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1. Mussolin L, Pillon M, Bonato P, Leszl A, Franceschetto G, Di Meglio A, d'Amore ES, Sainati L, Rosolen A: Cytogenetic analysis of pediatric anaplastic large cell lymphoma. Pediatr Blood Cancer; 2010 Sep;55(3):446-51
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  • [Title] Cytogenetic analysis of pediatric anaplastic large cell lymphoma.
  • BACKGROUND: Anaplastic large cell lymphoma (ALCL) constitutes approximately 15% of pediatric and 3% of adult non-Hodgkin lymphomas.
  • Most pediatric cases harbor the reciprocal translocation t(2;5)(p23;q35), involving the alk gene.
  • Cytogenetic studies of ALCL have mostly been published as case-reports.
  • The aim of this study was to determine the cytogenetic profiles of a series of pediatric ALCL and to compare them with pediatric and adult ALCL from the literature.
  • Comparative analysis was performed on our findings and on the karyotypes of 48 pediatric and 39 adult ALCL reported in the literature.
  • RESULTS: Karyotype was obtained in 16/18 ALCL: 9 showed translocation t(2;5) and 1 an alk variant form.
  • Trisomy 7 was found in 22% (13/59) of pediatric cases with abnormal karyotype and only in 5% (2/38) of adults; monosomy of chromosome 13 in 13% (5/38) of adults and only in 2% (1/59) of pediatric patients and monosomy of chromosome 15 in 16% (6/38) of adults and in none of the pediatric ALCL.
  • CONCLUSION: Our data suggest that pediatric and adult ALCL are characterized by different numerical chromosomal abnormalities.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Chromosome Aberrations. Diploidy. Female. Humans. Male. Monosomy. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic. Trisomy

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20658615.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 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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2. 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.
  • More recently, genomic DNA amplification and protein overexpression, as well as activating point mutations, of ALK have been described in neuroblastomas.
  • In addition to those cancers for which a causative role for aberrant ALK activity is well validated, more circumstantial links implicate the full-length, normal ALK receptor in the genesis of other malignancies - including glioblastoma and breast cancer - via a mechanism of receptor activation involving autocrine and/or paracrine growth loops with the reported ALK ligands, pleiotrophin and midkine.
  • This review summarizes normal ALK biology, the confirmed and putative roles of ALK in the development of human cancers and efforts to target ALK using small-molecule kinase inhibitors.

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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
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3. 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


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4. Ezra N, Van Dyke GS, Binder SW: CD30 positive anaplastic large-cell lymphoma mimicking Langerhans cell histiocytosis. J Cutan Pathol; 2010 Jul;37(7):787-92
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  • [Title] CD30 positive anaplastic large-cell lymphoma mimicking Langerhans cell histiocytosis.
  • The presence of CD 1a+ dendritic cells (DC) has been well described in T-cell lymphoproliferative disorders, and the presence of large numbers of DCs has rarely been reported as a mimicker of Langerhans cell histiocytsis (LCH).
  • We present the case of a 56-year-old female with a solitary nodule on the chin whose case was referred to our institution for confirmation of the diagnosis of LCH.
  • Skin biopsy showed an ulcerated nodule containing a wedge-shaped infiltrate comprised of large atypical cells and cells with prominent grooved nuclei.
  • The constellation of histologic and immunologic features favored a CD30 lymphoproliferative disorder of T-cell lineage even though there were accompanying numerous dendritic histiocytes and CD1a positive Langerhans cells.
  • The sheets of CD30 positive atypical lymphoid cells which express T-cell markers were consistent with CD30 positive lymphoproliferative disease and favor CD30 positive anaplastic large-cell lymphoma (ALCL) over Langerhans histiocytosis.
  • The absence of Anaplastic Lymphoma Kinase (ALK) staining favored a primary cutaneous origin.
  • This case signifies a CD 30+ ALCL of the skin which histopathologically mimics a LCH.
  • CD30 positive anaplastic large-cell lymphoma (ALCL) mimicking Langerhans cell histiocytosis (LCH).
  • [MeSH-major] Antigens, CD30 / biosynthesis. Histiocytosis, Langerhans-Cell / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Middle Aged


5. 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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  • [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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6. Szomor A, Al Saati T, Delsol G, Kereskai L, Szijártó Z, Losonczy H: Primary bone marrow T-cell anaplastic large cell lymphoma with triple M gradient. Pathol Oncol Res; 2007;13(3):260-2
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  • [Title] Primary bone marrow T-cell anaplastic large cell lymphoma with triple M gradient.
  • We present a case of a 60-year-old male patient with primary bone marrow anaplastic large cell lymphoma.
  • Bone marrow biopsy showed massive CD30-positive, ALK-negative large lymphoid cell infiltration of T-cell origin with anaplastic morphology.
  • PCR analysis of lymphoid cells separated from the bone marrow demonstrated the presence of a B/T hybrid genotype disorder with no evidence of the t(2;5), nor t(1;2) translocations.
  • [MeSH-major] Bone Marrow Neoplasms / diagnosis. Bone Marrow Neoplasms / immunology. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / immunology. T-Lymphocytes / immunology


7. 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.
  • In this study, we show that NPM-ALK expression increases matrix metalloproteinase-9 (MMP-9) expression.
  • 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.
  • The MMP inhibitor GM6001 and MMP-9 blocking antibodies abolished the invasiveness of NPM-ALK(+) cells.
  • 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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8. 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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9. Singh RR, Cho-Vega JH, Davuluri Y, Ma S, Kasbidi F, Milito C, Lennon PA, Drakos E, Medeiros LJ, Luthra R, Vega F: Sonic hedgehog signaling pathway is activated in ALK-positive anaplastic large cell lymphoma. Cancer Res; 2009 Mar 15;69(6):2550-8
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  • [Title] Sonic hedgehog signaling pathway is activated in ALK-positive anaplastic large cell lymphoma.
  • Deregulation of the sonic hedgehog (SHH) signaling pathway has been implicated in several cancers but has not been explored in T-cell lymphomas.
  • Here, we report that the SHH/GLI1 signaling pathway is activated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • We show that SHH, but not its transcriptional effector GLI1, is amplified in ALK+ ALCL tumors and cell lines, and that SHH and GLI1 proteins are highly expressed in ALK+ ALCL tumors and cell lines.
  • We also show that inhibition of SHH/GLI1 signaling with cyclopamine-KAAD, as well as silencing GLI1 gene expression by small interfering (si)RNA, decreased cell viability and clonogenicity of ALK+ ALCL cells.
  • Transfection of wild-type or mutant NPM-ALK into 293T cells showed that only wild-type NPM-ALK increased GLI1 protein levels and activated SHH/GLI1 signaling as shown by increase of CCND2 mRNA levels.
  • Inhibition of ALK tyrosine kinase and phosphatidylinositol 3-kinase (PI3K)/AKT or forced expression of pAKT down-regulated or up-regulated SHH/GLI1 signaling, respectively.
  • Inhibition of GSK3beta in 293T cells also increased protein levels of GLI1.
  • In conclusion, the SHH/GLI1 signaling pathway is activated in ALK+ ALCL.
  • SHH/GLI1 activation is the result of SHH gene amplification and is further mediated by NPM-ALK through activation of PI3K/AKT and stabilization of GLI1 protein.
  • There is a positive synergistic effect between the SHH/GLI1 and PI3K/AKT pathways that contributes to the lymphomagenic effect of NPM-ALK.
  • [MeSH-major] Hedgehog Proteins / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism
  • [MeSH-minor] Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / physiology. Enzyme Activation. Gene Amplification. Humans. Immunohistochemistry. Jurkat Cells. Phosphatidylinositol 3-Kinases / metabolism. Protein-Tyrosine Kinases / biosynthesis. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction. Transcription Factors / antagonists & inhibitors. Transcription Factors / biosynthesis. Transcription Factors / genetics. Transcription Factors / metabolism. Transcription, Genetic. Transfection

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  • (PMID = 19244133.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / SHH protein, human; 0 / Transcription Factors; 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 2.7.11.1 / Proto-Oncogene Proteins c-akt
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10. Siwicki JK, Rymkiewicz G, Błachnio K, Rygier J, Kuźniar P, Płoski R, Janusz A, Skurzak H, Chrzanowska K, Steffen J: Spontaneously immortalized T lymphocytes from Nijmegen Breakage Syndrome patients display phenotypes typical for lymphoma cells. Leuk Res; 2008 Apr;32(4):569-77
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  • [Title] Spontaneously immortalized T lymphocytes from Nijmegen Breakage Syndrome patients display phenotypes typical for lymphoma cells.
  • We found that the peripheral T lymphocytes from four of eight patients with the lymphoma predisposing Nijmegen Breakage Syndrome (NBS) acquired an unlimited growth potential following in vitro mitogen stimulation and subsequent interleukin-2-dependent propagation.
  • The immortal T cell lines revealed morphological and other features typical for anaplastic large cell lymphoma (ALCL).
  • In addition, multiple copies of ALK, but with no ALK gene rearrangements were found in a subpopulation of cells of one of the immortalized lines.
  • These cell lines may be useful for the in vitro elucidation of mechanisms involved in the development of ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Nijmegen Breakage Syndrome / pathology. T-Lymphocytes / pathology
  • [MeSH-minor] Cell Line, Transformed / pathology. Cells, Cultured. Flow Cytometry. Gene Rearrangement. Humans. Immunohistochemistry. Immunophenotyping. In Situ Hybridization, Fluorescence. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases

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  • (PMID = 17900685.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 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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11. 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


12. Merkel O, Hamacher F, Laimer D, Sifft E, Trajanoski Z, Scheideler M, Egger G, Hassler MR, Thallinger C, Schmatz A, Turner SD, Greil R, Kenner L: Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK)+ and ALK- anaplastic large-cell lymphoma. Proc Natl Acad Sci U S A; 2010 Sep 14;107(37):16228-33
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  • [Title] Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK)+ and ALK- anaplastic large-cell lymphoma.
  • Aberrant anaplastic lymphoma kinase (ALK) expression is a defining feature of many human cancers and was identified first in anaplastic large-cell lymphoma (ALCL), an aggressive non-Hodgkin T-cell lymphoma.
  • Since that time, many studies have set out to identify the mechanisms used by aberrant ALK toward tumorigenesis.
  • We have identified a distinct profile of micro-RNAs (miRNAs) that characterize ALCL; furthermore, this profile distinguishes ALK(+) from ALK(-) subtypes, and thus points toward potential mechanisms of tumorigenesis induced by aberrant ALK.
  • Using a nucleophosmin-ALK transgenic mouse model as well as human primary ALCL tumor tissues and human ALCL-derived cell lines, we reveal a set of overlapping deregulated miRNAs that might be implicated in the development and progression of ALCL.
  • Importantly, ALK(+) and ALK(-) ALCL could be distinguished by a distinct profile of "oncomirs": Five members of the miR-17-92 cluster were expressed more highly in ALK(+) ALCL, whereas miR-155 was expressed more than 10-fold higher in ALK(-) ALCL.
  • Moreover, miR-101 was down-regulated in all ALCL model systems, but its forced expression attenuated cell proliferation only in ALK(+) and not in ALK(-) cell lines, perhaps suggesting different modes of ALK-dependent regulation of its target proteins.
  • Furthermore, inhibition of mTOR, which is targeted by miR-101, led to reduced tumor growth in engrafted ALCL mouse models.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. MicroRNAs / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Base Sequence. Cell Line, Tumor. Cell Proliferation. Gene Expression Profiling. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Mice. Mice, Transgenic. Multigene Family. Receptor Protein-Tyrosine Kinases. Sirolimus / analogs & derivatives. Sirolimus / therapeutic use. Xenograft Model Antitumor Assays

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  • (PMID = 20805506.001).
  • [ISSN] 1091-6490
  • [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
  • [Grant] Austria / Austrian Science Fund FWF / / V 102
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MicroRNAs; 624KN6GM2T / temsirolimus; 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; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2941277
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13. Mergan F, Jaubert F, Sauvat F, Hartmann O, Lortat-Jacob S, Révillon Y, Nihoul-Fékété C, Sarnacki S: Inflammatory myofibroblastic tumor in children: clinical review with anaplastic lymphoma kinase, Epstein-Barr virus, and human herpesvirus 8 detection analysis. J Pediatr Surg; 2005 Oct;40(10):1581-6
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  • [Title] Inflammatory myofibroblastic tumor in children: clinical review with anaplastic lymphoma kinase, Epstein-Barr virus, and human herpesvirus 8 detection analysis.
  • Differential diagnosis with other tumor processes is sometimes difficult.
  • Similar anaplastic lymphoma kinase (ALK) gene abnormalities as in anaplastic large cell lymphoma have been reported.
  • Human herpesvirus 8 (HHV-8) DNA sequences have been described in adult pulmonary IMTs and Epstein-Barr virus (EBV) has been reported in splenic and hepatic IMTs, suggesting the importance of both viruses in IMT development.
  • This article aims to evaluate ALK, EBV, and HHV-8 expression in children with IMT and to correlate our findings with clinical features.
  • Formalin-fixed, paraffin-embedded archival tissues were stained for HHV-8 and ALK with immunohistochemistry.
  • ALK was positive in 3 (18.8%) cases and EBV in 1 pulmonary and 1 bladder tumor, all of them without recurrence or metastasis.
  • None of the cases were positive for HHV-8.
  • All patients are now disease-free with a mean follow-up of 4.2 years.
  • Larger multicentric studies would be necessary to understand the prognostic significance of ALK, EBV, and HHV-8 and their relationships with the origins of the tumor.
  • [MeSH-major] Granuloma, Plasma Cell / enzymology. Granuloma, Plasma Cell / virology. Herpesvirus 4, Human / isolation & purification. Herpesvirus 8, Human / isolation & purification. Protein-Tyrosine Kinases / analysis. Receptor Protein-Tyrosine Kinases / analysis

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  • (PMID = 16226988.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [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
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14. 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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15. Bakshi NA, Finn WG, Schnitzer B, Valdez R, Ross CW: Fascin expression in diffuse large B-cell lymphoma, anaplastic large cell lymphoma, and classical Hodgkin lymphoma. Arch Pathol Lab Med; 2007 May;131(5):742-7
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  • [Title] Fascin expression in diffuse large B-cell lymphoma, anaplastic large cell lymphoma, and classical Hodgkin lymphoma.
  • CONTEXT: Fascin is an actin-bundling protein involved in the formation of dendritic processes.
  • Fascin is a sensitive marker for classical Reed-Sternberg cells and has a high negative predictive value for diagnosis of classical Hodgkin lymphoma (CHL).
  • Fascin has been used to distinguish CHL from non-Hodgkin lymphoma.
  • Recently, it was shown that fascin might not help differentiate CHL from anaplastic large cell lymphoma (ALCL).
  • Moreover, fascin has not been extensively studied in the context of other large cell lymphomas.
  • OBJECTIVE: To analyze fascin expression in diffuse large B-cell lymphoma (DLBCL) and also reexamine its usefulness in discriminating CHL from ALCL.
  • DESIGN: Formalin-fixed, paraffin-embedded tissue samples from 41 cases of DLBCL, 30 cases of CHL, and 30 cases of ALCL were analyzed.
  • Fascin expression was compared across each type of lymphoma with additional correlation between fascin positivity and ALK-1 expression in ALCL performed.
  • RESULTS: Only 6 (14.6%) of 41 cases of DLBCL stained positively for fascin, with most neoplastic large cells exhibiting a weak staining pattern.
  • Fifteen (50%) of 30 cases of ALCL showed positivity for fascin, with most large cells staining strongly.
  • All 30 cases of CHL demonstrated intense positive staining.
  • Sixty percent of fascin-positive ALCLs were positive for ALK-1, while 66.7% of fascin-negative ALCLs were positive for ALK-1.
  • CONCLUSIONS: Fascin is highly sensitive for CHL and has a very high negative predictive value (100% in this series) for distinguishing CHL from DLBCL or ALCL.
  • However, the specificity and positive predictive value for fascin are much higher in distinguishing CHL from DLBCL than in distinguishing CHL from ALCL.
  • Expression of fascin appears more useful in the differential diagnosis of CHL versus DLBCL than in the differential diagnosis of CHL versus ALCL.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carrier Proteins / biosynthesis. Hodgkin Disease / metabolism. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Microfilament Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged. Predictive Value of Tests. Sensitivity and Specificity


16. Kadin ME: Current management of primary cutaneous CD30+ T-cell lymphoproliferative disorders. Oncology (Williston Park); 2009 Nov 30;23(13):1158-64
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  • [Title] Current management of primary cutaneous CD30+ T-cell lymphoproliferative disorders.
  • Primary cutaneous CD30+ T-cell lymphoproliferative disorders (PCLPDs) are the second most common type of cutaneous T-cell lymphoma.
  • These disorders comprise a spectrum of clinically benign lymphomatoidpapulosis (LyP) and primary cutaneous anaplastic large-cell lymphoma (ALCL).
  • The peak incidence of LyP is in the 5th decade of life, and the incidence of primary cutaneous ALCL peaks in the 6th decade, but children are also affected.
  • Both LyP and primary cutaneous ALCL have an excellent prognosis.
  • However, LyP is associated with development of malignant lymphoma (mycosis fungoides, Hodgkin lymphoma, or ALCL) in 20% of cases, and also with an increased risk of non-lymphoid cancers.
  • The diagnosis of LyP is difficult and often delayed.
  • Primary cutaneous ALCL must be distinguished from secondary skin lesions in systemic ALCL, which confer a poor prognosis.
  • Correlation of clinical findings with histopathology and immunopathology (stains for ALK kinase, epithelial membrane antigen, and cutaneous lymphocyte antigen) are important to achieve a correct diagnosis.
  • When a diagnosis of CD30+ PCLPD is established, minimal clinical staging is required.
  • Low-dose methotrexate (10-25 mg weekly) is the most effective therapy for PCLPD but is usually reserved for aggressive cases of LyP and multifocal lesions of cutaneous ALCL Many patients with LyP can be followed expectantly, with special attention to changes in character of the skin lesions or development of lymphadenopathy.
  • Patients with localized cutaneous ALCL can be treated with irradiation.
  • Extracutaneous spread of disease is an indication for multiagent chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Lymphoma, Primary Cutaneous Anaplastic Large Cell / drug therapy. Methotrexate / administration & dosage. Skin Neoplasms / drug therapy
  • [MeSH-minor] Antigens, CD30 / metabolism. Diagnosis, Differential. Humans

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  • (PMID = 20043465.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20RR018757
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 32
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17. Bard JD, Gelebart P, Anand M, Amin HM, Lai R: Aberrant expression of IL-22 receptor 1 and autocrine IL-22 stimulation contribute to tumorigenicity in ALK+ anaplastic large cell lymphoma. Leukemia; 2008 Aug;22(8):1595-603
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  • [Title] Aberrant expression of IL-22 receptor 1 and autocrine IL-22 stimulation contribute to tumorigenicity in ALK+ anaplastic large cell lymphoma.
  • One of the characteristic features of anaplastic lymphoma kinase (ALK)(+), anaplastic large cell lymphoma (ALK(+)ALCL) is the constitutive activation of signal transducers and activators of transcription-3 (STAT3), a defect believed to be important for the pathogenesis of these tumors.
  • In this report, we describe the existence of an autocrine stimulatory loop involving interleukin-22 (IL-22) that contributes to STAT3 activation and tumorigenicity of ALK(+)ALCL.
  • The IL-22 receptor, a heterodimer composed of IL-22R1 and IL-10R2, was expressed in all ALK(+)ALCL cell lines and tumors examined.
  • The expression of IL-22R1 in ALK(+)ALCL is aberrant, as this protein is absent in benign lymphocytes.
  • Although ALK(+)ALCL cells produce endogenous IL-22, addition of recombinant IL-22 to ALK(+)ALCL cell lines significantly increased STAT3 activation, cell proliferation and colony formation in soft agar.
  • Opposite biological effects were observed in cells treated with recombinant IL-22 binding protein (a naturally occurring IL-22 decoy) or IL-22-neutralizing antibody.
  • Nucleophosmin (NPM)-ALK, the characteristic fusion gene oncoprotein expressed in ALK(+)ALCL, directly contributes to the aberrant expression of IL-22R1, as transfection of NPM-ALK in Jurkat cells-induced IL-22R1 expression and IL-22-mediated STAT3 activation.
  • To conclude, for the first time, we demonstrate the importance of the IL-22 autocrine pathway in a lymphoid malignancy, and reveal yet another novel function of NPM-ALK.

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  • (PMID = 18509351.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395; United States / NCI NIH HHS / CA / CA114395
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Interleukins; 0 / RNA, Small Interfering; 0 / Receptors, Interleukin; 0 / STAT3 Transcription Factor; 0 / interleukin-22; 0 / interleukin-22 receptor
  • [Other-IDs] NLM/ NIHMS400234; NLM/ PMC3429118
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18. Benner MF, Jansen PM, Meijer CJ, Willemze R: Diagnostic and prognostic evaluation of phenotypic markers TRAF1, MUM1, BCL2 and CD15 in cutaneous CD30-positive lymphoproliferative disorders. Br J Dermatol; 2009 Jul;161(1):121-7
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  • [Title] Diagnostic and prognostic evaluation of phenotypic markers TRAF1, MUM1, BCL2 and CD15 in cutaneous CD30-positive lymphoproliferative disorders.
  • BACKGROUND: CD30 is expressed in various types of cutaneous lymphomas, including lymphomatoid papulosis (LyP), primary cutaneous anaplastic large cell lymphoma (C-ALCL), some cases of mycosis fungoides showing large cell transformation (MF-TR) and skin localizations of systemic anaplastic lymphoma kinase (ALK)-positive or ALK-negative ALCL.
  • OBJECTIVE: To evaluate the diagnostic and prognostic significance of these markers in a large group of cutaneous CD30-positive lymphoproliferations.
  • METHODS: An immunohistochemical study on the expression of TRAF1, MUM1, BCL2 and CD15 was performed on skin biopsies from 28 patients with C-ALCL, 39 patients with LyP, 11 patients with CD30-positive MF-TR, two with ALK-positive ALCL and six with ALK-negative ALCL.
  • RESULTS: TRAF1 was expressed in roughly 70-80% and MUM1 was expressed in 70-100% of all the groups of cutaneous CD30-positive lymphoproliferations.
  • Highest levels of BCL2 were expressed in MF-TR (73%), in contrast to 21% in C-ALCL and 36% in LyP.
  • Highest levels of CD15 were expressed in C-ALCL (43%), compared with 18% in LyP and 9% in MF-TR.
  • CONCLUSIONS: The results of the present study suggest that TRAF1, MUM1, BCL2 and CD15 cannot be considered as useful diagnostic or prognostic marker in cutaneous CD30-positive lymphoproliferations.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoproliferative Disorders / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD15 / analysis. Antigens, CD30 / analysis. Biopsy. Child. Female. Humans. Immunohistochemistry / methods. Interferon Regulatory Factors / analysis. Lymphoma, Primary Cutaneous Anaplastic Large Cell / chemistry. Lymphoma, Primary Cutaneous Anaplastic Large Cell / diagnosis. Lymphoma, Primary Cutaneous Anaplastic Large Cell / immunology. Lymphomatoid Papulosis / diagnosis. Lymphomatoid Papulosis / immunology. Lymphomatoid Papulosis / metabolism. Male. Middle Aged. Mycosis Fungoides / chemistry. Mycosis Fungoides / immunology. Mycosis Fungoides / pathology. Proto-Oncogene Proteins c-bcl-2 / analysis. TNF Receptor-Associated Factor 1 / analysis. Young Adult

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  • (PMID = 19416236.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD15; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TNF Receptor-Associated Factor 1; 0 / interferon regulatory factor-4
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19. Sebire NJ, Webb D, Ramsay AD: Anaplastic large cell lymphoma with ALK expression and presence of the t(2;5) translocation in a 5-month-old infant. Fetal Pediatr Pathol; 2005 Jan-Feb;24(1):63-70
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  • [Title] Anaplastic large cell lymphoma with ALK expression and presence of the t(2;5) translocation in a 5-month-old infant.
  • Anaplastic large cell lymphoma (ALCL) is a well-recognized subtype of non-Hodgkin lymphoma in childhood.
  • Several series report experience with the diagnosis and management of pediatric ALCL, the average age at diagnosis being 8 to 16 years, with a reported range of 1 to 15 years.
  • We present a case of ALCL affecting a 5-month-old infant in whom the diagnosis was confirmed by the nuclear and cytoplasmic immunohistochemical expression of ALK1, in addition to the presence of classical t(2;5)(p23;q35) translocation detected using reverse transcriptase-polymerase chain reaction.
  • This is the youngest case of ALCL thus far reported and hence expands the spectrum of infantile lymphoproliferative disorders.
  • [MeSH-major] Activin Receptors, Type I / biosynthesis. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Translocation, Genetic
  • [MeSH-minor] Activin Receptors, Type II. Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 5. Humans. Infant. Male

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  • (PMID = 16175752.001).
  • [ISSN] 1551-3815
  • [Journal-full-title] Fetal and pediatric pathology
  • [ISO-abbreviation] Fetal Pediatr Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type I; EC 2.7.11.30 / Activin Receptors, Type II
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20. Palmer RH, Vernersson E, Grabbe C, Hallberg B: Anaplastic lymphoma kinase: signalling in development and disease. Biochem J; 2009 Jun 15;420(3):345-61
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  • [Title] Anaplastic lymphoma kinase: signalling in development and disease.
  • RTKs (receptor tyrosine kinases) play important roles in cellular proliferation and differentiation.
  • In addition, RTKs reveal oncogenic potential when their kinase activities are constitutively enhanced by point mutation, amplification or rearrangement of the corresponding genes.
  • The ALK (anaplastic lymphoma kinase) RTK was originally identified as a member of the insulin receptor subfamily of RTKs that acquires transforming capability when truncated and fused to NPM (nucleophosmin) in the t(2;5) chromosomal rearrangement associated with ALCL (anaplastic large cell lymphoma).
  • To date, many chromosomal rearrangements leading to enhanced ALK activity have been described and are implicated in a number of cancer types.
  • Recent reports of the EML4 (echinoderm microtubule-associated protein like 4)-ALK oncoprotein in NSCLC (non-small cell lung cancer), together with the identification of activating point mutations in neuroblastoma, have highlighted ALK as a significant player and target for drug development in cancer.
  • In the present review we address the role of ALK in development and disease and discuss implications for the future.
  • [MeSH-major] Protein-Tyrosine Kinases / metabolism. Signal Transduction
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / pathology. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Models, Biological. Neuroblastoma / genetics. Neuroblastoma / metabolism. Neuroblastoma / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19459784.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 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
  • [Number-of-references] 237
  • [Other-IDs] NLM/ PMC2708929
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21. 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.
  • 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).
  • 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


22. Horie R: [Molecular basis of Hodgkin lymphoma and anaplastic large cell lymphoma and molecular targeting therapy by an NF-kappaB inhibitor]. Rinsho Ketsueki; 2007 Apr;48(4):255-61
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  • [Title] [Molecular basis of Hodgkin lymphoma and anaplastic large cell lymphoma and molecular targeting therapy by an NF-kappaB inhibitor].
  • [MeSH-major] Gene Targeting. Genetic Therapy. Hodgkin Disease / genetics. Hodgkin Disease / therapy. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / therapy. NF-kappa B / antagonists & inhibitors
  • [MeSH-minor] Antigens, CD30. Humans. Protein-Tyrosine Kinases


23. Vanhentenrijk V, Vanden Bempt I, Dierickx D, Verhoef G, Wlodarska I, De Wolf-Peeters C: Relationship between classic Hodgkin lymphoma and overlapping large cell lymphoma investigated by comparative expressed sequence hybridization expression profiling. J Pathol; 2006 Oct;210(2):155-62
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  • [Title] Relationship between classic Hodgkin lymphoma and overlapping large cell lymphoma investigated by comparative expressed sequence hybridization expression profiling.
  • There is a diagnostic grey zone between classic Hodgkin lymphoma (cHL) and some non-Hodgkin lymphoma (NHL), including primary mediastinal B cell lymphoma, diffuse large B cell lymphoma, and anaplastic large cell lymphoma.
  • To investigate this, we undertook an expression profiling study of these lymphomas using comparative expressed sequence hybridization.
  • This technique detects chromosomal regions that are differentially expressed between a test and a reference tissue in a manner similar to comparative genomic hybridization, and is particularly suitable when the number of informative biopsies is limited.
  • Using this approach, we identified a unique expression profile for all lymphoma types investigated.
  • Unsupervised hierarchical cluster analysis of the acquired data showed that cHL separates from all investigated NHLs, including ALCL-like HL.
  • Moreover, anaplastic lymphoma kinase (ALK)-negative ALCL clustered in a separate branch together with ALCL-like HL.
  • Thus, analysing the neoplastic cells concurrently with their microenvironment, ALK-negative ALCL and ALCL-like HL seem to be related to each other, while cHL constitutes a separate lymphoma entity.
  • [MeSH-major] Hodgkin Disease / genetics. Lymphoma, Large B-Cell, Diffuse / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Cluster Analysis. DNA, Neoplasm / genetics. Diagnosis, Differential. Female. Gene Expression Profiling / methods. Humans. Male. Middle Aged. Neoplasm Staging. Nucleic Acid Hybridization / methods

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  • (PMID = 16874743.001).
  • [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 / DNA, Neoplasm
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24. Ait-Tahar K, Barnardo MC, Pulford K: CD4 T-helper responses to the anaplastic lymphoma kinase (ALK) protein in patients with ALK-positive anaplastic large-cell lymphoma. Cancer Res; 2007 Mar 1;67(5):1898-901
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  • [Title] CD4 T-helper responses to the anaplastic lymphoma kinase (ALK) protein in patients with ALK-positive anaplastic large-cell lymphoma.
  • We have previously shown both humoral and CTL responses to anaplastic lymphoma kinase (ALK) in patients with ALK-positive anaplastic large-cell lymphoma (ALCL).
  • However, because CD4(+) T-helper (Th) cells also play a vital role in developing and maintaining tumor immunity, we investigated the presence of a CD4(+) Th response in ALK-positive ALCL.
  • Using an IFN-gamma ELISPOT assay, we identified two ALK-derived DRB1-restricted 24-mer promiscuous peptides, ALK1(278-301) and ALK2(233-256), as being immunogenic in six ALK-positive ALCL patients but not in two ALK-negative ALCL patients or five normal subjects.
  • A significant interleukin-4 response to the ALK peptides was detected in only one ALK-positive patient.
  • CD4(+) Th cell lines lysed ALK-positive ALCL cell lines in a MHC class II-restricted manner.
  • This first report of a CD4(+) Th response to ALK provides valuable information for developing future immunotherapeutic options for ALK-positive ALCL patients who fail to respond well to conventional therapies.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / immunology. Protein-Tyrosine Kinases / immunology. T-Lymphocytes, Helper-Inducer / immunology
  • [MeSH-minor] Adolescent. Adult. Cells, Cultured. Child, Preschool. Epitopes, T-Lymphocyte / immunology. Female. Humans. Male. Middle Aged. Peptide Fragments / immunology. Receptor Protein-Tyrosine Kinases

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  • (PMID = 17332315.001).
  • [ISSN] 0008-5472
  • [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 / Epitopes, T-Lymphocyte; 0 / Peptide Fragments; 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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25. Balachandran I, Walker JW Jr, Broman J: Fine needle aspiration cytology of ALK1(-), CD30+ anaplastic large cell lymphoma post renal transplantation: a case report and literature review. Diagn Cytopathol; 2010 Mar;38(3):213-6
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  • [Title] Fine needle aspiration cytology of ALK1(-), CD30+ anaplastic large cell lymphoma post renal transplantation: a case report and literature review.
  • Epstein-Barr virus (EBV) related non-Hodgkin's lymphomas of B-cell type is more common than those of T-cell origin.
  • CD30 positive Anaplastic Large Cell Lymphoma (ALCL) is a Non-Hodgkin's lymphoma (B or T cell type) that accounts for a small percentage of PTLD's.
  • ALCL of T-cell type are a spectrum of disease ranging from primary cutaneous to systemic nodal ALCL.
  • The systemic nodal ALCL is further subdivided into anaplastic lymphoma kinase-1 (ALK-1) positive or negative.
  • ALK-1 protein is a gene fusion product of translocation (2;5) and carries prognostic implications.
  • We present an unusual manifestation of ALK-1 negative CD30 positive ALCL in a post renal transplant patient in FNA cytology with all supportive adjuvant studies and differential diagnoses and review the cytology literature on this topic.
  • [MeSH-major] Antigens, CD30 / analysis. Kidney Transplantation / adverse effects. Lymphoma, Large-Cell, Anaplastic / pathology. Mediastinal Neoplasms / pathology. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Carcinoma / diagnosis. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Humans. Immunocompromised Host. Immunohistochemistry. Male. Melanoma / diagnosis. Postoperative Complications. Prednisone / therapeutic use. Receptor Protein-Tyrosine Kinases. Remission Induction. Seminoma / diagnosis. Seminoma / secondary. Testicular Neoplasms / diagnosis. Vincristine / therapeutic use

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  • (PMID = 19774614.001).
  • [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] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 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; VB0R961HZT / Prednisone; CHOP protocol
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26. Youssif C, Goldenbogen J, Hamoudi R, Carreras J, Viskaduraki M, Cui YX, Bacon CM, Burke GA, Turner SD: Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: a Children's Cancer and Leukaemia Group Study. Genes Chromosomes Cancer; 2009 Nov;48(11):1018-26
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  • [Title] Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: a Children's Cancer and Leukaemia Group Study.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) is a T-cell malignancy in which ALK expression is a consequence of the t(2;5) or a variant translocation involving Chromosome 2.
  • For the most part, this disease presents in the pediatric population and most, but not all, patients are successfully treated.
  • Although the t(2;5) product nucleophosmin-ALK has been extensively studied for its transforming properties, very little is known regarding cooperative genetic mutations that may contribute to lymphomagenesis and may predict survival outcome, specifically in a purely pediatric population.
  • We set out to determine the frequency and positions of genomic imbalances in this relatively rare disease.
  • We collected biopsy material from 15 UK-resident children with ALK-expressing ALCL.
  • A range of genomic imbalances exist in ALK-expressing ALCL of a pediatric origin, with a greater number associated with poorer overall survival.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cohort Studies. Comparative Genomic Hybridization / methods. DNA-Binding Proteins / genetics. Gene Deletion. Homeodomain Proteins / genetics. Humans. Inhibitor of Apoptosis Proteins. Kaplan-Meier Estimate. Markov Chains. Microtubule-Associated Proteins / genetics. Mutagenesis, Insertional. Receptor Protein-Tyrosine Kinases. Reproducibility of Results. Statistics, Nonparametric

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19691112.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / DDB1 protein, human; 0 / DNA-Binding Proteins; 0 / HOXB1 homeodomain protein; 0 / Homeodomain Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 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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27. Kelten C, Kabukcu S, Sen N, Teke Z, Yaren A, Erdem E, Duzcan E: Secondary involvement of the breast in T-cell non-Hodgkin lymphoma, an unusual example mimicking inflammatory breast carcinoma. Arch Gynecol Obstet; 2009 Jul;280(1):149-52
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  • [Title] Secondary involvement of the breast in T-cell non-Hodgkin lymphoma, an unusual example mimicking inflammatory breast carcinoma.
  • Non-Hodgkin lymphoma of the breast is a rare malignancy and present with almost equal frequency either as a primary or a secondary disease.
  • Survival is poor in most cases of secondary breast lymphoma because of their advanced stage.
  • The histologic and immunohistochemical features were diagnosed as an ALK (-) anaplastic large cell lymphoma.
  • A Computed Tomography examination was performed for staging the lymphoma and then chemotherapy was started.
  • Thirty months after the diagnosis, the patient is still alive with disease.
  • Because of the presence of systemic symptoms such as skin involvement and generalized lymphadenopathies (mediastinal, axillary or cervical), T cell lymphoma cases with breast involvement could mimic the clinical presentation of inflammatory breast carcinoma.
  • Pathologic examination is needed for the correct diagnosis.
  • [MeSH-major] Breast Neoplasms / secondary. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Lymph Nodes / pathology. Mammography. Neoplasm Staging. Tomography, X-Ray Computed


28. Siordia-Reyes AG, Ferman-Cano F, Rodríguez-Velasco A: [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case]. Gac Med Mex; 2005 Nov-Dec;141(6):531-4
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  • [Title] [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case].
  • [Transliterated title] Linfoma anaplásico de células grandes ALK-1 positivo, primario de pulmón. Informe de un caso pediátrico.
  • Ki-1 anaplastic large cell non-Hodgkin lymphoma is a well recognized clinical entity.
  • In the extranodal disease, which occurs in approximately half of the cases, the skin is the most common site; bone marrow, lung and central nervous system are generally not involved.
  • Anaplastic large cell lymphoma is more common among young people, in whom the prognosis is more favorable.
  • Primary anaplastic large cell lymphoma of the lung is a rare clinical entity.
  • Its clinical expression is similar to a high grade malignant lymphoma, and in most cases the diagnosis is made in advanced stages.
  • We present a pediatric case with ALK-1 positive anaplastic large cell lymphoma of the lung.
  • [MeSH-major] Lung Neoplasms / chemistry. Lymphoma, Large B-Cell, Diffuse / chemistry. Membrane Proteins / analysis
  • [MeSH-minor] Activin Receptors, Type II. Child. Humans. Male

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  • (PMID = 16381509.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
  • [Number-of-references] 16
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29. Hernández L, Campo E: Identification of anaplastic lymphoma kinase variant translocations using 5'RACE. Methods Mol Med; 2005;115:295-314
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  • [Title] Identification of anaplastic lymphoma kinase variant translocations using 5'RACE.
  • Anaplastic lymphoma kinase (ALK) is abnormally expressed in anaplastic large cell lymphoma (ALCL) and its expression associated with chromosomal translocations involving the ALK gene at 2p23.
  • These translocations lead to the synthesis of novel chimeric proteins that retain the C-terminal portion of ALK, where the tyrosine kinase domain is located.
  • In most of these tumors, the t(2;5)(p23;q35) translocation causes fusion of the ALK gene to the 5' region of the nucleophosmin (NPM) gene, but other different ALK partners have been identified, including nonmuscle tropomyosin (TPM3), TRK-fused gene (TFG), 5' aminoimidazole-4-carboxamide ribonucleotide formyltranferase/IMP cyclohydrolase (ATIC), clathrin heavy chain gene (CLTC), and moesin (MSN).
  • The characterization of these ALK partners has been performed using different molecular methods, including the 5' Rapid Amplification of complementary deoxyribonucleic acid (cDNA) Ends (5'RACE) polymerase chain reaction (PCR)-based technique.
  • In ALK translocations, identification of the 5' gene involved has been performed using primers designed within the known 3' catalytic domain of the ALK.
  • Initial reaction consists in a first-strand cDNA synthesis primed using a gene-specific antisense primer (ALK1), performing the cDNA conversion of specific messenger ribonucleic acids, and maximizing the potential for complete extension to the 5'-end of the message.
  • Tailed cDNA is then amplified by PCR using a nested gene-specific primer (ALK2), which anneals 3' to ALK1, and a complementary homopolymer containing an anchor primer (i.e., AAP), which permits amplification from the homopolymeric tail.
  • The reamplification is achieved by using a nested gene-specific primer (ALK3), which anneals 3' to ALK2, and a universal amplification primer, which anneals to the 5' sequence previously introduced by the AAP primer.
  • [MeSH-major] DNA, Complementary / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 2 / genetics. Chromosomes, Human, Pair 5 / genetics. DNA, Neoplasm / analysis. DNA, Neoplasm / genetics. Humans. Polymerase Chain Reaction / methods. Receptor Protein-Tyrosine Kinases

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  • (PMID = 15998975.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA, Neoplasm; 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
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30. Macák J, Falková I, Smardová J, Kren L: [Lymphoma of the small intestine]. Cesk Patol; 2010 Jan;46(1):20-4
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  • [Title] [Lymphoma of the small intestine].
  • A series of eight small intestine lymphomas comprised two cases of follicular lymphoma (FL), one anaplastic large cell lymphoma (ALCL) ALK negative, and five cases of diffuse large B-cell lymphoma.
  • The lymphomas were diagnosed by routine hematoxylin-eosin staining, immunohistochemistry and the FISH method for translocation t(14;18).
  • Immunohistochemistry revealed that the diffuse large B-cell lymphomas were of the non-germinal center type (non GC-DLBCL).
  • In one case of follicular lymphoma, microscopic foci of tumor were found in the intestinal mucosa which spread far from the primary nodule and probably beyond the resection border.
  • It is difficult to ascertain whether this phenomenon represents colonization of pre-existing non-neoplastic follicles by lymphoma or spreading of the tumor within the same tissue.
  • In this case, surgical removal of the lymphoma is problematic.
  • [MeSH-major] Intestinal Neoplasms / pathology. Intestine, Small. Lymphoma, Follicular / pathology. Lymphoma, Large B-Cell, Diffuse / pathology

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  • (PMID = 21280278.001).
  • [ISSN] 1210-7875
  • [Journal-full-title] Československá patologie
  • [ISO-abbreviation] Cesk Patol
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
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31. 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.
  • Reverse transcription-polymerase chain reaction studies for ALK and ALK/nucleophosmin were also performed.
  • 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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32. Medeiros LJ, Elenitoba-Johnson KS: Anaplastic Large Cell Lymphoma. Am J Clin Pathol; 2007 May;127(5):707-22
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  • [Title] Anaplastic Large Cell Lymphoma.
  • Session 8 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop was devoted to anaplastic large cell lymphoma (ALCL).
  • Most cases submitted were anaplastic lymphoma kinase (ALK)+ ALCL highlighting unusual clinical settings, histologic variants, and variant translocation partners.
  • Cases submitted as ALK- ALCL emphasized the immunohistochemical overlap with classical Hodgkin lymphoma (eg, CD15+/CD30+).
  • It was also clear that consensus histologic and immunohistochemical criteria for the diagnosis of ALK-ALCL are lacking.
  • Many expressed the opinion that ALK-ALCL is not a distinct entity at the immunophenotypic or genetic level and is better designated as peripheral T-cell lymphoma (PTCL), unspecified.
  • Others suggested that the histologic features of ALK-ALCL are distinctive nevertheless and that this diagnosis has meaning that is lost by designating these neoplasms as PTCL, unspecified.
  • This session also included CD30+ anaplastic lymphomas involving skin in which the differential diagnosis included cutaneous ALCL and systemic ALK-ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Antigens, CD30 / analysis. Flow Cytometry. Humans. Immunophenotyping. Receptor Protein-Tyrosine Kinases. Skin Neoplasms / pathology

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  • (PMID = 17511113.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 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] 40
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33. 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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  • [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.
  • These results were further validated in fibroblastic NIH-3T3 cells expressing a previously described chimeric epidermal growth factor receptor (EGFR)/ALK molecule that allows dissection of ALK enzymatic function under conditions of controlled ligand-induced activation.
  • 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.
  • Overall, our data indicate that alphaDGK activation is involved in the control of ALK-mediated mitogenic properties.
  • [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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34. 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).
  • The MS spectra were interpreted using SEQUEST to search the electronic UniProt protein database, and analyzed by ProteinProphet and INTERACT.
  • 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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35. Kotoula V, Bobos M, Kostopoulos I, Kaloutsi V, Koletsa T, Karayannopoulou G, Papadimitriou CS: In situ detection of hTERT variants in anaplastic large cell lymphoma. Leuk Lymphoma; 2006 Aug;47(8):1639-50
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  • [Title] In situ detection of hTERT variants in anaplastic large cell lymphoma.
  • The expression of hTERT and its isoforms is difficult to assess in lymphoma tissues with the commonly used reverse transcription-polymerase chain reaction (RT-PCR) methods, because non-neoplastic lymphocytes expressing hTERT are always present in the lymphomatous infiltrates.
  • The present study aimed to investigate hTERT mRNA variants in anaplastic large cell lymphoma (ALCL) (n = 38) with in situ hybridization (ISH), along with the immunodetection of hTERT protein.
  • Probes for the identification of mRNAs containing (Bplus) and lacking (Bdel) exons 7 and 8 of the hTERT mRNA were used.
  • Normal lymphocyte populations equally expressed both Bplus and Bdel mRNAs.
  • Although all ALCL examined were found positive for hTERT expression with RT-PCR, hTERT mRNAs were identified in 68% of these tumors with ISH, with a higher incidence in the group bearing ALK translocations (10 out of 11; 90.9%) compared to the ALK negative group (17 out of 27; 59.3%) (PPearson's = 0.002).
  • In approximately 50% of cases, only Bplus positive cells were identified, again with a higher incidence in the ALK positive compared to the ALK negative group (PPearson's = 0.016).
  • In conclusion, ISH for hTERT mRNAs appears to be a valuable tool for the investigation of hTERT expression in lymphomas.
  • Aberrations in hTERT variant profiles and a decline in the expression of the B deleted isoform may be associated with the pathogenesis of ALCL, especially with respect to ALK positive tumors.
  • [MeSH-major] Genetic Variation. In Situ Hybridization / methods. Lymphoma, Large-Cell, Anaplastic / genetics. Telomerase / genetics

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  • (PMID = 16966278.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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36. Nelson M, Horsman DE, Weisenburger DD, Gascoyne RD, Dave BJ, Loberiza FR, Ludkovski O, Savage KJ, Armitage JO, Sanger WG: Cytogenetic abnormalities and clinical correlations in peripheral T-cell lymphoma. Br J Haematol; 2008 May;141(4):461-9
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  • [Title] Cytogenetic abnormalities and clinical correlations in peripheral T-cell lymphoma.
  • Cytogenetic correlations among most types of peripheral T-cell lymphoma (PTCL) have not been very informative to date.
  • This study aimed to identify recurrent chromosomal abnormalities in angioimmunoblastic T-cell lymphoma (AITL), ALK-negative anaplastic large cell lymphoma (ALK-ALCL) and peripheral T-cell lymphoma, unspecified (PTCL-US), and to evaluate their prognostic value.
  • In ALK(-) ALCL, gains of 1q (50%) and 3p (30%), and losses of 16pter (50%), 6q13q21 (30%), 15 (30%), 16qter (30%) and 17p13 (30%) were frequent findings.
  • However, cases with complex karyotypes, most frequently observed in ALK(-) ALCL and PTCL-US, had a significantly shorter OS.
  • [MeSH-major] Chromosome Aberrations. Lymphoma, T-Cell, Peripheral / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Follow-Up Studies. Humans. Immunoblastic Lymphadenopathy / genetics. Karyotyping. Lymphoma, Large-Cell, Anaplastic / genetics. Male. Middle Aged. Prognosis. Survival Analysis

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  • (PMID = 18341637.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
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37. Savage KJ, Harris NL, Vose JM, Ullrich F, Jaffe ES, Connors JM, Rimsza L, Pileri SA, Chhanabhai M, Gascoyne RD, Armitage JO, Weisenburger DD, International Peripheral T-Cell Lymphoma Project: ALK- anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project. Blood; 2008 Jun 15;111(12):5496-504
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  • [Title] ALK- anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project.
  • The International Peripheral T-Cell Lymphoma Project is a collaborative effort designed to gain better understanding of peripheral T-cell and natural killer (NK)/T-cell lymphomas (PTCLs).
  • Of the 1314 eligible patients, 181 had anaplastic large-cell lymphoma (ALCL; 13.8%) on consensus review: One hundred fifty-nine had systemic ALCL (12.1%) and 22 had primary cutaneous ALCL (1.7%).
  • Patients with anaplastic lymphoma kinase-positive (ALK(+)) ALCL had a superior outcome compared with those with ALK(-) ALCL (5-year failure-free survival [FFS], 60% vs 36%; P = .015; 5-year overall survival [OS], 70% vs 49%; P = .016).
  • However, contrary to prior reports, the 5-year FFS (36% vs 20%; P = .012) and OS (49% vs 32%; P = .032) were superior for ALK(-) ALCL compared with PTCL, not otherwise specified (PTCL-NOS).
  • Patients with primary cutaneous ALCL had a very favorable 5-year OS (90%), but with a propensity to relapse (5-year FFS, 55%).
  • In summary, ALK(-) ALCL should continue to be separated from both ALK(+) ALCL and PTCL-NOS.
  • Although the prognosis of ALK(-) ALCL appears to be better than that for PTCL-NOS, it is still unsatisfactory and better therapies are needed.
  • Primary cutaneous ALCL is associated with an indolent course.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / mortality. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, T-Cell, Peripheral / mortality. Lymphoma, T-Cell, Peripheral / pathology. Protein-Tyrosine Kinases / immunology
  • [MeSH-minor] Adult. Asia. Diagnosis, Differential. Europe. Female. Follow-Up Studies. Humans. Immunophenotyping. International Cooperation. Male. Middle Aged. North America. Prognosis. Receptor Protein-Tyrosine Kinases. Recurrence. Retrospective Studies. Skin Neoplasms / immunology. Skin Neoplasms / mortality. Skin Neoplasms / pathology. Skin Neoplasms / therapy. Survival Analysis. Treatment Outcome

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  • (PMID = 18385450.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [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
  • [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; Zinzani PL; 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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38. Moreno L, Garzón L, Bautista FJ, Fernández Navarro JM, András MM, Verdeguer A: Diagnosis of paediatric anaplastic large-cell lymphoma: a historical perspective from a single institution. Clin Transl Oncol; 2009 May;11(5):318-21
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  • [Title] Diagnosis of paediatric anaplastic large-cell lymphoma: a historical perspective from a single institution.
  • INTRODUCTION: Anaplastic large-cell lymphoma (ALCL) is an infrequent childhood malignancy whose diagnosis and treatment have largely evolved since its initial description in 1985.
  • RESULTS: Our first patient was diagnosed shortly alter this entity was described based on morphology and Ki-1 positivity, while the diagnostic work-up for the last two children included accurate molecular diagnosis for ALK-NPM rearrangement.
  • After 156 months of median follow-up (range 4-245), 8 out of 9 children are alive, free of disease.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • (PMID = 19451065.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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39. Calista D, Valenzano F, Riccioni L: Unusual cutaneous presentation of ALK+ anaplastic large cell lymphoma mimicking syphilis on the glans penis. Eur J Dermatol; 2009 Jan-Feb;19(1):76-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual cutaneous presentation of ALK+ anaplastic large cell lymphoma mimicking syphilis on the glans penis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / diagnosis. Penile Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Fatal Outcome. Humans. Male. Protein-Tyrosine Kinases / analysis. Receptor Protein-Tyrosine Kinases. Syphilis / diagnosis

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  • (PMID = 19171536.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] France
  • [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
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40. Vranovsky A, Ladicka M, Lakota J: Autologous stem cell transplantation in first-line treatment of high-risk aggressive non-Hodgkin's lymphoma. Neoplasma; 2008;55(2):107-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous stem cell transplantation in first-line treatment of high-risk aggressive non-Hodgkin's lymphoma.
  • A single center, retrospective analysis evaluating the outcome of patients with poor-risk aggressive non-Hodgkin's lymphoma (NHL) treated with high-dose chemotherapy and autologous stem cell transplantation (ASCT) as a part of firstline therapy.
  • Forty-seven patients younger than 65 years with diffuse large B-cell lymphoma (DLBCL), mantle cell lymphoma (MCL), peripheral T-cell lymphoma (PTCL) or alk-negative anaplastic large cell lymphoma (ALCL) underwent ASCT between July 1997 and November 2005.
  • Patients with DLBCL and alk-negative ALCL had 2 or 3 age-adjusted International Prognostic Index risk factors.
  • Our results confirm the efficacy of high-dose therapy with ASCT during first-line treatment of patients with poor-prognosis aggressive lymphoma, with substantial number of patients cured by using this treatment approach.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, Non-Hodgkin / therapy

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  • (PMID = 18652043.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 11056-06-7 / Bleomycin; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; Q20Q21Q62J / Cisplatin; YL5FZ2Y5U1 / Methotrexate; DHAP protocol; MACOP-B regimen
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41. Daneshbod Y, Oryan A, Khojasteh HN, Rasekhi A, Ahmadi N, Mohammadianpanah M: Primary ALK-positive anaplastic large cell lymphoma of the breast: a case report and review of the literature. J Pediatr Hematol Oncol; 2010 Mar;32(2):e75-8
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  • [Title] Primary ALK-positive anaplastic large cell lymphoma of the breast: a case report and review of the literature.
  • BACKGROUND: Non-Hodgkin lymphomas of the breast are uncommon, which represent less than 1% of all breast malignancies and predominantly are of B-cell origin.
  • OBSERVATION: In this report, a rare case of anaplastic lymphoma kinase (ALK)-positive anaplastic large T-cell lymphoma in the breast of a 16-year-old female without breast implant is described.
  • The immunohistochemical profile showed positivity for CD30 and ALK and confirmed the diagnosis of ALK-positive anaplastic large T-cell lymphoma of the breast.
  • CONCLUSION: Anaplastic large T-cell lymphoma of the breast is rare, and can clinically mimic inflammatory breast carcinoma in adolescence.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Adolescent. Antigens, CD30 / analysis. Female. Humans. Receptor Protein-Tyrosine Kinases


42. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • It has similarity to the insulin receptor subfamily of kinases and is emerging as having increased pathologic and potential therapeutic importance in malignant disease.
  • 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-major] Chromosome Aberrations. Chromosomes, Human, Pair 2 / genetics. Neoplasms / genetics. Protein-Tyrosine Kinases / genetics
  • [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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43. Gudgin E, Rashbass J, Pulford KJ, Erber WN: Primary and isolated anaplastic large cell lymphoma of the bone marrow. Leuk Lymphoma; 2005 Mar;46(3):461-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary and isolated anaplastic large cell lymphoma of the bone marrow.
  • Anaplastic large cell lymphoma (ALCL) is a T-cell lymphoma in which the majority of patients present with advanced stage III or IV disease.
  • Here we report a case of ALCL where bone marrow was the only site of disease, in a 60-year-old man with pyrexia and pancytopenia.
  • The diagnosis of ALCL was made on detection of CD30-positive anaplastic cells in the bone marrow, together with prominent hemophagocytosis.
  • Genetics confirmed the clonal nature of the disease and showed it to be anaplastic lymphoma kinase (ALK) negative.
  • Primary isolated bone marrow ALCL should be considered in the diagnosis of pancytopenia associated with hemophagocytosis.
  • [MeSH-major] Bone Marrow / pathology. Lymphoma, Large-Cell, Anaplastic / pathology


44. Das P, Iyer VK, Mathur SR, Ray R: Anaplastic large cell lymphoma: a critical evaluation of cytomorphological features in seven cases. Cytopathology; 2010 Aug;21(4):251-8
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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 lymphoma: a critical evaluation of cytomorphological features in seven cases.
  • OBJECTIVE: Anaplastic large cell lymphoma (ALCL) is a rare subtype of non-Hodgkin's lymphoma that is difficult to diagnose on fine needle aspiration cytology (FNAC).
  • Detailed descriptions about the cytomorphological features of ALCL are few and do not illustrate the various categories of cells, which we have done in this study.
  • METHODS: Eight FNAC specimens from seven patients with biopsy-proven ALCL over a period of 6 years were reviewed.
  • Cytomorphological details were analysed and the various cell types identified were enumerated on Papanicolaou and May-Grünwald-Giemsa (MGG)-stained smears.
  • RESULTS: Of the seven cases, five were of conventional type, one of the lymphohistiocytic variant and one of the small cell variant.
  • Aspiration from the conventional type showed a mixed population of lymphoid cells with many plasma cells.
  • Aspiration from the lymphohistiocytic and small cell variants showed a small number of similar characteristic giant cells.
  • All cases were confirmed as ALK-1 positive.
  • CONCLUSIONS: The morphological spectrum of ALCL is wide and it may be misdiagnosed as a metastatic poorly differentiated malignant tumour on FNAC.
  • Identification of unusual giant cells on FNAC helps in establishing a diagnosis on an early lymph node biopsy.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Activin Receptors, Type II / metabolism. Adolescent. Adult. Biopsy, Fine-Needle. Female. Humans. Immunohistochemistry. Male. Middle Aged. Young Adult

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  • (PMID = 19744187.001).
  • [ISSN] 1365-2303
  • [Journal-full-title] Cytopathology : official journal of the British Society for Clinical Cytology
  • [ISO-abbreviation] Cytopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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45. Vinogradova IuE, Lutsenko IN, Kaplanskaia IB, Vorob'ev IA, Samoĭlova RS, Gorgidze LA, Ryzhikova NA, Valiev TT, Giliazitdinova EA, Dzhulakian UL, Egorova EK, Zvonkov EE, Krasil'nikova BB, Magomedova AU, Margolin OV, Mar'in DS, Kremenetskaia AM, Kravchenko SK, Vorob'ev AI: [Efficacy of therapy of different variants of anaplastic large T-cell lymphomas]. Ter Arkh; 2008;80(7):33-7
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  • [Title] [Efficacy of therapy of different variants of anaplastic large T-cell lymphomas].
  • AIM: To compare efficacy of NHL-BFM-90 and CHOP-like courses in the treatment of anaplastic large cell lymphoma (ALCL).
  • MATERIAL AND METHODS: Twenty-two patients with ALCL participated in the study.
  • The diagnosis was made basing on the findings of clinical, device, morphological, immunohistochemical and molecular-genetic examinations with application of a panel of monoclonal antibodies to CD30, ALK, CD3, CD4, CDS, CD7, CD34, CD15, CD68, CD20, CD45RO, CD45RA, Ki-67.
  • 14 cases of 22 were negative by kinase of anaplastic lymphocytes (ALK-) and 8 were positive (ALK+).
  • Mean age of ALK-ALCL patients was 39.6 +/- 4.1 years, of ALK+ALCL patients - 23.4 +/- 2.6 years.
  • All 14 patients treated according to NHL-BFM-90 had ALCL stages III-IV with B-symptoms.
  • Of 8 ALCL patients treated initially according to other schemes, a complete remission was achieved in 4 patients (2 had stage II).
  • Four patients who had failed to achieve complete remission died of the disease progression.
  • CONCLUSION: ALCL occurs more frequently in young and middle-aged patients.
  • The disease has an aggressive course with rapid generalization.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • (PMID = 18763592.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 3.5.1.1 / Asparaginase; Q573I9DVLP / Leucovorin; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; BEACOPP protocol; CHOP protocol; MACOP-B protocol; PVDA protocol
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46. Marschalkó M, Eros N, Holló P, Hársing J, Bottlik G, Bátai A, Csukly Z, Masszi T, Szentirmai Z, Fodor J, Kárpáti S, Matolcsy A, Csomor J: Secondary ALK negative anaplastic large cell lymphoma in a patient with lymphomatoid papulosis of 40 years duration. Am J Dermatopathol; 2010 Oct;32(7):708-12
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  • [Title] Secondary ALK negative anaplastic large cell lymphoma in a patient with lymphomatoid papulosis of 40 years duration.
  • At age 44, regional lymph node manifestation of anaplastic lymphoma kinase (ALK) anaplastic large cell lymphoma (ALCL) developed.
  • Four years later, systemic relapse was detected which was refractory to therapy.
  • Histology and immunohistochemistry showed congruent characteristics of multiple skin and lymph node biopsies: diffuse mixed infiltrate with large, anaplastic CD30 cells.
  • Immunophenotype and microscopic morphology suggested a common origin of the different manifestations-however, this could not be proven due to lack of T-cell receptor (TCR) gamma gene rearrangement in most of the samples.
  • The diagnosis of ALK-negative systemic ALCL with cutaneous symptoms was set up at the second flare up, however, the possibility of primary cutaneous ALCL was not excluded steadily.
  • Lymphomatoid papulosis, primary cutaneous ALCL, and systemic ALK ALCL are 3 different entities but the separation of them cannot be solved without distinctive diagnostic tools.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphomatoid Papulosis / pathology. Neoplasms, Second Primary / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fatal Outcome. Humans. Male. Middle Aged. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases


47. 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
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  • [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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48. Yakushijin Y, Shikata H, Kito K, Ohshima K, Kojima K, Hato T, Hasegawa H, Yasukawa M: Follicular dendritic cell tumor as an unknown primary tumor. Int J Clin Oncol; 2007 Feb;12(1):56-8
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  • [Title] Follicular dendritic cell tumor as an unknown primary tumor.
  • A 70-year-old Japanese man presented to our hospital with a 1-month history of progressive general fatigue and anorexia.
  • He eventually died without any diagnosis of his disease.
  • Immunohistochemical staining of his tumor after autopsy showed atypical cells that were negative for epithelial membrane antigen (EMA), keratin (AE1/3), keratin-20, vimentin, factor VIII, leukocyte common antigen (LCA/T200; CD45), myeloperoxidase (MPO), terminal deoxynucleotidyl transferase (TdT), lysozyme, CD1a, CD3, CD4, CD10, CD15, CD20 (L26), CD21, CD23, CD34, CD43, CD56, CD68, CD79a, CD138, and EBER-1 in situ.
  • Only a few scattered cells expressed CD30, but they showed no staining for anaplastic large-cell lymphoma kinase (ALK).
  • A few scattered cells expressed S-100 antigen and the majority of cells dominantly expressed dendritic cell-associated antigens (CD35, FDC, Ki-M1p).
  • In conclusion, we found this unknown primary tumor to be consistent with a follicular dendritic cell tumor with anaplastic features.


49. Bohling SD, Jenson SD, Crockett DK, Schumacher JA, Elenitoba-Johnson KS, Lim MS: Analysis of gene expression profile of TPM3-ALK positive anaplastic large cell lymphoma reveals overlapping and unique patterns with that of NPM-ALK positive anaplastic large cell lymphoma. Leuk Res; 2008 Mar;32(3):383-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of gene expression profile of TPM3-ALK positive anaplastic large cell lymphoma reveals overlapping and unique patterns with that of NPM-ALK positive anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) comprises a group of non-Hodgkin lymphomas characterized by the expression of the CD30/Ki-1 antigen.
  • A subset of ALCL is characterized by chromosomal translocations involving the anaplastic lymphoma kinase (ALK) gene on chromosome 2.
  • While the most common translocation is the t(2;5)(p23;q35) involving the nucleophosmin (NPM) gene on chromosome 5, up to 12 other translocations partners of the ALK gene have been identified.
  • One of these is the t(1;2)(q25;p23) which results in the formation of the chimeric protein TPM3-ALK.
  • While several of the signaling pathways induced by NPM-ALK have been elucidated, those involved in ALCLs harboring TPM3-ALK are largely unknown.
  • In order to investigate the expression profiles of ALCLs carrying the NPM-ALK and TPM3-ALK fusions, we carried out cDNA microarray analysis of two ALCL tissue samples, one expressing the NPM-ALK fusion protein and the other the TPM3-ALK fusion protein.
  • Quantitative fluorescence RT-PCR was performed to validate the cDNA microarray data on nine selected gene targets.
  • Our results show a significant overlap of genes deregulated in the NPM-ALK and TPM-ALK positive lymphomas.
  • These deregulated genes are involved in diverse cellular functions, such as cell cycle regulation, apoptosis, proliferation, and adhesion.
  • Interestingly, a subset of the genes was distinct in their expression pattern in the two types of lymphomas.
  • More importantly, many genes that were not previously associated with ALK positive lymphomas were identified.
  • Our results demonstrate the overlapping and unique transcriptional patterns associated with the NPM-ALK and TPM3-ALK fusions in ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Tropomyosin / genetics
  • [MeSH-minor] Adult. Child. Gene Expression Profiling. Humans. Male. Oligonucleotide Array Sequence Analysis. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 17720243.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; 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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50. Iqbal J, Weisenburger DD, Greiner TC, Vose JM, McKeithan T, Kucuk C, Geng H, Deffenbacher K, Smith L, Dybkaer K, Nakamura S, Seto M, Delabie J, Berger F, Loong F, Au WY, Ko YH, Sng I, Armitage JO, Chan WC, International Peripheral T-Cell Lymphoma Project: Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma. Blood; 2010 Feb 4;115(5):1026-36
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  • [Title] Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma.
  • Peripheral T-cell lymphoma (PTCL) is often challenging to diagnose and classify.
  • Gene expression profiling was performed on 144 cases of PTCL and natural killer cell lymphoma and robust molecular classifiers were constructed for angioimmunoblastic T-cell lymphoma (AITL), anaplastic lymphoma kinase-positive (ALK(+)) anaplastic large-cell lymphoma (ALCL), and adult T-cell leukemia/lymphoma.
  • PTCL-unclassifiable was molecularly heterogeneous, but we were able to identify a molecular subgroup with features of cytotoxic T lymphocytes and a poor survival compared with the remaining PTCL-not otherwise specified cases.
  • Many of the pathologic features and substantial components of the molecular signature of AITL are contributed by the follicular dendritic cells, B-cell, and other stromal components.
  • The expression of Th17-associated molecules in ALK(+) ALCL was noted and may represent aberrant activation of Th17-cell differentiation by abnormal cytokine secretion.
  • Adult T-cell leukemia/lymphoma has a homogeneous molecular signature demonstrating high expression of human T-lymphotropic virus type 1-induced genes.

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  • (PMID = 19965671.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE19069
  • [Grant] United States / NCI NIH HHS / CA / U01 CA114778; United States / NCI NIH HHS / CA / CA36727; United States / NCRR NIH HHS / RR / P20 RR016469; United States / NCI NIH HHS / CA / 5U01/CA114778; United States / NCI NIH HHS / CA / P30 CA036727
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [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
  • [Other-IDs] NLM/ PMC2817630
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51. Chiarle R, Martinengo C, Mastini C, Ambrogio C, D'Escamard V, Forni G, Inghirami G: The anaplastic lymphoma kinase is an effective oncoantigen for lymphoma vaccination. Nat Med; 2008 Jun;14(6):676-80
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  • [Title] The anaplastic lymphoma kinase is an effective oncoantigen for lymphoma vaccination.
  • For lymphoma, vaccination with subject-specific immunoglobulin idiotypes has had the most promising results.
  • Here we show that DNA vaccination with plasmids encoding portions of the cytoplasmic domain of anaplastic lymphoma kinase (ALK), which has been translocated in different fusion proteins necessary for the growth of anaplastic large cell lymphoma (ALCL), protects mice from local and systemic lymphoma growth.
  • The protection is potent and long lasting and elicits ALK-specific interferon-gamma responses and CD8+ T cell-mediated cytotoxicity.
  • A combination of chemotherapy and vaccination significantly enhanced the survival of mice challenged with ALK+ lymphomas.
  • These findings indicate that ALK represents an ideal tumor antigen for vaccination-based therapies of ALCL and possibly other ALK+ human tumors.
  • [MeSH-major] Antigens, Neoplasm / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Lymphoma, Large-Cell, Anaplastic / therapy. Protein-Tyrosine Kinases / immunology. Vaccination
  • [MeSH-minor] Animals. Cell Line, Transformed. Cell Line, Tumor. Cell Transformation, Neoplastic. Fluorescein-5-isothiocyanate / metabolism. Fluorescent Antibody Technique, Direct. Fluorescent Dyes / metabolism. Immunization, Secondary. Immunohistochemistry. Mice. Mice, Inbred BALB C. Mice, Transgenic. Mutation. Plasmids. Receptor Protein-Tyrosine Kinases


52. 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.
  • The most frequent translocation, t(2;5), generates the fusion protein nucleophosmin (NPM)-ALK with intrinsic tyrosine kinase activity.
  • Along with transformation, NPM-ALK induces morphologic changes in fibroblasts and lymphoid cells, suggesting a direct role of ALK in cell shaping.
  • In this study, we used a mass-spectrometry-based proteomic approach to search for proteins involved in cytoskeleton remodeling and identified p130Cas (p130 Crk-associated substrate) as a novel interactor of NPM-ALK.
  • 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.
  • Both of the effects were dependent on ALK kinase activity and on the adaptor protein growth factor receptor-bound protein 2 (Grb2), since no binding or phosphorylation was found with the kinase-dead mutant NPM-ALK(K210R) or in the presence of a Grb2 dominant-negative protein.
  • Phosphorylation of p130Cas by NPM-ALK was partially independent from Src (tyrosine kinase pp60c-src) kinase activity, as it was still detectable in Syf-/- cells.
  • 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.


53. Rassidakis GZ, Thomaides A, Atwell C, Ford R, Jones D, Claret FX, Medeiros LJ: JunB expression is a common feature of CD30+ lymphomas and lymphomatoid papulosis. Mod Pathol; 2005 Oct;18(10):1365-70
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  • [Title] JunB expression is a common feature of CD30+ lymphomas and lymphomatoid papulosis.
  • AP-1 is involved in cell proliferation and apoptosis.
  • Recent evidence suggests that Hodgkin and Reed-Sternberg cells overexpress JunB and that JunB facilitates constitutive CD30 expression by binding to an AP-1 site in the CD30 promoter.
  • In this study we surveyed JunB expression in a variety of CD30+ lymphoma types including 42 cases of anaplastic large cell lymphoma, 36 classical Hodgkin lymphoma, 15 cutaneous anaplastic large cell lymphoma, and 11 CD30+ diffuse large B-cell lymphoma.
  • In addition, seven cases of nodular lymphocyte-predominant Hodgkin lymphoma and 42 diffuse large B-cell lymphoma, known to be CD30-, were analyzed.
  • JunB expression was assessed using tissue microarrays, immunohistochemistry and a monoclonal antibody specific for JunB.
  • Expression of JunB was observed in 41 of 42 cases of anaplastic large cell lymphoma, including all 21 cases positive for anaplastic lymphoma kinase and 20 of 21 (95%) negative for anaplastic lymphoma kinase.
  • JunB was also expressed in all cases of classical Hodgkin lymphoma, cutaneous anaplastic large cell lymphoma and CD30+ diffuse large B-cell lymphoma, and in lymphomatoid papulosis.
  • By contrast, all nodular lymphocyte-predominant Hodgkin lymphomas and diffuse large B-cell lymphomas that were CD30- were also JunB-.
  • We conclude that JunB is expressed in virtually all CD30+ lymphomas and is a potential target for experimental therapy in patients with these tumors.
  • [MeSH-major] Antigens, CD30 / metabolism. Lymphoma / metabolism. Lymphomatoid Papulosis / metabolism. Proto-Oncogene Proteins c-jun / biosynthesis

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  • (PMID = 15920551.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090853
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-jun
  • [Other-IDs] NLM/ NIHMS8252; NLM/ PMC1382062
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54. Mussolin L, Pillon M, d'Amore ES, Santoro N, Lombardi A, Fagioli F, Zanesco L, Rosolen A: Prevalence and clinical implications of bone marrow involvement in pediatric anaplastic large cell lymphoma. Leukemia; 2005 Sep;19(9):1643-7
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  • [Title] Prevalence and clinical implications of bone marrow involvement in pediatric anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) harbors the reciprocal chromosomal translocation t(2;5)(p23;q35) in approximately 80% of the cases.
  • The genes involved are nucleophosmin (NPM) and anaplastic lymphoma kinase (ALK) and the resulting chimeric NPM-ALK protein is thought to play a key role in the pathogenesis of t(2;5) positive ALCL.
  • Few data on bone marrow (BM) involvement in ALCL have been published and they mostly rely on morphological examination of BM smears.
  • We studied 52 ALCL for NPM-ALK expression by RT-PCR: 47/52 biopsies were positive.
  • In 41 of the 47 cases we obtained the BM at diagnosis and investigated the prevalence of minimal BM infiltration by RT-PCR and real-time PCR.
  • Minimal disseminated disease was positive in 25/41 patients (61%), of whom six had morphologically infiltrated BM.
  • Survival analysis demonstrated a 5-year progression-free survival of 41 +/- 11% for patients with molecularly positive BM vs 100% for patients with negative BM (P = 0.001).
  • These results suggest that minimal BM involvement at diagnosis is a common event in pediatric ALCL and that minimal BM disease monitoring could identify patients at risk of relapse.
  • [MeSH-major] Bone Marrow / metabolism. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans. Infant. Male. Neoplasm, Residual. Nuclear Proteins / genetics. Prospective Studies. Protein-Tyrosine Kinases / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis

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  • (PMID = 16049513.001).
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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55. Costello R, Sanchez C, Le Treut T, Rihet P, Imbert J, Sébahoun G: Peripheral T-cell lymphoma gene expression profiling and potential therapeutic exploitations. Br J Haematol; 2010 Jul;150(1):21-7
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  • [Title] Peripheral T-cell lymphoma gene expression profiling and potential therapeutic exploitations.
  • Peripheral T-cell lymphomas constitute a heterogeneous group with regard to diagnosis, treatment and prognosis.
  • Molecular profiling has contributed to novel insights in the biology of T-cell lymphoma.
  • Regarding anaplastic large cell lymphoma, low expression T-cell receptor signalling and high STAT3 target signatures have been associated with the ALK-positive subgroup.
  • Gene expression profiling differentiates angioblastic T-cell lymphoma from other T-cell malignancies, suggests that the normal counterpart of lymphoma cells are follicular helper T cells, and supports the involvement of vascular endothelial growth factor deregulation in its physiopathology.
  • In peripheral T-cell lymphoma unspecified, gene profiling suggests the normal counterpart of tumour cells are activated CD4(+) or CD8(+) T-lymphocytes, delineates prognostic groups depending on the proliferative signature, and suggests therapeutic options aimed at regulating nuclear factor-kappaB and platelet-derived growth factor receptor-alpha phosphorylation.
  • Gene expression profiling of primary cutaneous T cell lymphomas highlighted the importance of abnormal methylation patterns, suggested a pivotal role for JUNB/AP-1, and defined a predictive model for response to interferon-alpha.
  • In conclusion, gene expression profiling is beginning to change the pathological classification, the prognosis profiles and the therapeutic approach in T-cell lymphomas.
  • [MeSH-major] Lymphoma, T-Cell, Peripheral / genetics
  • [MeSH-minor] Gene Expression Profiling. Humans. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / therapy. Oligonucleotide Array Sequence Analysis


56. Cooper PB, Auerbach A, Aguilera NS, Adair C, Moores L, Geyer D, Rushing EJ: Rare primary CNS anaplastic large cell lymphoma in an immunocompetent adult: a clinical-pathologic case report and review case of the literature. Clin Neuropathol; 2006 Sep-Oct;25(5):232-6
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  • [Title] Rare primary CNS anaplastic large cell lymphoma in an immunocompetent adult: a clinical-pathologic case report and review case of the literature.
  • OBJECTIVE AND IMPORTANCE: Isolated anaplastic large cell lymphoma (ALCL) presenting in the primary central nervous system is distinctly uncommon.
  • CLINICAL PRESENTATION: A 39-year-old immunocompetent male presented with seizures and a rapidly enlarging right occipital/parietal lesion.
  • Biopsy showed a proliferation of single cells and poorly cohesive groups of cells with large, pleomorphic nuclei, many containing prominent nucleoli, and a moderate amount of cytoplasm.
  • Immunohistochemical staining revealed CD-30 and ALK-positivity typical of ALCL, a rare form of T-cell lymphoma.
  • An extensive workup revealed neither systemic disease nor evidence of immunocompromise.
  • CONCLUSION: Reported in less than 20 patients, primary ALCL in an immunocompetent patient is rarely found intracranially; however, its ability to mimic glial neoplasms as well as other pathologies underlines its importance.
  • [MeSH-major] Brain Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biomarkers, Tumor / analysis. Combined Modality Therapy. Diagnosis, Differential. Glioma / pathology. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Radiotherapy. Seizures / etiology


57. Ahmed B, Estey E, Manning J, David C, Keating MJ, Kantarjian H, Tsimberidou AM: Anaplastic large cell lymphoma with involvement of the pancreas presenting as panniculitis in a patient with a history of acute myeloid leukemia--case report and review of the literature. Haematologica; 2006 Dec;91(12 Suppl):ECR55
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  • [Title] Anaplastic large cell lymphoma with involvement of the pancreas presenting as panniculitis in a patient with a history of acute myeloid leukemia--case report and review of the literature.
  • An autopsy of the pancreas revealed clusters of large, atypical cells, which morphologically and immunophenotypically were consistent with CD30 positive, ALK-negative anaplastic large cell lymphoma (ALCL) of T-cell lineage and multifocal fat necrosis (panniculitis) in the peripancreatic adipose tissue.
  • This is the first case of ALCL of the pancreas and panniculitis in a patient with history of AML.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Lymphoma, Large-Cell, Anaplastic / diagnosis. Neoplasms, Second Primary / diagnosis. Pancreas / pathology. Panniculitis / etiology
  • [MeSH-minor] Acute Disease. Aged. Fatal Outcome. Humans. Male. Neoplasm Proteins / analysis. Respiratory Insufficiency / etiology


58. Li HL, Jiang HY, Ji TH, Chu HJ, Liu F, Chen XY, Wang X, Zhang G, Zhao T: [Nuclear microarray combined with fluorescence in situ hybridization for detecting ALK gene translocation in paraffin-embedded anaplastic large cell lymphoma and its significance]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Apr;28(4):572-5
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  • [Title] [Nuclear microarray combined with fluorescence in situ hybridization for detecting ALK gene translocation in paraffin-embedded anaplastic large cell lymphoma and its significance].
  • OBJECTIVE: To compare the efficacy of nuclear microarray combined with fluorescence in situ hybridization (FISH) and immunohistochemistry in detecting ALK gene translocation and ALK fusion protein in anaplastic large cell lymphoma (ALCL).
  • METHODS: ALK gene translocation and ALK fusion protein in 17 paraffin-embedded ALCL specimens were detected using nuclear microarray combined with FISH and immunohistochemical straining, respectively.
  • RESULTS: The expression of ALK fusion protein was detected immunohistochemically with ALK antibody in 8 of the 17 specimens of systemic ALCL, including 4 with both nuclear and cytoplasmic positivity and 4 with only cytoplasmic positivity.
  • Dual-color FISH identified 6 positive specimens, including the 4 specimens with both nuclear and cytoplasmic positivity as identified immunohistochemically, and 2 with immunohistochemical cytoplasmic positivity.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Male. Microarray Analysis / methods. Middle Aged. Paraffin Embedding. Receptor Protein-Tyrosine Kinases. Reproducibility of Results. Young Adult

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  • (PMID = 18495593.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [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
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59. Tan BT, Seo K, Warnke RA, Arber DA: The frequency of immunoglobulin heavy chain gene and T-cell receptor gamma-chain gene rearrangements and Epstein-Barr virus in ALK+ and ALK- anaplastic large cell lymphoma and other peripheral T-cell lymphomas. J Mol Diagn; 2008 Nov;10(6):502-12
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  • [Title] The frequency of immunoglobulin heavy chain gene and T-cell receptor gamma-chain gene rearrangements and Epstein-Barr virus in ALK+ and ALK- anaplastic large cell lymphoma and other peripheral T-cell lymphomas.
  • We previously identified a relatively high frequency of B-cell proliferations along with simultaneous T-cell receptor gamma-chain gene (TRG) and immunoglobulin heavy chain gene (IGH) rearrangements in a series of angioimmunoblastic T-cell lymphoma and peripheral T-cell lymphoma, unspecified.
  • Here, we report on a series of 74 peripheral T-cell lymphoma (PTCL) cases composed entirely of specific PTCL subtypes, including 28 cases of ALK+ anaplastic large-cell lymphoma (ALCL), 35 cases of ALK- ALCL, and 11 cases that represent other specific PTCL subtypes.
  • We performed IGH and TRG gene rearrangement studies and in situ hybridization for Epstein-Barr virus (EBV) to determine the frequency of IGH clonality and to investigate the relationship between EBV, clonality, and associated B-cell proliferations.
  • Using BIOMED-2 PCR assays, we detected TRG clones in 64 of 74 (86%) cases and IGH clones in 6 of 74 (8%) cases, with all IGH-positive cases exhibiting a concurrent TRG clone.
  • Despite the detection of occasional IGH clones, there was no correlation between IGH clonality and EBV, and B-cell proliferations were not identified in any of the cases.
  • These findings suggest that other factors contribute to IGH clonality and demonstrate that, in the absence of an associated B-cell proliferation, IGH clonality occurs infrequently (8%) in specific PTCL subtypes.
  • [MeSH-major] Gene Rearrangement. Genes, T-Cell Receptor gamma. Herpesvirus 4, Human / immunology. Immunoglobulin Heavy Chains / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, T-Cell, Peripheral / genetics. Protein-Tyrosine Kinases / metabolism. Receptors, Antigen, T-Cell, gamma-delta / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Female. Humans. Male. Middle Aged. Receptor Protein-Tyrosine Kinases. Young Adult

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  • (PMID = 18832464.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell, gamma-delta; 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/ PMC2570633
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60. Qiu L, Lai R, Lin Q, Lau E, Thomazy DM, Calame D, Ford RJ, Kwak LW, Kirken RA, Amin HM: Autocrine release of interleukin-9 promotes Jak3-dependent survival of ALK+ anaplastic large-cell lymphoma cells. Blood; 2006 Oct 1;108(7):2407-15
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  • [Title] Autocrine release of interleukin-9 promotes Jak3-dependent survival of ALK+ anaplastic large-cell lymphoma cells.
  • The aberrant fusion protein NPM-ALK plays an important pathogenetic role in ALK+ anaplastic large-cell lymphoma (ALCL).
  • We previously demonstrated that Jak3 potentiates the activity of NPM-ALK.
  • Jak3 activation is restricted to interleukins that recruit the common gamma chain (gammac) receptor, including IL-9.
  • NPM-ALK was previously shown to promote widespread lymphomas in IL-9 transgenic mice by unknown mechanisms.
  • We hypothesized that IL-9 plays an important role in ALK+ ALCL via Jak3 activation.
  • Our studies demonstrate the expression of IL-9Ralpha and IL-9 in 3 ALK+ ALCL-cell lines and 75% and 83% of primary tumors, respectively.
  • IL-9 was detected in serum-free culture medium harvested from ALK+ ALCL-cell lines, supporting autocrine release of IL-9.
  • Treatment of these cells with an anti-IL-9-neutralizing antibody decreased pJak3 and its kinase activity, along with pStat3 and ALK kinase activity.
  • These effects were associated with decreased cell proliferation and colony formation in soft agar and cell-cycle arrest.
  • Evidence suggests that cell-cycle arrest can be attributed to up-regulation of p21 and down-regulation of Pim-1.
  • Our results illustrate that IL-9/Jak3 signaling plays a significant role in the pathogenesis of ALK+ ALCL and that it represents a potential therapeutic target for treating patients with ALK+ ALCL.

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  • (PMID = 16763206.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395; United States / NIAID NIH HHS / AI / AI053566; United States / NCI NIH HHS / CA / K08CA114395; United States / NCRR NIH HHS / RR / SG12RR008124
  • [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 / Interleukin-9; 0 / JAK3 protein, human; 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 / Jak3 protein, mouse; EC 2.7.10.2 / Janus Kinase 3
  • [Other-IDs] NLM/ PMC1895569
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61. 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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62. Lamant L, de Reyniès A, Duplantier MM, Rickman DS, Sabourdy F, Giuriato S, Brugières L, Gaulard P, Espinos E, Delsol G: Gene-expression profiling of systemic anaplastic large-cell lymphoma reveals differences based on ALK status and two distinct morphologic ALK+ subtypes. Blood; 2007 Mar 1;109(5):2156-64
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  • [Title] Gene-expression profiling of systemic anaplastic large-cell lymphoma reveals differences based on ALK status and two distinct morphologic ALK+ subtypes.
  • With the use of microarray gene-expression profiling, we analyzed a homogeneous series of 32 patients with systemic anaplastic large-cell lymphoma (ALCL) and 5 ALCL cell lines.
  • Unsupervised analysis classified ALCL in 2 clusters, corresponding essentially to morphologic subgroups (ie, common type vs small cell and "mixed" variants) and clinical variables.
  • Patients with a morphologic variant of ALCL had advanced-stage disease.
  • Supervised analysis showed that ALK+ALCL and ALK- ALCL have different gene-expression profiles, further confirming that they are different entities.
  • Among the most significantly differentially expressed genes between ALK+ and ALK- samples, we found BCL6, PTPN12, CEBPB, and SERPINA1 genes to be overexpressed in ALK+ ALCL.
  • This result was confirmed at the protein level for BCL-6, C/EBPbeta and serpinA1 through tissue microarrays.
  • The molecular signature of ALK- ALCL included overexpression of CCR7, CNTFR, IL22, and IL21 genes but did not provide any obvious clues to the molecular mechanism underlying this tumor subtype.
  • Once confirmed on a larger number of patients, the results of the present study could be used for clinical and therapeutic management of patients at the time of diagnosis.
  • [MeSH-major] Cell Shape. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Cell Line, Tumor. Humans. Immunohistochemistry. RNA, Messenger / genetics. Receptor Protein-Tyrosine Kinases. Tissue Array Analysis


63. Giuriato S, Faumont N, Bousquet E, Foisseau M, Bibonne A, Moreau M, Al Saati T, Felsher DW, Delsol G, Meggetto F: Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy. Cancer Biol Ther; 2007 Aug;6(8):1318-23
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  • [Title] Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy.
  • Overexpression and activation of TPM3-ALK tyrosine kinase fusion protein is a causal oncogenic event in the development of Anaplastic Large Cell Lymphoma and Inflammatory Myofibroblastic ALK-positive tumors.
  • Thus, the development of ALK specific tyrosine kinase inhibitors is a current therapeutic challenge.
  • Animal models are essential to assess, in vivo, the efficiency of ALK-oncogene inhibitors and to identify new and/or additional therapeutic targets in the ALK tumorigenesis pathway.
  • Using the tetracycline system to allow conditional and concomitant TPM3-ALK and luciferase expression, we have developed a unique transplant model for bioluminescent TPM3-ALK-induced fibroblastic tumors in athymic nude mice.
  • The reversible TPM3-ALK expression allowed us to demonstrate that this oncogene is essential for the tumor growth and its maintenance.
  • In addition, we showed that this model could be used to precisely assess tumor growth inhibition upon ALK chemical inactivation.
  • As proof of principle, we used the general tyrosine kinase inhibitor herbimycin A to inhibit ALK oncoprotein activity.
  • We conclude that this transplant model for TPM3-ALK-induced tumors represents a valuable tool not only to accurately and rapidly evaluate in vivo ALK-targeted therapies but also to gain insight into the mechanism of ALK-positive tumor development.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Disease Models, Animal. Lymphoma, Large-Cell, Anaplastic / drug therapy. Mice. Oncogene Proteins, Fusion / antagonists & inhibitors. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Tropomyosin / antagonists & inhibitors
  • [MeSH-minor] Animals. Benzoquinones / pharmacology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Drug Screening Assays, Antitumor / methods. Genes, Reporter. Lactams, Macrocyclic / pharmacology. Luciferases / analysis. Luciferases / genetics. Luminescent Agents / analysis. Mice, Nude. Neoplasm Transplantation. Receptor Protein-Tyrosine Kinases. Rifabutin / analogs & derivatives

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  • (PMID = 17660712.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Benzoquinones; 0 / Lactams, Macrocyclic; 0 / Luminescent Agents; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; 0 / Tpm3 protein, mouse; 0 / Tropomyosin; 1W306TDA6S / Rifabutin; 70563-58-5 / herbimycin; EC 1.13.12.- / Luciferases; 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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64. Asano N, Suzuki R, Ohshima K, Kagami Y, Ishida F, Yoshino T, Ogawa H, Morishima Y, Nakamura S: Linkage of expression of chemokine receptors (CXCR3 and CCR4) and cytotoxic molecules in peripheral T cell lymphoma, not otherwise specified and ALK-negative anaplastic large cell lymphoma. Int J Hematol; 2010 Apr;91(3):426-35
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  • [Title] Linkage of expression of chemokine receptors (CXCR3 and CCR4) and cytotoxic molecules in peripheral T cell lymphoma, not otherwise specified and ALK-negative anaplastic large cell lymphoma.
  • Peripheral T cell lymphoma not otherwise specified (PTCL-N) and ALK-negative anaplastic large cell lymphoma (ALCL) are heterogeneous categories with poor diagnostic reproducibility.
  • To clarify the biologic features of these categories, we investigated the expression of two chemokine receptors, type 1 (Th1/Tc1)-associated CXCR3 and type 2 (Th2/Tc2)-associated CCR4 in 110 PTCL-N and 35 ALK-negative ALCL cases, as well as the expression of cytotoxic molecules (CM).
  • CXCR3 and CCR4 were expressed in 69 (63%) and 37 (34%) of PTCL-N, and in 12 (34%) and 6 (17%) of ALK-negative ALCL, respectively.
  • In PTCL-N, type 1 pattern (CXCR3(+)CCR4(-)) was dominant (52%), whereas in ALK-negative ALCL, 54% were negative for both (P < 0.0001).
  • CM was expressed in 38% of PTCL-N and 51% of ALK-negative ALCL.
  • CM-positive PTCL-N consisted mostly of type 1 disease, which shows type 1 phenotype.
  • In contrast, type 2 pattern (CXCR3(-)CCR4(+)) was recognized in the CM-negative group only.
  • Among type 1 disease, CM-positive cases had a higher female ratio and more aggressive clinical features than CM-negative cases and a poorer prognosis (P = 0.006).
  • Multivariate analysis confirmed that the type 1 phenotype with CM expression was an independent prognostic factor.
  • In both PTCL-N and ALK-negative ALCL, CM-positive type 1 disease had an extremely poor prognosis.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, T-Cell / metabolism. Receptors, CCR4 / metabolism. Receptors, CXCR3 / metabolism


65. Grewal JS, Smith LB, Winegarden JD 3rd, Krauss JC, Tworek JA, Schnitzer B: Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature. Ann Hematol; 2007 Jul;86(7):499-508
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  • [Title] Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive neoplasm of T- or null cell phenotype and is recognized as a distinct clinicopathologic subtype of non-Hodgkin lymphoma (NHL) in the revised World Health Organization (WHO) classification of hematopoietic neoplasms.
  • Most cases with leukemic involvement are the small cell variant of ALCL.
  • These cases often lack the pleomorphism seen in the common variant of ALCL and may be misdiagnosed.
  • We report a series of three patients who presented with leukemic phase ALCL.
  • The patients included an 11-year-old boy, a 29-year-old man, and a 59-year-old woman.
  • The patients in our case series with leukemic phase ALCL exhibited rare clinical features.
  • The patients presented with massive extranodal disease involving cerebrospinal fluid (CSF), liver, spleen, lungs, and bone marrow.
  • Two of the patients had small cell variant and the third patient had common type ALCL.
  • The neoplastic cells in all three patients were ALK positive; however these patients died within months of diagnosis.
  • Leukemic phase ALCL is rare, and behaves in an aggressive manner.
  • Some, but not all, cases in the literature presenting with peripheral blood involvement had small cell variant ALCL, as seen in two of our cases.
  • The leukemic phase of ALCL should be considered when a T-cell leukemia with unusual morphologic features is encountered.
  • [MeSH-major] Leukemia / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Fatal Outcome. Female. Humans. Immunophenotyping. Male. Middle Aged. Receptor Protein-Tyrosine Kinases

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  • (PMID = 17396261.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [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] 91
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66. Beltran B, Castillo J, Salas R, Quiñones P, Morales D, Hurtado F, Riva L, Winer E: ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature. J Hematol Oncol; 2009;2:11
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature.
  • BACKGROUND: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma (ALK-DLBCL) is a rare lymphoma with several clinicopathological differences from ALK-positive anaplastic large cell lymphoma (ALCL).
  • The latest WHO classification of lymphomas recognizes ALK-DLBCL as a separate entity.
  • Two cases had primary extranodal disease (multifocal bone and right nasal fossa).
  • By immunohistochemistry, cases were positive for cytoplasmic ALK, MUM1, CD45, and EMA; they marked negative for CD3, CD30 and CD20.
  • CONCLUSION: ALK-DLBCL is a distinct variant of DLBCL with plasmacytic differentiation, which is characterized by a bimodal age incidence curve, primarily nodal involvement, plasmablastic morphology, lack of expression of CD20, aggressive behavior and poor response to standard therapies, although some cases can have prolonged survival as the cases reported in this study.
  • ALK-DLBCL does not seem associated to immunosuppression or the presence of EBV or HHV8.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD20 / metabolism. Female. Humans. Interferon Regulatory Factors / metabolism. Male. Prognosis. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19250532.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; 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] 39
  • [Other-IDs] NLM/ PMC2651189
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67. Chan JK, Kwong YL: Common misdiagnoses in lymphomas and avoidance strategies. Lancet Oncol; 2010 Jun;11(6):579-88
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  • [Title] Common misdiagnoses in lymphomas and avoidance strategies.
  • Lymphoma diagnosis integrates clinical, morphological, immunophenotypical, and molecular genetic features, as shown in WHO classifications of lymphoid malignancies.
  • Diagnosis of lymphoma is challenging.
  • Reactive lesions such as Kikuchi lymphadenitis, infectious mononucleosis, autoimmune lymphoproliferative syndrome, and immunoglobulin G4-related sclerosing disease can be misdiagnosed as lymphomas.
  • Anaplastic large-cell lymphoma variants that are positive for anaplastic lymphoma kinase, classical Hodgkin's lymphoma variants, and infarcted lymphomas might be misdiagnosed as reactive disorders.
  • Difficulties with classification of lymphomas are also encountered, such as the distinction of classical Hodgkin's lymphoma from anaplastic large-cell lymphoma that is negative for anaplastic lymphoma kinase.
  • Interpretation of immunophenotyping results is complicated in some cases by aberrant or cross-lineage expression of lymphoid antigens on lymphomas, and the occasional lymphoid antigen expression on non-lymphoid malignancies.
  • Molecular analysis can help to define clonality and lineage, but can be affected by the sensitivity and specificity of tests and cross-lineage gene rearrangement and pseudoclonality.
  • [MeSH-major] Diagnostic Errors. Lymphoma / diagnosis
  • [MeSH-minor] Antigens, CD20 / analysis. Antigens, CD3 / analysis. False Negative Reactions. Gene Rearrangement. Humans. Immunophenotyping. Polymerase Chain Reaction

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20227918.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, CD3
  • [Number-of-references] 74
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68. Matsushita H, Nakamura N, Asai S, Yabe M, Hayama N, Kondo Y, Urano T, Miyachi H: A leukemic change as an initial manifestation of the common variant type of ALK-positive anaplastic large cell lymphoma in a patient with lung adenocarcinoma. Intern Med; 2008;47(23):2057-62
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  • [Title] A leukemic change as an initial manifestation of the common variant type of ALK-positive anaplastic large cell lymphoma in a patient with lung adenocarcinoma.
  • We report an 81-year-old man who had leukemic presentation of ALK-positive anaplastic large cell lymphoma (ALCL) as an initial manifestation.
  • The peripheral blood smear and bone marrow aspiration revealed the infiltration of atypical large cells with horseshoe-shaped or lobulated nuclei.
  • The detection of CD30 expression and the t (2;5) (p23;q35) translocation in these cells was confirmatory of a diagnosis of common variant ALK-positive ALCL in a leukemic phase.
  • An adequate, prompt diagnosis is necessary for this rare disease status in oncologic emergency to improve the disease management.
  • [MeSH-major] Adenocarcinoma / diagnosis. Genetic Variation / genetics. Lung Neoplasms / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis
  • [MeSH-minor] Aged, 80 and over. Antigens, CD30 / genetics. Diagnosis, Differential. Humans. Male

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  • (PMID = 19043261.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Number-of-references] 20
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69. Cotta CV, Leventaki V, Atsaves V, Vidaki A, Schlette E, Jones D, Medeiros LJ, Rassidakis GZ: The helix-loop-helix protein Id2 is expressed differentially and induced by myc in T-cell lymphomas. Cancer; 2008 Feb 1;112(3):552-61
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  • [Title] The helix-loop-helix protein Id2 is expressed differentially and induced by myc in T-cell lymphomas.
  • BACKGROUND: Inhibitor of DNA binding 2 (Id2), a helix-loop-helix protein of the inhibitor of differentiation (ID) family, is involved in hematopoiesis, mainly through interaction with the E-family of transcription factors.
  • Recent studies have shown that Id2 is overexpressed in some types of B-cell lymphoma, including classical Hodgkin lymphoma.
  • The authors of the current study hypothesized that Id2 also is overexpressed in T-cell lymphomas.
  • METHODS: By using reverse-transcriptase polymerase chain reaction (RT-PCR) and Western blot analyses, high Id2 messenger RNA (mRNA) and protein levels, respectively, were detected in all 4 T-cell anaplastic large cell lymphoma (ALCL) cell lines that were tested.
  • RESULTS: Immunohistochemistry results indicated that Id2 was expressed strongly in 21 of 27 (78%) ALCL tumors (79% anaplastic lymphoma kinase [ALK]-negative and 75% ALK-positive), in 5 of 10 (50%) extranodal natural killer/T (NK/T)-cell lymphomas of the nasal type, in 2 of 8 (25%) cutaneous ALCLs, in 2 of 9 (22%) enteropathy type T-cell lymphomas, in 1 of 5 (20%) peripheral T-cell lymphomas not otherwise specified, and in 1 of 8 (13%) T-cell prolymphocytic leukemias.
  • Other types of T-cell lymphoma were negative for Id2.
  • Because it is known that myc is expressed in ALCL, myc was inhibited selectively in 2 ALCL cell lines, resulting in a concentration-dependent decrease in Id2 mRNA and protein levels.
  • Conversely, forced expression of myc in HEK 293T cells using an myc/green fluorescent protein adenoviral vector resulted in Id2 up-regulation.
  • CONCLUSIONS: Taken together, the current data suggest that Id2 commonly is overexpressed in highly proliferative T-cell lymphomas, and its expression may result from transcriptional activation of myc in these tumors.
  • [MeSH-major] Inhibitor of Differentiation Protein 2 / metabolism. Lymphoma, T-Cell / metabolism. Proto-Oncogene Proteins c-myc / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Gene Expression Regulation, Neoplastic / physiology. Hodgkin Disease / metabolism. Hodgkin Disease / pathology. Humans. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, Non-Hodgkin / metabolism. Lymphoma, Non-Hodgkin / pathology. Lymphomatoid Papulosis / metabolism. Lymphomatoid Papulosis / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Skin Neoplasms / metabolism. Skin Neoplasms / pathology. Up-Regulation / physiology

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  • (PMID = 18085637.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger
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70. Pant V, Jambhekar NA, Madur B, Shet TM, Agarwal M, Puri A, Gujral S, Banavali M, Arora B: Anaplastic large cell lymphoma (ALCL) presenting as primary bone and soft tissue sarcoma--a study of 12 cases. Indian J Pathol Microbiol; 2007 Apr;50(2):303-7
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  • [Title] Anaplastic large cell lymphoma (ALCL) presenting as primary bone and soft tissue sarcoma--a study of 12 cases.
  • This study highlights the rare presentation of anaplastic large cell lymphoma as primary bone and soft tissue tumour.
  • Clinical impression was non Hodgkin's lymphoma in 4 cases, sarcoma in 6 (osteosarcoma-2, Ewing's/primitive neuroectodermal tumour-1, and sarcoma NOS-3), and tuberculosis of thoracic spine in 1 and the last case involving the rib had a differential diagnosis of tuberculosis and NHL.
  • Immunohistochemically all tumours were CD30 positive and 8 of 9 cases (88.9%) showed ALK-1 positivity.
  • This alone will lead to an accurate recognition of ALCL and the appropriate chemotherapy.
  • [MeSH-major] Bone Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Sarcoma / pathology. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Activin Receptors, Type II / metabolism. Adolescent. Adult. Antigens, CD30 / metabolism. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male


71. Majhail NS, Burns LJ: Hematopoietic stem cell transplantation in the treatment of peripheral T-cell lymphomas. Curr Hematol Rep; 2005 Jul;4(4):252-9
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  • [Title] Hematopoietic stem cell transplantation in the treatment of peripheral T-cell lymphomas.
  • Peripheral T-cell lymphomas (PTCL) are a rare group of heterogeneous lymphoproliferative disorders with their origin in the post-thymic T cells.
  • Anaplastic large cell lymphoma (ALCL) has a better prognosis compared with other subtypes of PTCL.
  • As with aggressive B-cell non-Hodgkin's lymphoma, high-dose chemotherapy followed by autologous stem cell transplantation should be offered to patients with PTCL in their first relapse.
  • Patients with poor-risk features (alk-negative ALCL, histologic subtypes other than ALCL, and high International Prognostic Index score at presentation) may be candidates for autologous stem cell transplantation as first-line therapy.
  • Initial results of allogeneic stem cell transplantation, both with standard and nonmyeloablative conditioning, look promising.
  • Randomized, multi-institutional clinical trials are needed to optimally define the role of stem cell transplantation in PTCL.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, T-Cell, Peripheral / surgery
  • [MeSH-minor] Humans. Immunophenotyping. Prognosis. Stem Cell Transplantation. Transplantation, Autologous

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  • (PMID = 16009039.001).
  • [ISSN] 1541-0714
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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72. Khor TS, Alessandri AJ, Jevon GP: Infant anaplastic large cell lymphoma with hemophagocytic syndrome. Pediatr Dev Pathol; 2010 Jan-Feb;13(1):72-6
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  • [Title] Infant anaplastic large cell lymphoma with hemophagocytic syndrome.
  • Anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK)-positive, is uncommon in infancy.
  • We present an unusual occurrence of infant ALCL, ALK-positive, associated with hemophagocytic syndrome.
  • To the best of our knowledge, there have been no cases of infant ALCL, ALK-positive, described that have been associated with hemophagocytic syndrome.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Antigens, CD30 / metabolism. Biomarkers, Tumor / metabolism. Chromosomes, Human, Pair 2. Failure to Thrive. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Infant. Lymph Nodes / pathology. Male. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 19863446.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 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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73. Osajima-Hakomori Y, Miyake I, Ohira M, Nakagawara A, Nakagawa A, Sakai R: Biological role of anaplastic lymphoma kinase in neuroblastoma. Am J Pathol; 2005 Jul;167(1):213-22
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  • [Title] Biological role of anaplastic lymphoma kinase in neuroblastoma.
  • Anaplastic lymphoma kinase (ALK) is a tyrosine kinase receptor originally identified as part of the chimeric nucleophosmin-ALK protein in the t(2;5) chromosomal rearrangement associated with anaplastic large cell lymphoma.
  • We recently demonstrated that the ALK kinase is constitutively activated by gene amplification at the ALK locus in several neuroblastoma cell lines.
  • Forming a stable complex with hyperphosphorylated ShcC, activated ALK modifies the responsiveness of the mitogen-activated protein kinase pathway to growth factors.
  • In the present study, the biological role of activated ALK was examined by suppressing the expression of ALK kinase in neuroblastoma cell lines using an RNA interference technique.
  • The suppression of activated ALK in neuroblastoma cells by RNA interference significantly reduced the phosphorylation of ShcC, mitogen-activated protein kinases, and Akt, inducing rapid apoptosis in the cells.
  • By immunohistochemical analysis, the cytoplasmic expression of ALK was detected in most of the samples of neuroblastoma tissues regardless of the stage of the tumor, whereas significant amplification of ALK was observed in only 1 of 85 cases of human neuroblastoma samples.
  • These data demonstrate the limited frequency of ALK activation in the real progression of neuroblastoma.
  • [MeSH-major] Neuroblastoma / enzymology. Neuroblastoma / genetics. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Apoptosis / physiology. Blotting, Southern. Cell Line, Tumor. Child, Preschool. Enzyme Activation / physiology. Gene Amplification. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Infant. Mitogen-Activated Protein Kinases / metabolism. Neuropeptides / metabolism. Phosphorylation. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. RNA Interference. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. Shc Signaling Adaptor Proteins

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  • (PMID = 15972965.001).
  • [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 / Neuropeptides; 0 / Proto-Oncogene Proteins; 0 / SHC3 protein, human; 0 / Shc Signaling Adaptor Proteins; 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 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1603453
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74. Nguyen JT, Condron MR, Nguyen ND, De J, Medeiros LJ, Padula A: Anaplastic large cell lymphoma in leukemic phase: extraordinarily high white blood cell count. Pathol Int; 2009 May;59(5):345-53
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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 lymphoma in leukemic phase: extraordinarily high white blood cell count.
  • Anaplastic large cell lymphoma (ALCL) is a distinct type of T/null-cell non-Hodgkin lymphoma that commonly involves nodal and extranodal sites.
  • The World Health Organization of lymphoid neoplasms recognizes two types: anaplastic lymphoma kinase (ALK) positive or ALK negative, the former as a result of abnormalities involving the ALK gene at chromosome 2p23.
  • Patients with ALCL rarely develop a leukemic phase of disease, either at the time of initial presentation or during the clinical course.
  • Described herein is a patient with ALK+ ALCL, small cell variant, associated with the t(2;5)(p23;q35), who initially presented with leukemic involvement and an extraordinarily high leukocyte count of 529 x 10(9)/L, which subsequently peaked at 587 x 10(9)/L.
  • Despite chemotherapy the patient died 2(1/2) months after diagnosis.
  • In the literature review 20 well-documented cases are identified of ALCL in leukemic phase reported previously, with a WBC ranging from 15 to 151 x 10(9)/L.
  • Leukemic phase of ALCL occurs almost exclusively in patients with ALK+ ALCL, most often associated with the small cell variant and the t(2;5)(p23;q35), similar to the present case.
  • Patients with leukemic phase ALK+ ALCL appear to have a poorer prognosis than most patients with ALK+ ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / blood. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Flow Cytometry. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Leukocyte Count. Male. Polymerase Chain Reaction. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19432678.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Australia
  • [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] 19
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75. Cluzeau T, Pécuchet N, Mounier N, Vignot S: [Implications of ALK (anaplastic lymphoma kinase) in oncohematology]. Bull Cancer; 2010 Aug;97(8):991-6
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  • [Title] [Implications of ALK (anaplastic lymphoma kinase) in oncohematology].
  • [Transliterated title] Implications d'ALK (anaplastic lymphoma kinase) en oncohématologie.
  • The anaplastic lymphoma kinase gene (ALK) code for a receptor tyrosine-kinase.
  • The fusion proteins from the ALK gene have been identified in oncohaematology malignancies including ALK positive anaplastic lymphoma large cell and non small cells lung cancer with EML4-ALK fusion gene.
  • Constitutive activation generated by modification of this protein leads activation of anti apoptotic and survey pathways that makes it a prime target for these 2 subtypes of disease.
  • Strategies and therapeutic molecules targeting the fusion protein are under development and preliminary results are encouraging.
  • The best example is the chronic myeloid leukemia and the discovery of the fusion gene bcr-abl and of imatinib.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / enzymology. Lung Neoplasms / enzymology. Lymphoma, Large-Cell, Anaplastic / enzymology. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Fusion Proteins, bcr-abl / genetics. Humans. Nucleoplasmins / genetics. Nucleoplasmins / metabolism. Receptor Protein-Tyrosine Kinases

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  • (PMID = 20483705.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Nucleoplasmins; 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; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 27
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76. 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.
  • (1) a sensitive reverse transcription-polymerase chain reaction (RT-PCR) assay for various X-ALK fusion genes, (2) a 5' rapid amplification of cDNA ends (RACE) assay to identify unknown fusion partners, and (3) a real-time RT-PCR assay to quantify the amount of the NPM-ALK fusion transcript.
  • 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.
  • The 5' RACE assay detected ATIC-ALK fusion in the remaining case.
  • The real-time quantitative RT-PCR assay showed that the NPM-ALK transcript was over expressed in four of 20 quantifiable cases.
  • Patients with NPM-ALK overexpression showed a significantly unfavorable overall survival compared with those with a low expression of this transcript.
  • The RT-PCR and 5' RACE assays developed here may be useful for identification of known and unknown gene partners fused to the ALK gene.
  • 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
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor / biosynthesis. Child. Child, Preschool. Female. Fixatives. Formaldehyde. Humans. Infant. Male. Middle Aged. Paraffin Embedding. Predictive Value of Tests. Prognosis. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction

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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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77. 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).
  • Both transcriptional and post-translational mechanisms account for the constitutive expression of the protein, and the PI3K/Akt pathway is essential for this process.
  • Importantly, pharmacological inhibition of CDC25 dramatically inhibits the proliferation of NPM/ALK-expressing cells, while moderately affecting the proliferation of control Ba/F3 cells.
  • RNA interference-mediated downregulation of CDC25A confirmed that NPM/ALK-expressing cells are highly dependent on this protein for their proliferation.
  • 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
  •