezary cell-like (n = 3).
  • Immunostaining for T-cell leukemia-1 (TCL-1) was positive in specimens from 9 (64%) of 14 patients.
  • TCL-1 expression can aid in diagnosis at extramedullary sites.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, T-Cell / pathology. Lymphoid Tissue / pathology. Skin Neoplasms / pathology

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  • (PMID = 15716243.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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11. Bug S, Dürig J, Oyen F, Klein-Hitpass L, Martin-Subero JI, Harder L, Baudis M, Arnold N, Kordes U, Dührsen U, Schneppenheim R, Siebert R: Recurrent loss, but lack of mutations, of the SMARCB1 tumor suppressor gene in T-cell prolymphocytic leukemia with TCL1A-TCRAD juxtaposition. Cancer Genet Cytogenet; 2009 Jul;192(1):44-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent loss, but lack of mutations, of the SMARCB1 tumor suppressor gene in T-cell prolymphocytic leukemia with TCL1A-TCRAD juxtaposition.
  • In T-cell prolymphocytic leukemia (T-PLL), chromosomal imbalances affecting the long arm of chromosome 22 are regarded as typical chromosomal aberrations secondary to a TCRAD-TCL1A fusion due to inv(14) or t(14;14).
  • [MeSH-major] Chromosomal Proteins, Non-Histone / genetics. DNA-Binding Proteins / genetics. Gene Deletion. Leukemia, Prolymphocytic, T-Cell / genetics. Protein-Serine-Threonine Kinases / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 19480937.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / SMARCB1 protein, human; 0 / TCL1A protein, human; 0 / Transcription Factors; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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12. Crisostomo RH, Fernandez JA, Caceres W: Complex karyotype including chromosomal translocation (8;14) (q24;q32) in one case with B-cell prolymphocytic leukemia. Leuk Res; 2007 May;31(5):699-701
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  • [Title] Complex karyotype including chromosomal translocation (8;14) (q24;q32) in one case with B-cell prolymphocytic leukemia.
  • We report a case of a 64-year-old white female patient, who presented with symptomatic anemia (Hgb: 6.8g/dl), thrombocytopenia (platelets: 94,000/mcl) and leukocytosis (WBC: 156,000/mcl).
  • Peripheral blood smear revealed markedly increased white blood cell count with predominance of atypical lymphoid cells of intermediate size, moderately dense chromatin, and prominent large single nucleoli.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 8. Leukemia, B-Cell / genetics. Leukemia, Prolymphocytic / genetics. Translocation, Genetic

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  • (PMID = 16997373.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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13. 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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  • [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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14. Marie I, Robaday S, Kerleau JM, Jardin F, Levesque H: Typhlitis as a complication of alemtuzumab therapy. Haematologica; 2007 May;92(5):e62-3
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  • It is an effective immunotherapeutic agent in patients with malignancies such as non-Hodgkin lymphoma, B cell chronic lymphocytic leukemia and T cell pro- lymphocytic leukemia.
  • We recently observed a case of particular interest as the patient with T cell prolymphocytic leukaemia treated with alemtuzumab, exhibited symptomatic reactivation of CMV infection and developed subsequently typhlitis.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antibodies, Neoplasm / adverse effects. Antineoplastic Agents / adverse effects. Typhlitis / diagnosis. Typhlitis / etiology
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Female. Humans. Leukemia, Prolymphocytic / immunology. Leukemia, Prolymphocytic / therapy. Leukemia, T-Cell / immunology. Leukemia, T-Cell / therapy. Middle Aged

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  • (PMID = 17562596.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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15. Mahmoud IS, Sughayer MA, Mohammad HA, Awidi AS, EL-Khateeb MS, Ismail SI: The transforming mutation E17K/AKT1 is not a major event in B-cell-derived lymphoid leukaemias. Br J Cancer; 2008 Aug 5;99(3):488-90
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  • [Title] The transforming mutation E17K/AKT1 is not a major event in B-cell-derived lymphoid leukaemias.
  • Despite the major role of the AKT/PKB family of proteins in the regulation of many growth and survival mechanisms in the cell, and the increasing evidence suggesting that AKT disruption could play a key role in many human malignancies, no major mutations of AKT genes had been reported, until very recently when Carpten et al reported a novel transforming mutation (E17K) in the pleckstrin homology domain of the AKT1 gene in solid tumours.
  • Considering the importance of the PI3K/AKT pathway in mediating survival and antiapoptotic signals in the B-cell types of chronic lymphocytic leukaemia (CLL) and acute lymphoblastic leukaemia (ALL), we sequenced the AKT1 exon 3 for the above mentioned mutation in 87 specimens, representing 45 CLLs, 38 ALLs and 4 prolymphocytic leukaemia (PLL) cases, which are all of B-cell origin.
  • We conclude that this mutation is not a major event in B-cell-derived lymphoid leukaemias.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Transformation, Neoplastic / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Promyelocytic, Acute / genetics. Point Mutation. Proto-Oncogene Proteins c-akt / genetics

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  • (PMID = 18665177.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2527790
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16. Bonanni L, Adami F, Angelini A, Gurrieri C, Cutolo A, Ponchia A, Corbetti F, Thiene G, Semenzato G: Images in cardiovascular medicine. Right atrial mass in a patient with T-cell chronic lymphocytic leukemia: an unusual mechanism of thrombus formation. Circulation; 2007 Dec 18;116(25):e569-72
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  • [Title] Images in cardiovascular medicine. Right atrial mass in a patient with T-cell chronic lymphocytic leukemia: an unusual mechanism of thrombus formation.
  • [MeSH-major] Endocardium / pathology. Heart Neoplasms / pathology. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemic Infiltration / pathology. Thrombosis / pathology


17. McElreath DP, Angtuaco TL, Staggs B, Malik AH: T cell prolymphocytic leukemia: a rare cause of acute liver failure. Dig Dis Sci; 2006 Apr;51(4):819-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T cell prolymphocytic leukemia: a rare cause of acute liver failure.
  • [MeSH-major] Leukemia, Prolymphocytic / complications. Leukemia, Prolymphocytic / diagnosis. Liver Failure, Acute / etiology. Multiple Organ Failure / diagnosis
  • [MeSH-minor] Abdominal Pain / diagnosis. Abdominal Pain / etiology. Biopsy, Needle. Combined Modality Therapy. Disease Progression. Fatal Outcome. Humans. Immunohistochemistry. Liver Function Tests. Male. Middle Aged. Rare Diseases. Risk Assessment. Severity of Illness Index

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  • (PMID = 16615010.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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18. Bain BJ, Fawcett N: A T-lineage neoplasm-Which one? Am J Hematol; 2009 Oct;84(10):678
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Biomarkers, Tumor / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Antigens, CD / analysis. Antigens, CD / biosynthesis. Antigens, Neoplasm / analysis. Antigens, Neoplasm / biosynthesis. Diagnosis, Differential. Humans. Immunophenotyping. Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia, Prolymphocytic, T-Cell / immunology. Leukemia, Prolymphocytic, T-Cell / pathology. Male

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  • (PMID = 19373891.001).
  • [ISSN] 1096-8652
  • [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] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
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19. Moid F, Day E, Schneider MA, Goldstein K, DePalma L: An indolent case of T-prolymphocytic leukemia with t(3;22)(q21;q11.2) and elevated serum beta2-microglobulin. Arch Pathol Lab Med; 2005 Sep;129(9):1164-7
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  • [Title] An indolent case of T-prolymphocytic leukemia with t(3;22)(q21;q11.2) and elevated serum beta2-microglobulin.
  • We report a novel case of T-prolymphocytic leukemia, small cell variant, associated with complex cytogenetic findings including t(3;22)(q21;11.2) and elevated serum beta2-microglobulin.
  • The diagnosis is based on morphologic, immunophenotypic, cytogenetic, and molecular analysis of peripheral blood and bone marrow.
  • In contrast to most reported cases of T-prolymphocytic leukemia, this patient did not present with lymphadenopathy or organomegaly.
  • In the absence of any specific treatment, the patient is doing well, with a stable white blood cell count 12 months following presentation.
  • [MeSH-major] Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 3 / genetics. Leukemia, Prolymphocytic. Leukemia, Prolymphocytic, T-Cell. Translocation, Genetic / genetics. beta 2-Microglobulin / blood

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  • (PMID = 16119992.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / beta 2-Microglobulin
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20. Calfa CJ, Lossos IS, Ruiz P, Davis JL: Ocular involvement as the initial manifestation of T-cell chronic lymphocytic leukemia. Am J Ophthalmol; 2007 Aug;144(2):326-9
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  • [Title] Ocular involvement as the initial manifestation of T-cell chronic lymphocytic leukemia.
  • PURPOSE: To present a case of T-cell chronic lymphocytic leukemia (T-CLL) manifesting as an intraocular lymphoma.
  • Morphologic, immunohistochemical, flow cytometry, and molecular analysis by polymerase chain reaction of vitreous fluid, peripheral blood, bone marrow aspirate, and biopsy were performed.
  • RESULTS: Cytofluorographic and molecular analysis of vitreous cells demonstrated a monoclonal T-cell population consistent with a T-cell intraocular lymphoma.
  • Systemic evaluation established diagnosis of T-cell CLL.
  • CONCLUSION: T-CLL is a rare disease with an aggressive clinical course.
  • We present a case of T-cell intraocular lymphoma as the initial manifestation of an otherwise asymptomatic T-CLL.
  • [MeSH-major] Eye Neoplasms / diagnosis. Leukemia, Prolymphocytic, T-Cell / diagnosis. Lymphoma, T-Cell, Peripheral / diagnosis. Vitreous Body / pathology
  • [MeSH-minor] Aged. Antibiotics, Antineoplastic / therapeutic use. Biomarkers, Tumor / genetics. Biopsy. Bone Marrow Cells / pathology. DNA, Neoplasm / analysis. Diagnosis, Differential. Female. Flow Cytometry. Fluorescein Angiography. Follow-Up Studies. Fundus Oculi. Humans. Immunohistochemistry. Pentostatin / therapeutic use. Polymerase Chain Reaction. Tomography, Optical Coherence. Vitrectomy

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  • (PMID = 17659976.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109335
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 395575MZO7 / Pentostatin
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21. Ravandi F, O'brien S: Alemtuzumab in CLL and other lymphoid neoplasms. Cancer Invest; 2006 Nov;24(7):718-25
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  • A number of clinical trials have demonstrated the clinical activity of alemtuzumab in chronic lymphocytic leukemia (CLL), T-cell malignancies such as T-prolymphocytic leukemia (T-PLL) and cutaneous T-cell lymphoma (CTCL), and have examined its role as an immunosuppressive agent in transplantation and for the treatment of autoimmune disorders.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Lymphoma / therapy

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  • (PMID = 17118783.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [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 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  • [Number-of-references] 73
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22. Ibrahim RB, Abidi MH, Al-Kadhimi Z, Uberti JP, Edwards DJ: Tacrolimus disposition in the ascitic fluid of a bone marrow transplant patient. Ann Pharmacother; 2010 May;44(5):939-40
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  • [Title] Tacrolimus disposition in the ascitic fluid of a bone marrow transplant patient.
  • [MeSH-major] Ascitic Fluid / chemistry. Hematopoietic Stem Cell Transplantation. Immunosuppressive Agents / pharmacokinetics. Leukemia, Prolymphocytic, T-Cell / therapy. Tacrolimus / pharmacokinetics

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  • (PMID = 20371750.001).
  • [ISSN] 1542-6270
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; WM0HAQ4WNM / Tacrolimus
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23. O'Brien S, Ravandi F, Riehl T, Wierda W, Huang X, Tarrand J, O'Neal B, Kantarjian H, Keating M: Valganciclovir prevents cytomegalovirus reactivation in patients receiving alemtuzumab-based therapy. Blood; 2008 Feb 15;111(4):1816-9
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  • Diagnoses included chronic lymphocytic leukemia (29), T-cell prolymphocytic leukemia (3), hairy cell leukemia (1), adult T-cell leukemia/lymphoma (ATLL) (1), marginal zone leukemia (1), large granular lymphocyte leukemia (2), acute lymphoblastic leukemia (1), and T-cell lymphoma (2).
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Antiviral Agents / therapeutic use. Cytomegalovirus / physiology. Cytomegalovirus Infections / prevention & control. Ganciclovir / analogs & derivatives. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Virus Activation / physiology

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  • [CommentIn] Blood. 2008 Sep 1;112(5):2167 [18725576.001]
  • (PMID = 18039954.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00562770
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / valganciclovir; 3A189DH42V / alemtuzumab; P9G3CKZ4P5 / Ganciclovir
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24. Usher SG, Radford AD, Villiers EJ, Blackwood L: RAS, FLT3, and C-KIT mutations in immunophenotyped canine leukemias. Exp Hematol; 2009 Jan;37(1):65-77
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  • [Title] RAS, FLT3, and C-KIT mutations in immunophenotyped canine leukemias.
  • OBJECTIVE: To determine the frequency of FLT3, C-KIT, and RAS mutations in canine leukemia patients.
  • MATERIALS AND METHODS: Ethylenediamine tetra-acetic acid blood samples were recruited from dogs with suspected leukemia, categorized by quantitative and cytological evaluation and immunophenotyping.
  • RESULTS: Fifty-seven (77.0%) of 74 samples submitted from dogs with suspected leukemia had cytologically and immunophenotypically confirmed leukemia.
  • There were 36 (63.2%) acute leukemias, 16 (28.1%) chronic, 3 (5.3%) prolymphocytic, 1 natural killer cell, and 1 chronic leukemia undergoing blast transformation.
  • N-RAS mis-sense mutations were identified in 14 (25%) dogs with acute myeloid (AML) or lymphoid (ALL) leukemia, and also in one dog in the leukemic phase of lymphoma.
  • Sixty-one percent of dogs with acute leukemia harbored mutations in N/K-RAS, FLT3, or C-KIT.
  • CONCLUSION: RAS, FLT3, and C-KIT mutations, analogous to those found in human leukemia, occur commonly in acute canine leukemia.
  • [MeSH-major] Dog Diseases / genetics. Leukemia / genetics. Leukemia / veterinary. Mutation. Proto-Oncogene Proteins c-kit / genetics. fms-Like Tyrosine Kinase 3 / genetics. ras Proteins / genetics
  • [MeSH-minor] Acute Disease. Animals. Antigens, CD / genetics. Antigens, CD / metabolism. Chronic Disease. Dogs

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  • (PMID = 18977066.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / ras Proteins
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25. Krishnan B, Else M, Tjonnfjord GE, Cazin B, Carney D, Carter J, Ketterer N, Catovsky D, Ethell M, Matutes E, Dearden CE: Stem cell transplantation after alemtuzumab in T-cell prolymphocytic leukaemia results in longer survival than after alemtuzumab alone: a multicentre retrospective study. Br J Haematol; 2010 Jun;149(6):907-10
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  • [Title] Stem cell transplantation after alemtuzumab in T-cell prolymphocytic leukaemia results in longer survival than after alemtuzumab alone: a multicentre retrospective study.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Prolymphocytic, T-Cell / therapy

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  • (PMID = 20201944.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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26. Robak T: Novel drugs for chronic lymphoid leukemias: mechanism of action and therapeutic activity. Curr Med Chem; 2009;16(18):2212-34
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  • [Title] Novel drugs for chronic lymphoid leukemias: mechanism of action and therapeutic activity.
  • Chronic lymphoid leukemias include well defined mature B-cell and T-cell neoplasms with diverse natural history and specific morphological, immunophenotypic and molecular characteristics.
  • The most common adult leukemia in the Western world is chronic lymphocytic leukemia (CLL).
  • Rarer indolent lymphoid leukemias include prolymphocytic leukemia, hairy cell leukemia, large granular lymphocyte leukemia and T-cell leukemia/lymphoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Design. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

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  • (PMID = 19519388.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 230
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27. Matutes E: Adult T-cell leukaemia/lymphoma. J Clin Pathol; 2007 Dec;60(12):1373-7
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  • [Title] Adult T-cell leukaemia/lymphoma.
  • Adult T-cell leukaemia/lymphoma (ATLL) is a mature T-cell neoplasm of post-thymic lymphocytes aetiologically linked to the human T-cell lymphotropic virus, HTLV-I, and with a distinct geographical distribution.
  • The disease manifests with leukaemia in greater than two thirds of patients, while the remaining patients have a lymphomatous form.
  • According to the disease manifestations, various forms which differ in clinical course and prognosis have been recognised: acute, chronic, smouldering and lymphoma.
  • Organomegaly, skin involvement, circulating atypical lymphocytes ("flower" cells) with a CD4+ CD25+ phenotype and hypercalcaemia are the most common disease features.
  • The diagnosis should be based on a constellation of clinical features and laboratory investigations.
  • The differential diagnosis of ATLL includes other mature T-cell neoplasms such as T-cell prolymphocytic leukaemia (T-PLL), Sézary syndrome (SS), peripheral T-cell lymphomas and occasionally healthy carriers of the virus or Hodgkin disease.
  • Despite major advances in understanding the pathogenesis of the disease, management of these patients remains a challenge for clinicians as they do not respond or achieve only transient responses to therapies used in high-grade lymphomas.
  • The use of antiretroviral agents such as zidovudine in combination with interferon-alpha, with or without concomitant chemotherapy, has shown activity in this disease with improvement in survival and response rate.
  • Consolidation with high dose therapy and autologous or allogeneic stem-cell transplantation should be considered in young patients.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Antiviral Agents / therapeutic use. Biomarkers, Tumor / blood. Diagnosis, Differential. Drug Therapy, Combination. Humans. Immunophenotyping. Prognosis

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  • (PMID = 18042693.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / Biomarkers, Tumor
  • [Number-of-references] 42
  • [Other-IDs] NLM/ PMC2095573
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28. Belov L, Huang P, Chrisp JS, Mulligan SP, Christopherson RI: Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells. J Immunol Methods; 2005 Oct 20;305(1):10-9
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  • [Title] Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells.
  • We have developed a microarray (DotScan) that enables rapid immunophenotyping and classification of leukaemias and lymphomas by measuring the capture of cells by immobilized dots of 82 CD antibodies [Belov, L., de la Vega, O., dos Remedios, C.G., Mulligan, S.P., 2001.
  • Immunophenotyping of leukemia using a cluster of differentiation antibody microarray. Cancer Res.
  • Identification of repertoires of surface antigens on leukemias using an antibody microarray.
  • After blocking the remaining nitrocellulose surface, individual arrays were incubated with each of 7 cell types from a human leukaemia cell panel consisting of three cell lines, CCRF-CEM (a T-cell acute lymphocytic leukaemia), MEC-1 (derived from B-cell chronic lymphocytic leukaemia) and HL-60 (a promyelocytic leukaemia), and four leukaemias from patients: a T-cell prolymphocytic leukaemia, a B-cell chronic lymphocytic leukaemia, and two acute myeloid leukaemias.
  • Leukaemia cells were captured by those immobilized antibodies for which they expressed the corresponding surface molecule.
  • The data obtained show the unique expression profiles of the 7 cell types in the leukaemia cell panel obtained with the DotScan microarray, and the differential capture patterns for these 7 cell types screened against the 498 antibodies in the HLDA8 microarray constructed for this study.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antigens, CD / analysis. Leukemia / classification. Protein Array Analysis / methods
  • [MeSH-minor] Cell Line, Tumor. Collodion / chemistry. Flow Cytometry. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / immunology. Leukemia, Myeloid / classification. Leukemia, Myeloid / immunology. Leukemia, T-Cell / classification. Leukemia, T-Cell / immunology

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  • (PMID = 16125720.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 9004-70-0 / Collodion
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29. Ravandi F, Kantarjian H, Jones D, Dearden C, Keating M, O'Brien S: Mature T-cell leukemias. Cancer; 2005 Nov 1;104(9):1808-18
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  • [Title] Mature T-cell leukemias.
  • Mature T-cell and NK-cell leukemias are a group of relatively uncommon neoplasms derived from mature or postthymic T-cells accounting for a relatively small percentage of lymphoid malignancies.
  • The recent availability of modern immunophenotypic and molecular tools has allowed a better distinction of these disorders from their B-cell counterparts.
  • Herein, we review the clinical and pathological features of mature T-cell leukemias.
  • [MeSH-major] Leukemia, T-Cell / diagnosis
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Human T-lymphotropic virus 1. Humans. Immunophenotyping. Leukemia, Lymphoid. Leukemia, Prolymphocytic / diagnosis. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / genetics. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / virology. Middle Aged. Tumor Virus Infections

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 16136598.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 143
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30. Huh YO, Lin KI, Vega F, Schlette E, Yin CC, Keating MJ, Luthra R, Medeiros LJ, Abruzzo LV: MYC translocation in chronic lymphocytic leukaemia is associated with increased prolymphocytes and a poor prognosis. Br J Haematol; 2008 Jul;142(1):36-44
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  • [Title] MYC translocation in chronic lymphocytic leukaemia is associated with increased prolymphocytes and a poor prognosis.
  • Chromosomal translocations that involve MYC, characteristic of Burkitt lymphoma, are rare in chronic lymphocytic leukaemia (CLL).
  • Six cases were classified as CLL with increased prolymphocytes (CLL/PL; prolymphocytes 10-55%), and two were classified as CLL in prolymphocytic transformation (CLL/PT; prolymphocytes >55%).
  • Two developed Epstein-Barr virus (EBV)-associated diffuse large B-cell lymphomas (DLBCL) that were clonally unrelated to the CLL.
  • At follow-up, two patients are alive, four died of underlying disease, one died of EBV-associated DLBCL, and one died of an unrelated cancer.
  • [MeSH-major] Genes, myc / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Female. Humans. Immunophenotyping. Lymphoid Progenitor Cells / pathology. Male. Middle Aged. Mutation / genetics. Prognosis

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  • (PMID = 18477041.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] England
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31. Khot A, Dearden C: T-cell prolymphocytic leukemia. Expert Rev Anticancer Ther; 2009 Mar;9(3):365-71
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  • [Title] T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia is a rare post-thymic lymphoid disorder, which has distinctive clinical, morphologic, immunophenotypic and cytogenetic features.
  • However, responses are transient and allogeneic hematopoietic progenitor-cell transplantation remains the only potential curative option.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / therapy
  • [MeSH-minor] Antibodies, Monoclonal / genetics. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / genetics. Antibodies, Neoplasm / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diagnosis, Differential. Drug Administration Schedule. Hematopoietic Stem Cell Transplantation. Humans. Prognosis. Stem Cell Transplantation. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 19275513.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Number-of-references] 46
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32. Tempescul A, Feuerbach J, Ianotto JC, Dalbies F, Marion V, Le Bris MJ, De Braekeleer M, Berthou C: A combination therapy with fludarabine, mitoxantrone and rituximab induces complete immunophenotypical remission in B-cell prolymphocytic leukaemia. Ann Hematol; 2009 Jan;88(1):85-8
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  • [Title] A combination therapy with fludarabine, mitoxantrone and rituximab induces complete immunophenotypical remission in B-cell prolymphocytic leukaemia.
  • [MeSH-major] Antibodies, Monoclonal. Antineoplastic Combined Chemotherapy Protocols. Leukemia, Prolymphocytic, B-Cell / drug therapy. Mitoxantrone. Vidarabine / analogs & derivatives

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  • (PMID = 18654781.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; BZ114NVM5P / Mitoxantrone; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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33. Tsimberidou AM, Keating MJ: Richter syndrome: biology, incidence, and therapeutic strategies. Cancer; 2005 Jan 15;103(2):216-28
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  • Richter's transformation denotes the development of high-grade non-Hodgkin lymphoma, prolymphocytic leukemia, Hodgkin disease, or acute leukemia in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma.
  • Multiple genetic defects, such as mutations of the p53 tumor suppressor gene, p16INK4A, and p21, loss of p27 expression, deletion of retinoblastoma, increased copy number of C-MYC, and decreased expression of the A-MYB gene, have been described.
  • Therapeutic strategies include intensive chemotherapy, monoclonal antibodies, and stem cell transplantation.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Humans. Male. Prognosis. Risk Assessment. Severity of Illness Index. Stem Cell Transplantation / methods. Survival Analysis. Syndrome. Treatment Outcome

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  • [Copyright] (c) 2004 American Cancer Society.
  • (PMID = 15578683.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 159
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34. Li ZQ, Chen HS, Liu EB, Sun Q, Fang LH, Sun FJ, Zhang PH, Yang QY, Qiu LG: [Clinicopathologic study of 15 splenectomy specimens of patients with hairy cell leukemia]. Zhonghua Bing Li Xue Za Zhi; 2009 Nov;38(11):769-73
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  • [Title] [Clinicopathologic study of 15 splenectomy specimens of patients with hairy cell leukemia].
  • OBJECTIVE: To investigate the clinicopathologic features, diagnosis, differential diagnosis and the prognosis of hairy cell leukemia (HCL).
  • The abundant cytoplasm and prominent cell border resulted in a "fried egg" appearance.
  • Definite diagnosis of HCL requires a combined histological and immunohistochemical assessment of the splenectomy specimen, bone marrow biopsy and aspirate.
  • [MeSH-major] Leukemia, Hairy Cell / metabolism. Leukemia, Hairy Cell / pathology. Lymphoma, B-Cell, Marginal Zone / pathology. Spleen / pathology. Splenectomy
  • [MeSH-minor] Adult. Aged. Annexin A1 / metabolism. Antigens, CD11c / metabolism. Antigens, CD20 / metabolism. Antigens, CD45 / metabolism. Antigens, CD79 / metabolism. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Ki-67 Antigen / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Prolymphocytic / metabolism. Leukemia, Prolymphocytic / pathology. Lymphoma, Follicular / metabolism. Lymphoma, Follicular / pathology. Lymphoma, Mantle-Cell / metabolism. Lymphoma, Mantle-Cell / pathology. Male. Middle Aged. Retrospective Studies. Survival Rate

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  • (PMID = 20079018.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Annexin A1; 0 / Antigens, CD11c; 0 / Antigens, CD20; 0 / Antigens, CD79; 0 / Ki-67 Antigen; EC 3.1.3.48 / Antigens, CD45
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35. Kurihara K, Harashima N, Hanabuchi S, Masuda M, Utsunomiya A, Tanosaki R, Tomonaga M, Ohashi T, Hasegawa A, Masuda T, Okamura J, Tanaka Y, Kannagi M: Potential immunogenicity of adult T cell leukemia cells in vivo. Int J Cancer; 2005 Mar 20;114(2):257-67
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  • [Title] Potential immunogenicity of adult T cell leukemia cells in vivo.
  • Experimental vaccines targeting human T cell leukemia virus type-I (HTLV-I) Tax have been demonstrated in a rat model of HTLV-I-induced lymphomas.
  • However, the scarcity of HTLV-I-expression and the presence of defective HTLV-I-proviruses in adult T cell leukemia (ATL) cells have raised controversy about the therapeutic potential of HTLV-I-targeted immunotherapy in humans.
  • In flow cytometric analysis, we found that 3 of 5 acute-type and six of fifteen chronic-type ATL patients tested showed significant induction of HTLV-I Tax and Gag in their ATL cells in a 1-day culture.
  • Representative CTL epitopes restricted by HLA-A2 or A24 were conserved in 4 of 5 acute-type ATL patients tested.
  • Furthermore, spleen T cells from rats, which had been subcutaneously inoculated with formalin-fixed uncultured ATL cells, exhibited a strong interferon gamma-producing helper T cell responses specific for HTLV-I Tax-expressing cells.
  • Our study indicated that ATL cells from about half the patients tested readily express HTLV-I antigens including Tax in vitro, and that ATL cells express sufficient amounts of Tax or Tax-induced antigens to evoke specific T cell responses in vivo.
  • [MeSH-minor] Adult. Aged. Animals. Base Sequence. DNA Primers. Female. Humans. Japan. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemia, Prolymphocytic, T-Cell / virology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology. Male. Middle Aged. Polymerase Chain Reaction. Rats. Rats, Inbred F344. Reference Values. Transplantation, Heterologous / pathology

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551352.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers
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36. Machii T, Chou T, Suzuki M, Ohe Y, Katagiri S, Kitano EK, Kitano K, Fujiyama Y, Izumi T, Shimazaki C, Nanba K, Ohashi Y, Kitani T, Cladribine Study Group: Phase II clinical study of cladribine in the treatment of hairy cell leukemia. Int J Hematol; 2005 Oct;82(3):230-5
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  • [Title] Phase II clinical study of cladribine in the treatment of hairy cell leukemia.
  • We conducted a phase II clinical study to evaluate the therapeutic efficacy of cladribine (2-chlorodeoxyadenosine [2-CdA]) in the treatment of Japanese patients with hairy cell leukemia (HCL).
  • Seven patients with classic HCL and 3 with a prolymphocytic HCL variant were administered 2-CdA (0.09 mg/kg per day) by continuous intravenous infusion for 7 days.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Cladribine / administration & dosage. Leukemia, Hairy Cell / drug therapy

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  • (PMID = 16207596.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 47M74X9YT5 / Cladribine
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37. Maeda A, Iwai K, Ishibashi T: [Successful treatment of T-cell prolymphocytic leukemia (T-PLL) with fludarabine monophosphate]. Rinsho Ketsueki; 2009 Aug;50(8):658-62
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  • [Title] [Successful treatment of T-cell prolymphocytic leukemia (T-PLL) with fludarabine monophosphate].
  • We report a 79-year-old woman with T-cell prolymphocytic leukemia (T-PLL) who was successfully treated with fludarabine monophosphate.
  • The reticulocyte count increased gradually, and she became free from red cell transfusions.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Leukemia, Prolymphocytic, T-Cell / drug therapy. Vidarabine Phosphate / analogs & derivatives

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  • (PMID = 19915381.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 106XV160TZ / Vidarabine Phosphate; 1X9VK9O1SC / fludarabine phosphate
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38. Hofbauer SW, Piñón JD, Brachtl G, Haginger L, Wang W, Jöhrer K, Tinhofer I, Hartmann TN, Greil R: Modifying akt signaling in B-cell chronic lymphocytic leukemia cells. Cancer Res; 2010 Sep 15;70(18):7336-44
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  • [Title] Modifying akt signaling in B-cell chronic lymphocytic leukemia cells.
  • Emerging evidence suggests that the survival of B-cell chronic lymphocytic leukemia (CLL) cells is dependent on microenvironmental influences such as antigenic stimulation and support by stromal cells.
  • We investigated the role of Akt and its modulation by the protooncogene T-cell leukemia 1a (Tcl1a) in the survival pathways of primary CLL samples and CLL-derived prolymphocytic cell lines MEC-1 and MEC-2.
  • Akt activation was increased by the protective presence of human bone marrow stromal cells and B-cell receptor mimicking signals but antagonized by direct Akt blockade with the novel specific inhibitor AiX, with preferential apoptosis induction in CLL cells with an unmutated immunoglobulin status, which predicts poor clinical outcome.
  • In contrast, decreasing Tcl1a levels by small interfering RNA reduced Akt activation in the fludarabine-insensitive CLL cell line MEC-2 and sensitized the malignant cells to fludarabine treatment.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Humans. Oxazines / pharmacology. RNA, Small Interfering / genetics. Signal Transduction. Transfection


39. Dai HP, Xue YQ, Zhang J, Wu YF, Pan JL, Wang Y, Shen J: Translocation t(2;8)(p12;q24) in two patients with B Cell chronic lymphocytic leukemia. Acta Haematol; 2008;120(4):232-6
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  • [Title] Translocation t(2;8)(p12;q24) in two patients with B Cell chronic lymphocytic leukemia.
  • In this study, we report for the first time on 2 cases of chronic lymphocytic leukemia (CLL) with t(2;8).
  • They were diagnosed as having typical CLL (case 1) and CLL/prolymphocytic leukemia (case 2), respectively, based on morphology and immunophenotyping.
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 8. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Translocation, Genetic

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19246886.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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40. Herling M, Patel KA, Teitell MA, Konopleva M, Ravandi F, Kobayashi R, Jones D: High TCL1 expression and intact T-cell receptor signaling define a hyperproliferative subset of T-cell prolymphocytic leukemia. Blood; 2008 Jan 1;111(1):328-37
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  • [Title] High TCL1 expression and intact T-cell receptor signaling define a hyperproliferative subset of T-cell prolymphocytic leukemia.
  • The T-cell leukemia 1 (TCL1) oncoprotein is overexpressed by chromosomal rearrangement in the majority of cases of T-cell prolymphocytic leukemia (T-PLL).
  • In vitro, TCL1 can modulate the activity of the serine-threonine kinase AKT, a downstream effector of T-cell receptor (TCR) signaling.
  • High-level TCL1 in TCR-expressing T-PLL is associated with higher presenting white blood cell counts, faster tumor cell doubling, and enhanced in vitro growth response to TCR engagement.
  • In primary tumors and TCL1-transfected T-cell lines, TCR engagement leads to rapid recruitment of TCL1 and AKT to transient membrane activation complexes that include TCR-associated tyrosine kinases, including LCK.
  • Pharmacologic inhibition of AKT activation alters the localization, stability, and levels of these transient TCL1-AKT complexes and reduces tumor cell growth.

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  • (PMID = 17890451.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA90571; United States / NCI NIH HHS / CA / R01 CA107300; United States / NCI NIH HHS / CA / R01 CA090571; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA107300
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Receptors, Antigen, T-Cell; 0 / TCL1A protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2200815
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41. Dong HY, Weisberger J, Liu Z, Tugulea S: Immunophenotypic analysis of CD103+ B-lymphoproliferative disorders: hairy cell leukemia and its mimics. Am J Clin Pathol; 2009 Apr;131(4):586-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotypic analysis of CD103+ B-lymphoproliferative disorders: hairy cell leukemia and its mimics.
  • CD103 is characteristically expressed in hairy cell leukemia (HCL), a B-lymphoproliferative disorder highly responsive to treatment with purine analogs.
  • Other CD103+ diseases are rare and do not respond well to the same therapy, including HCL variant (HCLv) and splenic marginal zone B-cell lymphoma (SMZL) variants.
  • The CD25- cases had variable morphologic features ranging from HCLv and SMZL to prolymphocytic leukemia and diffuse large B-cell lymphoma.
  • Clinically, patients with CD25- disease tended to be older (P= .001), typically had leukocytosis (P= .014), and did not respond well to cladribine or pentostatin.
  • While HCL coexpresses CD25 and annexin-A1, diseases lacking CD25 and annexin-A1 behave clinically differently and can be separated from HCL on diagnosis.
  • [MeSH-major] Antigens, CD / biosynthesis. Integrin alpha Chains / biosynthesis. Interleukin-2 Receptor alpha Subunit / biosynthesis. Leukemia, Hairy Cell / classification. Receptors, Peptide / biosynthesis
  • [MeSH-minor] Diagnosis, Differential. Flow Cytometry. Humans. Immunohistochemistry. Immunophenotyping. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology

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  • (PMID = 19289595.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Integrin alpha Chains; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Peptide; 0 / alpha E integrins; 0 / annexin-A1 receptor, human
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42. Wang ZY, Chen QS: [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Apr;13(2):169-73
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  • [Title] [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial].
  • One of the important approaches for further prolonging remission duration and eradicating minimal residual disease in acute leukemia is immunotherapy.
  • Four kinds of immunotherapy for acute leukemia are under investigation:.
  • (1) monoclonal antibodies, among them, Mylotarg (cytotoxic antibiotic calicheamicin linked to CD33 Mab) is given for the treatment of refractory or relapsed acute myeloid leukemia and molecular relapse in acute promyelocytic leukemia with good results, Campath-1H (antiCD52 Mab) is administered in the treatment of prolymphocytic leukemia and Rituximab (anti-CD20 Mab) in B-PLL with high complete remission rates.
  • Other Mabs under preclinical and clinical trials include anti-IL-2 receptor Mab for the treatment of acute T lymphocytic leukemia, anti-220 kD Mab-6G7 for acute leukemias, recombinant immune toxin BL22 (anti-CD22) for hairy cell leukemia and Mabs labeled with radio-isotopes for different types of acute leukemias;.
  • (2) adoptive cellular immunotherapy using cytokine-induced killer cell, alloreactive NK cells, allogeneic or autologous leukemic-specific CD8(+) cytotoxic T lymphocytes, and other immune effector cells;.
  • (4) leukemia vaccines of several different formulations including antigen-specific, leukemia cell-based, leukemia antigen-pulsed dendritic cell (DC) and leukemia-derived DC vaccines, the latter two formulations are more attractive.
  • In conclusion, up to now, the most effective example of immunotherapy in acute leukemia is provided by the administration of Mabs, and the majority of other approaches in immunotherapy for acute leukemia although promising, need further studies.

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  • (PMID = 15854271.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Editorial; English Abstract
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines
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43. Despouy G, Joiner M, Le Toriellec E, Weil R, Stern MH: The TCL1 oncoprotein inhibits activation-induced cell death by impairing PKCtheta and ERK pathways. Blood; 2007 Dec 15;110(13):4406-16
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  • [Title] The TCL1 oncoprotein inhibits activation-induced cell death by impairing PKCtheta and ERK pathways.
  • The TCL1/MTCP1 oncogenes were identified on the basis of their involvement in T-cell prolymphocytic leukemia (T-PLL).
  • We investigate the biologic functions of TCL1 in the T-cell lineage using various cell lines, and primary malignant and normal lymphocytes.
  • In the Jurkat cell line, expression of TCL1 had no effect in unstimulated cells, whereas it abrogated activation-induced cell death (AICD).
  • Secondly, the TCL1-driven T-cell leukemia cell line SUP-T11 was shown to have impaired PKCtheta and ERK phosphorylation upon stimulation, which were restored by TCL1 inhibition using RNA interference.
  • [MeSH-minor] Cell Death. Cell Line. Humans. Lymphocyte Activation. Oncogene Proteins / physiology. Phosphorylation / drug effects. Signal Transduction. Tumor Cells, Cultured

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  • (PMID = 17846228.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / MTCP1 protein, human; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human; 148374-93-0 / PRKCQ protein, human; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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44. Toyota S, Nakamura N, Dan K: Small cell variant of T-cell prolymphocytic leukemia with a gammadelta immunophenotype. Int J Hematol; 2005 Jan;81(1):66-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small cell variant of T-cell prolymphocytic leukemia with a gammadelta immunophenotype.
  • T-cell prolymphocytic leukemia (T-PLL) is a rare postthymic T-cell disorder.
  • The disease is characterized by lymphadenopathy, splenomegaly, skin lesions, a high white blood cell count, and an aggressive clinical course.
  • The small cell variant of T-PLL occurs in approximately 20% of patients.
  • Most T-PLL patients express membrane T-cell receptors (TCR) of the alphabeta phenotype.
  • The diagnosis of small cell variant T-PLL in a 56-year-old woman was based on the findings of abnormal lymphocytosis, immunophenotype, lymphadenopathy, and aggressive clinical behavior.
  • This case was typical T-PLL except for the morphologically small cell type and the lack of the typical chromosome aberration.
  • If cases accumulate in the future, the specific features of the gamma8 type of T-PLL will become clearer.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, T-Cell / pathology. Receptors, Antigen, T-Cell, gamma-delta / metabolism

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  • (PMID = 15717692.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, gamma-delta
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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Exceptions include splenic marginal zone lymphomas and hepatosplenic T-cell lymphomas that are typically diagnosed from histological findings.
  • In addition, hairy-cell leukemia, LGL leukemia and T-cell prolymphocytic leukemia typically show characteristic patterns of infiltration in the spleen which may be diagnostically useful.
  • [MeSH-minor] Antigens, CD / analysis. Diagnosis, Differential. Humans. Leukemia, Hairy Cell / pathology. Leukemia, Prolymphocytic, T-Cell / pathology. Lymphoma, T-Cell / pathology. Splenectomy

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  • (PMID = 18214484.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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46. Lundin J, Karlsson C, Celsing F: Alemtuzumab therapy for severe autoimmune hemolysis in a patient with B-cell chronic lymphocytic leukemia. Med Oncol; 2006;23(1):137-9
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  • [Title] Alemtuzumab therapy for severe autoimmune hemolysis in a patient with B-cell chronic lymphocytic leukemia.
  • B-cell chronic lymphocytic leukemia (B-CLL) is the most common cause of autoimmune hemolytic anemia (AIHA), and a subgroup of these patients who develop both these conditions fail to respond to corticosteroids, cytotoxic drugs, splenectomy, and iv immunoglobulins.
  • Alemtuzumab is a humanized anti-CD52 monoclonal antibody that is an effective therapy for B-CLL, mycosis fungoides, and T-cell prolymphocytic leukemia.
  • Here we present a case report of a 78-yr-old woman with B-CLL and progressive life-threatening AIHA with hemoglobin count 5.5 g/dL following fludarabine treatment, who was treated successfully with alemtuzumab.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / complications

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  • (PMID = 16645240.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
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47. Dearden CE: T-cell prolymphocytic leukemia. Med Oncol; 2006;23(1):17-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive post-thymic malignancy with poor response to conventional treatment and short survival.
  • It can readily be distinguished from other T-cell leukemias on the basis of the distinctive morphology, immunophenotype, and cytogenetics.
  • Consistent chromosomal translocations involving the T-cell receptor gene and one of two protooncogenes (TCL-1 and MTCP-1) are seen in the majority of cases and are likely to be involved in the pathogenesis of the disorder.
  • However, relapse is inevitable and strategies using both autologous and allogeneic stem cell transplantation are currently being explored.
  • [MeSH-major] Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy

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  • (PMID = 16645226.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 28
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48. Foucar K: Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome. Am J Clin Pathol; 2007 Apr;127(4):496-510
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome.
  • The 2005 Society for Hematopathology/European Association for Haematopathology Workshop Session 1 was devoted to case presentations with discussions of 3 types of mature T-cell leukemias--T-cell prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome.
  • The application of clinical, morphologic, immunophenotypic, and genetic studies to the assessment and characterization of these 3 disorders is presented, along with specific diagnostic recommendations and differential diagnostic considerations.
  • [MeSH-major] Leukemia, Prolymphocytic / diagnosis. Leukemia, T-Cell / diagnosis. Sezary Syndrome / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Antigens, CD / metabolism. Chromosome Aberrations. Diagnosis, Differential. Humans. Immunophenotyping

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  • (PMID = 17369126.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Congresses
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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49. Yee KW, Zeng Z, Konopleva M, Verstovsek S, Ravandi F, Ferrajoli A, Thomas D, Wierda W, Apostolidou E, Albitar M, O'Brien S, Andreeff M, Giles FJ: Phase I/II study of the mammalian target of rapamycin inhibitor everolimus (RAD001) in patients with relapsed or refractory hematologic malignancies. Clin Cancer Res; 2006 Sep 1;12(17):5165-73
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  • PURPOSE: Everolimus (RAD001, Novartis), an oral derivative of rapamycin, inhibits the mammalian target of rapamycin (mTOR), which regulates many aspects of cell growth and division.
  • RESULTS: Twenty-seven patients (9 acute myelogenous leukemia, 5 myelodysplastic syndrome, 6 B-chronic lymphocytic leukemia, 4 mantle cell lymphoma, 1 myelofibrosis, 1 natural killer cell/T-cell leukemia, and 1 T-cell prolymphocytic leukemia) received everolimus.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Prolymphocytic / drug therapy. Leukemia, T-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Myelodysplastic Syndromes / drug therapy. Sirolimus / analogs & derivatives

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  • (PMID = 16951235.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA55164
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / EIF4EBP1 protein, human; 0 / Phosphoproteins; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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50. Hiromura M, Suizu F, Narita M, Kinowaki K, Noguchi M: Identification of nerve growth factor-responsive element of the TCL1 promoter as a novel negative regulatory element. J Biol Chem; 2006 Sep 22;281(38):27753-64
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  • The serine/threonine kinase, Akt (protein kinase B) plays a central role in the regulation of intracellular cell survival.
  • Recently, we demonstrated that the proto-oncogene TCL1, overexpressed in human T-cell prolymphocytic leukemia, is an Akt kinase co-activator.
  • Nur77/NGFI-B, an orphan receptor superfamily transcription factor implicated in T-cell apoptosis, is a substrate for Akt.
  • In an electrophoretic mobility shift assay with chromosomal immunoprecipitation assays, wild-type Nur77, but not S350A mutant Nur77, could specifically bind to TCL1-NBRE.
  • To the best of our knowledge, TCL1-NBRE is the first direct target of Nur77 involving the regulation of intracellular cell death survival.

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  • (PMID = 16835233.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / FOXO3 protein, human; 0 / Forkhead Transcription Factors; 0 / NR4A1 protein, human; 0 / Nr4a1 protein, mouse; 0 / Nr4a1 protein, rat; 0 / Nuclear Receptor Subfamily 4, Group A, Member 1; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Steroid; 0 / TCL1A protein, human; 0 / Transcription Factors; 9061-61-4 / Nerve Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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51. Robak T: Emerging drugs for rarer chronic lymphoid leukemias. Expert Opin Emerg Drugs; 2008 Mar;13(1):95-118
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Emerging drugs for rarer chronic lymphoid leukemias.
  • BACKGROUND: Rarer indolent lymphoid leukemias include well defined mature B-cell and T-cell neoplasm with widely varying natural history and specific morphological, immunophenotypic and molecular characteristics.
  • Among these are prolymphocytic leukemia (PLL), hairy cell leukemia (HCL) and its variants, large granular lymphocyte leukemia (LGLL) and adult T-cell leukemia/lymphoma (ATLL).
  • OBJECTIVE: To present current therapies and emerging drugs potentially useful in the treatment of rarer chronic lymphoid leukemias.
  • Future research should focus on the novel therapeutic strategies based on the molecular pathogenic mechanisms and the development of new targeted therapies for each distinct chronic lymphoid leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drugs, Investigational / therapeutic use. Leukemia, Lymphoid / drug therapy
  • [MeSH-minor] Animals. Chronic Disease. Humans

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  • (PMID = 18321151.001).
  • [ISSN] 1744-7623
  • [Journal-full-title] Expert opinion on emerging drugs
  • [ISO-abbreviation] Expert Opin Emerg Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Investigational
  • [Number-of-references] 189
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52. Berz D, Freeman NJ: Extreme hyperlymphocytosis. J Clin Oncol; 2008 Feb 1;26(4):674-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / complications. Leukemia, Prolymphocytic, T-Cell / diagnosis. Lymphocytosis / etiology
  • [MeSH-minor] Aged. Diagnosis, Differential. Humans. Male. Syndrome

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  • (PMID = 18235128.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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53. Shimoda T, Aoki M, Takezaki S, Futagami A, Inokuchi K, Sugisaki Y, Kawana S: A case of erythrodermic-CTCL. Leuk Lymphoma; 2006 Aug;47(8):1708-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Leukemia, Prolymphocytic / diagnosis. Lymphoma, T-Cell, Cutaneous / diagnosis. Sezary Syndrome / diagnosis
  • [MeSH-minor] Aged. Biopsy. Dermatitis, Exfoliative / diagnosis. Dermatitis, Exfoliative / pathology. Diagnosis, Differential. Female. Humans. Immunophenotyping

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  • (PMID = 16966295.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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54. Gribben JG, Hallek M: Rediscovering alemtuzumab: current and emerging therapeutic roles. Br J Haematol; 2009 Mar;144(6):818-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The humanized anti-CD52 monoclonal antibody alemtuzumab belongs to the family of Campath-1 antibodies, which were initially developed for their ability to prevent graft-versus-host disease (GVHD) and graft rejection in stem cell transplantation.
  • Alemtuzumab is indicated for the treatment of chronic lymphocytic leukaemia (CLL) and has demonstrated considerable activity in relapsed/refractory disease and in previously untreated disease.
  • It has been shown to induce minimal residual disease-negative responses as a single agent or as part of consolidation therapy in a meaningful proportion of patients with CLL and has shown promising activity in patients with high-risk cytogenetic markers.
  • Alemtuzumab may also have significant activity in T-cell malignancies, such as mycosis fungoides and T-cell prolymphocytic leukaemia.
  • Recent studies also have evaluated alemtuzumab as part of a conditioning regimen to prevent GVHD in stem cell transplantation.
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, Neoplasm / immunology. Glycoproteins / immunology. Graft vs Host Disease / prevention & control. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Stem Cell Transplantation. Transplantation Conditioning

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  • (PMID = 19183194.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA081534
  • [Publication-type] Journal Article; Review
  • [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
  • [Number-of-references] 80
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55. Duek A, Shvidel L, Braester A, Berrebi A: Clinical and immunologic aspects of B chronic lymphocytic leukemia associated with autoimmune disorders. Isr Med Assoc J; 2006 Dec;8(12):828-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and immunologic aspects of B chronic lymphocytic leukemia associated with autoimmune disorders.
  • BACKGROUND: Autoimmune disorders often develop during the course of B chronic lymphocytic leukemia.
  • We evaluated the lymphocyte morphology, immunoglobulin G and beta-2-microglobulin serum levels and positivity of the CD38 and FMC7 markers, and compared these values with those of a matched CLL population without autoimmune disorder.
  • We found atypical prolymphocytic morphology in 22%, high expression of the activation antigens CD38 and/or FMC7 in 30%, and high level of immunoglobulin G (> 1000 mg/dl) and beta-2-microglobulin in 57% and 78% respectively.
  • When compared with a matched CLL population without an autoimmune disorder, these values were statistically significant.
  • CONCLUSIONS: Our data, which show activated lymphocyte morphology, high levels of IgG and beta-2-microglobulin, and increased expression of CD38 and/or FMC7 in a significant number of cases, suggest that some degree of activation of B cells may lead to the occurrence of an autoimmune disorder in CLL.
  • [MeSH-major] Autoimmune Diseases / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

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  • [CommentIn] Isr Med Assoc J. 2006 Dec;8(12):864 [17214107.001]
  • (PMID = 17214095.001).
  • [ISSN] 1565-1088
  • [Journal-full-title] The Israel Medical Association journal : IMAJ
  • [ISO-abbreviation] Isr. Med. Assoc. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Biomarkers; 0 / Immunoglobulin G; 0 / beta 2-Microglobulin; EC 3.2.2.5 / Antigens, CD38
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56. Chen J, Petrus M, Bryant BR, Nguyen VP, Goldman CK, Bamford R, Morris JC, Janik JE, Waldmann TA: Autocrine/paracrine cytokine stimulation of leukemic cell proliferation in smoldering and chronic adult T-cell leukemia. Blood; 2010 Dec 23;116(26):5948-56
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  • [Title] Autocrine/paracrine cytokine stimulation of leukemic cell proliferation in smoldering and chronic adult T-cell leukemia.
  • Adult T-cell leukemia (ATL), a heterogeneous disease, can be divided into smoldering, chronic, lymphoma, and acute types clinically.
  • Here, we demonstrated that smoldering/chronic ATL peripheral blood mononuclear cells spontaneously proliferated ex vivo in a cytokine (interleukin-12 [IL-12]/IL-9/IL-15)-dependent manner, while acute-type ATL peripheral blood mononuclear cells did not proliferate or proliferated independent of cytokines.
  • In conclusion, our data provide evidence that there is autocrine/paracrine cytokine stimulation of leukemic cell proliferation in patients with smoldering/chronic ATL that could be targeted for treatment.

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  • (PMID = 20858854.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cytokines
  • [Other-IDs] NLM/ PMC3031384
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57. Lundell R, Hartung L, Hill S, Perkins SL, Bahler DW: T-cell large granular lymphocyte leukemias have multiple phenotypic abnormalities involving pan-T-cell antigens and receptors for MHC molecules. Am J Clin Pathol; 2005 Dec;124(6):937-46
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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 leukemias have multiple phenotypic abnormalities involving pan-T-cell antigens and receptors for MHC molecules.
  • T-cell large granular lymphocyte (T-LGL) leukemias represent monoclonal T-cell expansions that express CD16, CD56, or CD57 and cause cytopenias.
  • The identification of T-LGL leukemias can be difficult because reactive T-LGL cells also can express CD16, CD56, and CD57, and many leukemia cases show only mild lymphocytoses.
  • In this study, 23 T-LGL leukemia cases were analyzed by 3- and 4-color flow cytometry to identify markers that could aid in discriminating leukemic from normal T-LGL.
  • In most cases (18/23), abnormalities (bright, dim, or negative expression) of 2 or more pan-T-cell antigens were identified, with all cases showing abnormal CD5 levels.
  • These studies help define abnormal phenotypic features typical of T-LGL leukemia that may have important diagnostic value.
  • [MeSH-major] Antigens, Differentiation, T-Lymphocyte / metabolism. Biomarkers, Tumor / analysis. Histocompatibility Antigens Class I / metabolism. Leukemia, Prolymphocytic, T-Cell / diagnosis. Receptors, Antigen, T-Cell / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD5 / metabolism. Female. Flow Cytometry. Humans. Immunophenotyping. Killer Cells, Natural / metabolism. Male. Middle Aged. NK Cell Lectin-Like Receptor Subfamily D / metabolism. Receptors, Immunologic / metabolism. Receptors, KIR. Receptors, KIR2DL1. Receptors, KIR2DL2. Receptors, KIR2DL3. Receptors, KIR3DL1. Receptors, KIR3DL2. T-Lymphocytes / metabolism

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  • (PMID = 16416744.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / Histocompatibility Antigens Class I; 0 / KIR2DL2 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily D; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Immunologic; 0 / Receptors, KIR; 0 / Receptors, KIR2DL1; 0 / Receptors, KIR2DL2; 0 / Receptors, KIR2DL3; 0 / Receptors, KIR3DL1; 0 / Receptors, KIR3DL2
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58. Telek B, Batár P, Rejto L, Udvardy M: [Successful treatment of B-cell prolymphocytic leukemia (B-PLL) with FCR-Lite (fludarabine, cyclophosphamide, rituximab) protocol]. Orv Hetil; 2010 Aug 1;151(31):1261-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful treatment of B-cell prolymphocytic leukemia (B-PLL) with FCR-Lite (fludarabine, cyclophosphamide, rituximab) protocol].
  • [Transliterated title] B-sejtes prolymphocytás leukaemia (B-PLL) sikeres kezelése FCR-Lite (fludarabin, cyclophosphamid, rituximab) protokoll alkalmazásával.
  • B-cell prolymphocytic leukemia (B-PLL) is a rare disorder characterized by marked lymphocytosis in the peripheral blood, matured lymphocytic infiltration in the bone marrow and splenomegaly.
  • The authors present a case of a patient with typical B-PLL treated with FCR-Lite (fludarabine, cyclophosphamide, rituximab) protocol achieving complete hematological (and immunophenotypic) remission.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Prolymphocytic, B-Cell / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Cyclophosphamide / administration & dosage. Diagnosis, Differential. Humans. Immunophenotyping. Male. Prognosis. Rituximab. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 20656663.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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59. Miyoshi I, Hatakeyama N, Daibata M, Taguchi H: Cutaneous and nodal cryptococcosis in an ATL Patient. Intern Med; 2006;45(19):1105-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Cryptococcosis / etiology. Leukemia, Prolymphocytic, T-Cell / complications. Leukemia-Lymphoma, Adult T-Cell / complications. Lymph Nodes. Lymphatic Diseases / etiology. Skin Diseases / etiology
  • [MeSH-minor] Aged. Disease Susceptibility. Humans. Male


60. Del Giudice I, Osuji N, Dexter T, Brito-Babapulle V, Parry-Jones N, Chiaretti S, Messina M, Morgan G, Catovsky D, Matutes E: B-cell prolymphocytic leukemia and chronic lymphocytic leukemia have distinctive gene expression signatures. Leukemia; 2009 Nov;23(11):2160-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B-cell prolymphocytic leukemia and chronic lymphocytic leukemia have distinctive gene expression signatures.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Prolymphocytic, B-Cell / genetics


61. Chaar BT, Petruska PJ: Complete response to alemtuzumab in a patient with B prolymphocytic leukemia. Am J Hematol; 2007 May;82(5):417
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete response to alemtuzumab in a patient with B prolymphocytic leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Prolymphocytic / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. B-Lymphocytes / pathology. Combined Modality Therapy. Humans. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Remission Induction. Transplantation, Autologous

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  • (PMID = 17160995.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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62. Narat S, Gandla J, Dogan A, Mehta A: Successful treatment of hairy cell leukemia variant with rituximab. Leuk Lymphoma; 2005 Aug;46(8):1229-32
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  • [Title] Successful treatment of hairy cell leukemia variant with rituximab.
  • Hairy cell leukemia (HCL) variant is a rare low-grade B-cell disorder affecting the elderly or middle-aged population with features intermediate between those of HCL and prolymphocytic leukemia.
  • We report a case of a 53-year-old man who had refractory thrombocytopenia and lymphocytosis for 8 years.
  • Investigations and analysis of spleen and bone marrow revealed a diagnosis of HCL variant.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Hairy Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Cell Count. Humans. Male. Middle Aged. Remission Induction / methods. Rituximab. Treatment Outcome

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  • (PMID = 16085567.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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63. Jeong KH, Lew BL, Sim WY: Generalized leukaemia cutis from a small cell variant of T-cell prolymphocytic leukaemia presenting with exfoliative dermatitis. Acta Derm Venereol; 2009;89(5):509-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Generalized leukaemia cutis from a small cell variant of T-cell prolymphocytic leukaemia presenting with exfoliative dermatitis.
  • T-cell prolymphocytic leukaemia (T-PLL) is a rare, aggressive neoplasm of mature T lymphocytes.
  • The small cell variant occurs in approximately 20% of T-PLL patients.
  • The skin findings of leukaemia consist of leukaemia-specific skin lesions, which are infiltrated by leukaemia cells, and non-specific lesions.
  • The former type of lesion signifies leukaemia cutis.
  • Leukaemia cutis presents clinically as tumours, nodules, or patches on the scalp, face and trunk.
  • We suspected a hidden malignancy and diagnosed small cell variant T-PLL through blood and bone marrow examination.
  • Most of the atypical lymphocytes stained positively with CD markers such as CD2, CD3, CD4, CD5, CD7 and CD8, thereby confirming the presence of leukaemia cells.
  • To our knowledge, this is the first case of generalized leukaemia cutis from small cell variant of T-PLL presenting with exfoliative dermatitis over the whole body.
  • [MeSH-major] Dermatitis, Exfoliative / etiology. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemic Infiltration. Skin / pathology. T-Lymphocytes / pathology

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  • (PMID = 19734979.001).
  • [ISSN] 1651-2057
  • [Journal-full-title] Acta dermato-venereologica
  • [ISO-abbreviation] Acta Derm. Venereol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; VB0R961HZT / Prednisone
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64. Krejcí M, Adam Z, Pour L, Brychtová Y, Mayer J, Vorlícek J: [B-cell chronic lymphocytic leukaemia and the similar states]. Vnitr Lek; 2009 Sep;55(9):746-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [B-cell chronic lymphocytic leukaemia and the similar states].
  • [Transliterated title] Chronická B-lymfatická leukemie a jí podobné stavy.
  • B-cell chronic lymphocytic leukaemia and the similar diseases are seen predominantly in patients above the age 50 years, i.e. at the age when the patients also have other co-morbidities.
  • The aim of the present review is to provide the medical community with the main information on this disease as patients with B-cell chronic lymphocytic leukaemia and similar disease states are of older age and very often suffer from a range of co-morbidities.
  • The aim of the following text is to present a clear overview of the basic information about this group of diseases that might be useful to all physicians who provide care to patients with B-cell chronic lymphocytic leukaemia and similar conditions.
  • Since monoclonal immunoglobulin is sometimes identified in patients with these diseases, it is important to consider these conditions in the differential diagnosis of the states with the presence of monoclonal immunoglobulin.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Leukemia, Hairy Cell / diagnosis. Leukemia, Prolymphocytic / diagnosis. Multiple Myeloma / diagnosis. Paraproteinemias / diagnosis

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  • (PMID = 19785372.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 41
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65. Morris JC, Waldmann TA: Antibody-based therapy of leukaemia. Expert Rev Mol Med; 2009;11:e29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antibody-based therapy of leukaemia.
  • Over the past decade, monoclonal antibodies have dramatically impacted the treatment of haematological malignancies, as evidenced by the effect of rituximab on the response rate and survival of patients with follicular and diffuse large B cell non-Hodgkin's lymphoma.
  • Currently, only two monoclonal antibodies - the anti-CD33 immunotoxin gemtuzumab ozogamicin and the CD52-directed antibody alemtuzumab - are approved for treatment of relapsed acute myeloid leukaemia in older patients and B cell chronic lymphocytic leukaemia, respectively.
  • Although not approved for such treatment, alemtuzumab is also active against T cell prolymphocytic leukaemia, cutaneous T cell lymphoma and Sézary syndrome, and adult T cell leukaemia and lymphoma.
  • In addition, rituximab has demonstrated activity against B cell chronic lymphocytic and hairy cell leukaemia.
  • Monoclonal antibodies targeting CD4, CD19, CD20, CD22, CD23, CD25, CD45, CD66 and CD122 are now being studied in the clinic for the treatment of leukaemia.
  • Improved interactions with Fc receptors on immune effector cells can enhance destruction of target cells through antibody-dependent cellular cytotoxicity and complement-mediated cell lysis.
  • The antibodies can also be armed with cellular toxins or radionuclides to enhance the destruction of leukaemia cells.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Hematologic Neoplasms / therapy. Immunologic Factors / therapeutic use. Immunotoxins / therapeutic use. Leukemia / therapy

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  • (PMID = 19788782.001).
  • [ISSN] 1462-3994
  • [Journal-full-title] Expert reviews in molecular medicine
  • [ISO-abbreviation] Expert Rev Mol Med
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Immunologic Factors; 0 / Immunotoxins
  • [Number-of-references] 193
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66. Absi A, Hsi E, Kalaycio M: Prolymphocytic leukemia. Curr Treat Options Oncol; 2005 May;6(3):197-208
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  • [Title] Prolymphocytic leukemia.
  • Prolymphocytic leukemia is a rare chronic lymphoproliferative disorder that includes two subtypes, B cell and T cell, each with its own distinct clinical, laboratory and pathological features.
  • T-cell prolymphocytic leukemia has an aggressive course with short median survival and poor response to chemotherapy.
  • We recommend alemtuzumab as initial therapy and offer stem cell transplant (SCT) to selected young, healthy patients who respond.
  • Although B-cell prolymphocytic leukemia is also a progressive disease, some patients can achieve a prolonged progression-free-survival with fludarabine.
  • Rituximab is a promising agent and further investigations are warranted to better define its role in treatment of this disorder.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, B-Cell / therapy. Leukemia, Prolymphocytic / therapy. Leukemia, T-Cell / therapy
  • [MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / administration & dosage. Female. Humans. Male. Pentostatin / administration & dosage. Rituximab. Stem Cell Transplantation

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  • (PMID = 15869731.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 54
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67. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Nair R, Sengar M, Nair C: Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia. Indian J Cancer; 2010 Apr-Jun;47(2):189-93
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  • [Title] Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia.
  • INTRODUCTION: Mature T/NK cell lymphomas (MTNKL) presenting as leukemia are rare and show considerable overlapping of clinical, morphological and immunophenotypic features.
  • MATERIALS AND METHODS: We reviewed 380 consecutive cases of mature lymphoid neoplasm that presented as leukemia and were diagnosed on morphology and immunophenotyping of bone marrow and/or peripheral blood samples.
  • MTNKL constituted 4% (nine cases) of all mature lymphoid neoplasms presenting as leukemia.
  • It included four cases of T-large granular leukemia (T-LGL), two of T-cell prolymphocytic leukemia small cell variant (T-PLL), two of adult T-cell leukemia/lymphoma (ATLL) and one of primary cutaneous gamma delta T-cell lymphoma (PCGDTCL).
  • One case of T- PLL small cell variant showed CD4+/CD8- phenotype, while the other revealed CD4-/CD8+ phenotype.
  • CONCLUSION: Mature nodal T/NK cell neoplasms are rare and MTNKL presenting as leukemia are even rarer.
  • There is an overlap between the immunophenotypic profiles of different MTNKL subtypes and elaborate T/NK cell panels are required for their evaluation.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, T-Cell / diagnosis
  • [MeSH-minor] Adult. Aged. Bone Marrow / immunology. Bone Marrow / pathology. Diagnosis, Differential. Female. Flow Cytometry. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 20448385.001).
  • [ISSN] 1998-4774
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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68. Noguchi M, Ropars V, Roumestand C, Suizu F: Proto-oncogene TCL1: more than just a coactivator for Akt. FASEB J; 2007 Aug;21(10):2273-84
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  • Recently, the proto-oncogene TCL1 (T cell leukemia 1), with a previously unknown physiological function, was shown to interact with the Akt pleckstrin homology domain, enhancing Akt kinase activity; hence, it functions as an Akt kinase coactivator.
  • [MeSH-major] Leukemia, Prolymphocytic / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 17360849.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Number-of-references] 109
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69. Krishnan B, Matutes E, Dearden C: Prolymphocytic leukemias. Semin Oncol; 2006 Apr;33(2):257-63
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  • [Title] Prolymphocytic leukemias.
  • T and B subtypes of prolymphocytic leukemias (PLLs) are rare, highly aggressive lymphoid malignancies with characteristic morphologic, immunophenotypical, cytogenetic, and molecular features.
  • Recent studies have highlighted the role of specific oncogenes such as TCL1, MTCP-1, and ATM in the case of T-cell and p53 mutations in the case of B-cell PLLs.
  • [MeSH-major] Leukemia, Prolymphocytic

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  • (PMID = 16616073.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 46
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70. Ravandi F, O'Brien S, Jones D, Lerner S, Faderl S, Ferrajoli A, Wierda W, Garcia-Manero G, Thomas D, Koller C, Verstovsek S, Giles F, Cortes J, Herling M, Kantarjian H, Keating M: T-cell prolymphocytic leukemia: a single-institution experience. Clin Lymphoma Myeloma; 2005 Nov;6(3):234-9
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  • [Title] T-cell prolymphocytic leukemia: a single-institution experience.
  • BACKGROUND: T-cell prolymphocytic leukemia is an uncommon, aggressive, mature T-cell leukemia characterized by proliferation of T-cell lymphocytes.
  • The recent availability of modern immunophenotypic and molecular tools has allowed a better distinction of this disorder from its B-cell counterpart and other mature T-cell leukemias.
  • PATIENTS AND METHODS: The clinical, pathologic, and cytogenetic features of 57 patients with T-PLL who were evaluated at the Department of Leukemia, M. D.
  • RESULTS: The most common cytogenetic abnormality was inv(14)(q11;q32), which was present in 7 patients.
  • In all 7 patients, this abnormality was associated with other chromosomal aberrations.
  • CONCLUSION: Treatment with alemtuzumab results in higher response rates and a better survival rate in patients with T-cell prolymphocytic leukemia.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Leukemia, Prolymphocytic / metabolism. Proto-Oncogene Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Chromosome Inversion. Disease-Free Survival. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies

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  • (PMID = 16354329.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human
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71. Brüggemann M, White H, Gaulard P, Garcia-Sanz R, Gameiro P, Oeschger S, Jasani B, Ott M, Delsol G, Orfao A, Tiemann M, Herbst H, Langerak AW, Spaargaren M, Moreau E, Groenen PJ, Sambade C, Foroni L, Carter GI, Hummel M, Bastard C, Davi F, Delfau-Larue MH, Kneba M, van Dongen JJ, Beldjord K, Molina TJ: Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936. Leukemia; 2007 Feb;21(2):215-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936.
  • Polymerase chain reaction (PCR) assessment of clonal T-cell receptor (TCR) and immunoglobulin (Ig) gene rearrangements is an important diagnostic tool in mature T-cell neoplasms.
  • To obtain reference values for Ig/TCR rearrangement patterns, 19 European laboratories investigated 188 T-cell malignancies belonging to five World Health Organization-defined entities.
  • TCR clonality was detected in 99% (143/145) of all definite cases of T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia, peripheral T-cell lymphoma (unspecified) and angioimmunoblastic T-cell lymphoma (AILT), whereas nine of 43 anaplastic large cell lymphomas did not show clonal TCR rearrangements.
  • Our study indicates that the BIOMED-2 multiplex PCR tubes provide a powerful strategy for clonality assessment in T-cell malignancies assisting the firm diagnosis of T-cell neoplasms.
  • The detected TCR gene rearrangements can also be used as PCR targets for monitoring of minimal residual disease.
  • [MeSH-major] Genes, Immunoglobulin. Leukemia, T-Cell / genetics. Lymphoma, T-Cell / genetics. Polymerase Chain Reaction / methods. Receptors, Antigen, T-Cell / genetics
  • [MeSH-minor] Gene Amplification. Gene Rearrangement. Genotype. Humans. Immunohistochemistry. Leukemia, Prolymphocytic / genetics. Leukemia, Prolymphocytic / immunology. Leukemia, Prolymphocytic / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Large B-Cell, Diffuse / pathology. T-Lymphocytes / immunology

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  • (PMID = 17170730.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
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72. Jamet D, Quinio D, Moalic E, Ianotto JC, Dalbies F, Guillerm G, Marion V, Berthou C, Nevez G: [Systemic microsporidiosis and toxoplasmosis in a patient with T prolymphocytic leukemia]. Med Mal Infect; 2009 Jun;39(6):406-8
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  • [Title] [Systemic microsporidiosis and toxoplasmosis in a patient with T prolymphocytic leukemia].
  • [Transliterated title] Microsporidiose et toxoplasmose disséminées chez une patiente présentant une leucémie prolymphocytaire T.
  • We report a case of microsporidiosis in a 72-year-old woman presenting with prolymphocytic leukemia.
  • The underlying conditions 7 months after leukemia was diagnosed were pancytopenia and immunosuppression due to alemtuzumab and pentostatin.
  • The present case in a patient with lymphoid leukemia is the first to be reported.
  • [MeSH-major] Encephalitozoonosis / complications. Leukemia, Prolymphocytic, T-Cell / complications

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  • (PMID = 19046839.001).
  • [ISSN] 0399-077X
  • [Journal-full-title] Médecine et maladies infectieuses
  • [ISO-abbreviation] Med Mal Infect
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] F4216019LN / Albendazole
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73. Dungarwalla M, Matutes E, Dearden CE: Prolymphocytic leukaemia of B- and T-cell subtype: a state-of-the-art paper. Eur J Haematol; 2008 Jun;80(6):469-76
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  • [Title] Prolymphocytic leukaemia of B- and T-cell subtype: a state-of-the-art paper.
  • Prolymphocytic leukaemias of B and T cell subtype are rare diseases.
  • Despite recent advances in immunophenotyping and molecular cytogenetics, leading to a better understanding of the underlying cell biology of the prolymphocytic leukaemias, prognosis for these patients remains poor.
  • Purine analogues and monoclonal antibodies have shown efficacy in B-cell prolymphocytic leukaemia although further studies are warranted.
  • Monoclonal antibody therapy with alemtuzumab has significantly improved outcome in T-cell prolymphocytic leukaemia (T-PLL) but responses are still transient and further disease progression is inevitable.
  • While allogeneic stem cell transplant is an attractive option, due to the older age group of T-PLL patients the morbidity and mortality associated with the procedure is significant.
  • [MeSH-major] B-Lymphocytes / immunology. Leukemia, Lymphoid / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Disease Progression. Humans

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  • (PMID = 18331594.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Number-of-references] 49
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74. Reindl L, Bacher U, Dicker F, Alpermann T, Kern W, Schnittger S, Haferlach T, Haferlach C: Biological and clinical characterization of recurrent 14q deletions in CLL and other mature B-cell neoplasms. Br J Haematol; 2010 Oct;151(1):25-36
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  • [Title] Biological and clinical characterization of recurrent 14q deletions in CLL and other mature B-cell neoplasms.
  • 14q-deletions have been repeatedly described in mature B-cell neoplasms, but not yet characterized in a larger cohort.
  • Based on chromosome banding analysis, the present study identified 47 del(14q) cases in 3054 mature B-cell neoplasms (1·5%) (chronic lymphocytic leukaemia [CLL]: 1·9%; CLL/prolymphocytic leukaemia [PL]: 9·0%; others: 0·2%).
  • In conclusion, the del(14q) is a rare recurrent alteration in diverse mature B-cell neoplasms, shows variable size but distinct clustering of breakpoints, and is associated with short time to treatment.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 14 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Prolymphocytic / genetics

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20649559.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region
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75. Friedenson B: The BRCA1/2 pathway prevents hematologic cancers in addition to breast and ovarian cancers. BMC Cancer; 2007;7:152
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  • BACKGROUND: The present study was designed to test the hypothesis that inactivation of virtually any component within the pathway containing the BRCA1 and BRCA2 proteins would increase the risks for lymphomas and leukemias.
  • These kinds of rearrangements are typically associated with some lymphomas and leukemias.
  • RESULTS: Deleterious mutations of genes encoding proteins virtually anywhere within the BRCA pathway increased risks up to nearly 2000 fold for certain leukemias and lymphomas.
  • Cancers with large increases in risk included mantle cell lymphoma, acute myeloid leukemia, acute lymphocytic leukemia, chronic lymphocytic leukemia, and prolymphocytic leukemia.
  • Mantle cell lymphoma is defined by a characteristic rearrangement of DNA fragments interchanged between chromosomes 11 and 14.
  • CONCLUSION: An important function of the BRCA pathway is to prevent a subgroup of human leukemias and lymphomas that may involve non-random, characteristic gene rearrangements.
  • Inactivation of a single gene within the pathway can increase risks for multiple cancers and inactivation of a different gene in the same pathway may have similar effects.
  • [MeSH-minor] Adult. Child. Fanconi Anemia / genetics. Female. Genetic Predisposition to Disease. Humans. Leukemia / genetics. Lymphoma / genetics. Male. Translocation, Genetic

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  • (PMID = 17683622.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / BRCA2 Protein
  • [Number-of-references] 77
  • [Other-IDs] NLM/ PMC1959234
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76. Mod H, Prasiko G, Jha AK, Chaurasia PP, Srivastava R: Radiotherapy for splenomegaly. JNMA J Nepal Med Assoc; 2005 Jul-Sep;44(159):97-9
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  • Massive splenomegaly may be seen in CML, CLL, hairy cell leukemia and splenic marginal zone lymphomas, prolymphocytic leukemia, myeloproliferative disorders such as polycythaemia rubra, polycythaemia vera or essential thrombocytosis or myelofibrosis.
  • [MeSH-major] Brachytherapy. Palliative Care. Primary Myelofibrosis / diagnosis. Splenomegaly / radiotherapy

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  • (PMID = 16554863.001).
  • [ISSN] 0028-2715
  • [Journal-full-title] JNMA; journal of the Nepal Medical Association
  • [ISO-abbreviation] JNMA J Nepal Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Nepal
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77. Abrams SL, Steelman LS, Shelton JG, Chappell W, Bäsecke J, Stivala F, Donia M, Nicoletti F, Libra M, Martelli AM, McCubrey JA: Enhancing therapeutic efficacy by targeting non-oncogene addicted cells with combinations of signal transduction inhibitors and chemotherapy. Cell Cycle; 2010 May;9(9):1839-46
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  • The effects of inhibition of the Raf/MEK/ERK and PI3K/Akt/mTOR signaling pathways and chemotherapeutic drugs on cell cycle progression and drug sensitivity were examined in cytokine-dependent FL5.12 hematopoietic cells.
  • When cytokine-dependent FL5.12 cells were cultured in the presence of IL-3, which stimulated multiple proliferation and anti-apoptotic cascades, MEK, PI3K and mTOR inhibitors transiently suppressed but did not totally inhibit cell cycle progression or induce apoptosis while chemotherapeutic drugs such as doxorubicin and paclitaxel were more effective in inducing cell cycle arrest and apoptosis.
  • Doxorubicin was more effective in inducing cell death than paclitaxel.
  • It is important to develop methods to inhibit the growth of such cytokine-dependent cells as they may resemble the leukemia stem cell and other cancer initiating cells.

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  • (PMID = 20436269.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098195; United States / NCI NIH HHS / CA / R01CA098195
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Butadienes; 0 / Chromones; 0 / Interleukin-3; 0 / Intracellular Signaling Peptides and Proteins; 0 / Morpholines; 0 / Nitriles; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; P88XT4IS4D / Paclitaxel; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC3781183
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78. Schweighofer CD, Fätkenheuer G, Staib P, Hallek M, Reiser M: Lyme disease in a patient with chronic lymphocytic leukemia mimics leukemic meningeosis. Onkologie; 2007 Nov;30(11):564-6
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  • [Title] Lyme disease in a patient with chronic lymphocytic leukemia mimics leukemic meningeosis.
  • BACKGROUND: Involvement of the central nervous system (CNS) is a rare complication of chronic lymphocytic leukemia (CLL) and seems to be more frequent in patients with Richter's syndrome or prolymphocytic transformation.
  • PATIENT AND METHODS: We present the case of a 75-year-old male patient who was admitted to a rural hospital with ataxia, disorientation, and signs of progressive CLL disease.
  • RESULTS: When referred to our center, careful immunophenotyping of the CNS lymphocytes as well as assessment for infectious causes of lymphocytic meningitis led to the diagnosis of Lyme disease/neuroborreliosis.
  • CONCLUSION: In conclusion, this case report should alert clinicians that lymphocytic meningeal involvement in CLL patients accounts for the rare leukemic meningeosis only if cerebrospinal fluid cells show a predominating immunophenotype of typical BCLL cells, i.e. by flow cytometry, and if any infectious cause including Lyme disease has been ruled out.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Lyme Disease / complications. Lyme Disease / diagnosis. Meningitis / complications. Meningitis / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged


79. de Oliveira FM, Tone LG, Simões BP, Rego EM, Marinato AF, Jácomo RH, Falcão RP: Translocations t(X;14)(q28;q11) and t(Y;14)(q12;q11) in T-cell prolymphocytic leukemia. Int J Lab Hematol; 2009 Aug;31(4):453-6
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  • [Title] Translocations t(X;14)(q28;q11) and t(Y;14)(q12;q11) in T-cell prolymphocytic leukemia.
  • We report a case of T-cell prolymphocytic leukemia (T-PLL) in a 41-year-old male.
  • Classical cytogenetic, spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH) studies of a blood sample obtained at diagnosis revealed the co-existence of t(X;14)(q28;q11), t(Y;14)(q12;q11) and a ring chromosome derived from i(8)(q10).
  • Immunophenotypic studies revealed involvement of T-cell lineage, with proliferation of CD4(-) CD8+.
  • Chromosomal instability associated with the disease progression may have allowed the emergence of cell clones with translocations involving the sex chromosomes and the ring chromosome observed.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, X / genetics. Chromosomes, Human, Y / genetics. Leukemia, Prolymphocytic, T-Cell / genetics. Ring Chromosomes. Translocation, Genetic

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  • (PMID = 18294235.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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80. Gallipoli P, Clark A, Leach M: The evolving management of a rare lymphoproliferative disorder-T-cell prolymphocytic leukemia. Am J Hematol; 2009 Nov;84(11):750-3
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  • [Title] The evolving management of a rare lymphoproliferative disorder-T-cell prolymphocytic leukemia.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / diagnosis

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  • (PMID = 19714590.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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81. Fidani L, Hatzitolios AI, Goulas A, Savopoulos C, Basayannis C, Kotsis A: Cholesteryl ester transfer protein TaqI B and lipoprotein lipase Ser447Ter gene polymorphisms are not associated with ischaemic stroke in Greek patients. Neurosci Lett; 2005 Aug 12-19;384(1-2):102-5
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  • Cholesteryl ester transfer protein (CETP) and lipoprotein lipase (LPL) are both key players in plasma lipoprotein homeostasis and, as such, genetically induced alterations in their respective activities may affect susceptibility to cerebrovascular diseases.
  • In this study, we examined the distribution of two common polymorphisms, namely CETP TaqI B and LPL Ser447Ter in a cohort of Greek clinically diagnosed late-onset ischaemic stroke patients (n = 98) and an ethnicity-, age- and sex-matched control group with no manifestations of vascular disease (n = 100).
  • [MeSH-minor] Aged. Aged, 80 and over. Case-Control Studies. Cholesterol Ester Transfer Proteins. Female. Gene Frequency. Genetic Predisposition to Disease. Greece / epidemiology. Humans. Male. Odds Ratio

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  • (PMID = 15896905.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CETP protein, human; 0 / Carrier Proteins; 0 / Cholesterol Ester Transfer Proteins; 0 / Glycoproteins; 452VLY9402 / Serine; EC 3.1.1.34 / Lipoprotein Lipase
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82. Herling M, Valbuena JR, Jones D, Medeiros LJ: Skin involvement in T-cell prolymphocytic leukemia. J Am Acad Dermatol; 2007 Sep;57(3):533-4
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  • [Title] Skin involvement in T-cell prolymphocytic leukemia.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, Prolymphocytic, T-Cell / pathology. Skin / pathology

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  • [CommentOn] J Am Acad Dermatol. 2006 Sep;55(3):467-77 [16908353.001]
  • (PMID = 17707160.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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83. Kalaycio ME, Kukreja M, Woolfrey AE, Szer J, Cortes J, Maziarz RT, Bolwell BJ, Buser A, Copelan E, Gale RP, Gupta V, Maharaj D, Marks DI, Pavletic SZ, Horowitz MM, Arora M: Allogeneic hematopoietic cell transplant for prolymphocytic leukemia. Biol Blood Marrow Transplant; 2010 Apr;16(4):543-7
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  • [Title] Allogeneic hematopoietic cell transplant for prolymphocytic leukemia.
  • The poor prognosis of patients with prolymphocytic leukemia (PLL) has led some clinicians to recommend allogeneic hematopoietic cell transplant (HCT).
  • Further study of a larger population of patients is needed to determine which patients are more likely to benefit.

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  • [Copyright] Copyright (c) 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 19961946.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / 5U01HL069294; United States / NCI NIH HHS / CA / U24 CA076518; United States / NCI NIH HHS / CA / U24 CA076518-12; United States / NCI NIH HHS / CA / U24 CA76518; United States / NHLBI NIH HHS / HL / U01 HL069294; United States / NCI NIH HHS / CA / CA076518-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS162699; NLM/ PMC2839005
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84. Urbánková H, Holzerová M, Balcárková J, Raida L, Procházka V, Pikalová Z, Papajík T, Indrák K, Jarosová M: Array comparative genomic hybridization in the detection of chromosomal abnormalities in T-cell prolymphocytic leukemia. Cancer Genet Cytogenet; 2010 Oct 1;202(1):58-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Array comparative genomic hybridization in the detection of chromosomal abnormalities in T-cell prolymphocytic leukemia.
  • [MeSH-major] Chromosome Aberrations / classification. Comparative Genomic Hybridization / methods. Leukemia, Prolymphocytic, T-Cell / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-akt / genetics

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  • (PMID = 20804923.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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85. Okamura K, Ikeda T, Shimakura Y, Yoshiba F, Kishi K, Ando K, Hotta T: [Allogeneic bone marrow transplantation for chemotherapy-resistant T-prolymphocytic leukemia]. Rinsho Ketsueki; 2005 Jul;46(7):527-31
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  • [Title] [Allogeneic bone marrow transplantation for chemotherapy-resistant T-prolymphocytic leukemia].
  • Leukocyte count at diagnosis was 17,900/microl with 58% atypical lymphocytes having a convoluted nucleus and prominent nucleoli.
  • The patient was treated with Ara-C and etoposide before conditioning to decrease the high leukemia burden.
  • Because 9.4% of residual recipient type T-cells was seen with STR analysis on day 22, we decreased the dose of Cs'A.
  • After the occurrence of mild acute GVHD, the residual T-cell number decreased.
  • [MeSH-major] Bone Marrow Transplantation. Graft vs Leukemia Effect. Leukemia, Prolymphocytic / therapy. Leukemia, T-Cell / therapy
  • [MeSH-minor] Adult. Combined Modality Therapy. Female. Graft vs Host Disease / prevention & control. Humans. Remission Induction. Transplantation Conditioning. Transplantation, Homologous

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  • (PMID = 16440747.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 9
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86. Dürig J, Bug S, Klein-Hitpass L, Boes T, Jöns T, Martin-Subero JI, Harder L, Baudis M, Dührsen U, Siebert R: Combined single nucleotide polymorphism-based genomic mapping and global gene expression profiling identifies novel chromosomal imbalances, mechanisms and candidate genes important in the pathogenesis of T-cell prolymphocytic leukemia with inv(14)(q11q32). Leukemia; 2007 Oct;21(10):2153-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined single nucleotide polymorphism-based genomic mapping and global gene expression profiling identifies novel chromosomal imbalances, mechanisms and candidate genes important in the pathogenesis of T-cell prolymphocytic leukemia with inv(14)(q11q32).
  • T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive lymphoma derived from mature T cells, which is, in most cases, characterized by the presence of an inv(14)(q11q32)/t(14;14)(q11;q32) and a characteristic pattern of secondary chromosomal aberrations.
  • DNA microarray technology was employed to compare the transcriptomes of eight immunomagnetically purified CD3+ normal donor-derived peripheral blood cell samples, with five highly purified inv(14)/t(14;14)-positive T-PLL blood samples.
  • Between the two experimental groups, 734 genes were identified as differentially expressed, including functionally important genes involved in lymphomagenesis, cell cycle regulation, apoptosis and DNA repair.
  • In conclusion, combined transcriptional and molecular cytogenetic profiling identified novel specific chromosomal loci and genes that are likely to be involved in disease progression and suggests a gene dosage effect as a pathogenic mechanism in T-PLL.
  • [MeSH-major] Chromosome Inversion. Chromosome Mapping / methods. Chromosomes, Human, Pair 14. Gene Expression Profiling. Leukemia, Prolymphocytic / genetics. Leukemia, T-Cell / genetics. Polymorphism, Single Nucleotide
  • [MeSH-minor] Antigens, CD3 / biosynthesis. Apoptosis. Chromosome Aberrations. DNA Repair. Disease Progression. Gene Dosage. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 17713554.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3
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87. Sohani AR, Ferry JA, Chang PS, Abramson JS: Epstein-barr virus-positive diffuse large B-cell lymphoma during therapy with alemtuzumab for T-cell prolymphocytic leukemia. J Clin Oncol; 2010 Feb 10;28(5):e69-72
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  • [Title] Epstein-barr virus-positive diffuse large B-cell lymphoma during therapy with alemtuzumab for T-cell prolymphocytic leukemia.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antibodies, Neoplasm / adverse effects. Antineoplastic Agents / adverse effects. Herpesvirus 4, Human / isolation & purification. Leukemia, Prolymphocytic, T-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / chemically induced
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Examination. Disease Progression. Fatal Outcome. Female. Humans. Magnetic Resonance Imaging. Middle Aged. Treatment Failure

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  • (PMID = 19917859.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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88. de Lavallade H, Faucher C, Fürst S, El-Cheikh J, Vey N, Coso D, Bouabdallah R, Stoppa AM, Gastaut JA, Blaise D, Mohty M: Allogeneic stem cell transplantation after reduced-intensity conditioning in a patient with T-cell prolymphocytic leukemia: graft-versus-tumor effect and long-term remission. Bone Marrow Transplant; 2006 Apr;37(7):709-10
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  • [Title] Allogeneic stem cell transplantation after reduced-intensity conditioning in a patient with T-cell prolymphocytic leukemia: graft-versus-tumor effect and long-term remission.
  • [MeSH-major] Graft vs Tumor Effect. Leukemia, Prolymphocytic / therapy. Leukemia, T-Cell / therapy. Stem Cell Transplantation / adverse effects
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Follow-Up Studies. Graft vs Host Disease / diagnosis. Graft vs Host Disease / therapy. HLA Antigens / analysis. Humans. Male. Prednisone / therapeutic use. Remission Induction. Siblings. Time Factors. Tissue Donors. Transplantation Conditioning / methods. Transplantation, Homologous. Treatment Outcome. Vincristine / therapeutic use

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  • (PMID = 16474410.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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89. Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M: Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma. Int J Hematol; 2007 Apr;85(3):212-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
  • We analyzed NOTCH1 gene mutation in 53 adults with mature T-cell leukemia/lymphoma: 21 patients with adult T-cell leukemia (ATL), 25 with T-cell non-Hodgkin's lymphoma (T-NHL), and 7 with T-cell prolymphocytic leukemia.
  • We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an ATL patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-cell lymphoma-unspecified (PTCL-u).
  • These findings suggest that nonsense mutation in the PEST domain in the ATL case was associated with NOTCH1 signaling through a pathway different from that for T-cell acute lymphoblastic leukemia (T-ALL).
  • Although NOTCH1 mutation occurs infrequently in mature T-cell leukemia/lymphoma, NOTCH1 may be involved in leukemogenesis associated with various forms of T-cell leukemia/lymphoma rather than only with T-ALL.
  • [MeSH-major] Codon, Nonsense. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Receptor, Notch1 / genetics

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  • (PMID = 17483057.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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90. Babadoko AA, Hassan A, Ahmed AJ, Isah HA, Suleiman AM: Splenic lymphoma with villous lymphocytes: case report and literature review. Niger J Med; 2007 Jan-Mar;16(1):71-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Splenic lymphoma with villous lymphocytes (SLVL) is a rare but recognized distinct disease entity among chronic B lymphoproliferative disorders.
  • It is frequently misdiagnosed as chronic lymphocytic leukaemia, (CLL) Prolymphocytic leukaemia or Hairy Cell leukaemia.
  • METHOD: The case records of a sixty year old Nigerian male with a splenic lymphoma and a review of the literature on the subject using MEDLINE, other internet sources and manual library search was utilized.
  • CONCLUSION: Adequate morphologic evaluation is advocated particularly in the resource limited settings were Cytogenetics, immunohistochemistry and immunophenotyping are not available.
  • [MeSH-major] B-Lymphocytes / pathology. Lymphoma / diagnosis. Lymphoproliferative Disorders / diagnosis. Splenic Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Male. Middle Aged

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  • (PMID = 17563973.001).
  • [ISSN] 1115-2613
  • [Journal-full-title] Nigerian journal of medicine : journal of the National Association of Resident Doctors of Nigeria
  • [ISO-abbreviation] Niger J Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Nigeria
  • [Number-of-references] 9
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91. Osuji N, Matutes E, Dearden C, Catovsky D: Pregnancy improves neutropenia in T-cell large granular lymphocyte leukaemia. Br J Haematol; 2005 Mar;128(5):645-8
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  • [Title] Pregnancy improves neutropenia in T-cell large granular lymphocyte leukaemia.
  • The effect of pregnancy on T-cell large granular lymphocyte (LGL) leukaemia has not been previously described.
  • We retrospectively reviewed the clinical features of three patients with T-cell LGL leukaemia; each of them had one or more pregnancies during disease evolution.
  • A similar effect, induced by exogenous progesterone in one patient, suggests a role for progesterone in overcoming mechanisms of neutropenia in this disease.
  • Pregnancy thus appears to have a beneficial effect on neutrophil count in T-cell LGL leukaemia.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / immunology. Pregnancy Complications, Neoplastic / immunology

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  • (PMID = 15725086.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 4G7DS2Q64Y / Progesterone; 83HN0GTJ6D / Cyclosporine
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92. Osuji N, Matutes E, Catovsky D, Lampert I, Wotherspoon A: Histopathology of the spleen in T-cell large granular lymphocyte leukemia and T-cell prolymphocytic leukemia: a comparative review. Am J Surg Pathol; 2005 Jul;29(7):935-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histopathology of the spleen in T-cell large granular lymphocyte leukemia and T-cell prolymphocytic leukemia: a comparative review.
  • We review retrospectively the spleen histology in 8 patients with T-cell large granular lymphocyte (LGL) leukemia and 4 with T-cell prolymphocytic leukemia (T-PLL) to identify characteristic patterns of involvement and to distinguish such patterns from those described in other low grade B- and T-cell malignancies.
  • Moderate splenic enlargement with red pulp expansion due to lymphocytic infiltration was characteristic of LGL leukemia.
  • Unlike in hairy cell leukemia, the main differential diagnosis for red pulp lymphocytosis, the white pulp was not only preserved in T-cell LGL leukemia but showed germinal center hyperplasia with expansion of the mantle zones.
  • T-cell prolymphocytes did not express cytotoxic granule proteins or NK-cell markers, were CD5+, CD45RO+ like normal spleen T cells, were CD2+, CD3+, CD45+, CD43+, TCRbeta+, but CD25-, CD30-, ALK-1-, TRAP-, DBA44-, and TdT-.
  • These observations on the morphologic and immunohistochemical appearances of the spleen in T-cell LGL leukemia and T-PLL may aid diagnosis of these uncommon T-cell disorders, particularly T-cell LGL leukemia, where presentation may be cryptic and where unique pathognomonic features, are absent.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, T-Cell / pathology. Spleen / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Lymphocytes / metabolism. Lymphocytes / pathology. Male. Middle Aged. Retrospective Studies

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  • (PMID = 15958859.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 23
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93. Lau SK, Weiss LM, Zhang Y, Huang Q: Prolymphocytoid transformation of follicular lymphoma with coexpression of CD5 and CD10. Leuk Lymphoma; 2006 Mar;47(3):541-7
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  • Histologic transformation of follicular lymphoma is usually to a diffuse large B-cell lymphoma.
  • We present a rare example of a histologic transformation of follicular lymphoma manifested by prolymphocytoid morphology and an unusual immunophenotype characterized by coexpression of CD5 and CD10.
  • Prolymphocytoid transformation, similar to other histologic forms of transformation of follicular lymphoma, appears to accompany clinical progression of disease.
  • [MeSH-major] Antigens, CD5 / biosynthesis. Cell Transformation, Neoplastic / pathology. Leukemia, Prolymphocytic / pathology. Lymphoma, Follicular / pathology. Neoplasms, Second Primary / pathology. Neprilysin / biosynthesis
  • [MeSH-minor] Adult. Disease Progression. Fatal Outcome. Female. Humans. Immunophenotyping. Remission Induction. Treatment Failure

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  • (PMID = 16396778.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD5; EC 3.4.24.11 / Neprilysin
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94. Le Toriellec E, Despouy G, Pierron G, Gaye N, Joiner M, Bellanger D, Vincent-Salomon A, Stern MH: Haploinsufficiency of CDKN1B contributes to leukemogenesis in T-cell prolymphocytic leukemia. Blood; 2008 Feb 15;111(4):2321-8
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  • [Title] Haploinsufficiency of CDKN1B contributes to leukemogenesis in T-cell prolymphocytic leukemia.
  • T-cell prolymphocytic leukemia (T-PLL) is consistently associated with inactivation of the ATM gene and chromosomal re-arrangements leading to an overexpression of MTCP1/TCL1 oncoproteins.
  • The absence of biallelic inactivation of CDKN1B for most patients suggested a haploinsufficiency mechanism for tumor suppression, which was investigated in an animal model of the disease.
  • [MeSH-major] Chromosomes, Human, Pair 12. Intracellular Signaling Peptides and Proteins / deficiency. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Prolymphocytic, T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Animals. Ataxia Telangiectasia Mutated Proteins. Cell Cycle Proteins / genetics. Chromosome Mapping. Cyclin-Dependent Kinase Inhibitor p27. DNA Primers. DNA-Binding Proteins / genetics. Gene Deletion. Humans. Mice. Mice, Transgenic. Open Reading Frames. Polymerase Chain Reaction. Polymorphism, Single Nucleotide. Protein-Serine-Threonine Kinases / genetics. Tumor Cells, Cultured. Tumor Suppressor Proteins / genetics

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  • (PMID = 18073348.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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95. Curtin NJ, Schwarer AP: Nonmyeloablative peripheral blood stem cell transplant for T-cell prolymphocytic leukaemia complicated by fulminant haemolysis and acute renal failure at engraftment secondary to minor ABO incompatibility. Clin Lab Haematol; 2005 Jun;27(3):206-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonmyeloablative peripheral blood stem cell transplant for T-cell prolymphocytic leukaemia complicated by fulminant haemolysis and acute renal failure at engraftment secondary to minor ABO incompatibility.
  • We present a 54-year-old man who underwent human leucocyte antigen-identical sibling nonmyeloablative peripheral blood stem cell transplant for primary refractory T-cell prolymphocytic leukaemia (T-PLL).
  • [MeSH-major] ABO Blood-Group System / adverse effects. Acute Kidney Injury / etiology. Blood Group Incompatibility / complications. Hematopoietic Stem Cell Transplantation / adverse effects. Hemolysis. Leukemia, Prolymphocytic / complications. Leukemia, T-Cell / complications

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  • (PMID = 15938729.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABO Blood-Group System
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96. Meeuse JJ, Sprenger HG, van Assen S, Leduc D, Daenen SM, Arends JP, van der Werf TS: Rhodococcus equi infection after alemtuzumab therapy for T-cell prolymphocytic leukemia. Emerg Infect Dis; 2007 Dec;13(12):1942-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rhodococcus equi infection after alemtuzumab therapy for T-cell prolymphocytic leukemia.
  • [MeSH-major] Actinomycetales Infections / etiology. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / adverse effects. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Leukemia, Prolymphocytic, T-Cell / drug therapy. Rhodococcus equi

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  • (PMID = 18258054.001).
  • [ISSN] 1080-6040
  • [Journal-full-title] Emerging infectious diseases
  • [ISO-abbreviation] Emerging Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ PMC2876741
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97. Abbi KK, Rizvi SM, Sivik J, Thyagarajan S, Loughran T, Drabick JJ: Guillain-Barré syndrome after use of alemtuzumab (Campath) in a patient with T-cell prolymphocytic leukemia: a case report and review of the literature. Leuk Res; 2010 Jul;34(7):e154-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Guillain-Barré syndrome after use of alemtuzumab (Campath) in a patient with T-cell prolymphocytic leukemia: a case report and review of the literature.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antibodies, Neoplasm / adverse effects. Guillain-Barre Syndrome / chemically induced. Leukemia, Prolymphocytic, T-Cell / drug therapy

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  • (PMID = 20362332.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Immunoglobulins, Intravenous; 3A189DH42V / alemtuzumab
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98. Maljaei SH, Asvadi-E-Kermani I, Eivazi-E-Ziaei J, Nikanfar A, Vaez J: Usefulness of CD45 density in the diagnosis of B-cell chronic lymphoproliferative disorders. Indian J Med Sci; 2005 May;59(5):187-94
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  • [Title] Usefulness of CD45 density in the diagnosis of B-cell chronic lymphoproliferative disorders.
  • BACKGROUND: Although many B-cell chronic lymphoproliferative disorders (BCLPDs) including B-cell chronic lymphocytic leukemia (B-CLL) have characteristic clinical and biological features, the overlapping morphologic and immunophenotypic profiles of various BCLPDs, is still the main problem.
  • MATERIALS AND METHODS: The expression of CD45 in 37 patients with BCLPD including typical B-CLL (Group I), atypical B-CLL and CLL/PLL (II), and hairy cell leukemia (HCL), B-prolymphocytic leukemia (B-PLL), and B-non Hodgkin's lymphoma (B-NHL) as non-CLL BCLPDs (III) and in eight healthy age matched controls (IV) was quantitatively compared by flow cytometric CD45/RALS gating strategy.
  • [MeSH-major] Antigens, CD45 / immunology. Leukemia, B-Cell / diagnosis. Membrane Proteins / biosynthesis. Phosphoproteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. B-Lymphocytes / immunology. B-Lymphocytes / metabolism. Biomarkers / blood. Diagnosis, Differential. Female. Flow Cytometry. Fluorescent Antibody Technique, Direct. Follow-Up Studies. Humans. Intracellular Signaling Peptides and Proteins. Male. Middle Aged. Prospective Studies

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  • (PMID = 15985726.001).
  • [ISSN] 0019-5359
  • [Journal-full-title] Indian journal of medical sciences
  • [ISO-abbreviation] Indian J Med Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / PTPRCAP protein, human; 0 / Phosphoproteins; EC 3.1.3.48 / Antigens, CD45
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99. Trageser D, Iacobucci I, Nahar R, Duy C, von Levetzow G, Klemm L, Park E, Schuh W, Gruber T, Herzog S, Kim YM, Hofmann WK, Li A, Storlazzi CT, Jäck HM, Groffen J, Martinelli G, Heisterkamp N, Jumaa H, Müschen M: Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function. J Exp Med; 2009 Aug 3;206(8):1739-53
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  • [Title] Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function.
  • B cell lineage acute lymphoblastic leukemia (ALL) arises in virtually all cases from B cell precursors that are arrested at pre-B cell receptor-dependent stages.
  • Here, we demonstrate that the pre-B cell receptor functions as a tumor suppressor upstream of IKAROS through induction of cell cycle arrest in Ph(+) ALL cells.
  • Pre-B cell receptor-mediated cell cycle arrest in Ph(+) ALL cells critically depends on IKAROS function, and is reversed by coexpression of the dominant-negative IKAROS splice variant IK6.
  • IKAROS also promotes tumor suppression through cooperation with downstream molecules of the pre-B cell receptor signaling pathway, even if expression of the pre-B cell receptor itself is compromised.
  • In this case, IKAROS redirects oncogenic BCR-ABL1 tyrosine kinase signaling from SRC kinase-activation to SLP65, which functions as a critical tumor suppressor downstream of the pre-B cell receptor.
  • These findings provide a rationale for the surprisingly high frequency of IKAROS deletions in Ph(+) ALL and identify IKAROS-mediated cell cycle exit as the endpoint of an emerging pathway of pre-B cell receptor-mediated tumor suppression.

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  • (PMID = 19620627.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009659-16; None / None / / R01 CA137060-01A1; United States / NCI NIH HHS / CA / T32 CA009659; United States / NCI NIH HHS / CA / R01 CA090321; United States / NCI NIH HHS / CA / R01CA090321; United States / NCI NIH HHS / CA / R21 CA152497; None / None / / R01 CA137060-02; None / None / / R01 CA139032-01; United States / NCI NIH HHS / CA / R01CA137060; United States / NCI NIH HHS / CA / R01 CA139032-02; None / None / / R01 CA139032-02; United States / NCI NIH HHS / CA / R01 CA139032-01; United States / NCI NIH HHS / CA / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA137060-02; United States / NCI NIH HHS / CA / R01 CA137060-01A1; None / None / / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA139032; United States / NCI NIH HHS / CA / R01CA139032; United States / NCI NIH HHS / CA / R01 CA137060
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / IKZF1 protein, human; 0 / Pre-B Cell Receptors; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC2722172
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100. Beck C, Humpe A, Harder S, Schmid M, Horst HA: Myelodysplastic syndrome of donor origin subsequent to successful treatment of myeloid/NK-cell precursor leukaemia with allogeneic PBSCT: two very rare conditions in one patient. Ann Hematol; 2005 Sep;84(9):616-8
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  • [Title] Myelodysplastic syndrome of donor origin subsequent to successful treatment of myeloid/NK-cell precursor leukaemia with allogeneic PBSCT: two very rare conditions in one patient.
  • We report a 36-year-old male with myeloid/natural killer (NK)-cell precursor acute leukaemia with a complex aberrant karyotype, who was treated according to an acute-myeloid-leukaemia (AML) treatment protocol (idarubicine, cytarabine, and etoposide) followed by high-dose cytarabine consolidation and achieved complete remission.
  • He underwent allogeneic matched unrelated donor (MUD) peripheral blood stem-cell transplantation (PBSCT) and remained in remission throughout his remaining life.
  • This patient represents one of the few cases published achieving remission for a significant period of time after being diagnosed with myeloid/NK-cell precursor acute leukaemia, a very rare malignant disease.
  • In addition, the development of a myelodysplastic syndrome of donor origin is extremely rare and only very few cases are published worldwide.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Myeloid / pathology. Leukemia, Myeloid / therapy. Leukemia, Prolymphocytic, T-Cell / pathology. Myelodysplastic Syndromes / etiology. Peripheral Blood Stem Cell Transplantation / methods
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Fatal Outcome. Humans. Infection. Male. Remission Induction / methods. Thrombocytopenia. Tissue Donors. Transplantation, Homologous. Treatment Outcome






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