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35. Burmeister T, Macleod RA, Reinhardt R, Mansmann V, Loddenkemper C, Marinets O, Drexler HG, Thiel E, Blau IW: A novel sporadic Burkitt lymphoma cell line (BLUE-1) with a unique t(6;20)(q15;q11.2) rearrangement. Leuk Res; 2006 Nov;30(11):1417-23
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  • [Title] A novel sporadic Burkitt lymphoma cell line (BLUE-1) with a unique t(6;20)(q15;q11.2) rearrangement.
  • We report the establishment and characterization, including HLA-typing, immunophenotypic and molecular cytogenetic analysis, of a novel EBV-negative cell line (BLUE-1) derived from adult relapsed sporadic Burkitt lymphoma.
  • BLUE-1 carries the pathognomonic t(8;14)(q24;q32) effecting MYC/IgHJ fusion and a novel t(6;20)(q15;q11.2) originally present in the patient, analysis of which may facilitate identification of gene target(s) of recurrent 6q rearrangements in B-cell neoplasia.
  • Our findings are discussed in light of the current understanding of endemic and sporadic Burkitt lymphoma.
  • BLUE-1 grows well in culture and should be a useful lymphoma research tool.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Line, Tumor. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 6 / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Cytogenetic Analysis / methods. HLA Antigens / genetics. Histocompatibility Testing. Humans. Immunohistochemistry. Immunophenotyping. Male. Oligonucleotide Array Sequence Analysis / methods

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  • (PMID = 16697040.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens
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36. An Q, Wright SL, Moorman AV, Parker H, Griffiths M, Ross FM, Davies T, Harrison CJ, Strefford JC: Heterogeneous breakpoints in patients with acute lymphoblastic leukemia and the dic(9;20)(p11-13;q11) show recurrent involvement of genes at 20q11.21. Haematologica; 2009 Aug;94(8):1164-9
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  • [Title] Heterogeneous breakpoints in patients with acute lymphoblastic leukemia and the dic(9;20)(p11-13;q11) show recurrent involvement of genes at 20q11.21.
  • The dic(9;20)(p11-13;q11) is a recurrent chromosomal abnormality in patients with acute lymphoblastic leukemia.
  • From an initial cohort of 58 with acute lymphoblastic leukemia patients with this translocation, breakpoint mapping with fluorescence in situ hybridization on 26 of them revealed breakpoint heterogeneity of both chromosomes.
  • This study provides insight into the breakpoint complexity underlying dicentric chromosomal formation in acute lymphoblastic leukemia and highlights putative target gene loci.
  • [MeSH-major] Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. B-Cell-Specific Activator Protein / genetics. Base Sequence. Centromere / genetics. Child. Child, Preschool. Chromosome Breakage. Chromosome Mapping. Cohort Studies. Female. Genetic Heterogeneity. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Molecular Sequence Data. Nuclear Proteins / genetics. Recurrence. Repressor Proteins / genetics. Sequence Homology, Nucleic Acid. Transcription Factors / genetics. Young Adult

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  • (PMID = 19586940.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / B-Cell-Specific Activator Protein; 0 / FRG1 protein, human; 0 / Nuclear Proteins; 0 / PAX5 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / ZCCHC7 protein, human
  • [Other-IDs] NLM/ PMC2719040
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37. Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP: Cooperative genetic defects in TLX3 rearranged pediatric T-ALL. Leukemia; 2008 Apr;22(4):762-70
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  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del(19)(p13.2).
  • From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases.
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

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  • (PMID = 18185524.001).
  • [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 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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38. Sinclair P, Harrison CJ, Jarosová M, Foroni L: Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36). Haematologica; 2005 May;90(5):602-11
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  • [Title] Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).
  • BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia.
  • In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • RESULTS: Six of seven breakpoints in ALL and two in a single case of AML were localized to within a 10.5 Mb hotspot at 6q22-q23 with five analyzed to the level of a single probe.
  • INTERPRETATION AND CONCLUSIONS: We identified a new primary recurrent translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL.
  • Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be recurrent and may contribute to leukemogenesis through a novel mechanism.
  • [MeSH-major] Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15921375.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion
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39. Manoukian G, Hagemeister F: Denileukin diftitox: a novel immunotoxin. Expert Opin Biol Ther; 2009 Nov;9(11):1445-51
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  • RESULTS: In 1999, the FDA approved the use of denileukin diftitox for patients with persistent or relapsed CD25-positive cutaneous T-cell lymphoma (CTCL), but Ontak has been reported to be an effective therapy for other neoplastic and non-neoplastic conditions.
  • Oncological uses include therapy for CD25-negative T-cell lymphoma, recurrent and refractory chronic lymphocytic leukemia (CLL), non-Hodgkin's B-cell lymphoma (NHL), and human T-cell lymphotropic virus- 1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATL).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Diphtheria Toxin / therapeutic use. Interleukin-2 / therapeutic use. Lymphoma, T-Cell / drug therapy

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  • (PMID = 19817678.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 37
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40. Huang Y, de Reyniès A, de Leval L, Ghazi B, Martin-Garcia N, Travert M, Bosq J, Brière J, Petit B, Thomas E, Coppo P, Marafioti T, Emile JF, Delfau-Larue MH, Schmitt C, Gaulard P: Gene expression profiling identifies emerging oncogenic pathways operating in extranodal NK/T-cell lymphoma, nasal type. Blood; 2010 Feb 11;115(6):1226-37
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  • [Title] Gene expression profiling identifies emerging oncogenic pathways operating in extranodal NK/T-cell lymphoma, nasal type.
  • Biopsies and cell lines of natural killer/T-cell lymphoma, nasal type (NKTCL) were subject to combined gene expression profiling and array-based comparative genomic hybridization analyses.
  • Compared with peripheral T-cell lymphoma, not otherwise specified, NKTCL had greater transcript levels for NK-cell and cytotoxic molecules, especially granzyme H.
  • Notably, platelet-derived growth factor receptor alpha and its phosphorylated form were confirmed at the protein level, and in vitro the MEC04 NKTCL cell line was sensitive to imatinib.
  • Deregulation of the AKT, Janus kinase-signal transducers and activators of transcription, and nuclear factor-kappaB pathways was corroborated by nuclear expression of phosphorylated AKT, signal transducers and activators of transcription 3, and RelA in NKTCL, and several deregulated genes in these pathways mapped to regions of recurrent copy number aberrations (AKT3 [1q44], IL6R [1q21.3], CCL2 [17q12], TNFRSF21 [6p12.3]).
  • [MeSH-major] Epstein-Barr Virus Infections / genetics. Gene Expression Profiling. Killer Cells, Natural / pathology. Lymphoma, Extranodal NK-T-Cell / genetics. Nasopharyngeal Neoplasms / genetics. Oncogenes / physiology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Cell Proliferation. Cells, Cultured. Comparative Genomic Hybridization. Female. Herpesvirus 4, Human / physiology. Humans. Immunoenzyme Techniques. Male. Middle Aged. Nasal Mucosa / metabolism. Nasal Mucosa / pathology. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Platelet-Derived Growth Factor / genetics. Receptors, Platelet-Derived Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Ubiquitin-Protein Ligases / genetics. Ubiquitin-Protein Ligases / metabolism


41. Rutar T, Cockerham KP: Periorbital zygomycosis (mucormycosis) treated with posaconazole. Am J Ophthalmol; 2006 Jul;142(1):187-188
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  • RESULTS: A 22-year-old male undergoing induction chemotherapy for acute lymphoblastic leukemia presented with periorbital cellulitis attributable to Rhizopus.
  • Despite recurrent profound neutropenia, the periorbital infection resolved, he tolerated reconstructive procedures, and he did not develop orbital invasion.
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Humans. Male. Microbial Sensitivity Tests. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Tomography, X-Ray Computed

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  • (PMID = 16815283.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Triazoles; 6TK1G07BHZ / posaconazole
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42. Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA: WT1 mutations in T-ALL. Blood; 2009 Jul 30;114(5):1038-45
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  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • We used single nucleotide polymorphism array analysis to analyze paired diagnostic and relapsed T-ALL samples to identify recurrent genetic alterations in T-ALL.
  • This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.
  • In addition, we identified deletions and associated mutations in the WT1 tumor suppressor gene in 2 of 9 samples.
  • Subsequent analysis showed WT1 mutations in 28 of 211 (13.2%) of pediatric and 10 of 85 (11.7%) of adult T-ALL cases.
  • Survival analysis demonstrated that WT1 mutations do not confer adverse prognosis in pediatric and adult T-ALL.
  • Overall, these results identify the presence of WT1 mutations as a recurrent genetic alteration in T-ALL.
  • [MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

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  • (PMID = 19494353.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE15931
  • [Grant] United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2721784
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43. Jung SI, Cho HS, Lee CH, Jung BC: A case of adult B lymphoblastic leukemia with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3). Korean J Lab Med; 2010 Dec;30(6):585-90
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  • [Title] A case of adult B lymphoblastic leukemia with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3).
  • In B lymphoblastic leukemia/lymphoma (B-ALL/LBL), t(9;22)(q34;q11.2) and t(1;19)(q23;p13.3) are recurrent cytogenetic abnormalities.
  • Here, we report a case of adult B-ALL with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3).
  • This abnormality is specific to precursor B-lymphoid neoplasms, such as B-ALL or B-lymphoid blast phase of CML, and is associated with disease progression or short survival.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Translocation, Genetic

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  • (PMID = 21157143.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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4. Higuchi M, Muta T, Karube KN, Eto T, Yamano Y, Ohshima K: Epstein-Barr virus-positive blastoid variant of mantle cell lymphoma in an adult with recurrent infectious mononucleosis-like symptoms: a case report. Int J Hematol; 2007 Apr;85(3):219-22
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  • [Title] Epstein-Barr virus-positive blastoid variant of mantle cell lymphoma in an adult with recurrent infectious mononucleosis-like symptoms: a case report.
  • Epstein-Barr virus (EBV) is closely associated with several lymphomas, such as Burkitt lymphoma, natural killer/T-cell lymphoma, peripheral T-cell lymphoma, and Hodgkin's lymphoma; however, whether EBV is implicated in mantle cell lymphoma (MCL) has not been established.
  • We report the case of an adult with recurrent infectious mononucleosis (IM)-like symptoms who developed an EBV-positive blastoid variant of MCL.
  • He had a history of recurrent IM-like symptoms (prolonged fever and cervical lymphadenopathy) for at least 1 year.
  • EBV was detected in most of the lymphoma cells and in the peripheral blood.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Herpesvirus 4, Human / pathogenicity. Infectious Mononucleosis / virology. Lymph Nodes / pathology. Lymphoma, Mantle-Cell / virology

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  • (PMID = 17483058.001).
  • [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
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45. Elstrom RL, Martin P, Ostrow K, Barrientos J, Chadburn A, Furman R, Ruan J, Shore T, Schuster M, Cerchietti L, Melnick A, Coleman M, Leonard JP: Response to second-line therapy defines the potential for cure in patients with recurrent diffuse large B-cell lymphoma: implications for the development of novel therapeutic strategies. Clin Lymphoma Myeloma Leuk; 2010 Jun;10(3):192-6
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  • [Title] Response to second-line therapy defines the potential for cure in patients with recurrent diffuse large B-cell lymphoma: implications for the development of novel therapeutic strategies.
  • BACKGROUND: Patients with diffuse large B-cell lymphoma (DLBCL) who are not cured by initial therapy sometimes experience disease-free survival after autologous stem cell transplantation.
  • PATIENTS AND METHODS: We identified patients with relapsed or refractory DLBCL at Weill Cornell Medical Center for whom data on responses to second-line chemotherapy were available.
  • RESULTS: A total of 74 patients with relapsed or refractory DLBCL who underwent second-line chemotherapy between 1996 and 2007 were identified.
  • CONCLUSION: Our data demonstrate that patients with recurrent DLBCL not responding to second-line chemotherapy demonstrate dismal outcomes.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / surgery. Neoplasm Recurrence, Local / surgery. Salvage Therapy / methods
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Stem Cell Transplantation. Treatment Outcome. Young Adult

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  • (PMID = 20511164.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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46. Bittencourt AL, de Oliveira Mde F: Cutaneous manifestations associated with HTLV-1 infection. Int J Dermatol; 2010 Oct;49(10):1099-110
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  • [Title] Cutaneous manifestations associated with HTLV-1 infection.
  • Skin lesions are frequent in human T-cell lymphotropic virus type 1 (HTLV-1) infection and may constitute an alert for the diagnosis of this condition.
  • The most severe skin diseases related to this virus are adult T-cell leukemia/lymphoma (ATLL), an aggressive form of leukemia/lymphoma that fails to respond to chemotherapy, and infective dermatitis associated with HTLV-1 (IDH), a severe and recurrent form of eczema occurring in childhood.
  • IDH may progress to HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and to ATLL.
  • Adult onset IDH and reactional and inflammatory dermatoses found in carriers and also in patients with HAM/TSP will be considered.
  • Other dermatological diseases that occur more frequently in HTLV-1-infected individuals such as xerosis, acquired ichthyosis, seborrheic dermatitis and infectious and parasitic dermatoses will also be discussed.
  • [MeSH-major] Lymphoma, T-Cell / pathology. Lymphoma, T-Cell / virology
  • [MeSH-minor] Antiviral Agents / therapeutic use. Carrier State. Diagnosis, Differential. Drug Resistance, Neoplasm. HTLV-I Infections. Human T-lymphotropic virus 1. Humans. Ichthyosis / diagnosis. Ichthyosis / virology. Immunohistochemistry. Interferon-alpha / therapeutic use. Scabies / diagnosis. Skin / pathology. Skin Diseases, Viral / diagnosis. Treponemal Infections / diagnosis. Zidovudine / therapeutic use

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  • [Copyright] © 2010 The International Society of Dermatology.
  • (PMID = 20883400.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 4B9XT59T7S / Zidovudine
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47. Soulier J, Clappier E, Cayuela JM, Regnault A, García-Peydró M, Dombret H, Baruchel A, Toribio ML, Sigaux F: HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL). Blood; 2005 Jul 1;106(1):274-86
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  • [Title] HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL).
  • Using a combination of molecular cytogenetic and large-scale expression analysis in human T-cell acute lymphoblastic leukemias (T-ALLs), we identified and characterized a new recurrent chromosomal translocation, targeting the major homeobox gene cluster HOXA and the TCRB locus.
  • Inclusion of HOXA-translocated cases in a general molecular portrait of 92 T-ALLs based on large-scale expression analysis shows that this rearrangement defines a new homogeneous subgroup, which shares common biologic networks with the TLX1- and TLX3-related cases.
  • Because T-ALLs derive from T-cell progenitors, expression profiles of the distinct T-ALL subgroups were analyzed with respect to those of normal human thymic subpopulations.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Differentiation / genetics. Child. Child, Preschool. Female. Gene Expression Profiling. Humans. Infant. Male. Middle Aged. Multigene Family. T-Lymphocytes / cytology. T-Lymphocytes / physiology

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  • (PMID = 15774621.001).
  • [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 / Homeodomain Proteins; 157907-48-7 / HoxA protein
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48. Samassekou O, Ntwari A, Hébert J, Yan J: Individual telomere lengths in chronic myeloid leukemia. Neoplasia; 2009 Nov;11(11):1146-54
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  • [Title] Individual telomere lengths in chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a neoplasia characterized by proliferation of a myeloid cell lineage and chromosome translocation t(9;22) (q34;q11.2).
  • We observed recurrent telomere length changes as well as telomere length maintenance and elongation in some individual telomeres.
  • We suggest that individual telomere length maintenance is chromosome arm-specific associated with leukemia cells.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Telomere / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Young Adult


49. Murakami Y, Saigo K, Takashima H, Minami M, Okanoue T, Bréchot C, Paterlini-Bréchot P: Large scaled analysis of hepatitis B virus (HBV) DNA integration in HBV related hepatocellular carcinomas. Gut; 2005 Aug;54(8):1162-8
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  • HBV integration recurrently targeted the human telomerase reverse transcriptase gene (three cases) and genes belonging to distinct pathways: calcium signalling related genes, 60s ribosomal protein encoding genes, and platelet derived growth factor and mixed lineage leukaemia encoding genes.
  • CONCLUSIONS: In 61/68 (89.7%) cases, HBV DNA was integrated into cellular genes potentially providing cell growth advantage.
  • Identification of recurrent viral integration sites into genes of the same family allows recognition of common cell signalling pathways activated in hepatocarcinogenesis.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Calcium Signaling / genetics. DNA Transposable Elements / genetics. DNA-Binding Proteins. Female. Genes, Tumor Suppressor. Humans. Leukemia / genetics. Male. Middle Aged. Neoplasm Proteins / genetics. Platelet-Derived Growth Factor / genetics. Polymerase Chain Reaction / methods. Ribosomal Proteins / genetics. Telomerase / genetics. Viral Proteins / genetics

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  • (PMID = 16009689.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Transposable Elements; 0 / DNA, Viral; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Platelet-Derived Growth Factor; 0 / Ribosomal Proteins; 0 / Viral Proteins; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC1774867
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50. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
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  • [Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
  • Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).
  • In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.
  • Mutation analysis in 4 of these del(17)(q11.2)-positive patients revealed that mutations in the remaining NF1 allele were present in 3 patients, confirming its role as a tumor-suppressor gene in cancer.
  • NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics


51. Bashey A, Medina B, Corringham S, Pasek M, Carrier E, Vrooman L, Lowy I, Solomon SR, Morris LE, Holland HK, Mason JR, Alyea EP, Soiffer RJ, Ball ED: CTLA4 blockade with ipilimumab to treat relapse of malignancy after allogeneic hematopoietic cell transplantation. Blood; 2009 Feb 12;113(7):1581-8
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  • [Title] CTLA4 blockade with ipilimumab to treat relapse of malignancy after allogeneic hematopoietic cell transplantation.
  • Relapse of malignancy after allogeneic hematopoietic cell transplantation (allo-HCT) remains a therapeutic challenge.
  • Twenty-nine patients with malignancies that were recurrent or progressive after allo-HCT, received ipilimumab as a single infusion at dose cohorts between 0.1 and 3.0 mg/kg.
  • Organ-specific immune adverse events (IAE) were seen in 4 patients (grade 3 arthritis, grade 2 hyperthyroidism, recurrent grade 4 pneumonitis).
  • Three patients with lymphoid malignancy developed objective disease responses following ipilimumab: complete remission (CR) in 2 patients with Hodgkin disease and partial remission (PR) in a patient with refractory mantle cell lymphoma.

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  • (PMID = 18974373.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00060372
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 9389-01A1
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / ipilimumab
  • [Other-IDs] NLM/ PMC2644086
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52. Karst C, Gross M, Haase D, Wedding U, Höffken K, Liehr T, Mkrtchyan H: Novel cryptic chromosomal rearrangements detected in acute lymphoblastic leukemia detected by application of new multicolor fluorescent in situ hybridization approaches. Int J Oncol; 2006 Apr;28(4):891-7
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  • [Title] Novel cryptic chromosomal rearrangements detected in acute lymphoblastic leukemia detected by application of new multicolor fluorescent in situ hybridization approaches.
  • However, it is often difficult to obtain good karyotypes, especially of cells from cases with acute lymphoblastic leukemia (ALL) because of poor morphology and spreading.
  • Thus, we detected the following recurrent cryptic chromosomal aberrations: del(12)(pter) [8 cases], del(9)(qter) [3 cases], and del(11)(pter) [2 cases].
  • In summary, mMCB and subCTM were proven to be powerful methods in the screening for new cryptic chromosomal aberrations, which considerably increased the accuracy of cytogenetic diagnosis.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Spectral Karyotyping / methods. Translocation, Genetic / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosome Banding / methods. Female. Humans. Male. Middle Aged. Telomere / genetics

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  • (PMID = 16525638.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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53. Oshiro A, Tagawa H, Ohshima K, Karube K, Uike N, Tashiro Y, Utsunomiya A, Masuda M, Takasu N, Nakamura S, Morishima Y, Seto M: Identification of subtype-specific genomic alterations in aggressive adult T-cell leukemia/lymphoma. Blood; 2006 Jun 1;107(11):4500-7
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  • [Title] Identification of subtype-specific genomic alterations in aggressive adult T-cell leukemia/lymphoma.
  • Aggressive adult T-cell leukemia/lymphoma (ATLL) such as acute and lymphoma types are fatal diseases with poor prognosis.
  • We performed array-based comparative genomic hybridization for 17 acute and 49 lymphoma cases as well as real-time quantitative polymerase chain reaction (PCR) to identify the target genes of recurrently amplified regions.
  • Comparison of the genome profiles of acute and lymphoma types revealed that the lymphoma type had significantly more frequent gains at 1q, 2p, 4q, 7p, and 7q, and losses of 10p, 13q, 16q, and 18p, whereas the acute type showed a gain of 3/3p.
  • Of the recurrent high-level amplifications found at 1p36, 6p25, 7p22, 7q, and 14q32 in the lymphoma type, we were able to demonstrate that CARMA1 is a possible target gene of the 7p22 amplification for the lymphoma type but not for the acute type.
  • Furthermore, we found BCL11B overexpression in the acute type regardless of the 14q32 gain/amplification, but no or low expression of the gene in the lymphoma type.
  • These results suggest that acute and lymphoma types are genomically distinct subtypes, and thus may develop tumors via distinct genetic pathways.
  • [MeSH-major] Gene Amplification. Genome, Human. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis Regulatory Proteins / genetics. CARD Signaling Adaptor Proteins. Chromosomes. DNA-Binding Proteins / genetics. Female. Gene Dosage. Gene Expression Regulation, Neoplastic. Guanylate Cyclase / genetics. Humans. Lymphoma / genetics. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction. Repressor Proteins / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 16484591.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BCL11B protein, human; 0 / CARD Signaling Adaptor Proteins; 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
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54. Gué M, Sun JS, Boudier T: Simultaneous localization of MLL, AF4 and ENL genes in interphase nuclei by 3D-FISH: MLL translocation revisited. BMC Cancer; 2006;6:20
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  • MLL translocation in acute leukaemia) and two models have been proposed to explain the origins of recurrent reciprocal translocation.
  • METHODS: Using triple labeling 3D FISH experiments, we have determined the relative positions of MLL, AF4 and ENL genes, in two lymphoblastic and two myeloid human cell lines.
  • RESULTS: In all cell lines, the ENL gene is significantly closer to the MLL gene than the AF4 gene (with P value < 0.0001).
  • [MeSH-major] Cell Nucleus / chemistry. DNA-Binding Proteins / genetics. Genes. Imaging, Three-Dimensional. In Situ Hybridization, Fluorescence / methods. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Transformed / chemistry. Cell Line, Transformed / ultrastructure. Cell Line, Tumor / chemistry. Cell Line, Tumor / ultrastructure. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 19 / ultrastructure. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 4 / ultrastructure. HL-60 Cells / chemistry. HL-60 Cells / ultrastructure. Herpesvirus 4, Human. Histone-Lysine N-Methyltransferase. Humans. Interphase. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Male. Models, Genetic. Multiple Myeloma / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic

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  • (PMID = 16433901.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1388228
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55. Owatari S, Uozumi K, Tokunaga M, Tokunaga M, Haraguchi K, Suzuki S, Arima N: Adult T-cell leukemia/lymphoma in a 21-year-old man. Clin Lab Haematol; 2006 Apr;28(2):141-4
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  • [Title] Adult T-cell leukemia/lymphoma in a 21-year-old man.
  • Adult T-cell leukemia/lymphoma (ATL) is malignancy of mature T cells that caused by infection with human T-cell leukemia virus type I (HTLV-I).
  • Leukemogenesis of ATL cells considered to involve a multistep oncogenic process, resulting in a very long latency period.
  • But, we report here the case of a 21-year-old man having suffered from recurrent stomatititis who has already developed acute-type ATL.
  • ATL generally occurs after a long latency period, and the present case in a young man is thus very rare.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Blotting, Southern. HTLV-I Antibodies / blood. Humans. Male

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  • (PMID = 16630222.001).
  • [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 / HTLV-I Antibodies
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56. van Grotel M, Meijerink JP, Beverloo HB, Langerak AW, Buys-Gladdines JG, Schneider P, Poulsen TS, den Boer ML, Horstmann M, Kamps WA, Veerman AJ, van Wering ER, van Noesel MM, Pieters R: The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols. Haematologica; 2006 Sep;91(9):1212-21
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  • [Title] The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols.
  • BACKGROUND AND OBJECTIVES: Subgroups of T-cell acute lymphoblastic leukemia (T-ALL), defined according to recurrent cytogenetic aberrations, may have different prognoses.
  • RESULTS: In our cohort study, CALM-AF10 was associated with an immature immunophenotype and poor outcome (p=0.005).
  • HOX11L2 was associated with both immunophenotypically immature cases as well as cases committed to the gammadelta-lineage.
  • HOX11L2 was significantly associated with poor outcome (p=0.01), independently of the expression of CD1 or the presence of NOTCH1 mutations.
  • TAL1 abnormalities were associated with alphabeta-lineage commitment, and tended to be associated with a good outcome.
  • In relation to the expression of early T-cell transcription factors, high TAL1 levels were found in immunophenotypically-advanced cases, whereas high LYL1 levels were found in immature subgroups.
  • In our cohort, this cytogenetic aberration was associated with a poor outcome.
  • Our data on CALM-AF10 rearranged T-ALL, albeit based on only three patients, suggest that this type of leukemia is associated with a poor outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Cytogenetic Analysis. Leukemia-Lymphoma, Adult T-Cell / diagnosis


57. Strefford JC, Worley H, Barber K, Wright S, Stewart AR, Robinson HM, Bettney G, van Delft FW, Atherton MG, Davies T, Griffiths M, Hing S, Ross FM, Talley P, Saha V, Moorman AV, Harrison CJ: Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization. Oncogene; 2007 Jun 21;26(29):4306-18
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  • [Title] Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization.
  • Chromosomal abnormalities are important for the classification and risk stratification of patients with acute lymphoblastic leukemia (ALL).
  • However, approximately 30% of childhood and 50% of adult patients lack abnormalities with clinical relevance.
  • Deletions of 6q (del(6q)) were heterogeneous in size, in agreement with previous data, demonstrating the sensitivity of aCGH to measure CNA.
  • Six patients showed del(12p), with a common region encompassing the ETV6 gene.
  • Chromosome 21 CNA shared a common region of gain, with associated subtelomeric deletions.
  • Other recurrent findings included dim(13q), dim(16q) and enh(17q).
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Expression Profiling. Genome, Human. Leukemia-Lymphoma, Adult T-Cell / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Gene Dosage. Humans. Infant. Male. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 17237825.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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58. Nakashima Y, Tagawa H, Suzuki R, Karnan S, Karube K, Ohshima K, Muta K, Nawata H, Morishima Y, Nakamura S, Seto M: Genome-wide array-based comparative genomic hybridization of natural killer cell lymphoma/leukemia: different genomic alteration patterns of aggressive NK-cell leukemia and extranodal Nk/T-cell lymphoma, nasal type. Genes Chromosomes Cancer; 2005 Nov;44(3):247-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide array-based comparative genomic hybridization of natural killer cell lymphoma/leukemia: different genomic alteration patterns of aggressive NK-cell leukemia and extranodal Nk/T-cell lymphoma, nasal type.
  • Natural killer (NK) cell lymphomas/leukemias are highly aggressive lymphoid malignancies, but little is known about their genomic alterations, and thus there is an urgent need for identification and analysis of NK cell lymphomas/leukemias.
  • We performed an array CGH analysis for 27 NK-cell lymphoma/leukemia cases that were classified into two disease groups based on the World Health Organization Classification (10 aggressive NK-cell leukemia cases and 17 extranodal NK/T-cell [NK/T] lymphomas, nasal type).
  • The recurrent regions characteristic of the aggressive NK-cell leukemia group compared with those of the extranodal NK/T lymphoma, nasal-type group, were gain of 1q and loss of 7p15.1-p22.3 and 17p13.1.
  • Recurrent regions characteristic of the extranodal NK/T lymphoma, nasal-type group, compared with those of the other group were gain of 2q, and loss of 6q16.1-q27, 11q22.3-q23.3, 5p14.1-p14.3, 5q34-q35.3, 1p36.23-p36.33, 2p16.1-p16.3, 4q12, and 4q31.3-q32.1.
  • Our results can be expected to provide further insights into the genetic basis of lymphomagenesis and the clinicopathologic features of NK-cell lymphomas/leukemias.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Genome, Human. Killer Cells, Natural / pathology. Leukemia, T-Cell / genetics. Lymphoma, T-Cell / genetics. Nose Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Chromosomes, Artificial, Bacterial. DNA, Neoplasm / analysis. Female. Humans. Immunoenzyme Techniques. Karyotyping. Male. Middle Aged. Nucleic Acid Hybridization


59. Clappier E, Cuccuini W, Cayuela JM, Vecchione D, Baruchel A, Dombret H, Sigaux F, Soulier J: Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias. Leukemia; 2006 Jan;20(1):82-6
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  • [Title] Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias.
  • While the cyclin D1 and D3 genes (CCND1 and CCND3) are recurrently involved in genomic rearrangements, especially in B-cell lymphoid neoplasias, no clear involvement of the cyclin D2 gene (CCND2) has been reported to date.
  • Here, we identified chromosomal translocations targeting the CCND2 locus at 12p13, and the T-cell receptor beta (TCRB) or the TCRA/D loci in T-cell acute lymphoblastic leukemias (T-ALLs).
  • In order to evaluate dysregulation in T-ALL with respect to normal T-cell differentiation, we analyzed CCND2 expression in normal purified human thymic subpopulations.
  • CCND2 levels were downregulated through progression from the early stages of human T-cell differentiation, further suggesting that the massive and sustained expression in the CCND2-rearranged T-ALL cases was oncogenic.
  • This report is the first clear evidence of a direct involvement of cyclin D2 in human cancer due to recurrent somatic genetic alterations.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Cyclins / biosynthesis. Cyclins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Cell Separation. Child. Cyclin D2. Cytogenetic Analysis. DNA Mutational Analysis. Gene Rearrangement. Humans

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  • (PMID = 16270038.001).
  • [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 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell
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60. Yamamoto K, Nagata K, Morita Y, Inagaki K, Hamaguchi H: Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10). Leuk Res; 2007 May;31(5):713-8
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  • [Title] Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10).
  • We describe here the first case of acute lymphoblastic leukemia (ALL) with an isodicentric Philadelphia [idic(Ph)] chromosome.
  • The idic(Ph) chromosome was spindle-shaped and supposed to be formed by two Ph chromosomes joined at their q terminals, whereas idic(Ph) chromosomes in chronic myelogenous leukemia (CML) have been shown to be fused at the satellite regions of p arms.
  • Furthermore, considering other three reported cases, der(7;12)(q10;q10) may be one of the recurrent translocations in ALL.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male

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  • (PMID = 16979235.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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61. Le QH, Thomas X, Ecochard R, Iwaz J, Lhéritier V, Michallet M, Fiere D: Proportion of long-term event-free survivors and lifetime of adult patients not cured after a standard acute lymphoblastic leukemia therapeutic program: adult acute lymphoblastic leukemia-94 trial. Cancer; 2007 May 15;109(10):2058-67
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  • [Title] Proportion of long-term event-free survivors and lifetime of adult patients not cured after a standard acute lymphoblastic leukemia therapeutic program: adult acute lymphoblastic leukemia-94 trial.
  • BACKGROUND: In adult acute lymphoblastic leukemia, treatment results generally are expressed in terms of overall survival or disease-free survival at 3 years.
  • In this investigation, the authors attempted to express the results in terms of the proportion of long-term disease-free survivors and in terms of lifetime in patients who developed recurrent disease or died.
  • METHODS: Univariate and multivariate analyses were used to assess the influence of different covariates on the 2 result criteria in 922 participants in the Adult Acute Lymphoblastic Leukemia-94 multicenter trial.
  • The proportion decreased with increasing age, white blood cell count, and lactate dehydrogenase level.
  • It was longer in men than in women and was shorter with increasing age, performance status, hemoglobin level, and white blood cell count.
  • CONCLUSIONS: The results of this study highlighted and specified the importance of some classic prognostic factors in patients with acute lymphoblastic leukemia.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Genes, abl / genetics. Humans. Karyotyping. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Odds Ratio. Oncogene Proteins, Fusion / genetics. Prognosis. Risk Factors. Survival Rate. Treatment Failure

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  • [Copyright] (c) 2007 American Cancer Society
  • (PMID = 17407135.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 1.1.1.27 / L-Lactate Dehydrogenase
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62. Fujiwara SI, Yamashita Y, Nakamura N, Choi YL, Ueno T, Watanabe H, Kurashina K, Soda M, Enomoto M, Hatanaka H, Takada S, Abe M, Ozawa K, Mano H: High-resolution analysis of chromosome copy number alterations in angioimmunoblastic T-cell lymphoma and peripheral T-cell lymphoma, unspecified, with single nucleotide polymorphism-typing microarrays. Leukemia; 2008 Oct;22(10):1891-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-resolution analysis of chromosome copy number alterations in angioimmunoblastic T-cell lymphoma and peripheral T-cell lymphoma, unspecified, with single nucleotide polymorphism-typing microarrays.
  • Angioimmunoblastic T-cell lymphoma (AILT) and peripheral T-cell lymphoma, unspecified (PTCL-u) are relatively frequent subtypes of T- or natural killer cell lymphoma.
  • To characterize the structural anomalies of chromosomes associated with these disorders, we here determined chromosome copy number alterations (CNAs) and loss of heterozygosity (LOH) at >55,000 single nucleotide polymorphism loci for clinical specimens of AILT (n=40) or PTCL-u (n=33).
  • Recurrent copy number gain common to both conditions was detected on chromosomes 8, 9 and 19, whereas common LOH was most frequent for a region of chromosome 2.
  • [MeSH-major] Chromosome Aberrations. Loss of Heterozygosity. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Oligonucleotide Array Sequence Analysis. Polymorphism, Single Nucleotide
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. CARD Signaling Adaptor Proteins / genetics. DNA-Binding Proteins / genetics. Female. Guanylate Cyclase / genetics. Humans. Ikaros Transcription Factor / genetics. Male. Middle Aged. Neprilysin / analysis. Prognosis. Transcription Factors / genetics

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  • (PMID = 18633432.001).
  • [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 / CARD Signaling Adaptor Proteins; 0 / DNA-Binding Proteins; 0 / IKZF2 protein, human; 0 / MYCBP protein, human; 0 / Transcription Factors; 148971-36-2 / Ikaros Transcription Factor; EC 3.4.24.11 / Neprilysin; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
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63. Robak T, Lech-Maranda E, Janus A, Blonski J, Wierzbowska A, Gora-Tybor J: Cladribine combined with cyclophosphamide and mitoxantrone is an active salvage therapy in advanced non-Hodgkin's lymphoma. Leuk Lymphoma; 2007 Jun;48(6):1092-101
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  • [Title] Cladribine combined with cyclophosphamide and mitoxantrone is an active salvage therapy in advanced non-Hodgkin's lymphoma.
  • The aim of this study was to determine the feasibility, efficacy and toxicity of the combined therapy consisting of cladribine (2-CdA), mitoxantrone and cyclophosphamide (CMC regimen) in patients with refractory or relapsed non-Hodgkin's lymphoma (NHL).
  • Thirty six patients, 14 with mantle cell lymphoma (MCL), 10 with diffuse large B-cell lymphoma (DLBCL), 5 with follicular lymphoma (FL), 3 with small lymphocytic lymphoma (SLL), and 4 with T-cell lymphoma were enrolled to the study.
  • The CMC protocol consisted of 2-CdA at a dose of 0.12 mg/kg in a 2-hour infusion on days 1 through 3, mitoxantrone 10 mg/m(2) i.v. on day 1 and cyclophosphamide 650 mg/m(2) i.v. on day 1.
  • When different disease status before CMC treatment was considered, a trend toward longer survival of recurrent patients was observed (log rank test, P = 0.08).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cladribine / adverse effects. Cladribine / therapeutic use. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Feasibility Studies. Female. Humans. Male. Middle Aged. Mitoxantrone / adverse effects. Mitoxantrone / therapeutic use. Salvage Therapy / adverse effects. Survival Analysis. Treatment Outcome

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  • (PMID = 17577772.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; CMC protocol 2
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64. Yanada M, Kiyoi H, Murata M, Suzuki M, Iwai M, Yokozawa T, Baba H, Emi N, Naoe T: Micafungin, a novel antifungal agent, as empirical therapy in acute leukemia patients with febrile neutropenia. Intern Med; 2006;45(5):259-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Micafungin, a novel antifungal agent, as empirical therapy in acute leukemia patients with febrile neutropenia.
  • RESULTS: A total of 31 patients with acute leukemia who developed febrile neutropenia were enrolled in the study.
  • Among them, 18 patients fulfilling the protocol-defined criteria, including 10 with persistent fever and 8 with recurrent fever, received MCFG empirically.
  • Underlying diseases consisted of acute myeloid leukemia (n=15) and acute lymphoblastic leukemia (n=3).
  • [MeSH-minor] Adolescent. Adult. Algorithms. Echinocandins. Female. Fever / etiology. Humans. Leukemia, Myeloid / complications. Lipopeptides. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Prospective Studies

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  • (PMID = 16595990.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Lipopeptides; 0 / Lipoproteins; 0 / Peptides, Cyclic; R10H71BSWG / micafungin
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65. De Keersmaecker K, Marynen P, Cools J: Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia. Haematologica; 2005 Aug;90(8):1116-27
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  • [Title] Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia.
  • Over the past 20 years, a large number of genes involved in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL) has been identified by molecular characterization of recurrent chromosomal aberrations and more subtle genetic defects.
  • When reviewing the current list of oncogenes and tumor suppressor genes, it becomes clear that these can be grouped into four classes of mutations, which are involved in: (i) cell cycle deregulation;.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 16079112.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 129
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66. Micci F, Panagopoulos I, Tjønnfjord GE, Kolstad A, Delabie J, Beiske K, Heim S: Molecular cytogenetic characterization of t(14;19)(q32;p13), a new recurrent translocation in B cell malignancies. Virchows Arch; 2007 May;450(5):559-65
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  • [Title] Molecular cytogenetic characterization of t(14;19)(q32;p13), a new recurrent translocation in B cell malignancies.
  • Translocations involving an immunoglobulin (IG) locus are a recurring theme in B cell neoplasia.
  • We present here three cases of B cell neoplasia that showed a t(14;19)(q32;p13) by karyotypic analysis.
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 19. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Combined Modality Therapy. Cytogenetics. Female. Genes, Immunoglobulin Heavy Chain. Humans. In Situ Hybridization, Fluorescence. Male. Mediastinal Neoplasms / genetics. Mediastinal Neoplasms / pathology. Mediastinal Neoplasms / therapy. Molecular Diagnostic Techniques. Spectral Karyotyping. Treatment Outcome

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  • (PMID = 17406891.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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67. Fortune AF, Kelly K, Sargent J, O'Brien D, Quinn F, Chadwick N, Flynn C, Conneally E, Browne P, Crotty GM, Thornton P, Vandenberghe E: Large granular lymphocyte leukemia: natural history and response to treatment. Leuk Lymphoma; 2010 May;51(5):839-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large granular lymphocyte leukemia: natural history and response to treatment.
  • Large granular lymphocyte leukemia (T-LGL) is an indolent T lymphoproliferative disorder that was difficult to diagnose with certainty until clonality testing of the T cell receptor gene became routinely available.
  • We studied the natural history and response to treatment in 25 consecutive patients with T-LGL diagnosed between 2004 and 2008 in which the diagnosis was confirmed by molecular analysis, to define an effective treatment algorithm.
  • The median age at diagnosis was 61 years (range 27-78), with a male to female ratio of 1:1.8 and presenting features of fatigue (n = 13), recurrent infections (n = 9), and/or abnormal blood counts (n = 5).
  • The overall survival (OS) and progression-free survival (PFS) 37 months from diagnosis were 80% and 52%, respectively.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclosporine / therapeutic use. Immunosuppressive Agents / therapeutic use. Leukemia, Large Granular Lymphocytic / drug therapy
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / administration & dosage. Drug Therapy, Combination. Female. Humans. Male. Methotrexate / administration & dosage. Middle Aged. Pentostatin / administration & dosage. Survival Rate. Treatment Outcome

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  • (PMID = 20367569.001).
  • [ISSN] 1029-2403
  • [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 / Immunosuppressive Agents; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 83HN0GTJ6D / Cyclosporine; YL5FZ2Y5U1 / Methotrexate
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