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1. Shi X, Franko B, Frantz C, Amin HM, Lai R: JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells. Br J Haematol; 2006 Oct;135(1):26-32
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  • [Title] JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells.
  • As STAT3 activation is pathogenetically important in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ ALCL), we investigated whether JSI-124 can mediate significant inhibitory effects in this cell type.
  • In two ALK+ ALCL cell lines (Karpas 299 and SU-DHL-1), JSI-124 significantly reduced the number of viable cells to 50% of that of negative controls at a dose of 5-10 micromol/l at 24 h and 1-1.25 micromol/l at 48 h.
  • Interestingly, JSI-124 also dramatically decreased the protein levels of JAK3 and nucleophosmin (NPM)-ALK, and these effects were reversible by MG132.
  • Our data support that JSI-124 is a potentially useful therapeutic agent for ALK+ ALCL.
  • In addition to its role as a tyrosine kinase inhibitor, JSI-124 appears to be involved in regulating proteosome degradation for proteins such as JAK3 and NPM-ALK.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Triterpenes / pharmacology
  • [MeSH-minor] Blotting, Western. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Janus Kinase 3. Signal Transduction / drug effects. Tumor Cells, Cultured


2. Kelleher FC, McDermott R: The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene. Eur J Cancer; 2010 Sep;46(13):2357-68
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  • [Title] The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene.
  • The anaplastic lymphoma kinase gene (ALK) is a gene on chromosome 2p23 that has expression restricted to the brain, testis and small intestine but is not expressed in normal lymphoid tissue.
  • This gene was originally established as being implicated in the pathogenesis of rare diseases including inflammatory myofibroblastic tumour (IMT) and ALK-positive anaplastic large cell lymphoma, which is a subtype of non-Hodgkin's lymphoma.
  • Recently the number of diseases in which ALK is implicated in their pathogenesis has increased.
  • In 2007, an inversion of chromosome 2 involving ALK and a fusion partner gene in a subset of non-small cell lung cancer was discovered.
  • In 2008, publications emerged implicating ALK in familial and sporadic cases of neuroblastoma, a childhood cancer of the sympatho-adrenal system.
  • Chromosomal abnormalities involving ALK are translocations, amplifications or mutations.
  • Chromosomal translocations are the longest recognised ALK genetic abnormality.
  • When translocations occur a fusion gene is created between ALK and a gene partner.
  • This has been described in ALK-positive anaplastic large cell lymphoma in which ALK is fused to NPM (nucleolar protein gene) and in non-small cell lung cancer where ALK is fused to EML4 (Echinoderm microtubule-associated protein 4).
  • The most frequently described partner genes in inflammatory myofibroblastic tumour are tropomyosin 3/4 (TMP3/4), however in IMTs a diversity of ALK fusion partners have been found, with the ability to homodimerise a common characteristic.
  • Point mutations and amplification of the ALK gene occur in the childhood cancer neuroblastoma.
  • Therapeutic targeting of ALK fusion genes using tyrosine kinase inhibition, vaccination using an ALK specific antigen and treatment using viral vectors for RNAi are emerging potential therapeutic possibilities.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / therapy. Drug Synergism. Gene Amplification. Humans. Lung Neoplasms / genetics. Lung Neoplasms / therapy. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Mutation / genetics. Neuroblastoma / genetics. Neuroblastoma / therapy. Pyrimidines / therapeutic use. Pyrroles / therapeutic use. Receptor Protein-Tyrosine Kinases. Receptor, IGF Type 1 / antagonists & inhibitors

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20451371.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GSK 1838705A; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase
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3. Sausville EA, Arbuck SG, Messmann R, Headlee D, Bauer KS, Lush RM, Murgo A, Figg WD, Lahusen T, Jaken S, Jing X, Roberge M, Fuse E, Kuwabara T, Senderowicz AM: Phase I trial of 72-hour continuous infusion UCN-01 in patients with refractory neoplasms. J Clin Oncol; 2001 Apr 15;19(8):2319-33
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  • Therefore, nine patients received drug on the initial 2-week schedule, and 38 received drug on the recommended 4-week schedule.
  • One partial response was observed in a patient with melanoma, and one protracted period ( > 2.5 years) of disease stability was observed in a patient with alk-positive anaplastic large-cell lymphoma.
  • [MeSH-major] Alkaloids / adverse effects. Antineoplastic Agents / adverse effects. Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. DNA Damage. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance, Neoplasm. Female. Humans. Hyperglycemia / chemically induced. Hypotension / chemically induced. Infusions, Intravenous. Lymphoma, Large B-Cell, Diffuse / drug therapy. Male. Melanoma / drug therapy. Middle Aged. Nausea / chemically induced. Skin Neoplasms / drug therapy. Staurosporine / analogs & derivatives. Vomiting / chemically induced

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  • (PMID = 11304786.001).
  • [ISSN] 0732-183X
  • [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] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Antineoplastic Agents; 7BU5H4V94A / 7-hydroxystaurosporine; H88EPA0A3N / Staurosporine
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4. Reimer P, Hentrich M: [Peripheral T-cell lymphoma: diagnosis and treatment]. Dtsch Med Wochenschr; 2006 Mar 31;131(13):685-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Peripheral T-cell lymphoma: diagnosis and treatment].
  • Peripheral T/NK-cell lymphomas (PTCL) comprise a heterogeneous group of rare diseases accounting for approximately 10-15% of all non-Hodgkin"s lymphomas.
  • Compared to B-cell lymphomas, PTCL more frequently involve extranodal sites and have a worse prognosis.
  • Because of their usually indolent course, primary cutaneous T/NK-cell lymphomas should be distinguished from the other PTCL.
  • The International Prognostic Index, established for aggressive B-cell lymphomas, has also proved relevant for PTCL.
  • Apart from (ALK-positive) anaplastic large cell lymphoma it thus gives poorer results than those obtained in patients with aggressive B-cell lymphomas.
  • Data for high-dosage therapy with autologous stem cell transplantation (autoSCT) for relapsing and refractory PTCL are similar to those reported for aggressive B-cell lymphomas.
  • Allogeneic stem cell transplantation following reduced conditioning regimens has also given promising results in patients with relapse.
  • However, the impact of high-dosage strategies and the implementation of newer agents, such as alemtuzumab, in first-line treatment are still uncertain.
  • [MeSH-major] Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / therapy
  • [MeSH-minor] Humans. Stem Cell Transplantation. Survival Analysis. Transplantation, Homologous

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  • [CommentIn] Dtsch Med Wochenschr. 2006 Aug 25;131(34-35):1884; author reply 1884 [16915558.001]
  • (PMID = 16555177.001).
  • [ISSN] 0012-0472
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 56
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5. Hwang YY, Liang RH: An update in management of noncutaneous T-cell lymphomas. Adv Hematol; 2010;2010:424786
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  • [Title] An update in management of noncutaneous T-cell lymphomas.
  • T-cell lymphoma is a heterogeneous group of diseases.
  • Except for ALK positive anaplastic large cell lymphoma, T-cell lymphoma responds to conventional chemotherapy unfavourably, and most patients carry poor prognosis.
  • In recent years, efforts have been made to improve the outcome of T-cell lymphoma patients.
  • Novel agents, high-dose therapy, and allogeneic stem cell transplantation are studied, and various results are reported in literature.
  • This paper looks into the prognostication and treatment approach of different entities of noncutaneous T-cell lymphoma and would focus on the latest updates in its management.

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  • (PMID = 21188274.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3003949
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6. Vega F, Medeiros LJ, Leventaki V, Atwell C, Cho-Vega JH, Tian L, Claret FX, Rassidakis GZ: Activation of mammalian target of rapamycin signaling pathway contributes to tumor cell survival in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma. Cancer Res; 2006 Jul 1;66(13):6589-97
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  • [Title] Activation of mammalian target of rapamycin signaling pathway contributes to tumor cell survival in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) frequently carries the t(2;5)(p23;q35) resulting in aberrant expression of chimeric nucleophosmin-ALK.
  • Previously, nucleophosmin-ALK has been shown to activate phosphatidylinositol 3-kinase (PI3K) and its downstream effector, the serine/threonine kinase AKT.
  • In this study, we hypothesized that the mammalian target of rapamycin (mTOR) pathway, which functions downstream of AKT, mediates the oncogenic effects of activated PI3K/AKT in ALK+ ALCL.
  • Here, we provide evidence that mTOR signaling phosphoproteins, including mTOR, eukaryotic initiation factor 4E-binding protein-1, p70S6K, and ribosomal protein S6, are highly phosphorylated in ALK+ ALCL cell lines and tumors.
  • In addition, pharmacologic inhibition of PI3K/AKT down-regulates the activation of the mTOR signaling pathway.
  • We also show that inhibition of mTOR with rapamycin, as well as silencing mTOR gene product expression using mTOR-specific small interfering RNA, decreased phosphorylation of mTOR signaling proteins and induced cell cycle arrest and apoptosis in ALK+ ALCL cells.
  • Cell cycle arrest was associated with modulation of G(1)-S-phase regulators, including the cyclin-dependent kinase inhibitors p21(waf1) and p27(kip1).
  • Apoptosis following inhibition of mTOR expression or function was associated with down-regulation of antiapoptotic proteins, including c-FLIP, MCL-1, and BCL-2.
  • These findings suggest that the mTOR pathway contributes to nucleophosmin-ALK/PI3K/AKT-mediated tumorigenesis and that inhibition of mTOR represents a potential therapeutic strategy in ALK+ ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Kinases / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / physiology. Chromones / pharmacology. Down-Regulation. Enzyme Activation. Humans. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. Receptor Protein-Tyrosine Kinases. Signal Transduction. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Transfection


7. Han Y, Amin HM, Frantz C, Franko B, Lee J, Lin Q, Lai R: Restoration of shp1 expression by 5-AZA-2'-deoxycytidine is associated with downregulation of JAK3/STAT3 signaling in ALK-positive anaplastic large cell lymphoma. Leukemia; 2006 Sep;20(9):1602-9
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  • [Title] Restoration of shp1 expression by 5-AZA-2'-deoxycytidine is associated with downregulation of JAK3/STAT3 signaling in ALK-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALK+ ALCL) is characterized by constitutive activation of the Janus kinase (JAK)3/signal transducers and activators of transcription 3 (STAT3) signaling pathway.
  • SHP1, a tyrosine phosphatase that negatively regulates JAK/STAT, is frequently absent in ALK+ ALCL owing to gene methylation.
  • To test the hypothesis that loss of SHP1 contributes to JAK3/STAT3 activation in ALK+ ALCL cells, we induced SHP1 expression using 5-aza-2'-deoxycytidine (5-AZA), an inhibitor of DNA methyltransferase, in ALK+ ALCL cell lines, and correlated with changes in the JAK3/STAT3 pathway.
  • 5-AZA induced no significant increase in apoptosis but it sensitized ALCL cells to doxorubicin-induced apoptosis.
  • Our findings support the concept that loss of SHP1 contributes to the constitutive activation of JAK3/STAT3 in ALK+ ALCL cells.
  • [MeSH-major] Azacitidine / analogs & derivatives. Down-Regulation / drug effects. Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / metabolism. STAT3 Transcription Factor / metabolism. Signal Transduction
  • [MeSH-minor] Apoptosis / drug effects. Base Sequence. Blotting, Western. Cell Cycle. Cell Line. DNA Primers. Doxorubicin / pharmacology. Humans. Janus Kinase 3. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Receptor Protein-Tyrosine Kinases

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  • (PMID = 16871283.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Intracellular Signaling Peptides and Proteins; 0 / JAK3 protein, human; 0 / STAT3 Transcription Factor; 776B62CQ27 / decitabine; 80168379AG / Doxorubicin; 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 / Janus Kinase 3; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.48 / Protein Tyrosine Phosphatases; M801H13NRU / Azacitidine
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8. Drakos E, Atsaves V, Schlette E, Li J, Papanastasi I, Rassidakis GZ, Medeiros LJ: The therapeutic potential of p53 reactivation by nutlin-3a in ALK+ anaplastic large cell lymphoma with wild-type or mutated p53. Leukemia; 2009 Dec;23(12):2290-9
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  • [Title] The therapeutic potential of p53 reactivation by nutlin-3a in ALK+ anaplastic large cell lymphoma with wild-type or mutated p53.
  • p53 is expressed frequently, but is rarely mutated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) tumours.
  • We show that nutlin-3a activates p53 in ALK+ ALCL cells carrying a wild type (wt) or mutated but partially functional p53 gene resulting in p53-dependent cell-cycle arrest and apoptosis.
  • Cell-cycle arrest was associated with upregulation of the cyclin-dependent kinase inhibitor p21.
  • Nutlin-3a-induced apoptotic cell death was accompanied by Bax and Puma upregulation, downregulation of Bcl-xl, survivin, and caspase-3 cleavage, and this was reduced when p53-dependent transactivation activity was inhibited by pifithrin-alpha, or when pifithrin-mu was used to inhibit direct p53 targeting of mitochondria.
  • Nutlin-3a sensitized the activation of the extrinsic apoptotic pathway in wt-p53 ALK+ ALCL cells, in part, through upregulation of DR-5 and downregulation of c-Flip(S/L), and was synergistic with TRAIL in cell death induction.
  • In addition, nutlin-3a treatment enhanced doxorubicin cytotoxicity against ALK+ ALCL cells harbouring mt p53, and this was associated with p73 upregulation.
  • These data suggest that disruption of the p53-mdm2 interaction by nutlin-3a offers a novel therapeutic approach for ALK+ ALCL patients.
  • [MeSH-major] Imidazoles / pharmacology. Lymphoma, Large-Cell, Anaplastic / drug therapy. Mutation. Piperazines / pharmacology. Tumor Suppressor Protein p53 / drug effects
  • [MeSH-minor] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. Cell Cycle. Cell Line, Tumor. Doxorubicin / pharmacology. Drug Synergism. Humans. TNF-Related Apoptosis-Inducing Ligand / pharmacology


9. Vose J, Armitage J, Weisenburger D, International T-Cell Lymphoma Project: International peripheral T-cell and natural killer/T-cell lymphoma study: pathology findings and clinical outcomes. J Clin Oncol; 2008 Sep 1;26(25):4124-30
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  • [Title] International peripheral T-cell and natural killer/T-cell lymphoma study: pathology findings and clinical outcomes.
  • PURPOSE: Peripheral T-cell lymphoma (PTCL) and natural killer/T-cell lymphoma (NKTCL) are rare and heterogeneous forms of non-Hodgkin's lymphoma (NHL) that, in general, are associated with a poor clinical outcome.
  • RESULTS: A diagnosis of PTCL or NKTCL was confirmed in 1,153 (87.8%) of the cases.
  • The most common subtypes were PTCL not otherwise specified (NOS; 25.9%), angioimmunoblastic type (18.5%), NKTCL (10.4%), and adult T-cell leukemia/lymphoma (ATLL; 9.6%).
  • Misclassification occurred in 10.4% of the cases including Hodgkin's lymphoma (3%), B-cell lymphoma (1.4%), unclassifiable lymphoma (2.8%), or a diagnosis other than lymphoma (2.3%).
  • The use of an anthracycline-containing regimen was not associated with an improved outcome in PTCL-NOS or angioimmunoblastic type, but was associated with an improved outcome in anaplastic large-cell lymphoma, ALK positive.
  • However, expert hematopathology review is important for accurate diagnosis.
  • The clinical outcome for patients with most of these lymphoma subtypes is poor with standard therapies, and novel agents and new modalities are needed to improve survival.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / mortality. T-Lymphocytes / pathology

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  • (PMID = 18626005.001).
  • [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; Multicenter Study
  • [Publication-country] United States
  • [Investigator] Savage K; Connors J; Gascoyne R; Chhanabhai M; Wilson W; Jaffe E; Armitage J; Vose J; Weisenburger D; Anderson J; Ullrich F; Bast M; Hochberg E; Harris N; Levine A; Nathwani B; Miller T; Rimsza L; Montserrat E; Lopez-Guillermo A; Campo E; Cuadros M; Alvarez Ferreira J; Martinez Delgado B; Holte H; Delabie J; Rüdiger T; Müller-Hermelink K; Reimer P; Adam P; Wilhelm M; Schmitz N; Nerl C; Lister A; Norton A; MacLennan KA; Luigi Zinzani P; Pileri S; Federico M; Bellei M; Coiffier B; Berger F; Tanin I; Wannakrairot P; Au W; Liang R; Loong F; Rajan S; Sng I; Tobinai K; Matsuno Y; Morishima Y; Nakamura S; Seto M; Tanimoto M; Yoshino T; Suzumiya J; Ohshima K; Kim WS; Ko YH
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10. Matsubara K, Tanaka T, Taki T, Nakagawa A, Nigami H, Tamura A, Fukaya T: [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature]. Rinsho Ketsueki; 2008 May;49(5):325-30
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  • [Title] [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature].
  • We report a 10-year-old girl with ATIC-anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • Pathological findings showed that staining of ALK was restricted to the cytoplasm of ALCL cells.
  • ATIC-ALK chimeric transcripts were detected by reverse transcriptase polymerase chain reaction.
  • The patient was assigned to the standard risk group proposed by the international multicenter study for pediatric ALCL, ALCL99.
  • To date, 7 genes have been identified as a fusion partner of ALK, with the highest frequency in nucleophosmin (NPM).
  • Little is known about the clinical implications of subtypes of ALCL harboring each of the 7 fusion genes, especially those of variant fusion genes other than NPM-ALK.
  • In this paper, we review 9 patients with ATIC-ALK-positive ALCL in the literature in addition to discussing our patient.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Oncogene Proteins, Fusion / analysis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Child. Drug Administration Schedule. Female. Humans. Remission Induction. Treatment Outcome

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  • (PMID = 18572809.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 18
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11. ten Berge RL, Snijdewint FG, von Mensdorff-Pouilly S, Poort-Keesom RJ, Oudejans JJ, Meijer JW, Willemze R, Hilgers J, Meijer CJ: MUC1 (EMA) is preferentially expressed by ALK positive anaplastic large cell lymphoma, in the normally glycosylated or only partly hypoglycosylated form. J Clin Pathol; 2001 Dec;54(12):933-9
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  • [Title] MUC1 (EMA) is preferentially expressed by ALK positive anaplastic large cell lymphoma, in the normally glycosylated or only partly hypoglycosylated form.
  • AIMS: To investigate whether MUC1 mucin, a high molecular weight transmembrane glycoprotein, also known as epithelial membrane antigen (EMA), differs in its expression and degree of glycosylation between anaplastic large cell lymphoma (ALCL) and classic Hodgkin's disease (HD), and whether MUC1 immunostaining can be used to differentiate between CD30 positive large cell lymphomas.
  • METHODS/RESULTS: Using five different monoclonal antibodies (E29/anti-EMA, DF3, 139H2, VU-4H5, and SM3) that distinguish between various MUC1 glycoforms, high MUC1 expression (50-95% of tumour cells positive) was found in 13 of 17 anaplastic lymphoma kinase (ALK) positive systemic nodal ALCLs, and in one of 20 cases of classic HD.
  • Scattered or focal staining (< 25% of tumour cells) was seen in two additional ALK positive systemic ALCLs, two additional classic HD cases, and in three of 20 cases of ALK negative systemic nodal ALCL.
  • Primary cutaneous ALCL showed no staining with the anti-MUC1 antibodies.
  • Antibodies detecting hypoglycosylated MUC1 were found to be absent in all lymphomas (SM3) or present in only six of 15 ALK positive ALCLs (VU-4H5).
  • CONCLUSIONS: MUC1 is preferentially expressed by a subtype of systemic nodal ALCL, characterised by ALK expression, but is found in only a few cases of classic HD and ALK negative ALCL.
  • Therefore, although MUC1 could be used in a panel of markers for CD30 positive lymphomas, it is probably not a valuable tool to differentiate between ALK negative CD30 positive large cell lymphomas.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / chemistry. Mucin-1 / analysis. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Antibodies, Monoclonal. Diagnosis, Differential. Glycosylation. Hodgkin Disease / metabolism. Humans. Immunohistochemistry / methods. Leukocytes, Mononuclear / chemistry. Leukocytes, Mononuclear / drug effects. Lymphocyte Activation. Lymphoma, B-Cell / chemistry. Lymphoma, T-Cell / chemistry. Protein Isoforms / analysis. Receptor Protein-Tyrosine Kinases. Tetradecanoylphorbol Acetate / pharmacology

  • Genetic Alliance. consumer health - Anaplastic Large Cell Lymphoma.
  • Genetic Alliance. consumer health - Lymphoma, large-cell.
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  • (PMID = 11729213.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / Mucin-1; 0 / Protein Isoforms; 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; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ PMC1731330
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