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1. Barete S, Francés C, Charlotte F, Barrou B, Leblond V, Dereure O: Fatal outcome of deep-penetrating lower limb primary cutaneous anaplastic large cell lymphomas in two immunocompromised patients. Acta Derm Venereol; 2009 Nov;89(6):627-30
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  • [Title] Fatal outcome of deep-penetrating lower limb primary cutaneous anaplastic large cell lymphomas in two immunocompromised patients.
  • The occurrence of primary cutaneous anaplastic large cell lymphoma (PCALCL) in immunocompromised patients is rare.
  • Only 11 cases have been reported to date, all of them in organ transplant recipients and none in patient with idiopathic CD4+ T-cell lymphocytopaenia.
  • We describe here the original clinical pattern of deep, fascia and muscle-penetrating PCALCL of the lower limb in two immunocompromised patients, one in a renal transplant recipient, the other in a patient with idiopathic CD4+ T-cell lymphocytopaenia.
  • Both patients experienced a negative outcome, contrasting with the usually indolent course of PCALCL in immunocompetent patients, since both died of complications related to the lymphoma 30 and 13 months later, respectively.
  • [MeSH-major] Immunocompromised Host. Lymphoma, Primary Cutaneous Anaplastic Large Cell / pathology. Skin Neoplasms / pathology

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  • (PMID = 19997696.001).
  • [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
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2. Piva R, Chiarle R, Manazza AD, Taulli R, Simmons W, Ambrogio C, D'Escamard V, Pellegrino E, Ponzetto C, Palestro G, Inghirami G: Ablation of oncogenic ALK is a viable therapeutic approach for anaplastic large-cell lymphomas. Blood; 2006 Jan 15;107(2):689-97
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  • [Title] Ablation of oncogenic ALK is a viable therapeutic approach for anaplastic large-cell lymphomas.
  • Anaplastic large-cell lymphomas (ALCLs) carry chromosome translocations in which the anaplastic lymphoma kinase (ALK) gene is fused to several partners, most frequently, the NPM1 gene.
  • The ablation of ALK leads to the down-modulation of known ALK downstream effectors, cell growth arrest, and reversion of the transformed phenotype of ALK(+) mouse embryonic fibroblasts in vitro and in vivo.
  • In human ALCL cells lentiviral-mediated ALK knock-down leads to G(1) cell-cycle arrest and apoptosis in vitro and tumor growth inhibition and regression in vivo.
  • Using a specific approach we have demonstrated that the survival and growth of ALK(+) ALCLs are strictly dependent on ALK activation and signaling.
  • Therefore, ALK is a viable target for therapeutic intervention and its inactivation might represent a pivotal approach for the treatment of ALK lymphomas and other ALK-dependent human tumors.

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  • (PMID = 16189272.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [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 / RNA, Small Interfering; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC1895619
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3. Feldman AL, Law ME, Inwards DJ, Dogan A, McClure RF, Macon WR: PAX5-positive T-cell anaplastic large cell lymphomas associated with extra copies of the PAX5 gene locus. Mod Pathol; 2010 Apr;23(4):593-602

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PAX5-positive T-cell anaplastic large cell lymphomas associated with extra copies of the PAX5 gene locus.
  • Cell lineage is the major criterion by which lymphomas are classified.
  • Immunohistochemistry has greatly facilitated lymphoma diagnosis by detecting expression of lineage-associated antigens.
  • Anaplastic large cell lymphoma is a T-cell lymphoma that shows morphologic and phenotypic overlap with classical Hodgkin's lymphoma, which is a tumor of B-cell derivation.
  • Staining for the B-cell transcription factor, paired box 5 (PAX5), has been suggested to be helpful in this differential, as it is positive in most classical Hodgkin's lymphomas, but absent in anaplastic large cell lymphomas.
  • In this study we report four systemic T-cell anaplastic large cell lymphomas that were positive for PAX5 by immunohistochemistry, with weak staining intensity similar to that observed in classical Hodgkin's lymphoma.
  • All diagnoses were confirmed by a combination of morphologic, phenotypic, and molecular criteria.
  • Three cases were anaplastic lymphoma kinase (ALK) negative and one was ALK positive.
  • PAX5 immunohistochemistry was negative in 198 additional peripheral T-cell lymphomas, including 66 anaplastic large cell lymphomas.
  • Unexpectedly, although PAX5 translocations were absent, all evaluable PAX5-positive anaplastic large cell lymphomas showed extra copies of the PAX5 gene locus by fluorescence in situ hybridization (FISH).
  • In contrast, only 4% of PAX5-negative peripheral T-cell lymphomas had extra copies of PAX5.
  • We conclude that aberrant expression of PAX5 occurs rarely in T-cell anaplastic large cell lymphomas, and may be associated with extra copies of the PAX5 gene.
  • PAX5-positive lymphomas with morphologic features overlapping different lymphoma types should be evaluated with an extensive immunohistochemical panel and/or molecular studies to avoid diagnostic errors that could lead to inappropriate treatment.
  • As PAX5 overexpression causes T-cell neoplasms in experimental models, PAX5 may have contributed to lymphomagenesis in our cases.

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  • (PMID = 20118907.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA097274-08; United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / P50 CA097274-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ NIHMS167829; NLM/ PMC2848697
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4. d'Amore ES, Menin A, Bonoldi E, Bevilacqua P, Cazzavillan S, Donofrio V, Gambini C, Forni M, Gentile A, Magro G, Boldrini R, Pillon M, Rosolen A, Alaggio R: Anaplastic large cell lymphomas: a study of 75 pediatric patients. Pediatr Dev Pathol; 2007 May-Jun;10(3):181-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic large cell lymphomas: a study of 75 pediatric patients.
  • In this article, we describe the morphologic and immunophenotypic features of 75 cases of pediatric anaplastic large cell lymphoma (ALCL).
  • According to the World Health Organization classification, 49 cases were common subtype ALCL, and respectively, 3, 6, and 17 cases were small cell, lymphohistiocytic, or mixed histologic variants.
  • Anaplastic lymphoma kinase positivity was detected in 90.7% of the tumors and, using a panel of 9 T-cell surface markers, 88% could be assigned to the T-cell lineage.
  • A molecular analysis for the T-cell receptor gamma (TCR- gamma) and the heavy chain of the immunoglobulin H rearrangements was performed on 6/9 ALCLs with a null immunophenotype, and a TCR clonal pattern was detected in 5/6 cases.
  • Clusterin, CD83, and Pax5, respectively, expressed in 91.3%, 1.7%, and 0% of the ALCLs, were useful biomarkers for the differential diagnosis with Hodgkin's lymphomas.
  • [MeSH-major] Antigens, CD / immunology. Antigens, CD56 / immunology. B-Cell-Specific Activator Protein / immunology. Biomarkers, Tumor / immunology. Clusterin / immunology. Immunoglobulins / immunology. Lymphoma, Large B-Cell, Diffuse / immunology. Membrane Glycoproteins / immunology
  • [MeSH-minor] Child. Diagnosis, Differential. Female. Granzymes / immunology. Hodgkin Disease / diagnosis. Hodgkin Disease / immunology. Hodgkin Disease / pathology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocytes, Null / immunology. Lymphocytes, Null / pathology. Lymphoma, Large-Cell, Anaplastic / immunology. Lymphoma, Large-Cell, Anaplastic / pathology. Male. Perforin. Poly(A)-Binding Proteins / immunology. Pore Forming Cytotoxic Proteins / immunology. Receptors, Antigen, T-Cell, gamma-delta / immunology

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  • [CommentIn] Pediatr Dev Pathol. 2007 May-Jun;10(3):169-71 [17535094.001]
  • (PMID = 17535098.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD56; 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / CD83 antigen; 0 / CLU protein, human; 0 / Clusterin; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / PAX5 protein, human; 0 / Poly(A)-Binding Proteins; 0 / Pore Forming Cytotoxic Proteins; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / TIA1 protein, human; 126465-35-8 / Perforin; EC 3.4.21.- / Granzymes
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5. Rodig SJ, Ouyang J, Juszczynski P, Currie T, Law K, Neuberg DS, Rabinovich GA, Shipp MA, Kutok JL: AP1-dependent galectin-1 expression delineates classical hodgkin and anaplastic large cell lymphomas from other lymphoid malignancies with shared molecular features. Clin Cancer Res; 2008 Jun 1;14(11):3338-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AP1-dependent galectin-1 expression delineates classical hodgkin and anaplastic large cell lymphomas from other lymphoid malignancies with shared molecular features.
  • We recently found that Reed-Sternberg cell Gal1 promotes the immunosuppressive T-helper 2/T-regulatory cell-skewed microenvironment in classical Hodgkin lymphoma (cHL).
  • In addition, because there are common signaling and survival pathways in cHL and additional non-Hodgkin lymphomas, we also evaluated whether the AP1/Gal1 signature is shared by other molecularly or morphologically related lymphomas.
  • EXPERIMENTAL DESIGN: We evaluated 225 cases of primary cHL and non-Hodgkin lymphoma for evidence of a functional AP1/Gal1 signature by immunohistochemical techniques.
  • In contrast, diffuse large B-cell lymphoma, primary mediastinal large B-cell lymphoma, and another Hodgkin-related entity, nodular lymphocyte-predominant Hodgkin lymphoma, do not express Gal1.
  • However, anaplastic large cell lymphoma (ALCL), consistently expresses both Gal1 and its transcriptional regulator, c-Jun.
  • The presence of activated c-Jun, indicative of functional AP1 activity, was confirmed by phospho-c-Jun immunostaining in cHL and ALCL.
  • CONCLUSIONS: These findings establish a functional AP1 signature that includes Gal1 expression in cHL and ALCL and suggests a common mechanism for tumor immunotolerance in these diseases.
  • In addition, the combination of Gal1 and c-Jun serve as diagnostic biomarkers that delineate cHL and ALCL from other lymphomas with shared morphologic and/or molecular features.
  • [MeSH-major] Biomarkers, Tumor / analysis. Galectin 1 / biosynthesis. Hodgkin Disease / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoproliferative Disorders / metabolism. Transcription Factor AP-1 / metabolism
  • [MeSH-minor] Diagnosis, Differential. Gene Expression. Humans. Immunohistochemistry. Proto-Oncogene Proteins c-jun / metabolism. Reed-Sternberg Cells / metabolism

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  • (PMID = 18519761.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 1; 0 / Proto-Oncogene Proteins c-jun; 0 / Transcription Factor AP-1
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6. Jundt F, Raetzel N, Müller C, Calkhoven CF, Kley K, Mathas S, Lietz A, Leutz A, Dörken B: A rapamycin derivative (everolimus) controls proliferation through down-regulation of truncated CCAAT enhancer binding protein {beta} and NF-{kappa}B activity in Hodgkin and anaplastic large cell lymphomas. Blood; 2005 Sep 1;106(5):1801-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A rapamycin derivative (everolimus) controls proliferation through down-regulation of truncated CCAAT enhancer binding protein {beta} and NF-{kappa}B activity in Hodgkin and anaplastic large cell lymphomas.
  • In this study, we provide evidence that RAD has profound antiproliferative activity in vitro and in NOD/SCID mice in vivo against Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL) cells.
  • Moreover, we identified 2 molecular mechanisms that showed how RAD exerts antiproliferative effects in HL and ALCL cells.
  • Pharmacologic inhibition of the mTOR pathway by RAD therefore interferes with essential proliferation and survival pathways in HL and ALCL cells and might serve as a novel treatment option.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / metabolism. Cell Proliferation / drug effects. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. NF-kappa B / metabolism. Sirolimus / analogs & derivatives
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Down-Regulation / drug effects. Everolimus. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Transplantation, Heterologous

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  • (PMID = 15886325.001).
  • [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 / CCAAT-Enhancer-Binding Protein-beta; 0 / NF-kappa B; 9HW64Q8G6G / Everolimus; W36ZG6FT64 / Sirolimus
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7. Anastasov N, Bonzheim I, Rudelius M, Klier M, Dau T, Angermeier D, Duyster J, Pittaluga S, Fend F, Raffeld M, Quintanilla-Martinez L: C/EBPβ expression in ALK-positive anaplastic large cell lymphomas is required for cell proliferation and is induced by the STAT3 signaling pathway. Haematologica; 2010 May;95(5):760-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] C/EBPβ expression in ALK-positive anaplastic large cell lymphomas is required for cell proliferation and is induced by the STAT3 signaling pathway.
  • BACKGROUND: Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma is characterized by the t(2;5) chromosomal translocation, resulting in the expression of a fusion protein formed of nucleophosmin (NPM) and ALK.
  • Recently, we reported the abnormal expression of the transcription factor CCAAT/enhancer binding protein-beta (C/EBPbeta) in ALK-positive anaplastic large cell lymphomas, and demonstrated its dependence on NPM-ALK activity.
  • DESIGN AND METHODS: In this study, the role of C/EBPbeta in proliferation and survival of ALK-positive anaplastic large cell lymphomas was investigated, as well as the mechanism of its expression and activity.
  • RESULTS: Interference with C/EBPbeta expression resulted in a dramatic decrease in cell proliferation in ALK-positive anaplastic large cell lymphomas, with a mild induction of apoptosis after 6 days.
  • Down-regulation of STAT3 resulted in a marked decrease in C/EBPbeta mRNA and protein levels with impairment in cell proliferation and viability, underscoring the important role of these two proteins in ALK-mediated oncogenesis.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / biosynthesis. Cell Proliferation. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / enzymology. Receptor Protein-Tyrosine Kinases / biosynthesis. STAT3 Transcription Factor / physiology. Signal Transduction
  • [MeSH-minor] Animals. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cell Survival / genetics. Down-Regulation / genetics. Humans. Mice


8. Goteri G, Simonetti O, Rupoli S, Piccinini G, Rubini C, Stramazzotti D, Fazioli F, Capomagi C, Leoni P, Offidani AM, Lo Muzio L: Differences in survivin location and Bcl-2 expression in CD30+ lymphoproliferative disorders of the skin compared with systemic anaplastic large cell lymphomas: an immunohistochemical study. Br J Dermatol; 2007 Jul;157(1):41-8
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  • [Title] Differences in survivin location and Bcl-2 expression in CD30+ lymphoproliferative disorders of the skin compared with systemic anaplastic large cell lymphomas: an immunohistochemical study.
  • BACKGROUND: Cutaneous CD30+ lymphoproliferative disorders (LPDs) are a spectrum of disease associated with a favourable prognosis.
  • Systemic anaplastic large cell lymphoma (ALCL), although morphologically and phenotypically similar, differs in clinical presentation and has a less favourable biological behaviour.
  • Dysregulation of apoptosis, the process regulating cell population by programmed death, can explain the differences among these disorders.
  • OBJECTIVES: We investigated the expression of two inhibitors of apoptosis, survivin and Bcl-2 protein, in serial skin lesion samples from CD30+ LPDs compared with systemic ALCL.
  • METHODS: Immunohistochemical analysis with antibodies against anaplastic lymphoma kinase (ALK)-1 protein, survivin and Bcl-2 protein was performed in 10 cutaneous CD30+ LPDs (five lymphomatoid papulosis, five ALCL) and 18 systemic ALCLs.
  • RESULTS: Cutaneous CD30+ LPDs shared a heterogeneous expression of cytoplasmic survivin with all systemic ALCLs, and of Bcl-2 with systemic ALK- ALCLs; however, they differ from systemic ALK- ALCLs because they lack nuclear survivin (P = 0.045), and from systemic ALK+ ALCLs by a higher expression of Bcl-2 (P = 0.045) and a lack of ALK-1.
  • Overall, coexpression of Bcl-2 and nuclear survivin in CD30+ LPDs was associated with a less favourable disease survival.
  • CONCLUSIONS: The different patterns of expression of Bcl-2 and survivin in CD30+ LPDs might have an impact on their different biological and clinical behaviour.
  • Moreover, nuclear localization of survivin, similarly to ALK, may be a useful marker for predicting a systemic form of ALCL with cutaneous presentation.
  • [MeSH-major] Antigens, CD30 / metabolism. Lymphoproliferative Disorders / diagnosis. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cysteine Proteinase Inhibitors / pharmacology. Diagnosis, Differential. Female. Humans. Immunohistochemistry / methods. Inhibitor of Apoptosis Proteins. Lymphoma, Large B-Cell, Diffuse / diagnosis. Male. Middle Aged. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Skin

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  • [ErratumIn] Br J Dermatol. 2007 Aug;157(2):431. Lomuzio, L [corrected to Lo Muzio, L]
  • (PMID = 17484779.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / BIRC5 protein, human; 0 / Cysteine Proteinase Inhibitors; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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9. Eckerle S, Brune V, Döring C, Tiacci E, Bohle V, Sundström C, Kodet R, Paulli M, Falini B, Klapper W, Chaubert AB, Willenbrock K, Metzler D, Bräuninger A, Küppers R, Hansmann ML: Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma. Leukemia; 2009 Nov;23(11):2129-38
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  • [Title] Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is a main type of T-cell lymphomas and comprises three distinct entities: systemic anaplastic lymphoma kinase (ALK) positive, systemic ALK(-) and cutaneous ALK(-) ALCL (cALCL).
  • Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK(-) ALCL and classical Hodgkin lymphoma (cHL).
  • We conducted gene expression profiling of microdissected lymphoma cells of five ALK(+) and four ALK(-) systemic ALCL, seven cALCL and sixteen cHL, and of eight subsets of normal T and NK cells.
  • The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4(+), CD8(+) or CD30(+) T-cell origin.
  • Indeed, ALCL display a down-modulation of many T-cell characteristic molecules.
  • All ALCL types show significant expression of NFkappaB target genes and upregulation of genes involved in oncogenesis (e.g. EZH2).
  • Surprisingly, few genes are differentially expressed between systemic and cALCL despite their different clinical behaviour, and between ALK(-) ALCL and cHL despite their different cellular origin.
  • ALK(+) ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK.
  • This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Hodgkin Disease / genetics. Lymphoma, Large-Cell, Anaplastic / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line. Female. Humans. Immunohistochemistry. Killer Cells, Natural / cytology. Killer Cells, Natural / physiology. Male. Microdissection. Middle Aged. NF-kappa B / metabolism. Phenotype. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / cytology. T-Lymphocytes / physiology. Young Adult

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  • (PMID = 19657361.001).
  • [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 / NF-kappa B; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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10. Martín JM, Ricart JM, Monteagudo C, Alcácer J, Pinazo I, Tomás L, Rausell N, Jordá E: Primary cutaneous CD30+ anaplastic large-cell lymphomas mimicking keratoacanthomas. Clin Exp Dermatol; 2007 Nov;32(6):668-71
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  • [Title] Primary cutaneous CD30+ anaplastic large-cell lymphomas mimicking keratoacanthomas.
  • Primary cutaneous anaplastic large cell lymphoma (ALCL) may be associated with keratoacanthoma (KA)-like epithelial hyperplasia and dense eosinophilic and neutrophilic infiltrates.
  • Diagnosis in such cases is challenging both clinically and histologically, because the large atypical lymphoid cells may be obscured by the massive infiltrate of eosinophils and neutrophils, or confused with invasive squamous cell carcinoma or KA.
  • We recently encountered two cases of CD30+ ALCL presenting with a KA-like tumour on the eyelid and nose, respectively.
  • [MeSH-major] Facial Neoplasms / diagnosis. Keratoacanthoma / diagnosis. Lymphoma, Primary Cutaneous Anaplastic Large Cell / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Eyelid Neoplasms / diagnosis. Eyelid Neoplasms / pathology. Female. Humans. Male. Middle Aged. Nose Neoplasms / diagnosis. Nose Neoplasms / pathology

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  • (PMID = 17953637.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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11. Bovio IM, Allan RW: The expression of myeloid antigens CD13 and/or CD33 is a marker of ALK+ anaplastic large cell lymphomas. Am J Clin Pathol; 2008 Oct;130(4):628-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of myeloid antigens CD13 and/or CD33 is a marker of ALK+ anaplastic large cell lymphomas.
  • We retrospectively studied the immunophenotype by flow cytometry of 20 anaplastic large cell lymphomas (ALCLs) (9 anaplastic lymphoma kinase [ALK]+ and 11 ALK-) with a particular emphasis on the aberrant expression of the myeloid associated antigens CD13 and/or CD33.
  • All ALCLs expressed CD45, HLA-DR, and CD30.
  • Most (8/9) ALK+ ALCLs expressed at least 1 surface T-cell antigen (CD4, 6/9 [67%]; CD7, 6/9 [67%]; CD2, 5/9 [56%]; CD5, 2/9 [22%]; CD8, 2/9 [22%]; CD3, 1/9 [11%]).
  • All ALK-ALCLs expressed at least 1 surface T-cell antigen (CD3, 7/11 [64%]; CD4, 6/11 [55%]; CD2, 6/11 [55%]; CD7, 2/11 [18%]; CD5, 1/11 [9%]; CD8, 1/11 [9%]).
  • CD13 and/or CD33 were expressed in all (9/9) ALK+ ALCLs compared with 1 of 11 ALK-ALCLs (9%) (P < .0001).
  • Surface CD3 was more likely expressed in ALK-ALCLs (7/11) compared with ALK+ ALCLs (1/9) (P .03).
  • The myeloid-associated antigens CD13 and/or CD33 are sensitive but not entirely specific markers of ALK+ ALCLs and should not be misinterpreted as indicating myeloid sarcoma.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, CD13 / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Biomarkers, Tumor / analysis. Lymphoma, Large-Cell, Anaplastic / metabolism

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  • (PMID = 18794057.001).
  • [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, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.11.2 / Antigens, CD13
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12. Castillo J, Milani C, Pantanowitz L: HIV-associated anaplastic large cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19563

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIV-associated anaplastic large cell lymphoma.
  • : e19563 Background: Anaplastic large cell lymphoma (ALCL) is a CD30+ T-cell lymphoma that is generally unrelated to EBV in the non-HIV setting.
  • Based upon anaplastic lymphoma kinase (ALK) expression, the new WHO classification provisionally distinguishes between ALK+ (favorable) and ALK- (unfavorable) ALCL.
  • The characteristics of ALCL, such as ALK expression and EBV coinfection, in individuals with HIV infection have not been adequately evaluated.
  • The aim of this study was to investigate these features in HIV-associated ALCL cases.
  • METHODS: A MEDLINE search for all cases of HIV-associated non-cutaneous ALCL was undertaken.
  • Data regarding patient age, gender, HIV status (CD4 count, viral load, opportunistic infections), HAART, lymphoma features (B symptoms, stage, sites of involvement, immunophenotype, ALK expression, molecular studies), EBV coinfection, therapy and outcome (survival, cause of death) were extracted and analyzed.
  • ALCL was extranodal in 22 cases (96%) affecting most commonly lung, soft tissue and liver.
  • Many (78%) patients had stage IV disease and B symptoms were reported in 9 cases (50%).
  • T-cell receptor gene rearrangement was present in all cases, CD30 was positive in 22 (96%), and the vast majority (90%) were ALK-negative.
  • Therapy for ALCL was documented in 15 (67%) cases; 64% received CHOP.
  • Death was caused by either lymphoma progression (42%) or infection (58%).
  • CONCLUSIONS: HIV-associated non-cutaneous ALCL appears to affect younger individuals and is associated with EBV infection in a subset of cases.
  • Apart from marked immunosuppression, the poor prognosis of HIV-associated ALCL appears to be related to the absence of ALK expression, advanced stage at presentation with prominent extranodal disease, inadequate therapy including HAART, and poor response to CHOP.
  • Further research is needed to better understand and treat this unique HIV-associated lymphoma.

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  • (PMID = 27961064.001).
  • [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] Journal Article
  • [Publication-country] United States
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13. Goldman S, Coiffier B, Reiter A, Younes A, Cairo MS, International TLS Expert Panel: A medical decision tree for the prophylaxis (P) and treatment (T) of tumor lysis syndrome (TLS): An international TLS consensus panel. J Clin Oncol; 2009 May 20;27(15_suppl):e17575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Additionally, we recently reported an evidence based review of guidelines for the P and T of TLS (Coiffier et al, J Clin Oncol. 2008).
  • 2001) and a rapid reduction in UA in adults at high-risk of TLS (Coiffier et al, J Clin Oncol. 2003).
  • METHODS: We convened an international panel (N = 17) of experts in pediatric and adult hematological malignancies and solid tumors (ST) to develop a medical decision tree for the P and T of TLS based on the risk classification (low, medium, high) and management recommendations of Coiffier et al (J Clin Oncol.
  • 2008) Results: Patients without evidence of LTLS were assigned to either low-risk disease (LRD), medium-risk (MRD), or high-risk (HRD).
  • Risk factors included pathological classification stage, bulk, disease burden (WBC/LDH) and renal impairment/involvement.
  • MRD consisted of ALL ≤100K/mm<sup>3</sup>, AML 25-100K/mm<sup>3</sup>, BL/LL stage I/II and low LDH, childhood ALCL, DLBCL/PTCL/MCL/ATL non-bulky but elevated LDH, CLL treated with targeted therapy, and LRD with renal impairment/involvement.
  • CONCLUSIONS: This medical decision tree will facilitate the practice of management of the P and T of TLS and hopefully improve the quality of care in a cost effective manner.

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  • (PMID = 27963935.001).
  • [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] Journal Article
  • [Publication-country] United States
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14. Kwak EL, Camidge DR, Clark J, Shapiro GI, Maki RG, Ratain MJ, Solomon B, Bang Y, Ou S, Salgia R: Clinical activity observed in a phase I dose escalation trial of an oral c-met and ALK inhibitor, PF-02341066. J Clin Oncol; 2009 May 20;27(15_suppl):3509

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  • Tumor types included colorectal, pancreatic, sarcoma, ALCL and NSCLC.
  • Among 10 NSCLC pts whose tumors harbor EML4-ALK rearrangement, 1 pt has had a PR, 2 pts have achieved unconfirmed PR and 4 pts have had SD (3 have experienced reduction in tumor burden by ∼20% in measurable lesions and 1 has been treated for 28 weeks).

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  • (PMID = 27961297.001).
  • [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] Journal Article
  • [Publication-country] United States
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15. Rüdiger T, Bonzheim I, Geissinger E, Roth S, Zettl A, Marx A, Rosenwald A, Müller-Hermelink HK: [Anaplastic large cell lymphomas lack the expression of T-cell receptor molecules]. Verh Dtsch Ges Pathol; 2005;89:261-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Anaplastic large cell lymphomas lack the expression of T-cell receptor molecules].
  • Anaplastic large cell lymphoma (ALCL) designates a heterogeneous group of CD30+ (systemic or primary cutaneous) peripheral T-cell lymphomas (PTCLs).
  • A subgroup of systemic ALCL is transformed by anaplastic lymphoma kinase (ALK).
  • We compared 46 ALCL with 22 PTCLs in terms of T-cell receptor (TCR) rearrangements, expression of TCRs and TCR-associated molecules [CD3, ZAP-70 (zeta-associated protein 70)].
  • Despite their frequent clonal rearrangement for TCRbeta, only 4% of ALCLs expressed TCRbeta protein, whereas TCRs were detected in 86% of PTCLs.
  • Moreover, both TCRbeta+ ALCLs lacked CD3 and ZAP-70 (ie, molecules indispensable for the transduction of cognate TCR signals).
  • Defective expression of TCRs is a common characteristic of all types of ALCL, which may contribute to the dysregulation of intracellular signaling pathways controlling T-cell activation and survival.
  • This molecular hallmark of ALCL is analogous to defective immunoglobulin expression distinguishing Hodgkin lymphoma from other B-cell lymphomas.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / pathology. Receptors, Antigen, T-Cell / deficiency. Receptors, Antigen, T-Cell / genetics
  • [MeSH-minor] Antigens, CD / analysis. Antigens, CD30 / analysis. Humans. T-Lymphocytes / immunology

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  • (PMID = 18035700.001).
  • [ISSN] 0070-4113
  • [Journal-full-title] Verhandlungen der Deutschen Gesellschaft für Pathologie
  • [ISO-abbreviation] Verh Dtsch Ges Pathol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD30; 0 / Receptors, Antigen, T-Cell
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16. Blum KA, Smith M, Fung H, Zalevsky J, Combs D, Ramies DA, Younes A: Phase I study of an anti-CD30 Fc engineered humanized monoclonal antibody in Hodgkin lymphoma (HL) or anaplastic large cell lymphoma (ALCL) patients: Safety, pharmacokinetics (PK), immunogenicity, and efficacy. J Clin Oncol; 2009 May 20;27(15_suppl):8531

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of an anti-CD30 Fc engineered humanized monoclonal antibody in Hodgkin lymphoma (HL) or anaplastic large cell lymphoma (ALCL) patients: Safety, pharmacokinetics (PK), immunogenicity, and efficacy.
  • : 8531 Background: XmAb2513 is a novel 2<sup>nd</sup>-generation humanized monoclonal antibody (mAb) directed against CD30 (a cell surface antigen expressed on Reed-Sternberg cells of HL and ALCL), with an Fc region engineered to have increased binding affinity to Fcγ receptors (FcγRs) leading to improved FcγR-dependent effector cell functions.
  • In vitro, XmAb2513 was more potent and more efficacious than 1<sup>st</sup>-generation anti-CD30 mAbs (e.g., SGN-30 & MDX-060).
  • A Phase 1 study has been initiated to examine the safety and efficacy of XmAb2513 in patients (pts) with relapsed HL and ALCL.
  • Pts receive up to 4 cycles (8 infusions) with sample collections at regular intervals for safety, PK, soluble CD30 (sCD30) and detection of immunogenicity [i.e., human Abs to humanized Abs (HAHA)].
  • Half-life appeared to increase after multiple infusions and ranged from 5.3 - 30.2 days in the 1 and 3 mg/kg cohorts.

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  • (PMID = 27960926.001).
  • [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] Journal Article
  • [Publication-country] United States
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17. Andorsky DJ, Yamada R, Steward K, De Vos S, Said J, Timmerman J: Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells. J Clin Oncol; 2009 May 20;27(15_suppl):8526

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells.
  • METHODS: PD-L1 expression was analyzed in 16 NHL cell lines by flow cytometry (FC) and in 111 lymphoma specimens by immunohistochemistry (IHC) (n=92) or FC (n=19).
  • In functional studies, irradiated anaplastic large cell lymphoma (ALCL) cells were co-cultured with allogeneic T cells in the presence of anti-PD-L1 blocking antibody, and IFNγ secretion and thymidine incorporation was used to assess T cell function and proliferation.
  • To further test tumor-T cell interactions, malignant ascites from a patient with ALK+ ALCL and peripheral blood mononuclear cells from a patient with leukemic mantle cell lymphoma, both containing PD-L1-expressing tumor cells and tumor-associated T cells, were stimulated with phytohemagglutinin (a polyclonal T cell activator) and incubated with anti-PD-L1 antibody.
  • Levels of 16 inflammatory cytokines were measured as an assessment of T cell activity.
  • RESULTS: All 9 B cell lymphoma lines were negative for PD-L1, while all 5 ALCL cell lines were strongly positive.
  • One T-cell ALL line was positive, and one peripheral T cell lymphoma was negative.
  • Strong PD-L1 staining was detected by IHC in all 14 ALCL specimens and in 83% of diffuse large B cell lymphomas (DLBCL) analyzed (n=35).
  • Activity of allogeneic T cells co-cultured with irradiated ALCL cells, as measured by IFNγ secretion and proliferation, was markedly enhanced in the presence of anti-PD-L1 blocking antibody.
  • In the autologous setting using cultures of ALCL and mantle cell lymphoma specimens containing host T cells, secretion of inflammatory cytokines by tumor-associated T cells, including GMCSF, IFNγ, IL-1, IL-6, IL-8, TNFα, and MIP1α, were increased by incubation with anti-PD-L1 antibody.
  • CONCLUSIONS: PD-L1 is highly expressed in ALCL and in a majority of DLBCL.
  • PD-L1 may play a role in thwarting an effective anti-tumor immune response and represents an attractive target for lymphoma immunotherapy.

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  • (PMID = 27960901.001).
  • [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] Journal Article
  • [Publication-country] United States
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18. Oki M, Isozaki M, Nakamura N, Kikuchi A, Tsuchiya T, Arbogast P, Ogawa Y, Ando K: A multivariate analysis for the survival of nodal peripheral T-cell lymphoma (PTCL). J Clin Oncol; 2009 May 20;27(15_suppl):e19521

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multivariate analysis for the survival of nodal peripheral T-cell lymphoma (PTCL).
  • : e19521 Background: Nodal peripheral T-cell lymphoma (PTCL) is uncommon lymphoma with various subtypes and poor prognosis.
  • However, the superiority of high-dose chemotherapy followed by autologous stem cell transplantation (ASCT) has remained inconclusive.
  • The infrequency of PTCL is an obstacle to perform a large prospective study.
  • We conducted a retrospective study of fifty six patients with three major nodal PTCL, histologically classified as PTCL-not specified (NOS, n=29), angioimmunoblastic T-cell lymphoma (AITL, n=19), and ALK-negative anaplastic large cell lymphoma (ALCL, n=8) who underwent ASCT (n=14) or not (n=42) after CT in Tokai University Hospital, Ebina General Hospital, and Hadano Red Cross Hospital, Kanagawa, Japan between 1997 and 2008.
  • Hazard ratio (HR) of ASCT, IPI, and sIL-2R were 0.24 (95%CI: 0.08-0.76, p=0.02), 0.77 (95%CI: 0.34-1.77, p=0.54), and 1.45 (95%CI: 1.129-1.857, p=0.035), respectively.

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  • (PMID = 27960935.001).
  • [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] Journal Article
  • [Publication-country] United States
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19. Dueck GS, Chua N, Prasad A, Stewart D, White D, vanderJagt R, Johnston JB, Belch A, Reiman T: Activity of lenalidomide in a phase II trial for T-cell lymphoma: Report on the first 24 cases. J Clin Oncol; 2009 May 20;27(15_suppl):8524

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of lenalidomide in a phase II trial for T-cell lymphoma: Report on the first 24 cases.
  • : 8524 Background: Novel therapies are needed to improve outcomes in T-cell lymphomas.
  • We report the interim results of a prospective multicenter trial evaluating lenalidomide in T-cell lymphomas.
  • METHODS: Patients with relapsed and refractory T-cell lymphomas other than mycosis fungoides were prescribed oral lenalidomide (25mg daily) on days 1 to 21 of each 28 day cycle, with standardized dose reductions for toxicity.
  • Treatment continued until disease progression, death or unacceptable toxicity.
  • The histology was peripheral T-cell unspecified (PTCL-u, n=10), angioimmunoblastic (n=7), anaplastic large cell (n=5), enteropathic T-cell (n=1) and hepatosplenic gamma/delta (n=1).
  • Median number of prior therapies was 1 (range, 0-4), and three had prior autologous stem cell transplant.
  • Two patients had stable disease (SD) for ≥3 cycles.
  • Responses were seen in anaplastic, angioimmunoblastic, and PTCL-u histologies.
  • CONCLUSIONS: In relapsed and refractory T-cell lymphomas, oral lenalidomide monotherapy has clinical activity and toxicity is consistent with the known profile of lenalidomide.

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  • (PMID = 27960899.001).
  • [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] Journal Article
  • [Publication-country] United States
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20. Summers TA, Moncur JT: The small cell variant of anaplastic large cell lymphoma. Arch Pathol Lab Med; 2010 Nov;134(11):1706-10
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  • [Title] The small cell variant of anaplastic large cell lymphoma.
  • Anaplastic large cell lymphomas constitute a heterogeneous group of hematopoietic neoplasms that are characterized by immunopositivity for CD30 and the presence, in varying degrees, of large, pleomorphic "hallmark" cells.
  • Primary systemic anaplastic lymphoma kinase-positive anaplastic large cell lymphomas are a subset of this group.
  • Numerous heterogeneous histomorphologic patterns have been described in anaplastic lymphoma kinase-positive anaplastic large cell lymphomas, and all patterns tend to have a better prognosis than that found in anaplastic lymphoma kinase-negative cases.
  • We provide a short review of the small cell variant of anaplastic large cell lymphoma to facilitate the diagnosis of this difficult-to-recognize entity, which may be confused with reactive processes, commonly presents with disseminated disease, and pursues an aggressive clinical course.
  • [MeSH-major] Lymphocytes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Antigens, CD30 / metabolism. Diagnosis, Differential. Humans

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  • (PMID = 21043827.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30
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21. Salaverria I, Beà S, Lopez-Guillermo A, Lespinet V, Pinyol M, Burkhardt B, Lamant L, Zettl A, Horsman D, Gascoyne R, Ott G, Siebert R, Delsol G, Campo E: Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas. Br J Haematol; 2008 Mar;140(5):516-26
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  • [Title] Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is a T/null-cell neoplasm characterized by chromosomal translocations involving the anaplastic lymphoma kinase (ALK) gene (ALK).
  • The secondary chromosomal imbalances of these lymphomas are not well known.
  • We have examined 74 ALCL, 43 ALK-positive and 31 ALK-negative, cases by comparative genomic hybridization (CGH), and locus-specific alterations for TP53 and ATM were examined by fluorescence in situ hybridization and real-time quantitative polymerase chain reaction.
  • Chromosomal imbalances were detected in 25 (58%) ALK-positive and 20 (65%) ALK-negative ALCL.
  • ALK-positive ALCL with NPM-ALK or other ALK variant translocations showed a similar profile of secondary genetic alterations.
  • Gains of 17p and 17q24-qter and losses of 4q13-q21, and 11q14 were associated with ALK-positive cases (P = 0.05), whereas gains of 1q and 6p21 were more frequent in ALK-negative tumours (P = 0.03).
  • ALCL-negative tumours had a significantly worse prognosis than ALK-positive.
  • In conclusion, ALK-positive and negative ALCL have different secondary genomic aberrations, suggesting they correspond to different genetic entities.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromosome Aberrations. Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 18275429.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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22. Hu XF, Xing PX: MDX-060. Medarex. Curr Opin Investig Drugs; 2005 Dec;6(12):1266-71
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  • Medarex is developing the antibody MDX-060 for the potential treatment of CD30+ lymphomas, such as Hodgkin's disease and anaplastic large cell lymphomas.
  • [MeSH-major] Antibodies, Monoclonal. Antigens, CD30 / immunology. Antineoplastic Agents / therapeutic use. Hodgkin Disease / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy

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  • (PMID = 16370393.001).
  • [ISSN] 1472-4472
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / Antineoplastic Agents; 0 / iratumumab
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23. Colomba A, Courilleau D, Ramel D, Billadeau DD, Espinos E, Delsol G, Payrastre B, Gaits-Iacovoni F: Activation of Rac1 and the exchange factor Vav3 are involved in NPM-ALK signaling in anaplastic large cell lymphomas. Oncogene; 2008 Apr 24;27(19):2728-36
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  • [Title] Activation of Rac1 and the exchange factor Vav3 are involved in NPM-ALK signaling in anaplastic large cell lymphomas.
  • The majority of anaplastic large cell lymphomas (ALCLs) express the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion protein, which is oncogenic due to its constitutive tyrosine kinase activity.
  • Transformation by NPM-ALK not only increases proliferation, but also modifies cell shape and motility in both lymphoid and fibroblastic cells.
  • We report that the Rac1 GTPase, a known cytoskeletal regulator, is activated by NPM-ALK in ALCL cell lines (Karpas 299 and Cost) and transfected cells (lymphoid Ba/F3 cells, NIH-3T3 fibroblasts).
  • Moreover, Vav3 is phosphorylated in NPM-ALK positive biopsies from patients suffering from ALCL, demonstrating the pathological relevance of this observation.
  • The use of Vav3-specific shRNA and a dominant negative Rac1 mutant demonstrates the central role of GTPases in NPM-ALK elicited motility and invasion.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Lymphoma, Large-Cell, Anaplastic / enzymology. Protein-Tyrosine Kinases / metabolism. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction / physiology. rac1 GTP-Binding Protein / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. NIH 3T3 Cells. Nuclear Proteins / physiology. Phosphatidylinositol 3-Kinases / physiology. Receptor Protein-Tyrosine Kinases. src-Family Kinases / physiology

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  • (PMID = 17998938.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-vav; 0 / VAV3 protein, human; 0 / Vav3 protein, mouse; 117896-08-9 / nucleophosmin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases; EC 3.6.5.2 / rac1 GTP-Binding Protein
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24. Thornber K, Colomba A, Ceccato L, Delsol G, Payrastre B, Gaits-Iacovoni F: Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas. Oncogene; 2009 Jul 23;28(29):2690-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas.
  • The chimera nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), the tyrosine kinase activity of which is constitutively upregulated, is the causative agent of 75% of the anaplastic large-cell lymphomas (ALCLs).
  • Together, these data point to the ROS/LOX pathway as a potential new target for therapy in NPM-ALK-positive tumors.
  • [MeSH-major] Arachidonate 5-Lipoxygenase / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Humans. Lipoxygenase Inhibitors / pharmacology. Masoprocol / analysis

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  • (PMID = 19503098.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipoxygenase Inhibitors; 0 / Reactive Oxygen Species; 7BO8G1BYQU / Masoprocol; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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25. Thompson MA, Stumph J, Henrickson SE, Rosenwald A, Wang Q, Olson S, Brandt SJ, Roberts J, Zhang X, Shyr Y, Kinney MC: Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas. Hum Pathol; 2005 May;36(5):494-504
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  • [Title] Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive large T- or null-cell lymphoma.
  • Most ALCLs arising in children and young adults express a constitutively active receptor tyrosine kinase, anaplastic lymphoma kinase (ALK).
  • Anaplastic large cell lymphomas lacking ALK are clinically heterogeneous and their pathogenesis is unknown.
  • This study is the first complementary DNA (cDNA) microarray analysis using RNA extracted from tumor tissue (7 ALK+ ALCLs and 7 ALK- ALCLs) to identify genes differentially expressed or shared between the ALK+ and ALK- tumors.
  • Hierarchical clustering analysis using the 44 cDNAs with the greatest differential expression between ALK+ and ALK- RNAs grouped 6 of 7 ALK+ ALCLs together and 1 ALK+ ALCL with the ALK- group.
  • Cyclin D3 was overexpressed in the ALK+ group and the cell cycle inhibitor p19INK4D was decreased in the ALK- group, suggesting different mechanisms of promoting G 1 /S transition.
  • Genes highly expressed in both ALK- and ALK+ ALCLs included kinases (LCK, protein kinase C, vav2, and NKIAMRE) and antiapoptotic molecules, suggesting possible common pathogenetic mechanisms as well.
  • [MeSH-major] Gene Expression. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Child. Cyclin D3. Cyclin-Dependent Kinase Inhibitor p19. Cyclins / genetics. Cyclins / metabolism. Female. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction


26. Lansigan F, Cooper D, Seropian S, Foss F: Autologous and allogeneic transplantation for aggressive T-cell lymphomas: A single institution experience. J Clin Oncol; 2009 May 20;27(15_suppl):8558

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous and allogeneic transplantation for aggressive T-cell lymphomas: A single institution experience.
  • : 8558 Aggressive T-cell lymphomas (ATCL) represent 10-15% of non-Hodgkin lymphoma and have a worse prognosis than aggressive B-cell lymphomas.
  • Both autologous (Auto) and allogeneic (Allo) stem cell transplantation have been used as consolidation in first remission and at relapse, but the role of transplantation has not been clearly defined.
  • The Allo group consisted of 4 PTCLu, 3 angioimmunoblastic(AITL), 2 panniculitis-like, 2 cutaneous(CTCL) with large cell transformation, 2 NK-cell, 2 anaplastic large cell(ALCL), 1 hepatosplenic, 1 enteropathic, and 1 refractory CTCL.
  • The Auto group consisted of 6 PTCLu, 12 ALCL (5 Alk+, 5 Alk-, 2 Alk unk), 4 AITL, 1 CTCL with transformation, and 1 T-lymphoblastic lymphoma.
  • Median prior therapies were 3(Allo) and 1(Auto).
  • Median time from diagnosis to Allo or Auto was 18 and 8mo, respectively.
  • For patients with resistant or relapsed disease, Allo should be strongly considered rather than Auto.

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  • (PMID = 27960993.001).
  • [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] Journal Article
  • [Publication-country] United States
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27. Passoni L, Gallo B, Biganzoli E, Stefanoni R, Massimino M, Di Nicola M, Gianni AM, Gambacorti-Passerini C: In vivo T-cell immune response against anaplastic lymphoma kinase in patients with anaplastic large cell lymphomas. Haematologica; 2006 Jan;91(1):48-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo T-cell immune response against anaplastic lymphoma kinase in patients with anaplastic large cell lymphomas.
  • BACKGROUND AND OBJECTIVES: Anaplastic lymphoma kinase (ALK) oncogenic fusion proteins, expressed in about 60% of anaplastic large cell lymphomas (ALCL), are tumor-specific molecular targets for such a malignancy.
  • DESIGN AND METHODS: The frequency and the functional phenotype of the anti-ALK CD8 precursor repertoire in freshly isolated peripheral blood mononuclear cells (PBMC) from healthy donors and ALK-positive patients were determined by major histocompatibility complex (MHC)/tetrameric analyses.
  • In addition, the ability of the anti-ALK immune response to specifically lyse ALK-positive lymphoma cells was investigated by in vitro stimulation with ALK-derived peptide p280-89.
  • RESULTS: Tetrameric MHC/peptide complexes revealed high frequencies of CD8/ALK-tetramer-positive cells both in patients and in healthy individuals.
  • However, the functional phenotype of the CD8/ALK-tetramer-positive lymphocytes showed the presence of effector and memory T lymphocytes only in patients.
  • A polyclonal ALK-specific tumor-reactive T-cell line was isolated from patients' peripheral blood lymphocytes.
  • INTERPRETATION AND CONCLUSIONS: The presence of an anti-ALK effector/memory lymphocyte population in the peripheral blood of ALK-positive patients indicates an in vivo antigenic challenge.
  • Thus, ALK is a lymphoma-associated antigen suitable for immune interventions.
  • The high number of anti-ALK memory CD8 T cells present in patients' PBMC may represent a valid source of activated CTL suitable for cancer cell lysis.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Protein-Tyrosine Kinases / immunology

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  • (PMID = 16434370.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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28. Damm-Welk C, Klapper W, Oschlies I, Gesk S, Röttgers S, Bradtke J, Siebert R, Reiter A, Woessmann W: Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation. Br J Haematol; 2009 Aug;146(3):306-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation.
  • Anaplastic large cell lymphomas (ALCL) in children express anaplastic lymphoma kinase (ALK) fusion genes, most commonly NPM1-ALK.
  • The distribution of X-ALK among 66 childhood ALCLs was analysed.
  • One ALCL was ALK-negative.
  • The remaining seven ALCL stained for ALK in the cytoplasm only: two expressed TPM3-ALK, one ATIC-ALK, one MYH9-ALK; three no TPM3-, TFG-, ATIC-, CLTC- or MYH9-ALK.
  • Almost 90% of paediatric ALK-positive ALCLs express NPM1-ALK.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19545284.001).
  • [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 / ATIC-ALK fusion protein, human; 0 / MYH9 protein, human; 0 / Molecular Motor Proteins; 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; 0 / oncoprotein CLTCL-ALK; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.6.4.1 / Myosin Heavy Chains
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29. Turner SD, Alexander DR: What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis? Leukemia; 2005 Jul;19(7):1128-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is generated as a t(2;5) chromosomal breakpoint product, typically in CD30(+) anaplastic large cell lymphomas.
  • [MeSH-major] Lymphoma / immunology. Oncogene Proteins, Fusion / immunology. Protein-Tyrosine Kinases / immunology
  • [MeSH-minor] Animals. Disease Models, Animal. Humans. Mice. Mice, Transgenic. Phosphorylation. Signal Transduction / genetics. Signal Transduction / immunology

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  • (PMID = 15902287.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 65
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30. Chiarle R, Voena C, Ambrogio C, Piva R, Inghirami G: The anaplastic lymphoma kinase in the pathogenesis of cancer. Nat Rev Cancer; 2008 Jan;8(1):11-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The anaplastic lymphoma kinase in the pathogenesis of cancer.
  • However, few tyrosine kinases have been shown to have a well-defined pathogenetic role in lymphomas.
  • The anaplastic lymphoma kinase (ALK) is the oncogene of most anaplastic large cell lymphomas (ALCL), driving transformation through many molecular mechanisms.
  • [MeSH-major] Lymphoma / enzymology. Lymphoma / genetics. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Humans. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, T-Cell / enzymology. Lymphoma, T-Cell / genetics. Receptor Protein-Tyrosine Kinases / metabolism. Translocation, Genetic

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  • (PMID = 18097461.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 158
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31. Vera L, Reategui R, Beltran B, Morales D, Capellino A, Desposorio C, Castillo J: The clinicopathological spectrum of HIV-associated lymphoma: Eleven-year-experience in a general hospital in Peru. J Clin Oncol; 2009 May 20;27(15_suppl):e19561

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinicopathological spectrum of HIV-associated lymphoma: Eleven-year-experience in a general hospital in Peru.
  • : e19561 Background: The clinicopathological spectrum of HIV-associated lymphomas in developing countries has not been clearly defined.
  • METHODS: This is a retrospective review of the clinical records of patients with diagnosis of HIV in our institution from March 1997 to March 2008.
  • RESULTS: Forty-eight patients with HIV-associated lymphoma were identified.
  • Forty-four cases (92%) were diagnosed with non-Hodgkin lymphoma (NHL) and 4 cases (8%) with Hodgkin lymphoma (HL).
  • From the 44 NHL cases, 40 cases (91%) were of B-cell origin; 23 cases (57.5%) had diffuse large B-cell, 9 cases (22.5%) had Burkitt, 3 cases (7.5%) had plasmablastic, 2 cases (5%) had primary CNS, 2 cases (5%) had MALT and 1 case (2.5%) had primary effusion lymphoma.
  • The remaining 4 cases (9%) were of T-cell origin; 3 cases (75%) had peripheral T-cell lymphoma NOS and 1 case (25%) was ALK-negative anaplastic large cell lymphoma.
  • Only 16 patients (33%) were receiving HAART previously the diagnosis of NHL and 33 patients (68%) received any oncology treatment.
  • Also a high proportion of T-cells lymphomas are found.

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  • (PMID = 27961062.001).
  • [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] Journal Article
  • [Publication-country] United States
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32. Geissinger E, Sadler P, Roth S, Grieb T, Puppe B, Müller N, Reimer P, Vetter-Kauczok CS, Wenzel J, Bonzheim I, Rüdiger T, Müller-Hermelink HK, Rosenwald A: Disturbed expression of the T-cell receptor/CD3 complex and associated signaling molecules in CD30+ T-cell lymphoproliferations. Haematologica; 2010 Oct;95(10):1697-704
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  • [Title] Disturbed expression of the T-cell receptor/CD3 complex and associated signaling molecules in CD30+ T-cell lymphoproliferations.
  • BACKGROUND: CD30(+) T-cell lymphoproliferations comprise a spectrum of clinically heterogeneous entities, including systemic anaplastic large cell lymphomas (ALK(-) and ALK(+)) and primary cutaneous CD30(+) T-cell lymphoproliferative disorders.
  • While all these entities are characterized by proliferation of highly atypical, anaplastic CD30(+) T cells, the expression of T-cell specific antigens in the tumor cells is not consistently detectable.
  • DESIGN AND METHODS: We evaluated biopsies from 19 patients with primary cutaneous CD30(+) lymphoproliferative disorders, 38 with ALK(-) and 33 with ALK(+) systemic anaplastic large cell lymphoma.
  • The biopsies were examined for the expression of T-cell receptorαβ/CD3 complex (CD3γ, δ, ε, ζ), transcription factors regulating T-cell receptor expression (ATF1, ATF2, TCF-1, TCF-1α/LEF-1, Ets1), and molecules of T-cell receptor-associated signaling cascades (Lck, ZAP-70, LAT, bcl-10, Carma1, NFATc1, c-Jun, c-Fos, Syk) using immunohistochemistry.
  • RESULTS: In comparison to the pattern in 20 peripheral T-cell lymphomas, not otherwise specified, we detected a highly disturbed expression of the T-cell receptor/CD3 complex, TCF-1, TCF-1α/LEF-1, Lck, ZAP-70, LAT, NFATc1, c-Jun, c-Fos and Syk in most of the systemic anaplastic large cell lymphomas.
  • In addition, primary cutaneous CD30(+) lymphoproliferative disorders showed such a similar expression pattern to that of systemic anaplastic large cell lymphomas, that none of the markers we investigated can reliably distinguish between these CD30(+) T-cell lymphoproliferations.
  • CONCLUSIONS: Severely altered expression of the T-cell receptor/CD3 complex, T-cell receptor-associated transcription factors and signal transduction molecules is a common characteristic of systemic and cutaneous CD30(+) lymphoproliferations, although the clinical behavior of these entities is very different.
  • Since peripheral T-cell lymphomas, not otherwise specified retain the full expression program required for functioning T-cell receptor signaling, the differential expression of a subset of these markers might be of diagnostic utility in distinguishing peripheral T-cell lymphomas, not otherwise specified from the entire group of CD30(+) lymphoproliferations.
  • [MeSH-major] Antigens, CD3 / analysis. Antigens, CD30 / analysis. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, T-Cell, Cutaneous / diagnosis. Receptors, Antigen, T-Cell / analysis


33. Ries S, Rnjak L, Mitrović Z, Kuvezdić KG, Nola M, Sucić M: CD13+ anaplastic large cell lymphoma with leukemic presentation and additional chromosomal abnormality. Diagn Cytopathol; 2010 Feb;38(2):141-6
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  • [Title] CD13+ anaplastic large cell lymphoma with leukemic presentation and additional chromosomal abnormality.
  • Anaplastic large cell lymphoma (ALCL) is a highly malignant neoplasm characterized by pleomorphic appearance, different immunophenotypes and variable sites of involvement.
  • Expression of myeloid-associated markers in anaplastic large cell lymphomas may mislead the medical team and result in delay of diagnosis due to unusual phenotype.
  • It is important to diagnose this type of tumors and distinguish it from myeloid neoplasms (extramedullary myeloid cell tumors and histiocytic tumors) since therapy and prognosis are significantly different.A 16-year-old female patient presented with fever, lymphadenopathy, and high white blood cell count.
  • Diagnosing a CD13+ ALCL with leukemic presentation with additional cytogenetic abnormality (duplication 5q35) was a significant diagnostic challenge.This combination of features, unusual for lymphoma, should be considered in differential diagnosis of myeloid neoplasms and fatal infections.
  • [MeSH-major] Antigens, CD13 / biosynthesis. Chromosome Aberrations. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, Large-Cell, Anaplastic / physiopathology
  • [MeSH-minor] Adolescent. Cell Separation. Fatal Outcome. Female. Flow Cytometry. Humans. Immunohistochemistry. Immunophenotyping. In Situ Hybridization, Fluorescence

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  • (PMID = 19760763.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.11.2 / Antigens, CD13
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34. Kaliyadan F, Ray S, Mathew MK, Pai S, Sasikala L, Pai R: A rapidly progressing, fatal case of primary systemic anaplastic large cell lymphoma presenting as erythroderma--association with carbamazepine. Dermatol Online J; 2008;14(12):5
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  • [Title] A rapidly progressing, fatal case of primary systemic anaplastic large cell lymphoma presenting as erythroderma--association with carbamazepine.
  • A 73-year-old male patient admitted with erythroderma was diagnosed to have primary systemic Analpastic Lymphoma Kinase (ALK) positive, CD 30 positive, anaplastic large cell lymphoma.
  • The patient's condition deteriorated rapidly during the period after the diagnosis was confirmed, with subsequent death before chemotherapy could be started.
  • Here we highlight the possibility of carbamazepine inducing anaplastic large cell lymphomas and the need for a high level of suspicion to make an early diagnosis allowing rapid appropriate treatment in such cases.
  • [MeSH-major] Carbamazepine / adverse effects. Dermatitis, Exfoliative / complications. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / etiology
  • [MeSH-minor] Aged. Diabetic Neuropathies / drug therapy. Disease Progression. Fatal Outcome. Humans. Male. Tomography, X-Ray Computed

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  • (PMID = 19265618.001).
  • [ISSN] 1087-2108
  • [Journal-full-title] Dermatology online journal
  • [ISO-abbreviation] Dermatol. Online J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 33CM23913M / Carbamazepine
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35. Mühlhoff C, Rübben A, Gassler N, Megahed M: [Primary cutaneous CD30+ ALK(-) anaplastic large cell T-cell lymphoma]. Hautarzt; 2009 Dec;60(12):954-6
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  • [Title] [Primary cutaneous CD30+ ALK(-) anaplastic large cell T-cell lymphoma].
  • [Transliterated title] CD30(+) ALK(-) anaplastisch grosszelliges primär kutanes T-Zell-Lymphom.
  • Anaplastic large cell lymphomas (ALCL) are characterized by large, pleomorphic cells with a strong expression of cytokine receptor CD 30.
  • Based on clinical, histological and immunophenotypic criteria, the diagnosis of a primary cutaneous CD30(+) ALK(-) anaplastic large cell lymphoma was made.
  • [MeSH-major] Antigens, CD30 / analysis. Facial Neoplasms / pathology. Lymphoma, Primary Cutaneous Anaplastic Large Cell / pathology. Skin Neoplasms / pathology


36. Polgar D, Leisser C, Maier S, Strasser S, Rüger B, Dettke M, Khorchide M, Simonitsch I, Cerni C, Krupitza G: Truncated ALK derived from chromosomal translocation t(2;5)(p23;q35) binds to the SH3 domain of p85-PI3K. Mutat Res; 2005 Feb 15;570(1):9-15

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  • The chromosomal translocation t(2;5)(p23;q35) is associated with "Anaplastic large cell lymphomas" (ALCL), a Non Hodgkin Lymphoma occurring in childhood.
  • The fusion of the tyrosine kinase gene-ALK (anaplastic lymphoma kinase) on chromosome 2p23 to the NPM (nucleophosmin/B23) gene on chromosome 5q35 results in a 80 kDa chimeric protein, which activates the "survival" kinase PI3K.
  • This finding may be useful for the development of a new target-specific intervention.
  • [MeSH-minor] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 5. Humans. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Binding. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases

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  • (PMID = 15680399.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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37. Coronas S, Lagarrigue F, Ramel D, Chicanne G, Delsol G, Payrastre B, Tronchère H: Elevated levels of PtdIns5P in NPM-ALK transformed cells: implication of PIKfyve. Biochem Biophys Res Commun; 2008 Jul 25;372(2):351-5

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  • Here, we report the presence of higher levels of this lipid in cells expressing the oncogenic tyrosine kinase nucleophosmin anaplastic lymphoma kinase (NPM-ALK), a chimeric protein found in the large majority of anaplastic large cell lymphomas (ALCLs).
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Phosphatidylinositol Phosphates / metabolism. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 18501703.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phosphatidylinositol Phosphates; 0 / phosphatidylinositol 5-phosphate; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.1.137 / Pikfyve protein, mouse; EC 2.7.10.1 / Protein-Tyrosine Kinases
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38. Low SE, Stafford JS: Malignant histiocytosis: a case report of a rare tumour presenting with spontaneous splenic rupture. J Clin Pathol; 2006 Jul;59(7):770-2
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  • Cases previously reported as malignant histiocytosis were shown to be lymphomas of T or B lineage, especially anaplastic large-cell lymphomas.
  • At autopsy, a large quantity of fresh blood, originating from several ruptured nodules on the enlarged spleen, was seen in the peritoneal cavity.

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39. Sung CO, Ko YH, Park S, Kim K, Kim W: Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma. J Korean Med Sci; 2005 Dec;20(6):952-6
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  • [Title] Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma.
  • To verify the spectrum of CD99-expressing lymphoid malignancy, an immunohistochemical study for CD99 was carried out in 182 cases of non-Hodgkin's lymphoma, including 21 lymphoblastic lymphomas, 11 small lymphocytic lymphomas, 9 mantle cell lymphomas, 12 follicular lymphomas, 37 diffuse large B cell lymphomas, 18 Burkitt's lymphomas, 28 NK/T-cell lymphomas, 8 angioimmunoblastic T-cell lymphomas, 23 peripheral T-cell lymphomas, unspecified, and 15 systemic anaplastic large cell lymphomas.
  • CD99 was positive in all T-lymphoblastic lymphomas and in 60% of B-lymphoblastic lymphomas.
  • Majority of T and NK cell lymphomas were negative for CD99, except anaplastic large cell lymphomas (ALCLs).
  • Eight of 15 cases (54%) of ALCLs reacted with anti CD99 antibody.
  • Seven of 10 (70%) ALK positive ALCLs expressed CD99, whereas only 1 of 5 (20%) ALK negative ALCLs were positive.
  • Of the mature B-cell lymphomas, 5.4% (2/37) of diffuse large B cell lymphomas and 11.1% (2/18) of Burkitt's lymphomas expressed CD99.
  • In conclusion, CD99 is infrequently expressed in mature B and T cell lymphomas, except ALK-positive ALCL.
  • High expression of CD99 in ALK-positive ALCL is unexpected finding and its biologic and clinical significances have yet to be clarified.
  • [MeSH-major] Antigens, CD / metabolism. Cell Adhesion Molecules / metabolism. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Non-Hodgkin / immunology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16361803.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2779325
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40. Li C, Takino H, Eimoto T, Ishida T, Inagaki A, Ueda R, Suzuki R, Yoshino T, Nakagawa A, Nakamura S, Inagaki H: Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma. Mod Pathol; 2007 Jun;20(6):648-55
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  • [Title] Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma.
  • In anaplastic large-cell lymphomas positive for anaplastic lymphoma kinase (ALK) protein, the ALK gene is most commonly fused to the NPM gene, and less commonly to TPM3, TFG, ATIC, and other rare genes.
  • Although this lymphoma is generally associated with a favorable clinical outcome, 25% of the patients die of the disease within 5 years.
  • In 26 cases of ALK(+) anaplastic large-cell lymphoma, the RT-PCR assay showed that the ALK was fused to NPM in 21 cases, to TPM3 in three, and to TFG in one.
  • Overexpression of the NPM-ALK fusion transcript may be associated with a poor prognosis of the patients with ALK(+) anaplastic large-cell lymphomas.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Protein-Tyrosine Kinases / biosynthesis

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  • (PMID = 17464320.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Fixatives; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; 1HG84L3525 / Formaldehyde; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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41. Riera L, Lasorsa E, Ambrogio C, Surrenti N, Voena C, Chiarle R: Involvement of Grb2 adaptor protein in nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-mediated signaling and anaplastic large cell lymphoma growth. J Biol Chem; 2010 Aug 20;285(34):26441-50
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  • [Title] Involvement of Grb2 adaptor protein in nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-mediated signaling and anaplastic large cell lymphoma growth.
  • Most anaplastic large cell lymphomas (ALCL) express oncogenic fusion proteins derived from chromosomal translocations or inversions of the anaplastic lymphoma kinase (ALK) gene.
  • Frequently ALCL carry the t(2;5) translocation, which fuses the ALK gene to the nucleophosmin (NPM1) gene.
  • The transforming activity mediated by NPM-ALK fusion induces different pathways that control proliferation and survival of lymphoma cells.
  • Grb2 is an adaptor protein thought to play an important role in ALK-mediated transformation, but its interaction with NPM-ALK, as well as its function in regulating ALCL signaling pathways and cell growth, has never been elucidated.
  • Furthermore, Grb2 did not bind to a single region but rather to different regions of NPM-ALK, mainly Tyr(152-156), Tyr(567), and a proline-rich region, Pro(415-417).
  • Finally, shRNA knockdown experiments showed that Grb2 regulates primarily the NPM-ALK-mediated phosphorylation of SHP2 and plays a key role in ALCL cell growth.
  • [MeSH-major] Cell Proliferation. GRB2 Adaptor Protein / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / metabolism. Signal Transduction
  • [MeSH-minor] Binding Sites. Humans. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Phosphorylation. Protein Binding. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Receptor Protein-Tyrosine Kinases. Translocation, Genetic. Tumor Cells, Cultured

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  • (PMID = 20554525.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] International / European Research Council / / 242965
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GRB2 Adaptor Protein; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2924075
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42. Boudova L, Kazakov DV, Jindra P, Sima R, Vanecek T, Kuntscher V, Vera V, Bouda J, Michal M: Primary cutaneous histiocyte and neutrophil-rich CD30+ and CD56+ anaplastic large-cell lymphoma with prominent angioinvasion and nerve involvement in the forehead and scalp of an immunocompetent woman. J Cutan Pathol; 2006 Aug;33(8):584-9
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  • [Title] Primary cutaneous histiocyte and neutrophil-rich CD30+ and CD56+ anaplastic large-cell lymphoma with prominent angioinvasion and nerve involvement in the forehead and scalp of an immunocompetent woman.
  • BACKGROUND: Cutaneous lymphomas co-expressing CD56 and CD30 are very rare.
  • They share a clinicopathological overlap with natural killer- (NK)/T-cell lymphomas and anaplastic large-cell lymphomas (ALCLs), two entities with widely disparate clinical behavior.
  • METHODS: We present a case of an immunocompetent 57-year-old Caucasian woman with a rapidly growing, angiodestructive and neuroinvasive primary cutaneous ALCL (PCALCL).
  • The neoplastic population of large anaplastic CD30+ and CD56+ T cells was masked by a massive admixture of histiocytes and neutrophils.
  • Additionally, high-dose chemotherapy with autologous peripheral blood stem-cell transplantation was administered as a consolidation of complete remission, in which she has remained for 6 years.
  • CONCLUSIONS: This is the first CD30+ and CD56+ primary skin lymphoma to be reported on the head.
  • The presented case carries a remarkable combination of clinicopathological features of PCALCL and NK-/T-cell lymphoma.
  • [MeSH-major] Antigens, CD30 / analysis. Antigens, CD56 / analysis. Lymphoma, Large B-Cell, Diffuse / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Female. Forehead. Head and Neck Neoplasms / blood supply. Head and Neck Neoplasms / drug therapy. Head and Neck Neoplasms / immunology. Head and Neck Neoplasms / pathology. Histiocytes / cytology. Humans. Middle Aged. Neutrophils / cytology. Scalp / blood supply. Scalp / drug effects. Scalp / innervation. Scalp / pathology. Stem Cell Transplantation

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  • (PMID = 16919035.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antigens, CD56
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43. Cheng M, Ott GR: Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma. Anticancer Agents Med Chem; 2010 Mar;10(3):236-49
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  • [Title] Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was originally identified as the oncogenic NPM (nucleophosmin)-ALK fusion protein due to a t (2;5) chromosomal translocation in anaplastic large cell lymphomas.
  • The recent reports of EML4 (echinoderm microtubule-associated protein-like 4)-ALK oncogenic proteins in non-small cell lung cancer (NSCLC) and the identification of ALK activating point mutations and gene amplification in neuroblastoma have indicated ALK as a potential major therapeutic target for human cancers.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma, Large-Cell, Anaplastic / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors


44. Hsu FY, Zhao Y, Anderson WF, Johnston PB: Downregulation of NPM-ALK by siRNA causes anaplastic large cell lymphoma cell growth inhibition and augments the anti cancer effects of chemotherapy in vitro. Cancer Invest; 2007 Jun;25(4):240-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Downregulation of NPM-ALK by siRNA causes anaplastic large cell lymphoma cell growth inhibition and augments the anti cancer effects of chemotherapy in vitro.
  • The fusion protein, nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), results from the chromosome translocation t(2;5)(p23;q25) and is present in 50-70 percent of anaplastic large-cell lymphomas (ALCLs).
  • To examine if the NPM-ALK is a potential therapeutic target in ALCL, we used siRNA to specifically downregulate the expression of the NPM-ALK in ALCL cell lines.
  • In this report, we demonstrated viability loss in t(2;5)-positive ALCL cell lines, SUDHL-1 and Karpas 299 cells, but not in lymphoma cell lines without the chromosome translocation, Jurkat and Granta 519 cells.
  • Further study demonstrated that the downregulation of NPM-ALK resulted in decreased cell proliferation and increased cell apoptosis.
  • These results revealed the importance of continuous expression of NPM-ALK in maintaining the growth of ALCL cells.
  • Our data also suggested that the repression of the fusion gene might be a potential novel therapeutic strategy for NPM-ALK positive ALCLs.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. RNA, Small Interfering / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 5. Down-Regulation. Humans. Signal Transduction. Translocation, Genetic

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  • (PMID = 17612934.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59318
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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45. Koshiba S, Li H, Motoda Y, Tomizawa T, Kasai T, Tochio N, Yabuki T, Harada T, Watanabe S, Tanaka A, Shirouzu M, Kigawa T, Yamamoto T, Yokoyama S: Structural basis for the recognition of nucleophosmin-anaplastic lymphoma kinase oncoprotein by the phosphotyrosine binding domain of Suc1-associated neurotrophic factor-induced tyrosine-phosphorylated target-2. J Struct Funct Genomics; 2010 Jun;11(2):125-41
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  • [Title] Structural basis for the recognition of nucleophosmin-anaplastic lymphoma kinase oncoprotein by the phosphotyrosine binding domain of Suc1-associated neurotrophic factor-induced tyrosine-phosphorylated target-2.
  • The nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion oncoprotein, formed by the t(2;5) chromosomal translocation in anaplastic large-cell lymphomas, has constitutive tyrosine kinase activity and interacts with a number of signaling molecules.

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  • (PMID = 20454865.001).
  • [ISSN] 1570-0267
  • [Journal-full-title] Journal of structural and functional genomics
  • [ISO-abbreviation] J. Struct. Funct. Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Peptide Fragments; 21820-51-9 / Phosphotyrosine; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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46. Baumforth KR, Flavell JR, Reynolds GM, Davies G, Pettit TR, Wei W, Morgan S, Stankovic T, Kishi Y, Arai H, Nowakova M, Pratt G, Aoki J, Wakelam MJ, Young LS, Murray PG: Induction of autotaxin by the Epstein-Barr virus promotes the growth and survival of Hodgkin lymphoma cells. Blood; 2005 Sep 15;106(6):2138-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of autotaxin by the Epstein-Barr virus promotes the growth and survival of Hodgkin lymphoma cells.
  • A proportion of patients with Hodgkin lymphoma carry Epstein-Barr virus (EBV), an oncogenic herpesvirus, in their tumor cells.
  • Although it is generally assumed that EBV contributes to the malignant phenotype of Hodgkin lymphoma cells, direct evidence in support of this is lacking.
  • Here we show that EBV infection of Hodgkin lymphoma cells results in the induction of autotaxin, a secreted tumor-associated factor with lysophospholipase-D activity.
  • Up-regulation of autotaxin increased the generation of lysophosphatidic acid (LPA) and led to the enhanced growth and survival of Hodgkin lymphoma cells, whereas specific down-regulation of autotaxin decreased LPA levels and reduced cell growth and viability.
  • In lymphoma tissues, autotaxin expression was mainly restricted to CD30+ anaplastic large-cell lymphomas and Hodgkin lymphoma; in the latter, high levels of autotaxin were strongly associated with EBV positivity (P = .006).
  • Our results identify the induction of autotaxin and the subsequent generation of LPA as key molecular events that mediate the EBV-induced growth and survival of Hodgkin lymphoma cells and suggest that this pathway may provide opportunities for novel therapeutic intervention.
  • [MeSH-major] Cell Proliferation. Gene Expression Regulation, Neoplastic. Glucose-6-Phosphate Isomerase / genetics. Glycoproteins / genetics. Herpesvirus 4, Human / physiology. Hodgkin Disease / pathology. Hodgkin Disease / virology. Multienzyme Complexes / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Survival. Epstein-Barr Virus Infections / metabolism. Humans. Lysophospholipids / biosynthesis. Phosphodiesterase I. Phosphoric Diester Hydrolases. Pyrophosphatases. Up-Regulation

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  • (PMID = 15933052.001).
  • [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 / Glycoproteins; 0 / Lysophospholipids; 0 / Multienzyme Complexes; 22002-87-5 / lysophosphatidic acid; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.1 / Phosphodiesterase I; EC 3.1.4.39 / alkylglycerophosphoethanolamine phosphodiesterase; EC 3.6.1.- / Pyrophosphatases; EC 5.3.1.9 / Glucose-6-Phosphate Isomerase
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47. Rust R, Visser L, van der Leij J, Harms G, Blokzijl T, Deloulme JC, van der Vlies P, Kamps W, Kok K, Lim M, Poppema S, van den Berg A: High expression of calcium-binding proteins, S100A10, S100A11 and CALM2 in anaplastic large cell lymphoma. Br J Haematol; 2005 Dec;131(5):596-608
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of calcium-binding proteins, S100A10, S100A11 and CALM2 in anaplastic large cell lymphoma.
  • Anaplastic large cell lymphomas (ALCL) are characterised by the presence of CD30-positive large cells, which usually are of T-cell type.
  • Based on the presence or absence of translocations involving the anaplastic lymphoma kinase (ALK) locus, ALCL cases can be divided into two groups.
  • To gain more insight in the biology of ALCL, we applied serial analysis of gene expression (SAGE) on the Karpas299 cell line and identified 25 up- and 19 downregulated genes.
  • Quantitative reverse transcription polymerase chain reaction on 5 ALCL cell lines and 12 ALCL tissues confirmed the SAGE data for 13 out of 14 up- and one out of four downregulated genes.
  • Immunohistochemical staining confirmed the presence of S100A10, a calcium-binding protein, in three out of five ALK+ and all 7 ALK- ALCL cases.
  • S100A11 staining was confirmed in all ALK+ and six of seven ALK- ALCL cases.
  • Three of the upregulated genes represented calcium-binding proteins, which suggest that altered intracellular signaling might be associated with the oncogenesis of ALCL.
  • [MeSH-major] Annexin A2 / genetics. Calcium Signaling / genetics. Calmodulin / genetics. Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / genetics. S100 Proteins / genetics
  • [MeSH-minor] CD4-Positive T-Lymphocytes / metabolism. Cell Line, Tumor. Cells, Cultured. Down-Regulation. Galectin 1 / analysis. Galectin 1 / genetics. Gene Expression Profiling. Humans. Immunohistochemistry / methods. Membrane Proteins / genetics. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16351635.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A2; 0 / CALM2 protein, human; 0 / Calmodulin; 0 / Galectin 1; 0 / Membrane Proteins; 0 / S100 Proteins; 0 / S100 calcium binding protein A10; 146909-89-9 / S100A11 protein, human; 179801-28-6 / LAPTM5 protein, human
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48. Sabbatini P, Korenchuk S, Rowand JL, Groy A, Liu Q, Leperi D, Atkins C, Dumble M, Yang J, Anderson K, Kruger RG, Gontarek RR, Maksimchuk KR, Suravajjala S, Lapierre RR, Shotwell JB, Wilson JW, Chamberlain SD, Rabindran SK, Kumar R: GSK1838705A inhibits the insulin-like growth factor-1 receptor and anaplastic lymphoma kinase and shows antitumor activity in experimental models of human cancers. Mol Cancer Ther; 2009 Oct;8(10):2811-20
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  • [Title] GSK1838705A inhibits the insulin-like growth factor-1 receptor and anaplastic lymphoma kinase and shows antitumor activity in experimental models of human cancers.
  • GSK1838705A is a small-molecule kinase inhibitor that inhibits IGF-IR and the insulin receptor with IC(50)s of 2.0 and 1.6 nmol/L, respectively.
  • GSK1838705A blocks the in vitro proliferation of cell lines derived from solid and hematologic malignancies, including multiple myeloma and Ewing's sarcoma, and retards the growth of human tumor xenografts in vivo.
  • GSK1838705A also inhibits the anaplastic lymphoma kinase (ALK), which drives the aberrant growth of anaplastic large-cell lymphomas, some neuroblastomas, and a subset of non-small cell lung cancers.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology. Pyrroles / pharmacology. Receptor, IGF Type 1 / antagonists & inhibitors. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Proliferation / drug effects. Enzyme Activation / drug effects. Humans. Mice. Phosphorylation / drug effects. Receptor Protein-Tyrosine Kinases. Receptor, Insulin / metabolism. Signal Transduction / drug effects


49. Geissinger E, Bonzheim I, Roth S, Rosenwald A, Müller-Hermelink HK, Rüdiger T: CD52 expression in peripheral T-cell lymphomas determined by combined immunophenotyping using tumor cell specific T-cell receptor antibodies. Leuk Lymphoma; 2009 Jun;50(6):1010-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD52 expression in peripheral T-cell lymphomas determined by combined immunophenotyping using tumor cell specific T-cell receptor antibodies.
  • For peripheral T-cell lymphomas (PTCL), anti-CD52 (alemtuzumab) therapy is currently under investigation.
  • To accurately discriminate between the presumed mechanistically relevant CD52 expression in tumor versus bystander cells, we employed immunofluorescence double stains using CD52 in combination with an antibody directed against the rearranged T-cell receptor Vbeta-segment of the neoplastic clone in 6 angioimmunoblastic T-cell lymphomas (AITL) and 5 PTCL, unspecified (PTCL-NOS) and, in combination with CD30, in 18 anaplastic large cell lymphomas (ALCL).
  • Tumor cells in all AITL and PTCL-NOS were CD52 positive, while in 17 of 18 ALCL no specific staining was observed.
  • Conversely, the background T- and B-cell infiltrate showed a consistent positivity for CD52.
  • Our approach helps to precisely define CD52 expression in the tumor cell population of PTCL and might therefore be valuable when evaluating the response to alemtuzumab therapy in prospective clinical trials.
  • [MeSH-major] Antibodies / immunology. Antigens, CD / analysis. Antigens, Neoplasm / analysis. Glycoproteins / analysis. Immunophenotyping / methods. Lymphoma, T-Cell, Peripheral / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology
  • [MeSH-minor] Antigens, CD30 / analysis. Fluorescent Antibody Technique / methods. Humans. Lymphoma, Large-Cell, Anaplastic / immunology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 19479612.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD; 0 / Antigens, CD30; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Receptors, Antigen, T-Cell, alpha-beta
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50. Coluccia AM, Gunby RH, Tartari CJ, Scapozza L, Gambacorti-Passerini C, Passoni L: Anaplastic lymphoma kinase and its signalling molecules as novel targets in lymphoma therapy. Expert Opin Ther Targets; 2005 Jun;9(3):515-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase and its signalling molecules as novel targets in lymphoma therapy.
  • A crucial issue in the development of molecularly-targeted anticancer therapies is the identification of appropriate molecules whose targeting would result in tumour regression with a minimal level of systemic toxicity.
  • Anaplastic lymphoma kinase (ALK) is a transmembrane receptor tyrosine kinase, normally expressed at low levels in the nervous system.
  • As a consequence of chromosomal translocations involving the alk gene (2p23), ALK is also aberrantly expressed and constitutively activated in approximately 60% of CD30+ anaplastic large cell lymphomas (ALCLs).
  • Due to the selective overexpression of ALK in tumour cells, its direct involvement in the process of malignant transformation and its frequent expression in ALCL patients, the authors recognise ALK as a suitable candidate for the development of molecularly targeted strategies for the therapeutic treatment of ALK-positive lymphomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Lymphoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Signal Transduction / drug effects

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  • (PMID = 15948671.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 189
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51. Piva R, Pellegrino E, Inghirami G: Identification and validation of the anaplastic large cell lymphoma signature. Adv Exp Med Biol; 2007;604:129-36
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  • [Title] Identification and validation of the anaplastic large cell lymphoma signature.
  • Anaplastic large cell lymphomas (ALCL) represent a subset of lymphomas in which the anaplastic lymphoma kinase (ALK) gene is fused to several partners, most frequently to the NPM gene.
  • We have previously demonstrated that the constitutive expression and phosphorylation of ALK chimeric proteins is sufficient for cellular transformation, and its activity is strictly required for the survival of ALCL cells.
  • To unravel signaling pathways required for NPM-ALK-mediated transformation and tumor maintenance, we analyzed the transcriptomes of ALK positive ALCL cell lines through experimentally controlled approaches in which ALK signaling was abrogated by an inducible ALKshRNA or by ALK inhibitors.
  • A functional RNAi screening identified new ALK transcriptional targets instrumental to cell transformation and/or to sustain the growth and survival of ALK positive ALCL cells.
  • [MeSH-major] Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / genetics

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  • (PMID = 17695725.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [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 / RNA, Messenger
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52. Piva R, Pellegrino E, Mattioli M, Agnelli L, Lombardi L, Boccalatte F, Costa G, Ruggeri BA, Cheng M, Chiarle R, Palestro G, Neri A, Inghirami G: Functional validation of the anaplastic lymphoma kinase signature identifies CEBPB and BCL2A1 as critical target genes. J Clin Invest; 2006 Dec;116(12):3171-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional validation of the anaplastic lymphoma kinase signature identifies CEBPB and BCL2A1 as critical target genes.
  • Anaplastic large cell lymphomas (ALCLs) represent a subset of lymphomas in which the anaplastic lymphoma kinase (ALK) gene is frequently fused to the nucleophosmin (NPM) gene.
  • We previously demonstrated that the constitutive phosphorylation of ALK chimeric proteins is sufficient to induce cellular transformation in vitro and in vivo and that ALK activity is strictly required for the survival of ALK-positive ALCL cells.
  • To elucidate the signaling pathways required for ALK-mediated transformation and tumor maintenance, we analyzed the transcriptomes of multiple ALK-positive ALCL cell lines, abrogating their ALK-mediated signaling by inducible ALK RNA interference (RNAi) or with potent and cell-permeable ALK inhibitors.
  • Functional RNAi screening on a set of these ALK transcriptional targets revealed that the transcription factor C/EBPbeta and the antiapoptotic protein BCL2A1 are absolutely necessary to induce cell transformation and/or to sustain the growth and survival of ALK-positive ALCL cells.

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  • (PMID = 17111047.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [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 / BCL2-related protein A1; 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / STAT3 Transcription Factor; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC1636692
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53. Gualco G, Bacchi CE: B-cell and T-cell lymphomas of the breast: clinical--pathological features of 53 cases. Int J Surg Pathol; 2008 Oct;16(4):407-13
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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 and T-cell lymphomas of the breast: clinical--pathological features of 53 cases.
  • Breast involvement by non-Hodgkin lymphomas is rare.
  • We studied the morphological, immunophenotypical, and clinical features of 53 cases of malignant lymphomas involving the breast in a population of Brazilian patients.
  • Most of the cases were of B-cell phenotype.
  • Four of the patients with primary breast lymphomas had T-cell lymphomas, 3 had CD30-positive anaplastic large cell lymphomas, and 1 had panniculitis-like T-cell lymphoma.
  • Secondary breast lymphoma was seen in 19 patients and most commonly occurred as part of widespread nodal disease.
  • The most prevalent histological subtype was also diffuse large B-cell lymphoma, followed by follicular lymphoma.
  • This study shows that the broad morphological and immunophenotypical spectrum of malignant lymphoma of the breast occurring in a large series of Brazilian patients has many similarities with that seen in Western countries, with a higher proportion of high-grade lymphomas in both primary and secondary cases.
  • [MeSH-major] Breast Neoplasms / pathology. Breast Neoplasms, Male / pathology. Lymphoma, B-Cell / pathology. Lymphoma, T-Cell / pathology

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  • (PMID = 18480397.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 070058; United States / NCI NIH HHS / CA / CA082274
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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54. Geissinger E, Bonzheim I, Krenács L, Roth S, Reimer P, Wilhelm M, Müller-Hermelink HK, Rüdiger T: Nodal peripheral T-cell lymphomas correspond to distinct mature T-cell populations. J Pathol; 2006 Oct;210(2):172-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nodal peripheral T-cell lymphomas correspond to distinct mature T-cell populations.
  • Peripheral T-cell lymphomas (PTCL) have not been successfully correlated with specific developmental stages of reactive T-cells.
  • In this study, we evaluated lymph node biopsies from eight PTCL-not otherwise specified (PTCL-NOS), seven angioimmunoblastic T-cell lymphomas (AILT), and 15 anaplastic large cell lymphomas (ALCL).
  • Detection of tumour cells with antibodies that recognize specific rearranged T-cell receptor Vbeta segments allowed us to investigate the expression of various differentiation-associated molecules.
  • All AILT and ALCL showed a homogeneous effector cell phenotype (CD45RA(-)/CD45R0(+)/CD27(-)), but differed in the cytotoxic and activation markers expressed.
  • Several (5/8) PTCL-NOS clustered together; these cases all exhibited a CD4(+) central memory cell phenotype (CD45RA(-)/CD45R0(+)/CD27(+)) and four expressed the lymph node homing receptor CCR7.
  • In conclusion, AILT and ALCL tumour cells correspond to different subsets of effector cells, while a subset of PTCL-NOS correlates with a non-effector T-cell population.
  • [MeSH-major] Lymphoma, T-Cell, Peripheral / immunology. T-Lymphocyte Subsets / immunology
  • [MeSH-minor] Antigens, CD27 / metabolism. Antigens, CD45 / metabolism. CD4-Positive T-Lymphocytes / immunology. Cell Differentiation / immunology. Cluster Analysis. Humans. Immunoblastic Lymphadenopathy / immunology. Immunologic Memory. Immunophenotyping. Lymphoma, Large-Cell, Anaplastic / immunology. Receptors, CCR7. Receptors, Chemokine / metabolism

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  • (PMID = 16924587.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / CCR7 protein, human; 0 / Receptors, CCR7; 0 / Receptors, Chemokine; EC 3.1.3.48 / Antigens, CD45
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55. Karube K, Aoki R, Nomura Y, Yamamoto K, Shimizu K, Yoshida S, Komatani H, Sugita Y, Ohshima K: Usefulness of flow cytometry for differential diagnosis of precursor and peripheral T-cell and NK-cell lymphomas: analysis of 490 cases. Pathol Int; 2008 Feb;58(2):89-97

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Usefulness of flow cytometry for differential diagnosis of precursor and peripheral T-cell and NK-cell lymphomas: analysis of 490 cases.
  • Although various CD markers have been analyzed in T-cell and natural killer (NK)-cell lymphomas, the sensitivity and specificity of these phenotypic features have not been satisfactorily characterized.
  • Flow cytometry (FCM) was used to determine the phenotypic pattern of 490 T/NK-cell lymphomas with the aid of a set of surface antigens (CD2, CD3, CD4, CD5, CD7, CD8, CD10, CD11c, CD16, CD19, CD20, CD25, CD30, CD34, and CD56).
  • In data obtained from 319 patients, CD10 expression was detected in 57% of angioimmunoblastic T-cell lymphomas, CD30 in 93% of anaplastic large cell lymphomas, CD34 in 50% of lymphoblastic lymphomas, and CD56 in 100% of extranodal NK/T-cell lymphomas nasal type.
  • A total of 92% of adult T-cell leukemia/lymphomas (ATLL) had expression of CD25 and downregulation of CD7.
  • Of special interest is that 92 ATLL (50%) were CD4+CD7-CD25+ phenotype while only four peripheral T-cell lymphoma unspecified (9%) and one (9%) cutaneous T-cell lymphoma had this phenotype.
  • Phenotypic analysis using FCM was thus found to be useful for differential diagnosis of T-cell and NK-cell lymphomas.
  • [MeSH-major] Flow Cytometry / methods. Killer Cells, Natural / pathology. Lymphoma, T-Cell / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Antigens, CD / analysis. Biomarkers, Tumor / immunology. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Humans. Immunophenotyping. Lymph Nodes / immunology. Lymph Nodes / pathology

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  • (PMID = 18199158.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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56. Tamiolakis D, Maroulis G, Simopoulos C, Verettas D, Papadopoulos N, Venizelos J, Lambropoulou M, Koutsougeras G, Karpouzis A, Kouskoukis C: Human embryonal tissues of all three germ layers can express the CD30 antigen. An immunohistochemical study of 30 fetuses coming after therapeutic abortions from week 8th to week 16th of gestation. Cesk Patol; 2006 Jan;42(1):9-15

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human embryonal tissues of all three germ layers can express the CD30 antigen. An immunohistochemical study of 30 fetuses coming after therapeutic abortions from week 8th to week 16th of gestation.
  • Originally, expression of the CD30 antigen was shown to be typical of the tumor cells of Hodgkin disease and of anaplastic large cell lymphomas.
  • In reactive lymphoid tissue, CD30 is expressed only in a small population of activated lymphoid blasts.
  • Since then, several reports have been published describing CD30 expression in non lymphoid tissues and neoplasms, such as embryonal carcinomas, seminomas, cultivated macrophages, histiocytic neoplastic cells, deciduals cells, and mesothelioma cells.
  • In order to gain insight into the functions of CD30, given that it can mediate signals for cell proliferation and apoptosis, we studied the distribution of the antigen in different fetal archival paraffin-embedded tissues from week 8th to 16th of gestation.
  • We investigated the immunohistochemical expression of CD30 in 30 paraffin-embedded tissue samples representing all three germ layers, using the monoclonal antibody Ber-H2 CD30 is expressed early in human fetal development (8th-10th week) in a wide variety of tissues, with the exception of the skin and thymus in which it is expressed later on.
  • The finding of CD30 expression in the terminal period of organogenesis, period, which is highly hormone related, implies that the antigen has an important role in cell development, maturation, and pathway to terminal differentiation in almost all fetal tissues and structures.
  • [MeSH-major] Antigens, CD30 / analysis. Germ Layers / metabolism. Gestational Age. Organogenesis

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  • (PMID = 16506595.001).
  • [ISSN] 1210-7875
  • [Journal-full-title] Československá patologie
  • [ISO-abbreviation] Cesk Patol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Antigens, CD30
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57. Galkin AV, Melnick JS, Kim S, Hood TL, Li N, Li L, Xia G, Steensma R, Chopiuk G, Jiang J, Wan Y, Ding P, Liu Y, Sun F, Schultz PG, Gray NS, Warmuth M: Identification of NVP-TAE684, a potent, selective, and efficacious inhibitor of NPM-ALK. Proc Natl Acad Sci U S A; 2007 Jan 2;104(1):270-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Constitutive overexpression and activation of NPM-ALK fusion protein [t(2:5)(p23;q35)] is a key oncogenic event that drives the survival and proliferation of anaplastic large-cell lymphomas (ALCLs).
  • We have identified a highly potent and selective small-molecule ALK inhibitor, NVP-TAE684, which blocked the growth of ALCL-derived and ALK-dependent cell lines with IC(50) values between 2 and 10 nM.
  • NVP-TAE684 treatment resulted in a rapid and sustained inhibition of phosphorylation of NPM-ALK and its downstream effectors and subsequent induction of apoptosis and cell cycle arrest.
  • In vivo, NVP-TAE684 suppressed lymphomagenesis in two independent models of ALK-positive ALCL and induced regression of established Karpas-299 lymphomas.
  • NVP-TAE684 also induced down-regulation of CD30 expression, suggesting that CD30 may be used as a biomarker of therapeutic NPM-ALK kinase activity inhibition.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / drug therapy. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Antigens, CD30 / analysis. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line. Humans. Mice. Mice, SCID. Phosphorylation. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism. Signal Transduction / drug effects

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  • [ErratumIn] Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):2025
  • (PMID = 17185414.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / NVP-TAE684; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / STAT3 Transcription Factor; 0 / STAT5 Transcription Factor; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC1765448
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58. Ma L, Xu G, Sotnikova A, Szczepanowski M, Giefing M, Krause K, Krams M, Siebert R, Jin J, Klapper W: Loss of expression of LyGDI (ARHGDIB), a rho GDP-dissociation inhibitor, in Hodgkin lymphoma. Br J Haematol; 2007 Oct;139(2):217-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of expression of LyGDI (ARHGDIB), a rho GDP-dissociation inhibitor, in Hodgkin lymphoma.
  • Gene expression profiling of Hodgkin cell lines revealed that LyGDI expression was downregulated in these cell lines.
  • The present study evaluated the expression of LyGDI in Hodgkin cells in vivo and studied the function of LyGDI in Hodgkin cell lines in vitro.
  • Our results showed that virtually all Hodgkin and Reed-Sternberg cells in classical Hodgkin lymphoma lacked LyGDI protein expression.
  • On the other hand, almost all non-Hodgkin lymphomas, except for anaplastic large cell lymphomas, expressed LyGDI protein.
  • Transfection of the classical Hodgkin cell line L428 with a vector containing full-length LyGDI-induced apoptosis in a subset of cells.
  • [MeSH-major] Gene Expression Regulation. Guanine Nucleotide Dissociation Inhibitors / genetics. Hodgkin Disease / metabolism. Reed-Sternberg Cells / metabolism. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Flow Cytometry. Humans. Immunohistochemistry. Lymphoma, Non-Hodgkin / metabolism. Lymphoma, Non-Hodgkin / pathology. Mifepristone / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Transgenes. rho Guanine Nucleotide Dissociation Inhibitor alpha. rho Guanine Nucleotide Dissociation Inhibitor beta. rho-Specific Guanine Nucleotide Dissociation Inhibitors

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  • (PMID = 17897297.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ARHGDIA protein, human; 0 / ARHGDIB protein, human; 0 / Guanine Nucleotide Dissociation Inhibitors; 0 / Tumor Suppressor Proteins; 0 / rho Guanine Nucleotide Dissociation Inhibitor alpha; 0 / rho Guanine Nucleotide Dissociation Inhibitor beta; 0 / rho-Specific Guanine Nucleotide Dissociation Inhibitors; 320T6RNW1F / Mifepristone
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59. Jäger R, Hahne J, Jacob A, Egert A, Schenkel J, Wernert N, Schorle H, Wellmann A: Mice transgenic for NPM-ALK develop non-Hodgkin lymphomas. Anticancer Res; 2005 Sep-Oct;25(5):3191-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mice transgenic for NPM-ALK develop non-Hodgkin lymphomas.
  • BACKGROUND: The t(2;5)(p23;q35) translocation is associated with a high percentage of anaplastic large-cell lymphomas (ALCL) of T- or null-cell phenotype.
  • The translocation produces an 80 kDa hyperphosphorylated chimeric protein (p80) derived from the fusion of the anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM).
  • RESULTS: Mice rapidly developed large cell lymphoblastic lymphomas with a median latency of 8 weeks, primarily involving the thymus, with lymph node as well as histologically evident extranodal organ infiltration by large tumor cells.
  • [MeSH-major] Lymphoma, T-Cell / genetics. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Animals. Cell Lineage. Disease Models, Animal. Female. Humans. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Mice, Transgenic. Pregnancy. Promoter Regions, Genetic. T-Lymphocytes / cytology. T-Lymphocytes / physiology

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  • (PMID = 16101126.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck)
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60. Chang ST, Lu CL, Chuang SS: CD52 expression in non-mycotic T- and NK/T-cell lymphomas. Leuk Lymphoma; 2007 Jan;48(1):117-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD52 expression in non-mycotic T- and NK/T-cell lymphomas.
  • Campath-1H or alemtuzumab, a human anti-CD52, has been shown to be effective in T-cell malignancies; however, there is very limited information on CD52 expression in T-cell lymphoma (TCL).
  • Fourteen cases of angioimmunoblastic T-cell lymphoma (AITL) were excluded as there were no reliable criteria to differentiate whether the CD52-positive cells were neoplastic T-cells, which are usually small-sized, or the usually abundant, small-to-large residual/reactive B-cells in this lymphoma sub-type.
  • In the remaining 83 tumors, CD52 was expressed in 29 (35%) tumors including 8/17 (47%) NK/T-cell lymphomas, 14/35 (40%) unspecified peripheral TCLs and 4/18 (22%) anaplastic large cell lymphomas.
  • [MeSH-major] Antigens, CD / metabolism. Antigens, Neoplasm / metabolism. Glycoproteins / metabolism. Lymphoma, T-Cell / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Humans. Killer Cells, Natural / metabolism. Killer Cells, Natural / pathology. Male. Middle Aged. Retrospective Studies

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  • (PMID = 17325855.001).
  • [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 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins
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61. Chiarle R, Simmons WJ, Cai H, Dhall G, Zamo A, Raz R, Karras JG, Levy DE, Inghirami G: Stat3 is required for ALK-mediated lymphomagenesis and provides a possible therapeutic target. Nat Med; 2005 Jun;11(6):623-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Anaplastic large cell lymphomas (ALCLs) are caused by chromosomal translocations that juxtapose the anaplastic lymphoma kinase (ALK) proto-oncogene to a dimerization partner, resulting in constitutive expression of ALK and ALK tyrosine kinase activity.
  • One substrate of activated ALK in human ALCLs is the transcription factor Stat3, and its phosphorylation is accurately recapitulated in a new nucleophosmin (NPM)-ALK transgenic mouse model of lymphomagenesis.
  • Here we show by gene targeting that Stat3 is required for the transformation of mouse embryonic fibroblasts in vitro, for the development of B-cell lymphoma in transgenic mice and for the growth and survival of both human and mouse NPM-ALK-transformed B and T cells.
  • Pharmacological ablation of Stat3 represents a new candidate approach for the treatment of human lymphoma
  • [MeSH-major] Cell Transformation, Neoplastic. DNA-Binding Proteins / physiology. Lymphoma, Large B-Cell, Diffuse / physiopathology. Protein-Tyrosine Kinases / physiology. Trans-Activators / physiology
  • [MeSH-minor] Animals. Cell Line. Fibroblasts / physiology. Humans. Lymphoma, T-Cell / physiopathology. Mice. Mice, Inbred BALB C. Mice, Nude. Mice, Transgenic. Molecular Sequence Data. Multiple Myeloma / physiopathology. Oligonucleotides, Antisense / pharmacology. Receptor Protein-Tyrosine Kinases. STAT3 Transcription Factor

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  • [CommentIn] Nat Med. 2005 Jun;11(6):595-6 [15937466.001]
  • (PMID = 15895073.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF246978/ AY572796/ BC019168/ U04946
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oligonucleotides, Antisense; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Stat3 protein, mouse; 0 / Trans-Activators; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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62. d'Amore F, Jantunen E, Relander T: Hemopoietic stem cell transplantation in T-cell malignancies: who, when, and how? Curr Hematol Malig Rep; 2009 Oct;4(4):236-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hemopoietic stem cell transplantation in T-cell malignancies: who, when, and how?
  • Only in recent years has there been a specific focus on the treatment of T-cell lymphomas in general and peripheral T-cell lymphomas (PTCLs) in particular.
  • In this context, the role of hemopoietic stem cell transplantation-primarily autologous but also allogeneic-has been investigated.
  • High-dose therapy with autologous stem cell transplantation (HDT/ASCT) proved feasible in both relapsed/refractory and previously untreated PTCL.
  • Reported outcomes have varied, often depending on the number of anaplastic large-cell lymphomas in the cohort.
  • In addition, retrospective results usually focus on patients undergoing transplantation, whereas the fraction of patients with primary refractory or early relapsing disease is best described in the intention-to-treat analysis of prospective trials.
  • This article reviews the most recent results of upfront HDT/ASCT consolidation in different subtypes of systemic PTCL.
  • The data on allogeneic stem cell transplantation are more limited, but promising results have recently been reported in the setting of relapsed or primary refractory disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Lymphoma, T-Cell / therapy

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  • (PMID = 20425413.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 58
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63. Xiang YG, Lu SY, Gu MM, Wang SY, Ren SX, Fu G, Wang ZG: [Cloning and structural analysis of mouse genomic nucleophosmin gene]. Yi Chuan Xue Bao; 2005 Jun;32(6):641-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • NPM gene involved chromosomal translocations were found in the patients with anaplastic large cell lymphomas (ALCL), myelodysplastic syndrome (MDS), acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL).
  • A positive phage clone which contained the full-length NPM genomic DNA was obtained and the insert of 15.3 kb genomic DNA in this clone was sequenced with shotgun method.

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  • (PMID = 16018192.001).
  • [ISSN] 0379-4172
  • [Journal-full-title] Yi chuan xue bao = Acta genetica Sinica
  • [ISO-abbreviation] Yi Chuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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64. Settleman J: Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK). Semin Oncol; 2009 Apr;36(2 Suppl 1):S36-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK).
  • The potential broader significance of this relationship has been further highlighted in preclinical studies using tumor-derived cell lines as a model system that can faithfully recapitulate the association of specific genotypes with drug sensitivity, suggesting the utility of cancer cell lines to identify novel candidate biomarkers for predicting clinically responsive patient subsets for newly developed anticancer agents.
  • The case of the anaplastic lymphoma kinase (ALK) nicely exemplifies this, and cell line profiling has revealed that ALK mutations present in a subset of anaplastic large cell lymphomas (ALCLs), non-small cell lung cancers (NSCLCs), and neuroblastomas appear to sensitize cancer cells to treatment with selective ALK kinase inhibitors.

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  • (PMID = 19393834.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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65. Lagarrigue F, Dupuis-Coronas S, Ramel D, Delsol G, Tronchère H, Payrastre B, Gaits-Iacovoni F: Matrix metalloproteinase-9 is upregulated in nucleophosmin-anaplastic lymphoma kinase-positive anaplastic lymphomas and activated at the cell surface by the chaperone heat shock protein 90 to promote cell invasion. Cancer Res; 2010 Sep 1;70(17):6978-87
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  • [Title] Matrix metalloproteinase-9 is upregulated in nucleophosmin-anaplastic lymphoma kinase-positive anaplastic lymphomas and activated at the cell surface by the chaperone heat shock protein 90 to promote cell invasion.
  • Many anaplastic large cell lymphomas (ALCL) express the chimeric oncogene NPM-ALK, which drives malignant transformation and invasion.
  • Accordingly, we found that 100% of a large panel of ALK(+) ALCL biopsies examined were also MMP-9(+), in contrast to only 36.3% of ALK(-) tumors.
  • Interestingly, the hyaluronan receptor CD44 acted as a docking surface for MMP-9 and the chaperone heat shock protein 90 on the cell surface, where MMP-9 was cleaved and activated.
  • Taken together, our observations strengthen the concept that chaperones have a major extracellular role in the regulation of protein activation status, and reveal new factors that are crucial for spreading and invasion of ALK(+) ALCL.
  • They also point out new factors crucial for ALK(+) ALCL.
  • [MeSH-major] HSP90 Heat-Shock Proteins / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Matrix Metalloproteinase 9 / biosynthesis. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Antigens, CD44 / metabolism. Cell Line, Tumor. Cell Membrane / metabolism. Dipeptides / pharmacology. Enzyme Activation. Enzyme Precursors / metabolism. Humans. Matrix Metalloproteinase Inhibitors. Neoplasm Invasiveness. Up-Regulation. rac1 GTP-Binding Protein / metabolism

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  • (PMID = 20699364.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / CD44 protein, human; 0 / Dipeptides; 0 / Enzyme Precursors; 0 / HSP90 Heat-Shock Proteins; 0 / Matrix Metalloproteinase Inhibitors; 0 / N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide; 0 / RAC1 protein, human; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.4.24.- / pro-matrix metalloproteinase 9; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.5.2 / rac1 GTP-Binding Protein
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66. Gertner J, Wiedemann A, Poupot M, Fournié JJ: Human gammadelta T lymphocytes strip and kill tumor cells simultaneously. Immunol Lett; 2007 May 15;110(1):42-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here we investigated this topic using the model of human gammadelta lymphocytes co-incubated with anaplastic large cell lymphomas, a group of tumors with cytolytic T or null lineage.
  • By using flow cytometry and live cell imaging, we show that as soon as both cells were in contact, the TCR-mediated activation of gammadelta lymphocytes simultaneously triggered their secretion of lytic granules and stripping of lymphoma cell membranes, and both activities continued even after their cell death.
  • However reciprocally in such conjugates, resistant lymphoma failed to strip gammadelta cells and to kill them by untargeted secretion of their own lytic granules.
  • This indicated that secretion of lytic granules and target membrane stripping are associated in lytic cell conjugates, and that gammadelta T lymphocytes strip and kill their targets simultaneously.
  • [MeSH-major] Cell Death / immunology. Cell Membrane / immunology. Lymphoma, Large B-Cell, Diffuse / immunology. T-Lymphocytes / immunology

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  • (PMID = 17451812.001).
  • [ISSN] 0165-2478
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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67. Bacchiocchi R, Baldanzi G, Carbonari D, Capomagi C, Colombo E, van Blitterswijk WJ, Graziani A, Fazioli F: Activation of alpha-diacylglycerol kinase is critical for the mitogenic properties of anaplastic lymphoma kinase. Blood; 2005 Sep 15;106(6):2175-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activation of alpha-diacylglycerol kinase is critical for the mitogenic properties of anaplastic lymphoma kinase.
  • Oncogenic rearrangements of the tyrosine kinase receptor anaplastic lymphoma kinase (ALK), most commonly represented by the nucleophosmin/ALK fusion protein (NPM/ALK), are involved in the pathogenesis of anaplastic large-cell lymphomas (ALCLs).
  • In an effort to identify new intracellular transducers operative in ALK-positive malignancies, we have investigated the potential involvement of diacylglycerol kinase (DGK).
  • Here we show that alphaDGK is constitutively activated in the NPM/ALK-positive ALCL-derived cell line Karpas 299 and in NPM/ALK-infected 32D hematopoietic cells.
  • In this cell system, we also show that ALK-mediated alphaDGK activation is dependent on p60src tyrosine kinase, with which alphaDGK forms a complex.
  • The specific inhibition of alphaDGK, obtained by cell treatment with R59949, significantly reduced cellular growth in all cell lines.
  • [MeSH-major] Cell Proliferation. Diacylglycerol Kinase / metabolism. Lymphoma, Large B-Cell, Diffuse / etiology. Protein-Tyrosine Kinases / physiology
  • [MeSH-minor] Cell Line. Enzyme Activation. Enzyme Inhibitors / pharmacology. Humans. Oncogene Protein pp60(v-src) / metabolism. RNA, Small Interfering / pharmacology. Receptor Protein-Tyrosine Kinases. Up-Regulation

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  • (PMID = 15928040.001).
  • [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 / Enzyme Inhibitors; 0 / RNA, Small Interfering; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.1.107 / Diacylglycerol Kinase; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Oncogene Protein pp60(v-src)
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68. Paolo C, Lucia F, Anna D: Hematopoietic stem cell transplantation in peripheral T-cell lymphomas. Leuk Lymphoma; 2007 Aug;48(8):1496-501
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematopoietic stem cell transplantation in peripheral T-cell lymphomas.
  • Peripheral T-cell lymphomas (PTCL) are a rare entity with a dismal outcome.
  • After conventional chemotherapy they showed a worse prognosis compared with B-cell non-Hodgkin's lymphoma (NHL), except for anaplastic lymphoma-kinase (ALK)-positive anaplastic large cell lymphomas (ALCL).
  • High-dose chemotherapy followed by autologous stem cell transplantation (SCT) has been evaluated in relapsed patients as well as in the upfront setting.
  • Available data showed an advantage for patients who received transplant as first line treatment whereas results of autografting at relapse have been satisfactory only for ALK-positive ALCLs compared to other PTCL subtypes.
  • Based upon preliminary results, allogeneic SCT can be also considered as an alternative strategy in these lymphomas.
  • Whether or not the postulated graft-versus-lymphoma effect may overcome the poor prognosis of T-cell NHL patients has to be established.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, T-Cell, Peripheral / therapy

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  • (PMID = 17701579.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 38
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69. Sasikala PS, Nirmala K, Sundersingh S, Mahji U, Rajkumar T: Frequency and distribution of Epstein-Barr virus infection and its association with P53 expression in a series of primary nodal non-Hodgkin lymphoma patients from South India. Int J Lab Hematol; 2010 Feb;32(1 Pt 2):56-64
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  • [Title] Frequency and distribution of Epstein-Barr virus infection and its association with P53 expression in a series of primary nodal non-Hodgkin lymphoma patients from South India.
  • This study investigated the prevalence of Epstein-Barr virus (EBV) infection and its association with P53 expression in a panel of 87 previously untreated nodal non-Hodgkin lymphomas (NHLs) from India.
  • EBV, predominantly type A strain, was detected in 27/87 (31%) nodal lymphoid malignancies, 11/46 diffuse large B-cell lymphomas, 6/17 follicular lymphoma, 4/6 anaplastic large cell lymphomas (ALCL), 5/11 peripheral T-cell lymphomas (PTCL) and 1/7 lymphoblastic lymphomas.
  • EBV infection was more frequently observed in a specific subset of nodal NHL, suggesting a causative role of EBV infection in the pathogenesis of ALCL and PTCL.
  • [MeSH-major] Epstein-Barr Virus Infections / metabolism. Gene Expression Regulation. Lymphoma, Non-Hodgkin. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19055647.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EBV-encoded nuclear antigen 1; 0 / Epstein-Barr Virus Nuclear Antigens; 0 / Tumor Suppressor Protein p53
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70. Webb TR, Slavish J, George RE, Look AT, Xue L, Jiang Q, Cui X, Rentrop WB, Morris SW: Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy. Expert Rev Anticancer Ther; 2009 Mar;9(3):331-56
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  • [Title] Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was initially identified in constitutively activated oncogenic fusion forms - the most common being nucleophosmin-ALK - in anaplastic large-cell lymphomas, and subsequent studies have identified ALK fusions in diffuse large B-cell lymphomas, systemic histiocytosis, inflammatory myofibroblastic tumors, esophageal squamous cell carcinomas and non-small-cell lung carcinomas.

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  • (PMID = 19275511.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA069129-10; United States / NCI NIH HHS / CA / R01 CA69129; United States / NCI NIH HHS / CA / R01 CA069129; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA069129-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 134034-50-7 / pleiotrophin; 137497-38-2 / midkine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 304
  • [Other-IDs] NLM/ NIHMS105118; NLM/ PMC2780428
  •  go-up   go-down


71. Bonvini P, Zorzi E, Mussolin L, Monaco G, Pigazzi M, Basso G, Rosolen A: The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity. Haematologica; 2009 Jul;94(7):944-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity.
  • BACKGROUND: The loss of cell cycle regulation due to abnormal function of cyclin-dependent kinases (cdk) occurs in tumors and leads to genetic instability of chemotherapy-resistant cells.
  • In this study, we investigated the effect of the cdk inhibitor flavopiridol in anaplastic large cell lymphomas, in which unrestrained proliferation depends on NPM-ALK tyrosine kinase activity.
  • DESIGN AND METHODS: Effects of flavopiridol were examined in ALK-positive and -negative anaplastic large cell lymphoma cells by means of immunoblotting and immunofluorescence analyses to assess cdk expression and activity, quantitative real time reverse transcriptase polymerase chain reaction to measure drug-induced changes in transcription, and FACS analyses to monitor changes in proliferation and survival.
  • RESULTS: Treatment with flavopiridol resulted in growth inhibition of anaplastic large cell lymphoma cells, along with accumulation of subG(1) cells and disappearance of S phase without cell cycle arrest.
  • This correlated with induction of cell death through rapid mitochondrial damage, inhibition of DNA synthesis, and down-regulation of anti-apoptotic proteins and transcripts.
  • Notably, flavopiridol was less active in ALK-positive cells, as apoptosis was observed at higher concentrations and later time points, and resistance to treatment was observed in cells maintaining NPM-ALK signaling.
  • NPM-ALK inhibition affected proliferation but not survival of anaplastic large cell lym-phoma cells, whereas it resulted in a dramatic increase in apoptosis when combined with flavopiridol.
  • CONCLUSIONS: This work provides the first demonstration that targeting cdk is effective against anaplastic large cell lymphoma cells, and proves the critical role of NPM-ALK in the regulation of responsiveness of tumor cells with cdk dysregulation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Flavonoids / pharmacology. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / drug therapy. Piperidines / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis. Bromodeoxyuridine / pharmacology. Cell Cycle. Cell Separation. Cell Survival. Dose-Response Relationship, Drug. Humans. Reverse Transcriptase Polymerase Chain Reaction. Subcellular Fractions. Time Factors


72. Staber PB, Vesely P, Haq N, Ott RG, Funato K, Bambach I, Fuchs C, Schauer S, Linkesch W, Hrzenjak A, Dirks WG, Sexl V, Bergler H, Kadin ME, Sternberg DW, Kenner L, Hoefler G: The oncoprotein NPM-ALK of anaplastic large-cell lymphoma induces JUNB transcription via ERK1/2 and JunB translation via mTOR signaling. Blood; 2007 Nov 1;110(9):3374-83
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The oncoprotein NPM-ALK of anaplastic large-cell lymphoma induces JUNB transcription via ERK1/2 and JunB translation via mTOR signaling.
  • Anaplastic large cell lymphomas (ALCLs) are highly proliferating tumors that commonly express the AP-1 transcription factor JunB.
  • ALK fusions occur in approximately 50% of ALCLs, and among these, 80% have the t(2;5) translocation with NPM-ALK expression.
  • We report greater activity of JunB in NPM-ALK-positive than in NPM-ALK-negative ALCLs.
  • Specific knockdown of JUNB mRNA using small interfering RNA and small hairpin RNA in NPM-ALK-expressing cells decreases cellular proliferation as evidenced by a reduced cell count in the G2/M phase of the cell cycle.
  • Both NPM-ALK-positive and -negative ALCL tumors demonstrate active ERK1/2 signaling.
  • In contrast to NPM-ALK-negative ALCL, the mTOR pathway is active in NPM-ALK-positive lymphomas.
  • Pharmacological inhibition of mTOR in NPM-ALK-positive cells down-regulates JunB protein levels by shifting JUNB mRNA translation from large polysomes to monosomes and ribonucleic particles (RNPs), and decreases cellular proliferation.
  • Thus, JunB is a critical target of mTOR and is translationally regulated in NPM-ALK-positive lymphomas.
  • In conjunction with NPM-ALK, JunB enhances cell cycle progression and may therefore represent a therapeutic target.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Protein Kinases / physiology. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins c-jun / genetics. Proto-Oncogene Proteins c-jun / metabolism. Transcriptional Activation


73. Galietta A, Gunby RH, Redaelli S, Stano P, Carniti C, Bachi A, Tucker PW, Tartari CJ, Huang CJ, Colombo E, Pulford K, Puttini M, Piazza RG, Ruchatz H, Villa A, Donella-Deana A, Marin O, Perrotti D, Gambacorti-Passerini C: NPM/ALK binds and phosphorylates the RNA/DNA-binding protein PSF in anaplastic large-cell lymphoma. Blood; 2007 Oct 1;110(7):2600-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM/ALK binds and phosphorylates the RNA/DNA-binding protein PSF in anaplastic large-cell lymphoma.
  • The oncogenic fusion tyrosine kinase nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) induces cellular transformation in anaplastic large-cell lymphomas (ALCLs) carrying the t(2;5) chromosomal translocation.
  • The interaction between NPM/ALK and PSF was dependent on an active ALK kinase domain and PSF was found to be tyrosine-phosphorylated in NPM/ALK-expressing cell lines and in primary ALK(+) ALCL samples.

  • Genetic Alliance. consumer health - Anaplastic Large Cell Lymphoma.
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  • (PMID = 17537995.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092318; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / CA92318
  • [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-Binding Proteins; 0 / PTB-associated splicing factor; 0 / RNA-Binding Proteins; 21820-51-9 / Phosphotyrosine; 63231-63-0 / RNA; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC1988934
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74. Sjostrom C, Seiler C, Crockett DK, Tripp SR, Elenitoba Johnson KS, Lim MS: Global proteome profiling of NPM/ALK-positive anaplastic large cell lymphoma. Exp Hematol; 2007 Aug;35(8):1240-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Global proteome profiling of NPM/ALK-positive anaplastic large cell lymphoma.
  • OBJECTIVE: Constitutive overexpression of nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) is a key oncogenic event in anaplastic large cell lymphomas (ALCL) that carry the t(2;5)(p23;q35) translocation.
  • Global proteomic analysis of NPM/ALK-positive ALCL would improve understanding of the disease pathogenesis and yield new candidate targets for novel treatment and diagnostic strategies.
  • MATERIALS AND METHODS: To comprehensively determine the inventory of proteins from NPM/ALK-positive ALCL SUDHL-1 cells, the membrane, cytoplasm, and nuclear subcellular fractions were resolved by one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS).
  • Extensive annotation and systematic examination of the literature for information on 209 representative proteins indicated that 19.9% were reported to be expressed in T cells and 44.7% were reported to have important function in cancers, while only 4.3% were reported to be involved in ALCL pathogenesis.
  • CONCLUSION: We present an extensive catalog of proteins expressed by NPM/ALK-positive ALCL.
  • This study illustrates the potential for novel pathogenetic discovery in NPM/ALK-positive ALCL and the utility of combining cellular subfractionation, 1D SDS-PAGE, and LC-MS/MS for the comprehensive protein analysis of lymphoma.
  • [MeSH-major] Gene Expression Profiling. Lymphoma, Large B-Cell, Diffuse / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proteome
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. Humans. Molecular Sequence Data. Neoplasm Proteins / genetics

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  • (PMID = 17560012.001).
  • [ISSN] 0301-472X
  • [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 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proteome; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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75. Loddenkemper C, Longerich T, Hummel M, Ernestus K, Anagnostopoulos I, Dienes HP, Schirmacher P, Stein H: Frequency and diagnostic patterns of lymphomas in liver biopsies with respect to the WHO classification. Virchows Arch; 2007 May;450(5):493-502
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  • [Title] Frequency and diagnostic patterns of lymphomas in liver biopsies with respect to the WHO classification.
  • However, the applicability of this classification to a representative number of hepatic lymphomas in liver biopsy specimens has not yet been investigated.
  • The frequency and infiltration pattern of a series of 205 liver biopsies with lymphoma manifestations was analyzed with the aid of immunohistochemical and molecular pathological analyses.
  • Diffuse large B-cell lymphoma (DLBCL) was by far the most frequent entity, comprising 45% of the cases analyzed.
  • Using a previously published immunohistochemical algorithm, 35% of 80 DLBCL were assigned to a germinal center B-cell-like (GCB) and 65% to a non-GCB group.
  • Most B-cell lymphoma entities involving the liver revealed a characteristic infiltration pattern.
  • Diagnostically challenging entities were T-cell-rich B-cell lymphomas, anaplastic large cell lymphomas and peripheral T-cell lymphomas, which frequently required additional molecular clonality assessment.
  • Overall, the percentage of T-cell lymphomas in the liver (12%) was higher as compared to other extranodal sites except for the skin and the small intestine.
  • This study provides relevant data on the distribution of hepatic lymphomas and demonstrates the applicability of the WHO classification proposing a diagnostic algorithm for liver biopsies.
  • [MeSH-major] Liver Neoplasms / pathology. Lymphoma / pathology

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  • (PMID = 17431676.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC1888718
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76. Wu F, Wang P, Young LC, Lai R, Li L: Proteome-wide identification of novel binding partners to the oncogenic fusion gene protein, NPM-ALK, using tandem affinity purification and mass spectrometry. Am J Pathol; 2009 Feb;174(2):361-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), an oncogenic fusion gene protein that is characteristically found in a subset of anaplastic large cell lymphomas, promotes tumorigenesis through its functional and physical interactions with various biologically important proteins.
  • For the first time, we performed a proteome-wide identification of NPM-ALK-binding proteins using tandem affinity purification and a highly sensitive mass spectrometric technique.
  • [MeSH-minor] Amino Acid Sequence. Blotting, Western. Carrier Proteins / metabolism. Cell Line. Humans. Immunoprecipitation. Molecular Sequence Data. Reproducibility of Results. Sensitivity and Specificity. Tandem Mass Spectrometry. Transfection

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  • (PMID = 19131589.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC2630546
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77. Chow L, Lai R, Dabbagh L, Belch A, Young JD, Cass CE, Mackey JR: Analysis of human equilibrative nucleoside transporter 1 (hENT1) protein in non-Hodgkin's lymphoma by immunohistochemistry. Mod Pathol; 2005 Apr;18(4):558-64
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  • [Title] Analysis of human equilibrative nucleoside transporter 1 (hENT1) protein in non-Hodgkin's lymphoma by immunohistochemistry.
  • Since some nucleoside analogs have a role in treating patients with non-Hodgkin's lymphoma (NHL), this study was undertaken to assess hENT1 abundance in NHL.
  • Samples were considered positive when >or=50% of neoplastic cells showed immunostaining.
  • In NHL, a relatively high frequency of hENT1 positivity was found in Burkitt lymphoma/leukemia (63%), diffuse large B-cell lymphoma (DLCL; 45%), and follicular lymphoma (40%).
  • In DLCL, 26% of cases were positive for CD10, and CD10-positive DLCL cases were more likely to be hENT1 positive than CD10-negative cases (P=0.025).
  • A lower frequency of hENT1 positivity was found in mantle cell lymphoma (13%) and peripheral T-cell lymphomas (37%).
  • All marginal zone lymphomas (n=5), chronic lymphocytic leukemia small lymphocytic lymphomas (n=10), plasmacytoma (n=3), acute lymphoblastic lymphoma/leukemia, and anaplastic large-cell lymphomas (n=5) were negative.
  • [MeSH-major] Equilibrative Nucleoside Transporter 1 / analysis. Lymphoma, Non-Hodgkin / pathology

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  • (PMID = 15529184.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Equilibrative Nucleoside Transporter 1; 0 / SLC29A1 protein, human; EC 3.4.24.11 / Neprilysin
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78. Fernandez-Vidal A, Mazars A, Gautier EF, Prévost G, Payrastre B, Manenti S: Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation. Cell Cycle; 2009 May 1;8(9):1373-9
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  • [Title] Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation.
  • Here, we demonstrate that the expression of the dual specificity phosphatase CDC25A, a key regulator of cell cycle progression, is deregulated in Ba/F3 cells expressing the oncogenic protein NPM/ALK and in human cell lines derived from NPM/ALK-positive anaplastic large cell lymphomas (ALCL).
  • Altogether, our data point to the functional link between hematopoietic oncogenic tyrosine kinases and the G(1) cell cycle regulator CDC25A, and we propose that this protein may be a potential therapeutic target in ALCL and other hematological malignancies.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / pathology. Oncogenes. Protein-Tyrosine Kinases / metabolism. Up-Regulation. cdc25 Phosphatases / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. Oncogene Proteins, Fusion / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction

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  • (PMID = 19305144.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.16 / Cdc25a protein, mouse; EC 3.1.3.48 / CDC25A protein, human; EC 3.1.3.48 / cdc25 Phosphatases
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79. Ambrogio C, Voena C, Manazza AD, Piva R, Riera L, Barberis L, Costa C, Tarone G, Defilippi P, Hirsch E, Boeri Erba E, Mohammed S, Jensen ON, Palestro G, Inghirami G, Chiarle R: p130Cas mediates the transforming properties of the anaplastic lymphoma kinase. Blood; 2005 Dec 1;106(12):3907-16
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  • [Title] p130Cas mediates the transforming properties of the anaplastic lymphoma kinase.
  • Translocations of the anaplastic lymphoma kinase (ALK) gene have been described in anaplastic large-cell lymphomas (ALCLs) and in stromal tumors.
  • Along with transformation, NPM-ALK induces morphologic changes in fibroblasts and lymphoid cells, suggesting a direct role of ALK in cell shaping.
  • In 293 cells and in fibroblasts as well as in human ALK-positive lymphoma cell lines, NPM-ALK was able to bind p130Cas and to induce its phosphorylation.
  • Finally, p130Cas-/- (also known as Bcar1-/-) fibroblasts expressing NPM-ALK showed impaired actin filament depolymerization and were no longer transformed compared with wild-type cells, indicating an essential role of p130Cas activation in ALK-mediated transformation.

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  • (PMID = 16105984.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [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 / Crk-Associated Substrate Protein; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC1895100
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80. Dunphy CH, DeMello DE, Gale GB: Pediatric CD56+ anaplastic large cell lymphoma: a review of the literature. Arch Pathol Lab Med; 2006 Dec;130(12):1859-64
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  • [Title] Pediatric CD56+ anaplastic large cell lymphoma: a review of the literature.
  • CONTEXT: Anaplastic large cell lymphomas (ALCLs) are a heterogeneous group of CD30+ large cell lymphomas that, according to the World Health Organization classification, are defined as being of T-cell origin, based on immunophenotype, and/or the finding of a T-cell gene rearrangement by molecular studies.
  • Relatively recent data have suggested that some T-cell ALCLs are derived from cytolytic CD4+ cells, gammadelta T cells, or natural killer-like (CD56+ or CD57+) T cells.
  • We encountered a pediatric case of CD56+, anaplastic lymphoma kinase-positive ALCL of apparent natural killer-like T-cell origin (showing positivity for CD2, cytoplasmic CD3, surface CD3 partial positivity, CD7, CD8, CD56, TIA-1, and granzyme B).
  • OBJECTIVE: To review the current pediatric literature regarding the incidence, differential diagnosis, and clinical course of such cases.
  • CONCLUSIONS: Our review did not confirm a uniformly aggressive clinical course in pediatric cases of CD56+ ALCLs.
  • Such cases suggest the usefulness of the analysis of CD56-positivity in additional cases of ALCL in an attempt to accrue additional information on this condition.
  • [MeSH-major] Antigens, CD56 / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism

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  • (PMID = 17149964.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56
  • [Number-of-references] 22
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81. Perez-Pinera P, Zhang W, Chang Y, Vega JA, Deuel TF: Anaplastic lymphoma kinase is activated through the pleiotrophin/receptor protein-tyrosine phosphatase beta/zeta signaling pathway: an alternative mechanism of receptor tyrosine kinase activation. J Biol Chem; 2007 Sep 28;282(39):28683-90
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  • [Title] Anaplastic lymphoma kinase is activated through the pleiotrophin/receptor protein-tyrosine phosphatase beta/zeta signaling pathway: an alternative mechanism of receptor tyrosine kinase activation.
  • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (RTK) first discovered as the constitutively active nucleophosmin-ALK oncoprotein in anaplastic large cell lymphomas (ALCL).
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Differentiation / physiology. Enzyme Activation / drug effects. Enzyme Activation / physiology. HeLa Cells. Humans. Ligands. Neoplasms / metabolism. Phosphorylation / drug effects. Receptor Protein-Tyrosine Kinases. Receptor-Like Protein Tyrosine Phosphatases, Class 5

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  • (PMID = 17681947.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 2 T32 DK007022-26; United States / NCI NIH HHS / CA / CA84400
  • [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 / Carrier Proteins; 0 / Cytokines; 0 / Ligands; 134034-50-7 / pleiotrophin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.1.3.48 / PTPRZ1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 5
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82. Kansal R, Sait SN, Block AW, Ward PM, Kelly FL, Cheney RT, Czuczman M, Brecher ML, Barcos M: Extra copies of chromosome 2 are a recurring aberration in ALK-negative lymphomas with anaplastic morphology. Mod Pathol; 2005 Feb;18(2):235-43
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  • [Title] Extra copies of chromosome 2 are a recurring aberration in ALK-negative lymphomas with anaplastic morphology.
  • The purpose of this study was to evaluate fluorescence in situ hybridization abnormalities of the 2p23 anaplastic lymphoma kinase (ALK) gene loci in lymphomas with anaplastic morphology.
  • We studied 24 anaplastic large cell lymphomas (ALCL) classified by World Health Organization criteria [17 primary nodal/systemic (10 ALK+, 7 ALK-), seven primary cutaneous], and 17 additional non-Hodgkin's lymphomas [one ALK+ B-lineage lymphoma, 14 ALK- diffuse large B-cell lymphomas (seven anaplastic variants, five nonanaplastic, two secondary CD30+), two follicular lymphomas].
  • ALK- lymphomas with anaplastic morphology showed extra nonrearranged anaplastic lymphoma kinase gene loci (P=0.004) due to trisomy 2 irrespective of the following factors: B or T/null phenotype (P=0.315), diagnostic categories of systemic or cutaneous ALCL or the above-mentioned B-cell lymphomas (P=0.131), and CD30 positivity by immunohistochemistry (P=1.000).
  • Trisomy 2 was absent in all ALK+ lymphomas (P=0.009), which showed rearranged ALK gene loci (P<0.001).
  • Whether trisomy 2 is a primary or secondary event that leads to ALK- lymphomas cannot be determined from this study.
  • Its presence in secondary B-cell lymphomas suggests that trisomy 2 may be a secondary cytogenetic aberration in lymphomas in general.
  • Further investigation of this finding is necessary to further our understanding of the heterogeneous group of ALK- lymphomas.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 2 / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Antigens, CD15 / analysis. Antigens, CD30 / analysis. Child. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology. Male. Mucin-1 / analysis. Receptor Protein-Tyrosine Kinases. Statistics as Topic

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  • (PMID = 15475930.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD15; 0 / Antigens, CD30; 0 / Mucin-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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83. Heerema NA, Bernheim A, Lim MS, Look AT, Pasqualucci L, Raetz E, Sanger WG, Cairo MS: State of the Art and Future Needs in Cytogenetic/Molecular Genetics/Arrays in childhood lymphoma: summary report of workshop at the First International Symposium on childhood and adolescent non-Hodgkin lymphoma, April 9, 2003, New York City, NY. Pediatr Blood Cancer; 2005 Oct 15;45(5):616-22
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  • [Title] State of the Art and Future Needs in Cytogenetic/Molecular Genetics/Arrays in childhood lymphoma: summary report of workshop at the First International Symposium on childhood and adolescent non-Hodgkin lymphoma, April 9, 2003, New York City, NY.
  • BACKGROUND: A significant number of studies describe the cytogenetics and molecular genetics of adult non-Hodgkin lymphoma (NHL); however, similar knowledge is lacking regarding pediatric NHL.
  • METHODS: A workshop to discuss the "State of the Art and Future Needs in Cytogenetic/Molecular Genetics/Arrays" in pediatric NHL was held in conjunction with the First International Symposium on Childhood and Adolescent Non-Hodgkin Lymphoma on April 9, 2003 in New York City.
  • RESULTS: Cytogenetic characteristics of pediatric NHL include 14q11.2 rearrangements in T-cell lymphoblastic leukemia/lymphomas (LBL), ALK rearrangements in anaplastic large cell lymphomas (ALCL), and CMYC translocations in both Burkitt and Burkitt-like lymphomas (BL/BLL).
  • Pediatric diffuse large B-cell lymphoma (DLBCL) is cytogenetically different from DLBCL in adults, suggesting a different disease in children.
  • Microarray studies demonstrate three types of T-cell leukemia, the leukemic counterpart of LBL, that block T-cell differentiation at different stages of T-cell development, corresponding to LYL, TAL1, and HOX-expressing leukemias.
  • ALCL cell lines have a unique expression profile compared to normal T-cells.
  • Germinal centers of BL have CMYC expression signatures, indicating that CMYC expression is ectopic and does not reflect the physiology of the normal cell counterpart.
  • A greater understanding of pediatric NHL will lead to disease-specific and patient-individualized therapies of these diseases.
  • [MeSH-major] Lymphoma, Non-Hodgkin / genetics
  • [MeSH-minor] Adolescent. Basic Helix-Loop-Helix Transcription Factors. Burkitt Lymphoma / genetics. Child. Cytogenetic Analysis. DNA-Binding Proteins / genetics. Gene Rearrangement. Homeodomain Proteins / genetics. Humans. Intracellular Signaling Peptides and Proteins. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Microarray Analysis. Molecular Biology. Neoplasm Proteins / genetics. Oncogene Proteins / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16127683.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R13-CA10195-01
  • [Publication-type] Congresses; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / LYL1 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / STIL protein, human; 0 / TLX3 protein, human
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84. Mino-Kenudson M, Chirieac LR, Law K, Hornick JL, Lindeman N, Mark EJ, Cohen DW, Johnson BE, Jänne PA, Iafrate AJ, Rodig SJ: A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry. Clin Cancer Res; 2010 Mar 1;16(5):1561-71
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  • In the present study, we used novel antibodies to compare ALK protein expression in genetically defined lung cancers and anaplastic large cell lymphomas.
  • RESULTS: ALK protein is invariably and exclusively expressed in ALK-rearranged lung adenocarcinomas but at much lower levels than in the prototypic ALK-rearranged tumor, anaplastic large cell lymphoma, and as a result, is often not detected by conventional IHC.

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  • (PMID = 20179225.001).
  • [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 / P20 CA090578; United States / NCI NIH HHS / CA / CA090578; United States / NCI NIH HHS / CA / CA136851-01A1; United States / NCI NIH HHS / CA / R01 CA136851-01A1; United States / NCI NIH HHS / CA / R01CA136851; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R01 CA114465; United States / NCI NIH HHS / CA / R01 CA136851
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ NIHMS170973; NLM/ PMC2831135
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85. Voena C, Conte C, Ambrogio C, Boeri Erba E, Boccalatte F, Mohammed S, Jensen ON, Palestro G, Inghirami G, Chiarle R: The tyrosine phosphatase Shp2 interacts with NPM-ALK and regulates anaplastic lymphoma cell growth and migration. Cancer Res; 2007 May 1;67(9):4278-86
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  • [Title] The tyrosine phosphatase Shp2 interacts with NPM-ALK and regulates anaplastic lymphoma cell growth and migration.
  • Anaplastic large cell lymphomas (ALCL) are mainly characterized by the reciprocal translocation t(2;5)(p23;q35) that involves the anaplastic lymphoma kinase (ALK) gene and generates the fusion protein NPM-ALK with intrinsic tyrosine kinase activity.
  • NPM-ALK triggers several signaling cascades, leading to increased cell growth, resistance to apoptosis, and changes in morphology and migration of transformed cells.
  • We found that NPM-ALK was able to bind Shp2 in coprecipitation experiments and to induce its phosphorylation in the tyrosine residues Y542 and Y580 both in HEK293 cells and ALCL cell lines.
  • In primary lymphomas, antibodies against the phosphorylated tyrosine Y542 of Shp2 mainly stained ALK-positive cells.
  • In ALCL cell lines, Shp2-constitutive phosphorylation was dependent on NPM-ALK, as it significantly decreased after short hairpin RNA (shRNA)-mediated NPM-ALK knock down.
  • Shp2 knock down by specific shRNA decreased the phosphorylation of extracellular signal-regulated kinase 1/2 and of the tyrosine residue Y416 in the activation loop of Src, resulting in impaired ALCL cell proliferation and growth disadvantage.
  • Finally, migration of ALCL cells was reduced by Shp2 shRNA.
  • These findings show a direct involvement of Shp2 in NPM-ALK lymphomagenesis, highlighting its critical role in lymphoma cell proliferation and migration.
  • [MeSH-major] Cell Movement / physiology. Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Amino Acid Sequence. Apoptosis / physiology. Cell Growth Processes / physiology. Down-Regulation. Enzyme Activation. GRB2 Adaptor Protein / metabolism. Humans. K562 Cells. Mass Spectrometry. Molecular Sequence Data. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 11. RNA, Small Interfering / genetics. SH2 Domain-Containing Protein Tyrosine Phosphatases. Transfection

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  • [ErratumIn] Cancer Res. 2016 Mar 15;76(6):1669 [26979794.001]
  • (PMID = 17483340.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [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 / GAB2 protein, human; 0 / GRB2 Adaptor Protein; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / SH2 Domain-Containing Protein Tyrosine Phosphatases
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86. Meier C, Hoeller S, Bourgau C, Hirschmann P, Schwaller J, Went P, Pileri SA, Reiter A, Dirnhofer S, Tzankov A: Recurrent numerical aberrations of JAK2 and deregulation of the JAK2-STAT cascade in lymphomas. Mod Pathol; 2009 Mar;22(3):476-87
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  • [Title] Recurrent numerical aberrations of JAK2 and deregulation of the JAK2-STAT cascade in lymphomas.
  • The presence of JAK2 mutations in lymphomas has been addressed in larger cohorts, but there are little systemic data on numerical and structural JAK2 aberrations in lymphoid neoplasms.
  • To study the molecular epidemiology of these aberrations and the consecutive activation of the JAK2-STAT pathway in lymphomas, we examined 527 cases, covering the most common entities, in a tissue microarray by fluorescent in situ hybridization with breakable JAK2 probes, and immunohistochemistry for phosphorylated JAK2 (pJAK2) and its preferred downstream pSTAT3 and pSTAT5.
  • 9p24 gains were detected in 6/17 (35%) primary mediastinal B-cell lymphomas (PMBCLs), 25/77 (33%) Hodgkin's lymphomas (HLs), 3/16 (19%) angioimmunoblastic T-cell lymphomas (AILTs) and 1/5 ALK1(+) anaplastic large cell lymphomas (ALCLs); breaks were observed only in three cases. pJAK2 expression was most prevalent in PMBCL, peripheral T-cell lymphomas and HL. pSTAT3 predominated in ALCLs, HLs, AILTs, PMBCLs and peripheral T-cell lymphomas. pSTAT5 expression was detected frequently in follicular lymphomas, diffuse large B-cell lymphomas and AILTs.
  • In follicular lymphomas, concomitant expression of pJAK2 and pSTAT5 was linked to better prognosis, whereas expression of pSTAT3 in nongerminal center-like diffuse large B-cell lymphomas could identify a patient group with an inferior outcome.
  • Our findings stress that despite the rarity of activating JAK2 mutations in lymphomas, JAK2 is recurrently targeted by numerical, and rarely by structural, genetic aberrations in distinct lymphoma subtypes and that JAK2-STAT pathway may play a role in lymphomagenesis.
  • [MeSH-major] Janus Kinase 2 / genetics. Lymphoma / genetics. Lymphoma / metabolism. STAT Transcription Factors / metabolism. Signal Transduction / physiology

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  • (PMID = 19136931.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT Transcription Factors; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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87. Akimzhanov A, Krenacs L, Schlegel T, Klein-Hessling S, Bagdi E, Stelkovics E, Kondo E, Chuvpilo S, Wilke P, Avots A, Gattenlöhner S, Müller-Hermelink HK, Palmetshofer A, Serfling E: Epigenetic changes and suppression of the nuclear factor of activated T cell 1 (NFATC1) promoter in human lymphomas with defects in immunoreceptor signaling. Am J Pathol; 2008 Jan;172(1):215-24
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  • [Title] Epigenetic changes and suppression of the nuclear factor of activated T cell 1 (NFATC1) promoter in human lymphomas with defects in immunoreceptor signaling.
  • The nuclear factor of activated T cell 1 (Nfatc1) locus is a common insertion site for murine tumorigenic retroviruses, suggesting a role of transcription factor NFATc1 in lymphomagenesis.
  • Although NFATc1 is expressed in most human primary lymphocytes and mature human T- and B-cell neoplasms, we show by histochemical stainings that NFATc1 expression is suppressed in anaplastic large cell lymphomas and classical Hodgkin's lymphomas (HLs).
  • In HL cell lines, NFATc1 silencing correlated with a decrease in histone H3 acetylation, H3-K4 trimethylation, and Sp1 factor binding but with an increase in HP1 binding to the NFATC1 P1 promoter.
  • Together with DNA hypermethylation of the NFATC1 P1 promoter, which we detected in all anaplastic large cell lymphoma and many HL lines, these observations reflect typical signs of transcriptional silencing.
  • In several lymphoma lines, methylation of NFATC1 promoter DNA resulted in a "window of hypomethylation," which is flanked by Sp1-binding sites.
  • [MeSH-minor] Animals. DNA Methylation. Histones / metabolism. Hodgkin Disease / metabolism. Humans. Immunohistochemistry / methods. Mice. Signal Transduction. Sp1 Transcription Factor / metabolism. Transcription, Genetic

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  • (PMID = 18156209.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 0 / NFATC Transcription Factors; 0 / NFATC1 protein, human; 0 / Nfatc1 protein, mouse; 0 / Sp1 Transcription Factor
  • [Other-IDs] NLM/ PMC2189623
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88. McDermott U, Iafrate AJ, Gray NS, Shioda T, Classon M, Maheswaran S, Zhou W, Choi HG, Smith SL, Dowell L, Ulkus LE, Kuhlmann G, Greninger P, Christensen JG, Haber DA, Settleman J: Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors. Cancer Res; 2008 May 1;68(9):3389-95
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  • [Title] Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors.
  • We have established an automated platform for examining the sensitivity to various molecularly targeted inhibitors across a large panel of human tumor-derived cell lines to identify additional genotype-correlated responses that may be clinically relevant.
  • Among the inhibitors tested in a panel of 602 cell lines derived from a variety of human cancers, we found that a selective inhibitor of the anaplastic lymphoma kinase (ALK) potently suppressed growth of a small subset of tumor cells.
  • This subset included lines derived from anaplastic large cell lymphomas, non-small-cell lung cancers, and neuroblastomas.
  • ALK is a receptor tyrosine kinase that was first identified as part of a protein fusion derived from a chromosomal translocation detected in the majority of anaplastic large cell lymphoma patients, and has recently been implicated as an oncogene in a small fraction of non-small-cell lung cancers and neuroblastomas.
  • Significantly, sensitivity in these cell lines was well correlated with specific ALK genomic rearrangements, including chromosomal translocations and gene amplification.
  • Moreover, in such cell lines, ALK kinase inhibition can lead to potent suppression of downstream survival signaling and an apoptotic response.
  • These findings suggest that a subset of lung cancers, lymphomas, and neuroblastomas that harbor genomic ALK alterations may be clinically responsive to pharmacologic ALK inhibition.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzimidazoles / therapeutic use. Cell Line, Tumor. Cytogenetic Analysis. Drug Evaluation, Preclinical. Gene Amplification / physiology. Genomic Instability / drug effects. Humans. Mutation. Protein Kinase Inhibitors / therapeutic use. Pyridones / therapeutic use. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 18451166.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA115830; United States / NCI NIH HHS / CA / R01 CA115830
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BMS 536924; 0 / Benzimidazoles; 0 / NVP-TAE684; 0 / Protein Kinase Inhibitors; 0 / Pyridones; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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89. Cussac D, Pichereaux C, Colomba A, Capilla F, Pont F, Gaits-Iacovoni F, Lamant L, Espinos E, Burlet-Schiltz O, Monsarrat B, Delsol G, Payrastre B: Proteomic analysis of anaplastic lymphoma cell lines: identification of potential tumour markers. Proteomics; 2006 May;6(10):3210-22
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  • [Title] Proteomic analysis of anaplastic lymphoma cell lines: identification of potential tumour markers.
  • Anaplastic large-cell lymphomas (ALCL) are high grade lymphomas of T or null phenotype often associated with the t(2;5) translocation leading to the expression of a chimeric protein consisting of the N-terminal portion of nucleophosmin (NPM) and the intracellular domain of the anaplastic lymphoma kinase (ALK).
  • Although ALCL are recognized as distinct clinical, biological and cytogenetic entities, heterogeneities persist in this group of tumours, which exhibit a broad spectrum of morphological features.
  • Particularly, the common type tumour consisting in large cells contrast with the small cell variant that is sometimes associated with a leukemic phase.
  • The ALK-negative ALCL is often associated with a poor prognosis.
  • Here, we investigated the proteome of these subtypes of tumours using patient-derived cell lines.
  • We compared the proteome of the cytosolic fraction of NPM-ALK-positive versus NPM-ALK-negative cells on one hand, and the proteome of common cell type versus small cell variant on the other hand.
  • The identification of a set of proteins differentially expressed in the subtypes of ALCL points to new diagnosis/prognosis markers.
  • This study also provides interesting information on the molecular mechanisms responsible for the different subtypes of ALCL.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Lymphoma, Large B-Cell, Diffuse / metabolism. Proteome / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Cytosol / metabolism. Electrophoresis, Gel, Two-Dimensional. Humans. Immunohistochemistry. Nuclear Proteins / biosynthesis. Phenotype. Prognosis. Protein-Tyrosine Kinases / biosynthesis. Receptor Protein-Tyrosine Kinases. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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  • (PMID = 16596703.001).
  • [ISSN] 1615-9853
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Proteome; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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90. Bu X, Zheng Z, Wang C, Yu Y: Significance of C4d deposition in the follicular lymphoma and MALT lymphoma and their relationship with follicular dendritic cells. Pathol Res Pract; 2007;203(3):163-7
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  • [Title] Significance of C4d deposition in the follicular lymphoma and MALT lymphoma and their relationship with follicular dendritic cells.
  • We evaluated the deposition of C4d in follicular lymphomas (FL) and extranodal marginal zone B-cell lymphomas of mucosa-associated lymphoid tissue (MALT lymphoma).
  • Deposition of C4d was detected in 118 lymphoma tissues from patients with lymphoma and in 20 reactive hyperplasia lymphadens (RHL) using immunohistochemistical methods.
  • FL, MALT lymphoma, and RHL were studied using double staining for CD35/C4d and Bcl-2/C4d.
  • There was no significant difference between the positive ratio of C4d and the grades of FL.
  • We studied 12 MALT lymphoma tissues, six of which displayed C4d deposition.
  • There was no C4d deposition in diffuse large B-cell lymphomas, mantle cell lymphomas, B-small lymphocytic lymphomas, T-lymphoblastic lymphomas, peripheral T-cell lymphomas, and anaplastic large cell lymphomas.
  • C4d deposition in partially colonized follicles of MALT lymphoma was completely different from that in neoplastic follicles of FL, forming a key point for differential diagnosis.
  • [MeSH-major] Complement C4b / analysis. Dendritic Cells, Follicular / immunology. Lymphoma, B-Cell, Marginal Zone / immunology. Lymphoma, Follicular / immunology. Peptide Fragments / analysis. Pseudolymphoma / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Immunohistochemistry / methods. Male. Middle Aged. Neoplasm Staging. Proto-Oncogene Proteins c-bcl-2 / analysis. Receptors, Complement 3b / analysis

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  • (PMID = 17307308.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Complement 3b; 80295-50-7 / Complement C4b; 80295-52-9 / complement C4d
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91. Schlaf G, Altermann WW, Rothhoff A, Seliger B: Soluble CD30 serum level--an adequate marker for allograft rejection of solid organs? Histol Histopathol; 2007 11;22(11):1269-79
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  • [Title] Soluble CD30 serum level--an adequate marker for allograft rejection of solid organs?
  • The CD30 molecule, a 120 kDa cell surface glycoprotein, is a member of the tumor necrosis factor receptor (TNF-R) superfamily and was originally identified on the surface of Reed-Sternberg cells and anaplastic large cell lymphomas in Hodgkin's disease patients.
  • In addition to lymphoproliferative disorders the expression of CD30 was found in both activated CD8+ and CD4+ Th2 cells which lead to the activation of B-cells and consequently to the inhibition of the Th1-type cellular immunity.
  • The membrane-bound CD30 molecule can be proteolytically cleaved, thereby generating a soluble form (sCD30) of about 85 kDa.
  • Low serum levels of soluble CD30 were found in healthy humans, whereas increased sCD30 serum concentrations were detected under pathophysiological situations such as systemic lupus erythematosus, rheumatoid arthritis, certain viral infections and adult T cell leukaemia/lymphoma.
  • [MeSH-major] Antigens, CD30 / blood. Biomarkers / blood. Graft Rejection / blood. Graft Rejection / diagnosis. Monitoring, Immunologic / methods. Organ Transplantation

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  • (PMID = 17647199.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers
  • [Number-of-references] 76
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92. Jiang L, Yuan CM, Hubacheck J, Janik JE, Wilson W, Morris JC, Jasper GA, Stetler-Stevenson M: Variable CD52 expression in mature T cell and NK cell malignancies: implications for alemtuzumab therapy. Br J Haematol; 2009 Apr;145(2):173-9
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  • [Title] Variable CD52 expression in mature T cell and NK cell malignancies: implications for alemtuzumab therapy.
  • The anti-CD52 antibody alemtuzumab has been explored as a novel targeted therapy in T cell malignancies.
  • To assess the suitability of alemtuzumab therapy, we carried out a comprehensive study of CD52 expression using flow cytometry (FC) in 78 untreated patients diagnosed with mature T/natural killer (NK) cell neoplasms, including 34 adult T cell leukaemia/lymphomas (ATLL), two anaplastic large cell lymphomas (ALCL), three angioimmunoblastic T cell lymphomas (AITL), 16 cutaneous T cell lymphomas (CTCL), four extra-nodal T/NK cell lymphomas (ENT/NKCL), four hepatosplenic T cell lymphomas (HSTCL), 13 peripheral T cell lymphomas, not otherwise specified (PTCL-NOS) and two T-prolymphocytic leukaemia (T-PLL).
  • All AITL, HSTCL and T-PLL cases were CD52-positive and the frequency of CD52 expression was high in PTCL-NOS (92.3%), ATLL (94.1%) and CTCL (87.5%), implying a rational role for alemtuzumab in the treatment of these diseases; however, CD52 expression was low in ALCL (50%) and ENT/NKCL (25%).
  • FC testing for cell surface expression of CD52 is indicated in patients with T/NK cell malignancies being considered for alemtuzumab therapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / analysis. Antigens, Neoplasm / analysis. Antineoplastic Agents / therapeutic use. Glycoproteins / analysis. Lymphoma, T-Cell / immunology
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antigens, CD30 / analysis. Case-Control Studies. Flow Cytometry / methods. Humans. Immunophenotyping / methods. Killer Cells, Natural / immunology. Lymphoma, Extranodal NK-T-Cell / immunology. Prospective Studies. T-Lymphocytes / immunology. Treatment Failure

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  • (PMID = 19236377.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC011104-01
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, CD30; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ NIHMS416345; NLM/ PMC3487105
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93. Allouche M: ALK is a novel dependence receptor: potential implications in development and cancer. Cell Cycle; 2007 Jul 1;6(13):1533-8
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  • ALK (anaplastic lymphoma kinase) is a transmembrane receptor tyrosine kinase, initially discovered as part of the NPM-ALK fusion protein, resulting from a chromosomal rearrangement frequently associated with anaplastic large cell lymphomas.
  • However, an excessive or constitutive ALK tyrosine kinase activation can lead to deregulation of cell proliferation and survival, therefore to human cancers such as lymphomas and inflammatory myofibroblastic tumors.
  • Our observations could have important implications in the therapy of ALK-positive tumors harboring the chimeric or wild type ALK protein.
  • [MeSH-minor] Animals. Apoptosis / genetics. Cell Survival. Humans. Ligands. Models, Biological. Receptor Protein-Tyrosine Kinases. Signal Transduction

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  • (PMID = 17611412.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 61
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94. Pao-Chun L, Chan PM, Chan W, Manser E: Cytoplasmic ACK1 interaction with multiple receptor tyrosine kinases is mediated by Grb2: an analysis of ACK1 effects on Axl signaling. J Biol Chem; 2009 Dec 11;284(50):34954-63
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  • ACK1 (activated Cdc42-associated kinase 1), a cytoplsmic tyrosine kinase, is implicated in metastatic behavior, cell spreading and migration, and epidermal growth factor receptor (EGFR) signaling.
  • The function of ACK1 in the regulation of receptor tyrosine kinases requires a C-terminal region that demonstrates a significant homology to the EGFR binding domain of MIG6.
  • In this study, we have identified additional receptor tyrosine kinases, including Axl, leukocyte tyrosine kinase, and anaplastic lymphoma kinase, that can bind to the ACK1/MIG6 homology region.
  • The ability of ACK1 to modulate Axl and perhaps anaplastic lymphoma kinase (altered in anaplastic large cell lymphomas) might explain why ACK1 can promote metastatic and transformed behavior in a number of cancers.
  • [MeSH-minor] Amino Acid Sequence. Animals. COS Cells. Cell Membrane / metabolism. Cell Movement. Cercopithecus aethiops. Humans. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Molecular Sequence Data. Phylogeny. Proto-Oncogene Proteins. RNA Interference. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Sequence Alignment

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  • (PMID = 19815557.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GRB2 Adaptor Protein; 0 / Intercellular Signaling Peptides and Proteins; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 0 / growth arrest-specific protein 6; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / axl receptor tyrosine kinase; EC 2.7.10.2 / TNK2 protein, human
  • [Other-IDs] NLM/ PMC2787358
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95. Feldman AL, Law M, Remstein ED, Macon WR, Erickson LA, Grogg KL, Kurtin PJ, Dogan A: Recurrent translocations involving the IRF4 oncogene locus in peripheral T-cell lymphomas. Leukemia; 2009 Mar;23(3):574-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent translocations involving the IRF4 oncogene locus in peripheral T-cell lymphomas.
  • In contrast to myeloid and B-cell neoplasms, translocations in peripheral T-cell lymphomas (PTCLs) are poorly understood.
  • IRF4 translocations exist in myeloma and some B-cell lymphomas, but have not been reported earlier in PTCLs.
  • Two cases with t(6;14)(p25;q11.2) had translocations between IRF4 and the T-cell receptor-alpha (TCRA) locus.
  • In total, 8 of the remaining 10 cases were cutaneous anaplastic large-cell lymphomas (ALCLs) without TCRA rearrangements (57% of cutaneous ALCLs tested).
  • These findings identified IRF4 translocations as a novel recurrent genetic abnormality in PTCLs.
  • Translocations involving IRF4 but not TCRA appear to occur predominantly in cutaneous ALCLs.
  • Detecting these translocations may be useful in lymphoma diagnosis.

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  • (PMID = 18987657.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / P50 CA097274-07; United States / NCI NIH HHS / CA / P50 CA97274
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / interferon regulatory factor-4
  • [Other-IDs] NLM/ NIHMS70248; NLM/ PMC2656414
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96. Chang BH, Stork L, Fan G: A unique case of adolescent CD56-negative extranodal NK/T-cell lymphoma, nasal type. Pediatr Dev Pathol; 2008 Jan-Feb;11(1):50-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A unique case of adolescent CD56-negative extranodal NK/T-cell lymphoma, nasal type.
  • Mature T-cell neoplasms are unusual in the pediatric population.
  • The majority of these neoplasms in the United States are anaplastic large cell lymphomas (ALCL) characterized by CD30 and anaplastic lymphoma kinase-1 expression.
  • Extranodal natural killer/T (NK/T)-cell lymphomas, nasal type, are extremely rare.
  • Extranodal NK/T-cell lymphomas often express CD56, are associated with Epstein-Barr virus, and are negative for CD30.
  • Clinically, extranodal NK/T-cell lymphomas are much more aggressive than ALCL, and require different treatment strategies.
  • The authors present an adolescent male with a CD56 negative extranodal NK/T-cell lymphoma, nasal type.
  • The lymphoma was partially positive for CD30, diffusely positive for EBV by in situ hybridization, and clonal for T-cell receptor gene rearrangement and cytogenetic abnormalities.
  • More than 2 years from completion of the therapy, the patient remains disease free.
  • This case highlights the importance and difficulty of accurate identification of this type of rare tumor.
  • We further present the literature review and discuss the diagnostic criteria for extranodal NK/T lymphoma using morphologic, immunologic, molecular, and cytogenetic information.
  • [MeSH-major] Antigens, CD56 / metabolism. Lymphoma, Extranodal NK-T-Cell / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis
  • [MeSH-minor] Adolescent. Antigens, CD30 / metabolism. Chromosome Aberrations. Diagnosis, Differential. Gene Rearrangement. Herpesvirus 4, Human / isolation & purification. Humans. In Situ Hybridization. Male. Nose / pathology. Receptors, Antigen, T-Cell / genetics

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  • [CommentIn] Pediatr Dev Pathol. 2008 Jul-Aug;11(4):325; author reply 326 [18839448.001]
  • (PMID = 18237230.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antigens, CD56; 0 / Receptors, Antigen, T-Cell
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97. Mathas S, Jöhrens K, Joos S, Lietz A, Hummel F, Janz M, Jundt F, Anagnostopoulos I, Bommert K, Lichter P, Stein H, Scheidereit C, Dörken B: Elevated NF-kappaB p50 complex formation and Bcl-3 expression in classical Hodgkin, anaplastic large-cell, and other peripheral T-cell lymphomas. Blood; 2005 Dec 15;106(13):4287-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated NF-kappaB p50 complex formation and Bcl-3 expression in classical Hodgkin, anaplastic large-cell, and other peripheral T-cell lymphomas.
  • Transcription factor nuclear factor kappa B (NF-kappaB) plays a central role in the pathogenesis of classical Hodgkin lymphoma (cHL).
  • In anaplastic large-cell lymphomas (ALCLs), which share molecular lesions with cHL, the NF-kappaB system has not been equivalently investigated.
  • Here we describe constitutive NF-kappaB p50 homodimer [(p50)2] activity in ALCL cells in the absence of constitutive activation of the IkappaB kinase (IKK) complex.
  • Bcl-3, which is an inducer of nuclear (p50)2 and is associated with (p50)2 in ALCL and HRS cell lines, is abundantly expressed in ALCL and HRS cells.
  • Notably, a selective overexpression of Bcl-3 target genes is found in ALCL cells.
  • By immunohistochemical screening of 288 lymphoma cases, a strong Bcl-3 expression in cHL and in peripheral T-cell non-Hodgkin lymphoma (T-NHL) including ALCL was found.
  • In 3 of 6 HRS cell lines and 25% of primary ALCL, a copy number increase of the BCL3 gene locus was identified.
  • Together, these data suggest that elevated Bcl-3 expression has an important function in cHL and peripheral T-NHL, in particular ALCL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Hodgkin Disease / genetics. Hodgkin Disease / metabolism. Lymphoma, T-Cell, Peripheral / genetics. Lymphoma, T-Cell, Peripheral / metabolism. NF-kappa B p50 Subunit / metabolism. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Cell Line. Dimerization. Humans. I-kappa B Proteins / metabolism. Interleukin-9 / metabolism. Microarray Analysis. Oncogene Proteins v-rel / metabolism. Protein Binding. Transcription Factors

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  • [CommentIn] Blood. 2006 Jul 1;108(1):401-2; author reply 402-3 [16790585.001]
  • (PMID = 16123212.001).
  • [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 / I-kappa B Proteins; 0 / Interleukin-9; 0 / NF-kappa B p50 Subunit; 0 / Oncogene Proteins v-rel; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3
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98. Schain F, Schain D, Mahshid Y, Liu C, Porwit A, Xu D, Claesson HE, Sundström C, Björkholm M, Sjöberg J: Differential expression of cysteinyl leukotriene receptor 1 and 15-lipoxygenase-1 in non-Hodgkin lymphomas. Clin Lymphoma Myeloma; 2008 Dec;8(6):340-7
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of cysteinyl leukotriene receptor 1 and 15-lipoxygenase-1 in non-Hodgkin lymphomas.
  • We have recently reported that the cysteinyl leukotriene receptor 1 (CysLT1) and 15-lipoxygenase-1 (15-LO-1) are expressed by the malignant Hodgkin Reed-Sternberg cells of Hodgkin lymphoma and certain Hodgkin lymphoma cell lines, and that these cells convert arachidonic acid to the novel proinflammatory eoxins.
  • MATERIALS AND METHODS: The expression of the CysLT1 receptor and 15-LO-1 was investigated in a broad range of non-Hodgkin lymphomas (NHLs) by immunohistochemistry.
  • The functionality of the CysLT1 receptor in primary mediastinal B-cell lymphoma (PMBCL) cell lines was studied by calcium mobilization assays.
  • RESULTS: Primary mediastinal B-cell lymphoma was the only NHL entity showing tumor cells positive for the CysLT1 receptor (9 of 10 tumors), and the PMBCL cell line Med-B1 expressed functional CysLT1 receptors, responding with a robust calcium signal upon cysteinyl leukotriene challenge.
  • Furthermore, the tumor cells in 1 of 4 T-cell-derived anaplastic large-cell lymphomas, in contrast to all other studied NHLs, strongly expressed 15-LO-1.
  • Thus, this further corroborates the pathologic overlap between PMBCL and classical Hodgkin lymphoma.
  • [MeSH-major] Arachidonate 15-Lipoxygenase / metabolism. Lymphoma, Non-Hodgkin / metabolism. Receptors, Leukotriene / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biopsy. Calcium / metabolism. Cell Line, Tumor. Child. Child, Preschool. Female. Gene Expression. Humans. Immunohistochemistry. Leukotriene D4 / pharmacology. Male. Middle Aged

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  • (PMID = 19064398.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Leukotriene; 0 / leukotriene D4 receptor; 73836-78-9 / Leukotriene D4; EC 1.13.11.33 / Arachidonate 15-Lipoxygenase; SY7Q814VUP / Calcium
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99. Lim MS, Carlson ML, Crockett DK, Fillmore GC, Abbott DR, Elenitoba-Johnson OF, Tripp SR, Rassidakis GZ, Medeiros LJ, Szankasi P, Elenitoba-Johnson KS: The proteomic signature of NPM/ALK reveals deregulation of multiple cellular pathways. Blood; 2009 Aug 20;114(8):1585-95
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