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1. Turner SD, Merz H, Yeung D, Alexander DR: CD2 promoter regulated nucleophosmin-anaplastic lymphoma kinase in transgenic mice causes B lymphoid malignancy. Anticancer Res; 2006 Sep-Oct;26(5A):3275-9
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  • [Title] CD2 promoter regulated nucleophosmin-anaplastic lymphoma kinase in transgenic mice causes B lymphoid malignancy.
  • BACKGROUND: Nucleophosmin-anaplastic lymphoma kinase expression is associated with a lymphoid malignancy, anaplastic large cell lymphoma, and is characterized by a t(2;5) chromosomal translocation.
  • MATERIALS AND METHODS: We describe a novel transgenic mouse line in which NPM-ALK expression is targeted to the T-cell lineage using the CD2 promoter.
  • RESULTS: Surprisingly, the mice develop B cell lymphomas in the majority of cases.
  • [MeSH-major] Antigens, CD2 / genetics. Lymphoma, B-Cell / etiology. Lymphoma, Large B-Cell, Diffuse / etiology. Lymphoma, T-Cell / genetics. Promoter Regions, Genetic. Protein-Tyrosine Kinases / physiology
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cell Lineage. Female. Genotype. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Oncogene Proteins, Fusion / physiology. Polymerase Chain Reaction

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  • (PMID = 17094440.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD2; 0 / Oncogene Proteins, Fusion; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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2. Li S: Anaplastic lymphoma kinase-positive large B-cell lymphoma: a distinct clinicopathological entity. Int J Clin Exp Pathol; 2009;2(6):508-18
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  • [Title] Anaplastic lymphoma kinase-positive large B-cell lymphoma: a distinct clinicopathological entity.
  • Anaplastic lymphoma kinase-positive large B-cell lymphoma (ALK(+) LBCL) represents a distinct subtype of mature B-cell neoplasms in the most recent WHO classification of hematolymphoid neoplasms.
  • With the advent of new ALK inhibitors for possible targeted therapy clinical trials, it is important to recognize this new entity, particularly in the pediatric population because the prognosis is worse than the more common ALK+ anaplastic large cell lymphoma.

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  • (PMID = 19636398.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2713458
  • [Keywords] NOTNLM ; ALK / Anaplastic lymphoma kinase / CLTC/ALK / diffuse large B-cell lymphoma / t(2;17)
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3. Lagarrigue F, Dupuis-Coronas S, Ramel D, Delsol G, Tronchère H, Payrastre B, Gaits-Iacovoni F: Matrix metalloproteinase-9 is upregulated in nucleophosmin-anaplastic lymphoma kinase-positive anaplastic lymphomas and activated at the cell surface by the chaperone heat shock protein 90 to promote cell invasion. Cancer Res; 2010 Sep 1;70(17):6978-87
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  • [Title] Matrix metalloproteinase-9 is upregulated in nucleophosmin-anaplastic lymphoma kinase-positive anaplastic lymphomas and activated at the cell surface by the chaperone heat shock protein 90 to promote cell invasion.
  • Many anaplastic large cell lymphomas (ALCL) express the chimeric oncogene NPM-ALK, which drives malignant transformation and invasion.
  • Accordingly, we found that 100% of a large panel of ALK(+) ALCL biopsies examined were also MMP-9(+), in contrast to only 36.3% of ALK(-) tumors.
  • Interestingly, the hyaluronan receptor CD44 acted as a docking surface for MMP-9 and the chaperone heat shock protein 90 on the cell surface, where MMP-9 was cleaved and activated.
  • [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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4. Li R, Xue L, Zhu T, Jiang Q, Cui X, Yan Z, McGee D, Wang J, Gantla VR, Pickens JC, McGrath D, Chucholowski A, Morris SW, Webb TR: Design and synthesis of 5-aryl-pyridone-carboxamides as inhibitors of anaplastic lymphoma kinase. J Med Chem; 2006 Feb 9;49(3):1006-15
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  • [Title] Design and synthesis of 5-aryl-pyridone-carboxamides as inhibitors of anaplastic lymphoma kinase.
  • Anaplastic lymphoma kinase (ALK) is a promising new target for therapy of certain cancers such as anaplastic large-cell lymphoma (ALCL) and inflammatory myofibroblastic tumor (IMT).
  • Herein the details of the design process and synthesis of these novel pyridones, along with their enzymatic and cell-based activity, are discussed.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Combinatorial Chemistry Techniques. Databases, Factual. Drug Design. Humans. Mice. Models, Molecular. Receptor Protein-Tyrosine Kinases. Structure-Activity Relationship

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  • (PMID = 16451066.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / CA 69129
  • [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 / Amides; 0 / Antineoplastic Agents; 0 / Pyridones; 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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5. Bilsland JG, Wheeldon A, Mead A, Znamenskiy P, Almond S, Waters KA, Thakur M, Beaumont V, Bonnert TP, Heavens R, Whiting P, McAllister G, Munoz-Sanjuan I: Behavioral and neurochemical alterations in mice deficient in anaplastic lymphoma kinase suggest therapeutic potential for psychiatric indications. Neuropsychopharmacology; 2008 Feb;33(3):685-700
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  • [Title] Behavioral and neurochemical alterations in mice deficient in anaplastic lymphoma kinase suggest therapeutic potential for psychiatric indications.
  • The receptor tyrosine kinase product of the anaplastic lymphoma kinase (ALK) gene has been implicated in oncogenesis as a product of several chromosomal translocations, although its endogeneous role in the hematopoietic and neural systems has remained poorly understood.
  • [MeSH-minor] Animals. Anxiety / genetics. Anxiety / psychology. Bromodeoxyuridine. Cell Proliferation / drug effects. Chromatography, High Pressure Liquid. Depression / genetics. Depression / psychology. Dopamine / metabolism. Female. Flow Cytometry. Hindlimb Suspension. Immunohistochemistry. Male. Mice. Mice, Knockout. Motor Activity. Receptor Protein-Tyrosine Kinases. Recognition (Psychology) / physiology. Reverse Transcriptase Polymerase Chain Reaction. Serotonin / metabolism. Swimming / psychology. Thymidine / analogs & derivatives. Thymidine / pharmacology


6. Shi Y, Chen G, Zhou XG, Gong LP, Yu R, Zheng YY, Xie JL, Jin Y: [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study]. Zhonghua Bing Li Xue Za Zhi; 2010 Apr;39(4):235-9
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  • [Title] [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study].
  • OBJECTIVE: To study the clinicopathologic features of 66 cases of primary systemic anaplastic large cell lymphoma (ALCL), with emphasis on the differences between ALK-positive and ALK-negative cases.
  • Small cell variant and sarcomatoid subtype were found only in few cases (3 cases and 2 cases, respectively).On the other hand, common variant (17 cases) constituted the majority of ALK-negative ALCL.
  • ALK-positive ALCL more often expressed epithelial membrane antigen (100% versus 72%; P < 0.05) but less so for T-cell markers (including CD2, CD3, CD43 and CD45RO).
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 20654121.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 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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7. McDermott U, Iafrate AJ, Gray NS, Shioda T, Classon M, Maheswaran S, Zhou W, Choi HG, Smith SL, Dowell L, Ulkus LE, Kuhlmann G, Greninger P, Christensen JG, Haber DA, Settleman J: Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors. Cancer Res; 2008 May 1;68(9):3389-95
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  • [Title] Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors.
  • We have established an automated platform for examining the sensitivity to various molecularly targeted inhibitors across a large panel of human tumor-derived cell lines to identify additional genotype-correlated responses that may be clinically relevant.
  • Among the inhibitors tested in a panel of 602 cell lines derived from a variety of human cancers, we found that a selective inhibitor of the anaplastic lymphoma kinase (ALK) potently suppressed growth of a small subset of tumor cells.
  • This subset included lines derived from anaplastic large cell lymphomas, non-small-cell lung cancers, and neuroblastomas.
  • ALK is a receptor tyrosine kinase that was first identified as part of a protein fusion derived from a chromosomal translocation detected in the majority of anaplastic large cell lymphoma patients, and has recently been implicated as an oncogene in a small fraction of non-small-cell lung cancers and neuroblastomas.
  • Significantly, sensitivity in these cell lines was well correlated with specific ALK genomic rearrangements, including chromosomal translocations and gene amplification.
  • Moreover, in such cell lines, ALK kinase inhibition can lead to potent suppression of downstream survival signaling and an apoptotic response.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzimidazoles / therapeutic use. Cell Line, Tumor. Cytogenetic Analysis. Drug Evaluation, Preclinical. Gene Amplification / physiology. Genomic Instability / drug effects. Humans. Mutation. Protein Kinase Inhibitors / therapeutic use. Pyridones / therapeutic use. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 18451166.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA115830; United States / NCI NIH HHS / CA / R01 CA115830
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BMS 536924; 0 / Benzimidazoles; 0 / NVP-TAE684; 0 / Protein Kinase Inhibitors; 0 / Pyridones; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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8. Jiang YH, Cheng B, Ge MH, Cheng Y, Zhang G: Comparison of the clinical and immunohistochemical features, including anaplastic lymphoma kinase (ALK) and p53, in inflammatory myofibroblastic tumours. J Int Med Res; 2009 May-Jun;37(3):867-77
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  • [Title] Comparison of the clinical and immunohistochemical features, including anaplastic lymphoma kinase (ALK) and p53, in inflammatory myofibroblastic tumours.
  • This retrospective study evaluated 15 cases of inflammatory myofibroblastic tumours (IMTs) to determine histological atypicality, clinicopathological features, outcomes, and expression of anaplastic lymphoma kinase-1 (ALK1) and p53, to assess potential pathological prognostic indicators.

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  • (PMID = 19589272.001).
  • [ISSN] 0300-0605
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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9. Bossi RT, Saccardo MB, Ardini E, Menichincheri M, Rusconi L, Magnaghi P, Orsini P, Avanzi N, Borgia AL, Nesi M, Bandiera T, Fogliatto G, Bertrand JA: Crystal structures of anaplastic lymphoma kinase in complex with ATP competitive inhibitors. Biochemistry; 2010 Aug 17;49(32):6813-25
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  • [Title] Crystal structures of anaplastic lymphoma kinase in complex with ATP competitive inhibitors.
  • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase involved in the development of several human cancers and, as a result, is a recognized target for the development of small-molecule inhibitors for the treatment of ALK-positive malignancies.
  • [MeSH-minor] Animals. Cell Line. Enzyme Inhibitors / chemistry. Humans. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases. Spodoptera

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  • (PMID = 20695522.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NVP-TAE684; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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10. Wasik MA, Zhang Q, Marzec M, Kasprzycka M, Wang HY, Liu X: Anaplastic lymphoma kinase (ALK)-induced malignancies: novel mechanisms of cell transformation and potential therapeutic approaches. Semin Oncol; 2009 Apr;36(2 Suppl 1):S27-35
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  • [Title] Anaplastic lymphoma kinase (ALK)-induced malignancies: novel mechanisms of cell transformation and potential therapeutic approaches.
  • Among the many oncogenic variants of the anaplastic lymphoma kinase (ALK), nucleophosmin 1 (NPM)/ALK fusion protein expressed in the subset of T-cell lymphoma (ALK(+)TCL) is currently the best characterized.
  • Recent data indicate that NPM/ALK also promotes immune evasion of the ALK(+)TCL by inducing through STAT3 activation the expression of immunosuppressive cytokines interleukin-10 (IL-10) and transforming growth factor-beta (TGFss) and cell surface protein CD274 (PD-L1, B7-H1).
  • [MeSH-major] Lymphoma, T-Cell / drug therapy. Lymphoma, T-Cell / physiopathology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / physiology. Signal Transduction / physiology
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / enzymology. Cell Transformation, Neoplastic / drug effects. Humans. Mice. Receptor Protein-Tyrosine Kinases. STAT3 Transcription Factor / antagonists & inhibitors. STAT3 Transcription Factor / physiology

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  • (PMID = 19393833.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [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 / Protein Kinase Inhibitors; 0 / STAT3 Transcription Factor; 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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11. Webb TR, Slavish J, George RE, Look AT, Xue L, Jiang Q, Cui X, Rentrop WB, Morris SW: Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy. Expert Rev Anticancer Ther; 2009 Mar;9(3):331-56
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  • [Title] Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was initially identified in constitutively activated oncogenic fusion forms - the most common being nucleophosmin-ALK - in anaplastic large-cell lymphomas, and subsequent studies have identified ALK fusions in diffuse large B-cell lymphomas, systemic histiocytosis, inflammatory myofibroblastic tumors, esophageal squamous cell carcinomas and non-small-cell lung carcinomas.

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  • (PMID = 19275511.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA069129-10; United States / NCI NIH HHS / CA / R01 CA69129; United States / NCI NIH HHS / CA / R01 CA069129; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA069129-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 134034-50-7 / pleiotrophin; 137497-38-2 / midkine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 304
  • [Other-IDs] NLM/ NIHMS105118; NLM/ PMC2780428
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12. Vigil CE, Ayala E, Sokol L: Autologous stem cell transplant in peripheral T cell lymphomas: Single institution 10-year retrospective analysis. J Clin Oncol; 2009 May 20;27(15_suppl):e19538

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous stem cell transplant in peripheral T cell lymphomas: Single institution 10-year retrospective analysis.
  • : e19538 Background: Peripheral T-cell lymphoma is a rare entitydisease, compromising 10% of non-Hodgkin's lymphoma worldwide and 5% of all lymphoid neoplasms in the United States.
  • High-dose chemotherapy followed by autologous haematopoietic stem cell transplantation, has been explored in recent years with little experiences.
  • METHODS: A retrospective analysis on patients with diagnosis of peripheral T-cell lymphoma receiving autologous stem cell transplant was conducted (January 1997 to July 2008).
  • RESULTS: Twenty-nine subjects were identified, with a median age of 51; 13 patients had Anaplastic T cell, 18 patient had PTCL-nos, and 6 patients with angioimmunoblastic T cell lymphoma.

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  • (PMID = 27961010.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Li R, Morris SW: Development of anaplastic lymphoma kinase (ALK) small-molecule inhibitors for cancer therapy. Med Res Rev; 2008 May;28(3):372-412
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of anaplastic lymphoma kinase (ALK) small-molecule inhibitors for cancer therapy.
  • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (RTK) involved in the genesis of several human cancers; indeed, ALK was initially identified in constitutively activated and oncogenic fusion forms--the most common being nucleophosmin (NPM)-ALK--in a non-Hodgkin's lymphoma (NHL) known as anaplastic large-cell lymphoma (ALCL) and subsequent studies identified ALK fusions in the human sarcomas called inflammatory myofibroblastic tumors (IMTs).
  • In addition, two recent reports have suggested that the ALK fusion, TPM4-ALK, may be involved in the genesis of a subset of esophageal squamous cell carcinomas.
  • [MeSH-minor] Animals. Carrier Proteins / metabolism. Cytokines / metabolism. Disease Models, Animal. Drug Design. Humans. Lymphoma, Large-Cell, Anaplastic / enzymology. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Receptor Protein-Tyrosine Kinases

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  • [Copyright] Copyright (c) 2007 Wiley-Periodicals, Inc.
  • (PMID = 17694547.001).
  • [ISSN] 0198-6325
  • [Journal-full-title] Medicinal research reviews
  • [ISO-abbreviation] Med Res Rev
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / R01 CA69129
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Small Molecule Libraries; 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] 349
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14. Milkiewicz KL, Ott GR: Inhibitors of anaplastic lymphoma kinase: a patent review. Expert Opin Ther Pat; 2010 Dec;20(12):1653-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitors of anaplastic lymphoma kinase: a patent review.
  • IMPORTANCE OF THE FIELD: Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that belongs to the insulin receptor superfamily.
  • Aberrant ALK activity has been implicated in the oncogenesis of human cancers as a fusion protein in anaplastic large cell lymphoma, inflammatory myofibroblastic tumor, diffuse large B-cell lymphoma, systemic histiocytosis and NSCLC or through mutations in the full length protein in hereditary familial neuroblastoma.

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  • (PMID = 20961208.001).
  • [ISSN] 1744-7674
  • [Journal-full-title] Expert opinion on therapeutic patents
  • [ISO-abbreviation] Expert Opin Ther Pat
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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15. Kruczynski A, Mayer P, Marchand A, Vispé S, Fournier E, Annereau JP, Brel V, Barret JM, Delsol G, Imbert T, Fahy J, Bailly C: Antitumor activity of pyridoisoquinoline derivatives F91873 and F91874, novel multikinase inhibitors with activity against the anaplastic lymphoma kinase. Anticancer Drugs; 2009 Jun;20(5):364-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity of pyridoisoquinoline derivatives F91873 and F91874, novel multikinase inhibitors with activity against the anaplastic lymphoma kinase.
  • The anaplastic lymphoma kinase (ALK) is a validated target for the therapy of different malignancies.
  • Aberrant expression of constitutively active ALK chimeric proteins has been implicated in the pathogenesis of anaplastic large-cell lymphoma (ALCL) and has been detected in other cancers such as inflammatory myofibroblastic tumors, diffuse large B-cell lymphomas, certain non-small-cell lung cancers, rhabdomyosarcomas, neuroblastomas and glioblastomas.
  • F91873 and F91874 also inhibited nucleophosmin-ALK and signal transducer and activator of transcription 3 phosphorylation in the ALCL cell line COST with the same potency.
  • Both F91873 and F91874 behaved as ATP noncompetitive inhibitors and inhibited cell proliferation of the ALK(+) ALCL cell lines COST, PIO, and Karpas299 ALCL.
  • This growth inhibition effect was associated with a G1-phase cell cycle arrest.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinolizines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. Female. G1 Phase / drug effects. Lung Neoplasms / enzymology. Lung Neoplasms / pathology. Mice. Mice, Inbred ICR. Mice, SCID. Ovarian Neoplasms / enzymology. Ovarian Neoplasms / pathology. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases. Recombinant Fusion Proteins / antagonists & inhibitors. Xenograft Model Antitumor Assays

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  • (PMID = 19322071.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / F 91873; 0 / F 91874; 0 / Protein Kinase Inhibitors; 0 / Quinolizines; 0 / Recombinant Fusion Proteins; 0 / Thiazoles; 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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16. Li JF, Li GD, Liu WP, Wang Y, Cheng JR, Chen Y, Yang H, Tang HL, Bai YQ, Lin DG, DU LH, Peng FX, Yang YH, Zhao C: [Expression of anaplastic lymphoma kinase and survivin proteins in anaplastic large cell lymphoma and its significance]. Zhonghua Bing Li Xue Za Zhi; 2006 Apr;35(4):213-7
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  • [Title] [Expression of anaplastic lymphoma kinase and survivin proteins in anaplastic large cell lymphoma and its significance].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and survivin proteins in anaplastic large cell lymphoma (ALCL) and there clinical significance.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16776978.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm 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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17. Zhang Q, Wang HY, Bhutani G, Liu X, Paessler M, Tobias JW, Baldwin D, Swaminathan K, Milone MC, Wasik MA: Lack of TNFalpha expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15843-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of TNFalpha expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis.
  • Here we report that T-cell lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express the TNFalpha and frequently display DNA methylation of the TNFalpha gene promoter.
  • While only a subset of the ALK+ TCL-derived cell lines showed a high degree of the promoter methylation, all 6 showed low to nondetectable expression of the TNFalpha mRNA, and none expressed the TNFalpha protein.
  • Notably, the ALK+ TCL cell lines uniformly expressed the type 1 TNFalpha receptor (TNF-R1) protein known to transduce the TNFalpha-induced pro-apoptotic signals.
  • Moreover, exogenous TNFalpha inhibited growth of the ALK+ TCL cell lines in a dose-dependent manner and induced activation of the members of the cell apoptotic pathway: Caspase 8 and caspase 3.
  • They also suggest that treatment with TNFalpha may be highly effective in this type of lymphoma.

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  • (PMID = 19717436.001).
  • [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] United States / NCI NIH HHS / CA / R01 CA089194; United States / NCI NIH HHS / CA / R01 CA096856; United States / NCI NIH HHS / CA / R01-CA89194; United States / NCI NIH HHS / CA / R01-CA96856
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 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/ PMC2747206
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18. Perez-Pinera P, Chang Y, Astudillo A, Mortimer J, Deuel TF: Anaplastic lymphoma kinase is expressed in different subtypes of human breast cancer. Biochem Biophys Res Commun; 2007 Jun 29;358(2):399-403
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase is expressed in different subtypes of human breast cancer.
  • Pleiotrophin signals by inactivating its receptor, the receptor protein tyrosine phosphatase (RPTP)beta/zeta, and, recently, PTN was found to activate anaplastic lymphoma kinase (ALK) through the PTN/RPTPbeta/zeta signaling pathway in PTN-stimulated cells, not through a direct interaction of PTN with ALK and thus not through the PTN-enforced dimerization of ALK.
  • Since full-length ALK is activated in different malignant cancers and activated ALK is a potent oncogenic protein, we examined human breast cancers to test the possibility that ALK may be expressed in breast cancers and potentially activated through the PTN/RPTPbeta/zeta signaling pathway; we now demonstrate that ALK is strongly expressed in different histological subtypes of human breast cancer; furthermore, ALK is expressed in both nuclei and cytoplasm and, in the ;;dotted" pattern characteristic of ALK fusion proteins in anaplastic large cell lymphoma.

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  • (PMID = 17490616.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA084400-06; United States / NIDDK NIH HHS / DK / 2 T32 DK007022-26; United States / NCI NIH HHS / CA / R01 CA084400-06; United States / NCI NIH HHS / CA / CA88440; United States / NIDDK NIH HHS / DK / T32 DK007022
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cytokines; 134034-50-7 / pleiotrophin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.1.3.48 / PTPRZ1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 5
  • [Other-IDs] NLM/ NIHMS24272; NLM/ PMC1945107
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19. Passoni L, Gallo B, Biganzoli E, Stefanoni R, Massimino M, Di Nicola M, Gianni AM, Gambacorti-Passerini C: In vivo T-cell immune response against anaplastic lymphoma kinase in patients with anaplastic large cell lymphomas. Haematologica; 2006 Jan;91(1):48-55
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  • [Title] In vivo T-cell immune response against anaplastic lymphoma kinase in patients with anaplastic large cell lymphomas.
  • BACKGROUND AND OBJECTIVES: Anaplastic lymphoma kinase (ALK) oncogenic fusion proteins, expressed in about 60% of anaplastic large cell lymphomas (ALCL), are tumor-specific molecular targets for such a malignancy.
  • In addition, the ability of the anti-ALK immune response to specifically lyse ALK-positive lymphoma cells was investigated by in vitro stimulation with ALK-derived peptide p280-89.
  • A polyclonal ALK-specific tumor-reactive T-cell line was isolated from patients' peripheral blood lymphocytes.
  • Thus, ALK is a lymphoma-associated antigen suitable for immune interventions.
  • The high number of anti-ALK memory CD8 T cells present in patients' PBMC may represent a valid source of activated CTL suitable for cancer cell lysis.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Protein-Tyrosine Kinases / immunology

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  • (PMID = 16434370.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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20. Passoni L, Longo L, Collini P, Coluccia AM, Bozzi F, Podda M, Gregorio A, Gambini C, Garaventa A, Pistoia V, Del Grosso F, Tonini GP, Cheng M, Gambacorti-Passerini C, Anichini A, Fossati-Bellani F, Di Nicola M, Luksch R: Mutation-independent anaplastic lymphoma kinase overexpression in poor prognosis neuroblastoma patients. Cancer Res; 2009 Sep 15;69(18):7338-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutation-independent anaplastic lymphoma kinase overexpression in poor prognosis neuroblastoma patients.
  • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase predominantly expressed in the developing nervous system.
  • We investigated ALK genetic mutations, protein expression/phosphorylation, and functional inhibition both in NBL-derived cell lines and in 34 localized and 48 advanced/metastatic NBL patients.
  • No activation was found in cell lines with low expression of wild-type ALK.
  • After 72 hours of treatments, small molecule ALK inhibitor CEP-14083 (60 nmol/L) induced growth arrest and cell death in NBL cells overexpressing wild-type (viability: ALK(high) 12.8%, ALK(low) 73%, P = 0.0035; cell death: ALK(high) 56.4%, ALK(low) 16.2%, P = 0.0001) or mutated ALK.
  • [MeSH-minor] Carbazoles / pharmacology. Cell Death / drug effects. Cell Death / physiology. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line, Tumor. Disease Progression. Down-Regulation. Enzyme Activation. Humans. Immunohistochemistry. Phenylurea Compounds / pharmacology. Phosphorylation. Prognosis. Promoter Regions, Genetic. Protein Kinase Inhibitors / pharmacology. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19723661.001).
  • [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 / CEP 14083; 0 / Carbazoles; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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21. Kapur S, Tiemann M, Menke MA, Schubert C, Parwaresch R: The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases. Indian J Med Res; 2005 Jan;121(1):46-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases.
  • BACKGROUND AND OBJECTIVES: Molecular events that precede transformations from lymphomatoid palulosis (LyP) to mycosis fungoides (MF) or to cutaneous anaplastic large cell lymphoma (ALCL) in the CD 30(+) cutaneous lymphoproliferative diseases (LPDs) are not known.
  • Expression of the anaplastic lymphoma kinase (ALK) gene product has also been described as an important prognostic indicator in ALCL.

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  • (PMID = 15713979.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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22. Blum KA, Smith M, Fung H, Zalevsky J, Combs D, Ramies DA, Younes A: Phase I study of an anti-CD30 Fc engineered humanized monoclonal antibody in Hodgkin lymphoma (HL) or anaplastic large cell lymphoma (ALCL) patients: Safety, pharmacokinetics (PK), immunogenicity, and efficacy. J Clin Oncol; 2009 May 20;27(15_suppl):8531

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of an anti-CD30 Fc engineered humanized monoclonal antibody in Hodgkin lymphoma (HL) or anaplastic large cell lymphoma (ALCL) patients: Safety, pharmacokinetics (PK), immunogenicity, and efficacy.
  • : 8531 Background: XmAb2513 is a novel 2<sup>nd</sup>-generation humanized monoclonal antibody (mAb) directed against CD30 (a cell surface antigen expressed on Reed-Sternberg cells of HL and ALCL), with an Fc region engineered to have increased binding affinity to Fcγ receptors (FcγRs) leading to improved FcγR-dependent effector cell functions.

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  • (PMID = 27960926.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Boland JM, Erdogan S, Vasmatzis G, Yang P, Tillmans LS, Johnson MR, Wang X, Peterson LM, Halling KC, Oliveira AM, Aubry MC, Yi ES: Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas. Hum Pathol; 2009 Aug;40(8):1152-8
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  • [Title] Anaplastic lymphoma kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non-small cell lung carcinomas.
  • Recently, the fusion gene EML4-ALK was identified in non-small cell lung carcinoma, which could be a potential therapeutic target.
  • We investigated the prevalence of anaplastic lymphoma kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies.
  • Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of anaplastic lymphoma kinase immunostaining as a screening tool.
  • Florescence in situ hybridization for the ALK locus and reverse transcriptase-polymerase chain reaction for EML4-ALK were performed on tumors positive for anaplastic lymphoma kinase by immunohistochemistry.
  • These 2 cases were positive for anaplastic lymphoma kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative.
  • In the independent cohort, anaplastic lymphoma kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas.
  • The 6 cases positive for anaplastic lymphoma kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation.
  • In conclusion, anaplastic lymphoma kinase immunoreactivity in non-small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript.
  • Anaplastic lymphoma kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Lung Neoplasms / genetics. Protein-Tyrosine Kinases / genetics. Up-Regulation / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Aged. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Cohort Studies. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Male. Oncogene Proteins, Fusion / genetics. Receptor Protein-Tyrosine Kinases. Sequence Analysis, DNA. Transcription, Genetic

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  • [CommentIn] Hum Pathol. 2010 Apr;41(4):614-5; author reply 615-616 [20163822.001]
  • (PMID = 19386350.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 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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24. 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.
  • [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

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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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25. Oki M, Isozaki M, Nakamura N, Kikuchi A, Tsuchiya T, Arbogast P, Ogawa Y, Ando K: A multivariate analysis for the survival of nodal peripheral T-cell lymphoma (PTCL). J Clin Oncol; 2009 May 20;27(15_suppl):e19521

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  • [Title] A multivariate analysis for the survival of nodal peripheral T-cell lymphoma (PTCL).
  • : e19521 Background: Nodal peripheral T-cell lymphoma (PTCL) is uncommon lymphoma with various subtypes and poor prognosis.
  • However, the superiority of high-dose chemotherapy followed by autologous stem cell transplantation (ASCT) has remained inconclusive.
  • The infrequency of PTCL is an obstacle to perform a large prospective study.
  • We conducted a retrospective study of fifty six patients with three major nodal PTCL, histologically classified as PTCL-not specified (NOS, n=29), angioimmunoblastic T-cell lymphoma (AITL, n=19), and ALK-negative anaplastic large cell lymphoma (ALCL, n=8) who underwent ASCT (n=14) or not (n=42) after CT in Tokai University Hospital, Ebina General Hospital, and Hadano Red Cross Hospital, Kanagawa, Japan between 1997 and 2008.

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  • (PMID = 27960935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Andorsky DJ, Yamada R, Steward K, De Vos S, Said J, Timmerman J: Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells. J Clin Oncol; 2009 May 20;27(15_suppl):8526

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  • METHODS: PD-L1 expression was analyzed in 16 NHL cell lines by flow cytometry (FC) and in 111 lymphoma specimens by immunohistochemistry (IHC) (n=92) or FC (n=19).
  • In functional studies, irradiated anaplastic large cell lymphoma (ALCL) cells were co-cultured with allogeneic T cells in the presence of anti-PD-L1 blocking antibody, and IFNγ secretion and thymidine incorporation was used to assess T cell function and proliferation.
  • To further test tumor-T cell interactions, malignant ascites from a patient with ALK+ ALCL and peripheral blood mononuclear cells from a patient with leukemic mantle cell lymphoma, both containing PD-L1-expressing tumor cells and tumor-associated T cells, were stimulated with phytohemagglutinin (a polyclonal T cell activator) and incubated with anti-PD-L1 antibody.
  • Levels of 16 inflammatory cytokines were measured as an assessment of T cell activity.
  • RESULTS: All 9 B cell lymphoma lines were negative for PD-L1, while all 5 ALCL cell lines were strongly positive.
  • One T-cell ALL line was positive, and one peripheral T cell lymphoma was negative.
  • Strong PD-L1 staining was detected by IHC in all 14 ALCL specimens and in 83% of diffuse large B cell lymphomas (DLBCL) analyzed (n=35).
  • In the autologous setting using cultures of ALCL and mantle cell lymphoma specimens containing host T cells, secretion of inflammatory cytokines by tumor-associated T cells, including GMCSF, IFNγ, IL-1, IL-6, IL-8, TNFα, and MIP1α, were increased by incubation with anti-PD-L1 antibody.
  • PD-L1 may play a role in thwarting an effective anti-tumor immune response and represents an attractive target for lymphoma immunotherapy.

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  • (PMID = 27960901.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Mastini C, Martinengo C, Inghirami G, Chiarle R: Anaplastic lymphoma kinase: an oncogene for tumor vaccination. J Mol Med (Berl); 2009 Jul;87(7):669-77
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  • [Title] Anaplastic lymphoma kinase: an oncogene for tumor vaccination.
  • In addition, we will summarize some results on clinical trials that are currently exploiting selected antigens against tumors and on the recently identified anaplastic lymphoma kinase as a potential oncoantigen for selected types of human cancers.
  • [MeSH-minor] Animals. Humans. Immunotherapy. Lymphoma / therapy. Neoplasms / enzymology. Neoplasms / therapy. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19330473.001).
  • [ISSN] 1432-1440
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Vaccines, DNA; 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] 48
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28. Settleman J: Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK). Semin Oncol; 2009 Apr;36(2 Suppl 1):S36-41
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  • [Title] Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK).
  • The potential broader significance of this relationship has been further highlighted in preclinical studies using tumor-derived cell lines as a model system that can faithfully recapitulate the association of specific genotypes with drug sensitivity, suggesting the utility of cancer cell lines to identify novel candidate biomarkers for predicting clinically responsive patient subsets for newly developed anticancer agents.
  • The case of the anaplastic lymphoma kinase (ALK) nicely exemplifies this, and cell line profiling has revealed that ALK mutations present in a subset of anaplastic large cell lymphomas (ALCLs), non-small cell lung cancers (NSCLCs), and neuroblastomas appear to sensitize cancer cells to treatment with selective ALK kinase inhibitors.

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  • (PMID = 19393834.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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29. Mencía-Gutiérrez E, Gutiérrez-Díaz E, Salamanca J, Martínez-González MA: Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL). Int J Dermatol; 2006 Jun;45(6):766-9
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  • [Title] Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL).
  • AIM: To report an unusual case of cutaneous presentation on the eyelid of systemic (or nodal), CD30+, anaplastic large-cell lymphoma (ALCL).
  • RESULTS: The histopathologic and immunohistochemical diagnosis was ALCL, T-cell phenotype, strongly positive for CD43 and CD30, and negative for CD3, anaplastic lymphoma kinase (ALK), and B-cell antigens.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Eyelid Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / analysis

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  • (PMID = 16796648.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 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
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30. Shi YF, Liu CL, Zhou CJ, Gong LP, Dong LN, Li M, Huang X, Gao ZF: [Anaplastic lymphoma kinase gene abnormality and the expression of its fusion protein in primary systemic anaplastic large cell lymphoma]. Beijing Da Xue Xue Bao; 2008 Aug 18;40(4):380-6
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  • [Title] [Anaplastic lymphoma kinase gene abnormality and the expression of its fusion protein in primary systemic anaplastic large cell lymphoma].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and chromosome breakage of the anaplastic lymphoma kinase (ALK) gene retrospectively and to investigate their possible value as indicators of prognosis in primary systemic anaplastic large cell lymphomas (S-ALCL).
  • METHODS: Twenty-eight cases of S-ALCL were collected from the Lymphoma Lab, the Department of Pathology, Peking University Health Science Center and Beijing Children's Hospital.
  • [MeSH-major] Chromosome Breakage. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 18677384.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing 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] 0 / Recombinant Fusion 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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31. Chen CH, Chen SW, Shen WL, Chen TY, Tsao CJ, Huang WT: Successful allogeneic stem cell transplantation for an adult with refractory anaplastic lymphoma kinase-positive anaplastic large cell lymphoma. Int J Hematol; 2007 Feb;85(2):105-7
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  • [Title] Successful allogeneic stem cell transplantation for an adult with refractory anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK) expression exists in approximately 60% of anaplastic large cell lymphoma (ALCL) cases.
  • In the relapsed or refractory ALCL cases, high-dose chemotherapy followed by autologous stem cell transplantation has been widely used as a salvage therapy.
  • However, 40% of patients who received transplants after more than 2 complete remissions eventually experienced disease progression, despite receiving autologous stem cell transplantation.
  • Allogeneic stem cell transplantation has been proposed as a therapeutic option in refractory ALCL cases, but clinical reports of adult patients are rare.
  • Herein, we report the case of an adult with refractory ALK-positive ALCL who was successfully treated with salvage high-dose chemotherapy followed by allogeneic stem cell transplantation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, Large-Cell, Anaplastic / therapy. Stem Cell Transplantation

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  • (PMID = 17321986.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CEOP protocol 1; CVAD protocol
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32. Schönherr C, Yang HL, Vigny M, Palmer RH, Hallberg B: Anaplastic lymphoma kinase activates the small GTPase Rap1 via the Rap1-specific GEF C3G in both neuroblastoma and PC12 cells. Oncogene; 2010 May 13;29(19):2817-30
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  • [Title] Anaplastic lymphoma kinase activates the small GTPase Rap1 via the Rap1-specific GEF C3G in both neuroblastoma and PC12 cells.
  • Many different types of cancer originate from aberrant signaling from the anaplastic lymphoma kinase (ALK) receptor tyrosine kinase (RTK), arising through different translocation events and overexpression.
  • These results suggest that ALK activation of Rap1 may contribute to cell proliferation and oncogenesis of neuroblastoma driven by gain-of-function mutant ALK receptors.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Animals. Cell Proliferation. Cell Transformation, Neoplastic. Enzyme Activation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. GTPase-Activating Proteins / genetics. Gene Expression Regulation, Neoplastic. Gene Knockdown Techniques. Humans. Mice. Neurites / metabolism. Nuclear Proteins / metabolism. PC12 Cells. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. Rats. Receptor Protein-Tyrosine Kinases

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  • (PMID = 20190816.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CRKL protein; 0 / GTPase-Activating Proteins; 0 / Guanine Nucleotide-Releasing Factor 2; 0 / NVP-TAE684; 0 / Nuclear Proteins; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.2 / rap1 GTP-Binding Proteins
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33. Riera L, Lasorsa E, Ambrogio C, Surrenti N, Voena C, Chiarle R: Involvement of Grb2 adaptor protein in nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-mediated signaling and anaplastic large cell lymphoma growth. J Biol Chem; 2010 Aug 20;285(34):26441-50
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  • [Title] Involvement of Grb2 adaptor protein in nucleophosmin-anaplastic lymphoma kinase (NPM-ALK)-mediated signaling and anaplastic large cell lymphoma growth.
  • Most anaplastic large cell lymphomas (ALCL) express oncogenic fusion proteins derived from chromosomal translocations or inversions of the anaplastic lymphoma kinase (ALK) gene.
  • The transforming activity mediated by NPM-ALK fusion induces different pathways that control proliferation and survival of lymphoma cells.
  • Grb2 is an adaptor protein thought to play an important role in ALK-mediated transformation, but its interaction with NPM-ALK, as well as its function in regulating ALCL signaling pathways and cell growth, has never been elucidated.
  • Finally, shRNA knockdown experiments showed that Grb2 regulates primarily the NPM-ALK-mediated phosphorylation of SHP2 and plays a key role in ALCL cell growth.
  • [MeSH-major] Cell Proliferation. GRB2 Adaptor Protein / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / metabolism. Signal Transduction

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  • (PMID = 20554525.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] International / European Research Council / / 242965
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GRB2 Adaptor Protein; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2924075
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34. Mathivet T, Mazot P, Vigny M: In contrast to agonist monoclonal antibodies, both C-terminal truncated form and full length form of Pleiotrophin failed to activate vertebrate ALK (anaplastic lymphoma kinase)? Cell Signal; 2007 Dec;19(12):2434-43
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  • [Title] In contrast to agonist monoclonal antibodies, both C-terminal truncated form and full length form of Pleiotrophin failed to activate vertebrate ALK (anaplastic lymphoma kinase)?
  • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase essentially and transiently expressed during development in specific regions of the central and peripheral nervous system.
  • [MeSH-major] Antibodies, Monoclonal. Carrier Proteins / metabolism. Cytokines / metabolism. Glioblastoma / metabolism. Neuroblastoma / metabolism. Protein-Tyrosine Kinases / metabolism. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Movement. Enzyme Activation. Humans. Kinetics. Ligands. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Mutation. Phosphorylation. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases. Receptor-Like Protein Tyrosine Phosphatases, Class 5 / metabolism. Recombinant Proteins / metabolism. Transfection

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  • (PMID = 17904822.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Carrier Proteins; 0 / Cytokines; 0 / Ligands; 0 / Receptors, Cell Surface; 0 / Recombinant Proteins; 134034-50-7 / pleiotrophin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 5
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35. Hurley SP, Clary DO, Copie V, Lefcort F: Anaplastic lymphoma kinase is dynamically expressed on subsets of motor neurons and in the peripheral nervous system. J Comp Neurol; 2006 Mar 10;495(2):202-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase is dynamically expressed on subsets of motor neurons and in the peripheral nervous system.
  • In this study, we have characterized the spatial-temporal expression profile of a recently identified receptor tyrosine kinase, anaplastic lymphoma kinase (ALK), in embryonic chick by means of whole-mount in situ hybridization in conjunction with immunohistochemistry.
  • Expression within the spinal cord is coincident with the onset and duration of motor neuron programmed cell death and during the period of musculature innervation and synapse formation.

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
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  • (PMID = 16435287.001).
  • [ISSN] 0021-9967
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS035714-10; United States / NINDS NIH HHS / NS / NS035714-10; United States / NINDS NIH HHS / NS / NS35714; United States / NINDS NIH HHS / NS / R29 NS035714; United States / NINDS NIH HHS / NS / R01 NS035714
  • [Publication-type] Comparative Study; Journal Article; 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/ NIHMS69037; NLM/ PMC2566964
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36. Gómez-Román JJ, Cobo ML, Val-Bernal JF: Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma presenting as a bladder neoplasm. Pathol Int; 2008 Apr;58(4):249-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma presenting as a bladder neoplasm.
  • Malignant lymphoma presenting in the bladder has been classified in primary cases, as the first sign of disseminated disease and as a secondary infiltration.
  • Reported herein is the case of a 45-year-old man with an anaplastic large cell lymphoma (anaplastic lymphoma kinase (ALK) and granzyme B positive) that presented as a bladder neoplasm.
  • The morphological differential diagnosis was complex because the EMA-positive immunophenotype, CD45 and CD3 negativity and the clinical manifestation simulated a transitional cell carcinoma.
  • T-cell receptor-gamma clonal rearrangement could be also helpful in these cases.
  • Although bladder involvement by recurrent lymphoma is a sign of widely disseminated disease and it is associated with a very poor prognosis, it seems that chemotherapeutic regimens in this kind of ALK-positive lymphoma could be effective, given that the present patient had an impressive response to chemotherapy treatment.
  • [MeSH-major] Carcinoma, Transitional Cell / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis. Protein-Tyrosine Kinases / metabolism. Urinary Bladder Neoplasms / diagnosis

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  • (PMID = 18324919.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Mucin-1; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 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; Q20Q21Q62J / Cisplatin; X4W7ZR7023 / Methylprednisolone
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37. Stylianou DC, Auf der Maur A, Kodack DP, Henke RT, Hohn S, Toretsky JA, Riegel AT, Wellstein A: Effect of single-chain antibody targeting of the ligand-binding domain in the anaplastic lymphoma kinase receptor. Oncogene; 2009 Sep 17;28(37):3296-306
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of single-chain antibody targeting of the ligand-binding domain in the anaplastic lymphoma kinase receptor.
  • The tyrosine kinase receptor anaplastic lymphoma kinase (ALK) and its ligand, the growth factor pleiotrophin (PTN), are highly expressed during the development of the nervous system and have been implicated in the malignant progression of different tumor types.
  • Invasion of an intact endothelial cell monolayer by U87MG human glioblastoma cells was inhibited by the anti-ALK scFv.
  • [MeSH-minor] Amino Acid Sequence. Animals. Bacteria / cytology. Bacteria / immunology. Binding, Competitive. Brain Neoplasms / genetics. Brain Neoplasms / immunology. Brain Neoplasms / pathology. Carrier Proteins / genetics. Carrier Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. Computational Biology. Cytokines / genetics. Cytokines / metabolism. Endothelial Cells / pathology. Epitopes / immunology. Gene Expression Regulation, Neoplastic. Glioblastoma / pathology. Humans. Immunoglobulin Variable Region / immunology. Ligands. Mice. Models, Molecular. Molecular Sequence Data. Protein Binding / immunology. Protein Structure, Tertiary. Protein Tyrosine Phosphatases / genetics. Protein Tyrosine Phosphatases / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction / immunology

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  • (PMID = 19633684.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058185; United States / NCI NIH HHS / CA / R01 CA071508; United States / NCI NIH HHS / CA / R01 CA101811; United States / NCI NIH HHS / CA / R01 CA108440; United States / NCI NIH HHS / CA / R01 CA108440; United States / NCI NIH HHS / CA / T32 CA009686
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Carrier Proteins; 0 / Cytokines; 0 / Epitopes; 0 / Immunoglobulin Variable Region; 0 / Ligands; 0 / RNA, Messenger; 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; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  • [Other-IDs] NLM/ NIHMS462080; NLM/ PMC4312131
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38. Ambrogio C, Voena C, Manazza AD, Martinengo C, Costa C, Kirchhausen T, Hirsch E, Inghirami G, Chiarle R: The anaplastic lymphoma kinase controls cell shape and growth of anaplastic large cell lymphoma through Cdc42 activation. Cancer Res; 2008 Nov 1;68(21):8899-907
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The anaplastic lymphoma kinase controls cell shape and growth of anaplastic large cell lymphoma through Cdc42 activation.
  • Anaplastic large cell lymphoma (ALCL) is a non-Hodgkin's lymphoma that originates from T cells and frequently expresses oncogenic fusion proteins derived from chromosomal translocations or inversions of the anaplastic lymphoma kinase (ALK) gene.
  • Here we show that the kinase activity of the nucleophosmin (NPM)-ALK fusion regulated the shape of ALCL cells and F-actin filament assembly in a pattern similar to T-cell receptor-stimulated cells.
  • In vitro knockdown of VAV1 or Cdc42 by short hairpin RNA, as well as pharmacologic inhibition of Cdc42 activity by secramine, resulted in a cell cycle arrest and apoptosis of ALCL cells.
  • Thus, our data open perspectives for new therapeutic strategies by revealing a mechanism of regulation of ALCL cell growth through Cdc42.

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  • (PMID = 18974134.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033; United States / NCI NIH HHS / CA / CA090773-04; United States / NIGMS NIH HHS / GM / R01-GM075252-04; United States / NIGMS NIH HHS / GM / R01 GM075252-04; United States / NIGMS NIH HHS / GM / R01 GM075252; United States / NCI NIH HHS / CA / R01 CA090773-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-vav; 0 / VAV1 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 3.6.5.2 / cdc42 GTP-Binding Protein
  • [Other-IDs] NLM/ NIHMS69833; NLM/ PMC2596920
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39. Ardini E, Magnaghi P, Orsini P, Galvani A, Menichincheri M: Anaplastic Lymphoma Kinase: role in specific tumours, and development of small molecule inhibitors for cancer therapy. Cancer Lett; 2010 Dec 28;299(2):81-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic Lymphoma Kinase: role in specific tumours, and development of small molecule inhibitors for cancer therapy.
  • The Anaplastic Lymphoma Kinase (ALK) is a receptor tyrosine kinase first identified as the product of a gene rearrangement in Anaplastic Large Cell Lymphoma.
  • ALK has subsequently been found to be rearranged, mutated, or amplified in a further series of tumours including neuroblastoma, and Non-Small Cell Lung Cancer.

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  • [Copyright] Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20934803.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GSK 1838705A; 0 / NVP-TAE684; 0 / PF-2341066; 0 / Piperidines; 0 / Pyridines; 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 / anaplastic lymphoma kinase
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40. Ott GR, Tripathy R, Cheng M, McHugh R, Anzalone AV, Underiner TL, Curry MA, Quail MR, Lu L, Wan W, Angeles TS, Albom MS, Aimone LD, Ator MA, Ruggeri BA, Dorsey BD: Discovery of a potent inhibitor of anaplastic lymphoma kinase with in vivo antitumor activity. ACS Med Chem Lett; 2010 Dec 9;1(9):493-8
Guide to Pharmacology. gene/protein/disease-specific - unc-51 like kinase 3 - data and references .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Discovery of a potent inhibitor of anaplastic lymphoma kinase with in vivo antitumor activity.
  • A series of novel 7-amino-1,3,4,5-tetrahydrobenzo[b]azepin-2-one derivatives within the diaminopyrimidine class of kinase inhibitors were identified that target anaplastic lymphoma kinase (ALK).
  • These inhibitors are potent against ALK in an isolated enzyme assay and inhibit autophosphorylation of the oncogenic fusion protein NPM-ALK in anaplastic large cell lymphoma (ALCL) cell lines.


41. Gunby RH, Ahmed S, Sottocornola R, Gasser M, Redaelli S, Mologni L, Tartari CJ, Belloni V, Gambacorti-Passerini C, Scapozza L: Structural insights into the ATP binding pocket of the anaplastic lymphoma kinase by site-directed mutagenesis, inhibitor binding analysis, and homology modeling. J Med Chem; 2006 Sep 21;49(19):5759-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural insights into the ATP binding pocket of the anaplastic lymphoma kinase by site-directed mutagenesis, inhibitor binding analysis, and homology modeling.
  • Anaplastic lymphoma kinase (ALK) is a valid target for anticancer therapy; however, potent ALK inhibitors suitable for clinical use are lacking.

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  • (PMID = 16970400.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aniline Compounds; 0 / Benzamides; 0 / Nitriles; 0 / PD 173955; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyridones; 0 / Pyrimidines; 0 / Quinolines; 5018V4AEZ0 / bosutinib; 8A1O1M485B / Imatinib Mesylate; 8L70Q75FXE / Adenosine Triphosphate; 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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42. Damm-Welk C, Schieferstein J, Schwalm S, Reiter A, Woessmann W: Flow cytometric detection of circulating tumour cells in nucleophosmin/anaplastic lymphoma kinase-positive anaplastic large cell lymphoma: comparison with quantitative polymerase chain reaction. Br J Haematol; 2007 Aug;138(4):459-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flow cytometric detection of circulating tumour cells in nucleophosmin/anaplastic lymphoma kinase-positive anaplastic large cell lymphoma: comparison with quantitative polymerase chain reaction.
  • Quantification of occult circulating tumour cells in blood or bone marrow (BM) enables the identification of patients with a high risk for relapse in nucleophosmin/anaplastic lymphoma kinase (NPM-ALK)-positive anaplastic large cell lymphoma (ALCL).
  • When ALCL cells were admixed with normal peripheral blood or BM, ALK- and CD30-positive cells could be detected above background level at an added concentration of 10(-5) for all three cell lines tested.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Neoplastic Cells, Circulating / pathology

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  • (PMID = 17608768.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / Nuclear Proteins; 0 / RNA, Messenger; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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43. Schlaak M, Renner R, Treudler R, Harth W, Poenisch W, Kauer F, Grunewald S, Wittekind C, Simon JC: CD30+ anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with an unusual translocation t(11;22). Br J Dermatol; 2008 Jul;159(1):240-2
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  • [Title] CD30+ anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with an unusual translocation t(11;22).
  • [MeSH-major] Bone Neoplasms / genetics. Chromosomes, Human, Pair 11 / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. Translocation, Genetic / genetics

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  • (PMID = 18489597.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Review
  • [Publication-country] England
  • [Number-of-references] 9
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44. Kasprzycka M, Marzec M, Liu X, Zhang Q, Wasik MA: Nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) oncoprotein induces the T regulatory cell phenotype by activating STAT3. Proc Natl Acad Sci U S A; 2006 Jun 27;103(26):9964-9
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  • [Title] Nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) oncoprotein induces the T regulatory cell phenotype by activating STAT3.
  • The mechanisms of malignant cell transformation mediated by the oncogenic, chimeric nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) tyrosine kinase remain only partially understood.
  • Here we report that the NPM/ALK-carrying T cell lymphoma (ALK+TCL) cells secrete IL-10 and TGF-beta and express FoxP3, indicating their T regulatory (Treg) cell phenotype.

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  • [CommentIn] Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10151-2 [16801534.001]
  • (PMID = 16766651.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089194; United States / NCI NIH HHS / CA / R01 CA096856; United States / NCI NIH HHS / CA / R01 CA 89194; United States / NCI NIH HHS / CA / R01 CA 96856
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD28; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Oncogene Proteins, Fusion; 0 / Receptors, IgE; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Transforming Growth Factor beta; 130068-27-8 / Interleukin-10; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC1502562
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45. Salakos C, Nikolakopoulou NM, De Verney Y, Tsamandas AC, Ziambaras T, Petsas T, Papanastasiou DA: Anaplastic lymphoma kinase (ALK) positive inflammatory pseudotumor of the liver: conservative treatment and long-term follow-up. Eur J Pediatr Surg; 2010 Jul;20(4):278-80
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  • [Title] Anaplastic lymphoma kinase (ALK) positive inflammatory pseudotumor of the liver: conservative treatment and long-term follow-up.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Blood Transfusion / methods. Granuloma, Plasma Cell / enzymology. Liver Neoplasms / enzymology. Protein-Tyrosine Kinases / blood

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  • (PMID = 20178077.001).
  • [ISSN] 1439-359X
  • [Journal-full-title] European journal of pediatric surgery : official journal of Austrian Association of Pediatric Surgery ... [et al] = Zeitschrift für Kinderchirurgie
  • [ISO-abbreviation] Eur J Pediatr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 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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46. Voena C, Conte C, Ambrogio C, Boeri Erba E, Boccalatte F, Mohammed S, Jensen ON, Palestro G, Inghirami G, Chiarle R: The tyrosine phosphatase Shp2 interacts with NPM-ALK and regulates anaplastic lymphoma cell growth and migration. Cancer Res; 2007 May 1;67(9):4278-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The tyrosine phosphatase Shp2 interacts with NPM-ALK and regulates anaplastic lymphoma cell growth and migration.
  • Anaplastic large cell lymphomas (ALCL) are mainly characterized by the reciprocal translocation t(2;5)(p23;q35) that involves the anaplastic lymphoma kinase (ALK) gene and generates the fusion protein NPM-ALK with intrinsic tyrosine kinase activity.
  • NPM-ALK triggers several signaling cascades, leading to increased cell growth, resistance to apoptosis, and changes in morphology and migration of transformed cells.
  • We found that NPM-ALK was able to bind Shp2 in coprecipitation experiments and to induce its phosphorylation in the tyrosine residues Y542 and Y580 both in HEK293 cells and ALCL cell lines.
  • In ALCL cell lines, Shp2-constitutive phosphorylation was dependent on NPM-ALK, as it significantly decreased after short hairpin RNA (shRNA)-mediated NPM-ALK knock down.
  • Shp2 knock down by specific shRNA decreased the phosphorylation of extracellular signal-regulated kinase 1/2 and of the tyrosine residue Y416 in the activation loop of Src, resulting in impaired ALCL cell proliferation and growth disadvantage.
  • These findings show a direct involvement of Shp2 in NPM-ALK lymphomagenesis, highlighting its critical role in lymphoma cell proliferation and migration.
  • [MeSH-major] Cell Movement / physiology. Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Amino Acid Sequence. Apoptosis / physiology. Cell Growth Processes / physiology. Down-Regulation. Enzyme Activation. GRB2 Adaptor Protein / metabolism. Humans. K562 Cells. Mass Spectrometry. Molecular Sequence Data. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 11. RNA, Small Interfering / genetics. SH2 Domain-Containing Protein Tyrosine Phosphatases. Transfection

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  • [ErratumIn] Cancer Res. 2016 Mar 15;76(6):1669 [26979794.001]
  • (PMID = 17483340.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / GAB2 protein, human; 0 / GRB2 Adaptor Protein; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / SH2 Domain-Containing Protein Tyrosine Phosphatases
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47. Mourali J, Bénard A, Lourenço FC, Monnet C, Greenland C, Moog-Lutz C, Racaud-Sultan C, Gonzalez-Dunia D, Vigny M, Mehlen P, Delsol G, Allouche M: Anaplastic lymphoma kinase is a dependence receptor whose proapoptotic functions are activated by caspase cleavage. Mol Cell Biol; 2006 Aug;26(16):6209-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase is a dependence receptor whose proapoptotic functions are activated by caspase cleavage.
  • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase, initially discovered as part of the NPM-ALK fusion protein, resulting from the t(2;5) translocation that is frequently associated with anaplastic large-cell lymphomas.
  • In order to assess the role of ALK in neural cell-derived tissue, we transiently expressed ALK in the 13.S.1.24 rat neuroblast immortalized cell line.
  • ALK expression led to apoptotic cell death of the neuroblasts.
  • ALK ligation by specific activating antibodies decreased ALK-facilitated apoptosis in both lymphoid and neuronal cell lines.
  • [MeSH-major] Apoptosis. Caspases / metabolism. Protein-Tyrosine Kinases / metabolism. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Animals. Antibodies / immunology. Aspartic Acid / genetics. Caspase 3. Cell Line, Tumor. Cell Membrane / metabolism. Cerebral Cortex / cytology. Cerebral Cortex / enzymology. Doxorubicin / pharmacology. Enzyme Activation. Gene Expression. Humans. Jurkat Cells. Mice. Mutation / genetics. Neurons / cytology. Neurons / enzymology. Protein Processing, Post-Translational. Rats. Rats, Sprague-Dawley. Receptor Protein-Tyrosine Kinases. Transfection

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  • (PMID = 16880530.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Receptors, Cell Surface; 30KYC7MIAI / Aspartic Acid; 80168379AG / Doxorubicin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC1592804
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48. Tan LH, Tan PH, Tan SY, Ventura R, Yip GW, Zhou YC, Do E, Koay ES, Kwan C, Poh BK, Peh S: Inflammatory myofibroblastic tumour of the bladder may express anaplastic lymphoma kinase by translocation-dependent and translocation-independent mechanisms: a report of two cases. Histopathology; 2007 Jan;50(2):278-82
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  • [Title] Inflammatory myofibroblastic tumour of the bladder may express anaplastic lymphoma kinase by translocation-dependent and translocation-independent mechanisms: a report of two cases.

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  • (PMID = 17222259.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [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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49. Castillo J, Milani C, Pantanowitz L: HIV-associated anaplastic large cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19563

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIV-associated anaplastic large cell lymphoma.
  • : e19563 Background: Anaplastic large cell lymphoma (ALCL) is a CD30+ T-cell lymphoma that is generally unrelated to EBV in the non-HIV setting.
  • Based upon anaplastic lymphoma kinase (ALK) expression, the new WHO classification provisionally distinguishes between ALK+ (favorable) and ALK- (unfavorable) ALCL.
  • Data regarding patient age, gender, HIV status (CD4 count, viral load, opportunistic infections), HAART, lymphoma features (B symptoms, stage, sites of involvement, immunophenotype, ALK expression, molecular studies), EBV coinfection, therapy and outcome (survival, cause of death) were extracted and analyzed.
  • T-cell receptor gene rearrangement was present in all cases, CD30 was positive in 22 (96%), and the vast majority (90%) were ALK-negative.
  • Death was caused by either lymphoma progression (42%) or infection (58%).
  • Further research is needed to better understand and treat this unique HIV-associated lymphoma.

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  • (PMID = 27961064.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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50. 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.
  • 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.
  • 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.
  • [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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51. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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).
  • [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

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  • (PMID = 16818631.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [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 / Chromones; 0 / Morpholines; 0 / RNA, Small Interfering; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine 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; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS443817; NLM/ PMC4839264
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52. Laurent C, Do C, Gascoyne RD, Lamant L, Ysebaert L, Laurent G, Delsol G, Brousset P: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis. J Clin Oncol; 2009 Sep 1;27(25):4211-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis.
  • PURPOSE: Anaplastic lymphoma kinase (ALK) -positive diffuse large B-cell lymphoma (DLBCL) is a rare variant of DLBCL that has been described only in small case reports.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / analysis

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  • [ErratumIn] J Clin Oncol. 2010 Jan 1;28(1):182
  • (PMID = 19636007.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / oncoprotein CLTCL-ALK; 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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53. Camidge DR, Kono SA, Flacco A, Tan AC, Doebele RC, Zhou Q, Crino L, Franklin WA, Varella-Garcia M: Optimizing the detection of lung cancer patients harboring anaplastic lymphoma kinase (ALK) gene rearrangements potentially suitable for ALK inhibitor treatment. Clin Cancer Res; 2010 Nov 15;16(22):5581-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optimizing the detection of lung cancer patients harboring anaplastic lymphoma kinase (ALK) gene rearrangements potentially suitable for ALK inhibitor treatment.
  • PURPOSE: Anaplastic lymphoma kinase (ALK) rearrangements, associated with sensitivity to an experimental ALK/MET inhibitor, occur in 3% to 5% of non-small cell lung cancers.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 21062932.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058187; United States / NCI NIH HHS / CA / P50CA58187
  • [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 / Protein Kinase Inhibitors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ NIHMS375238; NLM/ PMC3395226
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54. Donella-Deana A, Marin O, Cesaro L, Gunby RH, Ferrarese A, Coluccia AM, Tartari CJ, Mologni L, Scapozza L, Gambacorti-Passerini C, Pinna LA: Unique substrate specificity of anaplastic lymphoma kinase (ALK): development of phosphoacceptor peptides for the assay of ALK activity. Biochemistry; 2005 Jun 14;44(23):8533-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unique substrate specificity of anaplastic lymphoma kinase (ALK): development of phosphoacceptor peptides for the assay of ALK activity.
  • The anaplastic lymphoma kinase (ALK), whose constitutively active fusion proteins are responsible for 5-10% of non-Hodgkin's lymphomas, shares with the other members of the insulin receptor kinase (IRK) subfamily an activation loop (A-loop) with the triple tyrosine motif Y-x-x-x-Y-Y.
  • [MeSH-minor] Amino Acid Sequence. Amino Acid Substitution. Cell Line, Tumor. Enzyme Activation. Humans. Lymphoma, Large-Cell, Anaplastic / enzymology. Molecular Sequence Data. Oligopeptides / chemical synthesis. Phosphorylation. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases / chemistry. Receptor Protein-Tyrosine Kinases / metabolism. Substrate Specificity. Tyrosine / metabolism

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  • (PMID = 15938644.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Peptides; 42HK56048U / Tyrosine; 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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55. Thompson MA, Stumph J, Henrickson SE, Rosenwald A, Wang Q, Olson S, Brandt SJ, Roberts J, Zhang X, Shyr Y, Kinney MC: Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas. Hum Pathol; 2005 May;36(5):494-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive large T- or null-cell lymphoma.
  • Most ALCLs arising in children and young adults express a constitutively active receptor tyrosine kinase, anaplastic lymphoma kinase (ALK).
  • Anaplastic large cell lymphomas lacking ALK are clinically heterogeneous and their pathogenesis is unknown.
  • Cyclin D3 was overexpressed in the ALK+ group and the cell cycle inhibitor p19INK4D was decreased in the ALK- group, suggesting different mechanisms of promoting G 1 /S transition.
  • [MeSH-major] Gene Expression. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Child. Cyclin D3. Cyclin-Dependent Kinase Inhibitor p19. Cyclins / genetics. Cyclins / metabolism. Female. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15948116.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM007753
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND3 protein, human; 0 / CDKN2D protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin D3; 0 / Cyclin-Dependent Kinase Inhibitor p19; 0 / Cyclins; 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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56. Wang WY, Ma ZG, Li GD, Liu WP, Zhong L, Wang Y, Li JM, Li L, Jiang W, Tang Y, Liao DY: [Diffuse large B-cell lymphoma with expression of anaplastic lymphoma kinase protein: clinicopathologic and immunohistochemical study of 5 cases]. Zhonghua Bing Li Xue Za Zhi; 2006 Sep;35(9):529-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diffuse large B-cell lymphoma with expression of anaplastic lymphoma kinase protein: clinicopathologic and immunohistochemical study of 5 cases].
  • OBJECTIVE: To study the clinicopathologic features of diffuse large B-cell lymphoma (DLBCL) with expression of anaplastic lymphoma kinase (ALK) protein.
  • Morphologic subtypes included centroblastic 2, anaplastic 1, immunoblastic with plasmacytoid differentiation 1 and plasmablastic 1.
  • Immunohistochemically, 4 cases were CD20 positive (including 2 centroblastic, 1 anaplastic and 1 immunoblastic cases).
  • As for ALK protein staining, a mixed membranous and cytoplasmic (1 immunoblastic case), granular cytoplasmic (2 centroblastic and 1 anaplastic cases) and mixed nuclear and cytoplasmic (1 plasmablastic case) patterns were observed.
  • CONCLUSIONS: Expression of ALK protein is a rare phenomenon in DLBCL and can be seen in centroblastic, anaplastic, immunoblastic and plasmablastic subtypes.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 17134546.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Immunoglobulin kappa-Chains; 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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57. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • [MeSH-major] DNA, Complementary / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Translocation, Genetic

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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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58. Regairaz M, Munier F, Sartelet H, Marty V, Castaing M, Michiels S, Fabre M, Roesel J, Vassal G: Role of ALK activation in the development and maintenance of the neoplastic phenotype in neuroblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):10008

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 10008 Background: Activating mutations of the Anaplastic Lymphoma Kinase (ALK) receptor could be responsible for most familial neuroblastoma cases and for up to 15% of somatic cases.
  • Effects of the ALK inhibitor TAE684 (Novartis) on cell proliferation and signaling was evaluated in wild-type or mutated ALK neuroblastoma cell lines and xenografts.
  • Inhibition of cell proliferation by TAE684 was detectible in all neuroblastoma cell lines, regardless of ALK status.

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  • (PMID = 27962533.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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59. Sterlacci W, Cappuzzo F, Savic S, Bubendorf L, Tzankov A: Anaplastic lymphoma kinase 1 detected by immunohistochemistry in non-small cell lung cancer: a promising feature? Hum Pathol; 2010 Apr;41(4):614-5; author reply 615-616
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase 1 detected by immunohistochemistry in non-small cell lung cancer: a promising feature?
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Cell Cycle Proteins / genetics. Humans. Immunohistochemistry. Microtubule-Associated Proteins / genetics. Receptor Protein-Tyrosine Kinases. Serine Endopeptidases / genetics

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  • [CommentOn] Hum Pathol. 2009 Aug;40(8):1152-8 [19386350.001]
  • (PMID = 20163822.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle 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; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases
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60. Costa V, Oliva T, Norton L: Successful treatment with daclizumab of refractory anaplastic lymphoma. Pediatr Blood Cancer; 2009 Dec;53(6):1130-1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment with daclizumab of refractory anaplastic lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is a relatively rare and highly malignant form of non-Hodgkin lymphoma (NHL) which accounts for 10-15% of these childhood lymphomas.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Immunoglobulin G / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • (PMID = 19598219.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; CUJ2MVI71Y / daclizumab
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61. Dueck GS, Chua N, Prasad A, Stewart D, White D, vanderJagt R, Johnston JB, Belch A, Reiman T: Activity of lenalidomide in a phase II trial for T-cell lymphoma: Report on the first 24 cases. J Clin Oncol; 2009 May 20;27(15_suppl):8524

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

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  • (PMID = 27960899.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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62. Bellezza G, Cavaliere A, Del Sordo R, Sidoni A: Inflammatory myofibroblastic tumor of the larynx with anaplastic lymphoma kinase (ALK) protein overexpression. A case report. Tumori; 2006 Sep-Oct;92(5):449-51
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  • [Title] Inflammatory myofibroblastic tumor of the larynx with anaplastic lymphoma kinase (ALK) protein overexpression. A case report.
  • It may be easily misinterpreted as a malignant epithelial or mesenchymal spindle cell neoplasm.
  • Immunohistochemical investigation revealed that the neoplastic cells expressed anaplastic lymphoma kinase (ALK) protein.

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  • (PMID = 17168442.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [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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63. Kunugi H, Hashimoto R, Okada T, Hori H, Nakabayashi T, Baba A, Kudo K, Omori M, Takahashi S, Tsukue R, Anami K, Hirabayashi N, Kosuga A, Tatsumi M, Kamijima K, Asada T, Harada S, Arima K, Saitoh O: Possible association between nonsynonymous polymorphisms of the anaplastic lymphoma kinase (ALK) gene and schizophrenia in a Japanese population. J Neural Transm (Vienna); 2006 Oct;113(10):1569-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possible association between nonsynonymous polymorphisms of the anaplastic lymphoma kinase (ALK) gene and schizophrenia in a Japanese population.
  • We examined, for the first time, the possible association between schizophrenia and the anaplastic lymphoma kinase (ALK) gene which plays an important role in neurodevelopment.

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  • (PMID = 16604305.001).
  • [ISSN] 0300-9564
  • [Journal-full-title] Journal of neural transmission (Vienna, Austria : 1996)
  • [ISO-abbreviation] J Neural Transm (Vienna)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [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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64. Makimoto Y, Nabeshima K, Iwasaki H, Ishiguro A, Miyoshi T, Shiraishi T, Iwasaki A, Shirakusa T: Inflammatory myofibroblastic tumor of the posterior mediastinum: an older adult case with anaplastic lymphoma kinase abnormalities determined using immunohistochemistry and fluorescence in situ hybridization. Virchows Arch; 2005 Apr;446(4):451-5
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  • [Title] Inflammatory myofibroblastic tumor of the posterior mediastinum: an older adult case with anaplastic lymphoma kinase abnormalities determined using immunohistochemistry and fluorescence in situ hybridization.
  • Anaplastic lymphoma kinase (ALK) abnormalities in IMT, determined using immunohistochemistry and/or molecular genetic studies, including fluorescence in situ hybridization (FISH), have almost been limited to children and young adults.

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  • (PMID = 15778844.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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65. Sabbatini P, Korenchuk S, Rowand JL, Groy A, Liu Q, Leperi D, Atkins C, Dumble M, Yang J, Anderson K, Kruger RG, Gontarek RR, Maksimchuk KR, Suravajjala S, Lapierre RR, Shotwell JB, Wilson JW, Chamberlain SD, Rabindran SK, Kumar R: GSK1838705A inhibits the insulin-like growth factor-1 receptor and anaplastic lymphoma kinase and shows antitumor activity in experimental models of human cancers. Mol Cancer Ther; 2009 Oct;8(10):2811-20
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  • [Title] GSK1838705A inhibits the insulin-like growth factor-1 receptor and anaplastic lymphoma kinase and shows antitumor activity in experimental models of human cancers.
  • GSK1838705A blocks the in vitro proliferation of cell lines derived from solid and hematologic malignancies, including multiple myeloma and Ewing's sarcoma, and retards the growth of human tumor xenografts in vivo.
  • GSK1838705A also inhibits the anaplastic lymphoma kinase (ALK), which drives the aberrant growth of anaplastic large-cell lymphomas, some neuroblastomas, and a subset of non-small cell lung cancers.
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Proliferation / drug effects. Enzyme Activation / drug effects. Humans. Mice. Phosphorylation / drug effects. Receptor Protein-Tyrosine Kinases. Receptor, Insulin / metabolism. Signal Transduction / drug effects


66. Takeshita H, Kawakami S, Okubo Y, Yamamoto S, Yonese J, Fukui I, Kono A, Kurata M, Inoshita N, Ishikawa Y: [A case of inflammatory myofibroblastic tumor of the urinary bladder finally diagnosed by anaplastic lymphoma kinase (ALK) immunostaining]. Hinyokika Kiyo; 2006 May;52(5):375-8
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  • [Title] [A case of inflammatory myofibroblastic tumor of the urinary bladder finally diagnosed by anaplastic lymphoma kinase (ALK) immunostaining].
  • Since the tumor cells showed spindle cell proliferation alone without epithelial growth and positive staining for anaplastic lymphoma kinase, we corrected the final diagnosis as an inflammatory myofibroblastic tumor of the urinary bladder.
  • [MeSH-major] Granuloma, Plasma Cell / pathology. Protein-Tyrosine Kinases / analysis. Urinary Bladder Neoplasms / pathology

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  • (PMID = 16758729.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [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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67. Cheng M, Ott GR: Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma. Anticancer Agents Med Chem; 2010 Mar;10(3):236-49
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  • [Title] Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was originally identified as the oncogenic NPM (nucleophosmin)-ALK fusion protein due to a t (2;5) chromosomal translocation in anaplastic large cell lymphomas.
  • The recent reports of EML4 (echinoderm microtubule-associated protein-like 4)-ALK oncogenic proteins in non-small cell lung cancer (NSCLC) and the identification of ALK activating point mutations and gene amplification in neuroblastoma have indicated ALK as a potential major therapeutic target for human cancers.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma, Large-Cell, Anaplastic / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors


68. 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).
  • CD4(+) Th cell lines lysed ALK-positive ALCL cell lines in a MHC class II-restricted manner.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / immunology. Protein-Tyrosine Kinases / immunology. T-Lymphocytes, Helper-Inducer / immunology

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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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69. Nasr MR, Laver JH, Chang M, Hutchison RE: Expression of anaplastic lymphoma kinase, tyrosine-phosphorylated STAT3, and associated factors in pediatric anaplastic large cell lymphoma: A report from the children's oncology group. Am J Clin Pathol; 2007 May;127(5):770-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of anaplastic lymphoma kinase, tyrosine-phosphorylated STAT3, and associated factors in pediatric anaplastic large cell lymphoma: A report from the children's oncology group.
  • In anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK) activates (phosphorylates) signal transducer and activator of transcription 3 (STAT3) with subsequent cytoplasmic expression, in some cases, of survivin and tissue inhibitor of metalloprotease 1 (TIMP1).
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / chemistry. Protein-Tyrosine Kinases / analysis. STAT3 Transcription Factor / analysis

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  • (PMID = 17439836.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 30969; United States / NCI NIH HHS / CA / CA 98543
  • [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 / Antigens, CD56; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / STAT3 Transcription Factor; 0 / Tissue Inhibitor of Metalloproteinase-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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70. Koshiba S, Li H, Motoda Y, Tomizawa T, Kasai T, Tochio N, Yabuki T, Harada T, Watanabe S, Tanaka A, Shirouzu M, Kigawa T, Yamamoto T, Yokoyama S: Structural basis for the recognition of nucleophosmin-anaplastic lymphoma kinase oncoprotein by the phosphotyrosine binding domain of Suc1-associated neurotrophic factor-induced tyrosine-phosphorylated target-2. J Struct Funct Genomics; 2010 Jun;11(2):125-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural basis for the recognition of nucleophosmin-anaplastic lymphoma kinase oncoprotein by the phosphotyrosine binding domain of Suc1-associated neurotrophic factor-induced tyrosine-phosphorylated target-2.
  • The nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion oncoprotein, formed by the t(2;5) chromosomal translocation in anaplastic large-cell lymphomas, has constitutive tyrosine kinase activity and interacts with a number of signaling molecules.

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  • (PMID = 20454865.001).
  • [ISSN] 1570-0267
  • [Journal-full-title] Journal of structural and functional genomics
  • [ISO-abbreviation] J. Struct. Funct. Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Peptide Fragments; 21820-51-9 / Phosphotyrosine; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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71. Moog-Lutz C, Degoutin J, Gouzi JY, Frobert Y, Brunet-de Carvalho N, Bureau J, Créminon C, Vigny M: Activation and inhibition of anaplastic lymphoma kinase receptor tyrosine kinase by monoclonal antibodies and absence of agonist activity of pleiotrophin. J Biol Chem; 2005 Jul 15;280(28):26039-48
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  • [Title] Activation and inhibition of anaplastic lymphoma kinase receptor tyrosine kinase by monoclonal antibodies and absence of agonist activity of pleiotrophin.
  • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that is transiently expressed in specific regions of the central and peripheral nervous systems, suggesting a role in its normal development and function.
  • Finally, in these cell systems, a mitogenic form of pleiotrophin, a proposed ligand of ALK, failed to activate this receptor.
  • [MeSH-minor] Animals. Cell Line. DNA, Complementary / metabolism. Dose-Response Relationship, Drug. Enzyme Activation. Humans. Ligands. MAP Kinase Signaling System. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Models, Biological. Neurons / metabolism. PC12 Cells. Phosphorylation. Plasmids / metabolism. Protein Structure, Tertiary. Rats. Receptor Protein-Tyrosine Kinases. Time Factors. Transfection. Tyrosine / chemistry

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  • (PMID = 15886198.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Carrier Proteins; 0 / Cytokines; 0 / DNA, Complementary; 0 / Enzyme Inhibitors; 0 / Ligands; 134034-50-7 / pleiotrophin; 42HK56048U / Tyrosine; 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 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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72. Ait-Tahar K, Damm-Welk C, Burkhardt B, Zimmermann M, Klapper W, Reiter A, Pulford K, Woessmann W: Correlation of the autoantibody response to the ALK oncoantigen in pediatric anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor dissemination and relapse risk. Blood; 2010 Apr 22;115(16):3314-9
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  • [Title] Correlation of the autoantibody response to the ALK oncoantigen in pediatric anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor dissemination and relapse risk.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) constitutes an ideal model disease to study tumor-specific immune responses.
  • Although antibodies and T-cell responses to ALK have previously been detected in ALK-positive ALCL patients, their prognostic significance is unknown.
  • We investigated a large cohort of uniformly treated ALK-positive pediatric ALCL patients to ascertain whether the titers of preexisting ALK autoantibodies correlated with clinical and histologic characteristics, tumor dissemination, and patient outcome.
  • Our results provide the first clinical evidence that a robust preexisting immune response to an oncoantigen resulting from an oncogenic chromosomal translocation inhibits lymphoma dissemination and decreases the risk of relapse.
  • [MeSH-major] Autoantibodies / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasm Recurrence, Local / immunology. Protein-Tyrosine Kinases / immunology

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  • (PMID = 20185586.001).
  • [ISSN] 1528-0020
  • [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 / Autoantibodies; 0 / Autoantigens; 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. Shi X, Franko B, Frantz C, Amin HM, Lai R: JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells. Br J Haematol; 2006 Oct;135(1):26-32
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  • [Title] JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells.
  • As STAT3 activation is pathogenetically important in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ ALCL), we investigated whether JSI-124 can mediate significant inhibitory effects in this cell type.
  • In two ALK+ ALCL cell lines (Karpas 299 and SU-DHL-1), JSI-124 significantly reduced the number of viable cells to 50% of that of negative controls at a dose of 5-10 micromol/l at 24 h and 1-1.25 micromol/l at 48 h.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Triterpenes / pharmacology

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  • (PMID = 16939498.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / JAK3 protein, human; 0 / Triterpenes; 2222-07-3 / cucurbitacin I; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 3
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74. Perez-Pinera P, Zhang W, Chang Y, Vega JA, Deuel TF: Anaplastic lymphoma kinase is activated through the pleiotrophin/receptor protein-tyrosine phosphatase beta/zeta signaling pathway: an alternative mechanism of receptor tyrosine kinase activation. J Biol Chem; 2007 Sep 28;282(39):28683-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase is activated through the pleiotrophin/receptor protein-tyrosine phosphatase beta/zeta signaling pathway: an alternative mechanism of receptor tyrosine kinase activation.
  • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (RTK) first discovered as the constitutively active nucleophosmin-ALK oncoprotein in anaplastic large cell lymphomas (ALCL).
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Differentiation / physiology. Enzyme Activation / drug effects. Enzyme Activation / physiology. HeLa Cells. Humans. Ligands. Neoplasms / metabolism. Phosphorylation / drug effects. Receptor Protein-Tyrosine Kinases. Receptor-Like Protein Tyrosine Phosphatases, Class 5

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  • (PMID = 17681947.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 2 T32 DK007022-26; United States / NCI NIH HHS / CA / CA84400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cytokines; 0 / Ligands; 134034-50-7 / pleiotrophin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.1.3.48 / PTPRZ1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 5
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75. Kuo AH, Stoica GE, Riegel AT, Wellstein A: Recruitment of insulin receptor substrate-1 and activation of NF-kappaB essential for midkine growth signaling through anaplastic lymphoma kinase. Oncogene; 2007 Feb 8;26(6):859-69
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recruitment of insulin receptor substrate-1 and activation of NF-kappaB essential for midkine growth signaling through anaplastic lymphoma kinase.
  • Anaplastic lymphoma kinase (ALK) is a transmembrane receptor tyrosine kinase in the insulin receptor superfamily.
  • [MeSH-minor] Animals. Binding Sites. Cell Line. Cell Proliferation. Cercopithecus aethiops. Enzyme Activation. Humans. Insulin Receptor Substrate Proteins. Mice. Mitogen-Activated Protein Kinases / metabolism. Phenotype. Protein Subunits / genetics. Protein Subunits / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. Receptor Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases / metabolism. Transcription, Genetic / genetics

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  • (PMID = 16878150.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / C06 RR14567; United States / NCI NIH HHS / CA / CA101811
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / IRS1 protein, human; 0 / Insulin Receptor Substrate Proteins; 0 / Irs1 protein, mouse; 0 / NF-kappa B; 0 / Phosphoproteins; 0 / Protein Subunits; 0 / RNA, Small Interfering; 137497-38-2 / midkine; EC 2.7.1.- / Ltk protein, mouse; 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 2.7.11.24 / Mitogen-Activated Protein Kinases
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76. Hegazy SA, Wang P, Anand M, Ingham RJ, Gelebart P, Lai R: The tyrosine 343 residue of nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) is important for its interaction with SHP1, a cytoplasmic tyrosine phosphatase with tumor suppressor functions. J Biol Chem; 2010 Jun 25;285(26):19813-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The tyrosine 343 residue of nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) is important for its interaction with SHP1, a cytoplasmic tyrosine phosphatase with tumor suppressor functions.
  • The cytoplasmic tyrosine phosphatase SHP1 has been shown to inhibit the oncogenic fusion protein nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK), and loss of SHP1 contributes to NPM-ALK-mediated tumorigenesis.

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  • (PMID = 20424160.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Tumor Suppressor Proteins; 117896-08-9 / nucleophosmin; 42HK56048U / Tyrosine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6
  • [Other-IDs] NLM/ PMC2888392
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77. Reiner DJ, Ailion M, Thomas JH, Meyer BJ: C. elegans anaplastic lymphoma kinase ortholog SCD-2 controls dauer formation by modulating TGF-beta signaling. Curr Biol; 2008 Aug 5;18(15):1101-9
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  • [Title] C. elegans anaplastic lymphoma kinase ortholog SCD-2 controls dauer formation by modulating TGF-beta signaling.
  • We map this defect in dauer response to a mutation in the scd-2 gene, which, we show, encodes the nematode anaplastic lymphoma kinase (ALK) homolog, a proto-oncogene receptor tyrosine kinase. scd-2 acts in a genetic pathway shown here to include the HEN-1 ligand, the RTK adaptor SOC-1, and the MAP kinase SMA-5.

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  • (PMID = 18674914.001).
  • [ISSN] 0960-9822
  • [Journal-full-title] Current biology : CB
  • [ISO-abbreviation] Curr. Biol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM030702; United States / NIGMS NIH HHS / GM / R01 GM048700; United States / NIGMS NIH HHS / GM / R01GM48700; United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Caenorhabditis elegans Proteins; 0 / DAF-3 protein, C elegans; 0 / HEN-1 protein, C elegans; 0 / Ligands; 0 / Nerve Tissue Proteins; 0 / Pheromones; 0 / SMA-5 protein, C elegans; 0 / Smad Proteins; 0 / Transforming Growth Factor beta; 0 / soc-1 protein, C elegans; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Scd-2 protein, C elegans
  • [Other-IDs] NLM/ NIHMS414520; NLM/ PMC3489285
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78. Hsu FY, Johnston PB, Burke KA, Zhao Y: The expression of CD30 in anaplastic large cell lymphoma is regulated by nucleophosmin-anaplastic lymphoma kinase-mediated JunB level in a cell type-specific manner. Cancer Res; 2006 Sep 15;66(18):9002-8
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  • [Title] The expression of CD30 in anaplastic large cell lymphoma is regulated by nucleophosmin-anaplastic lymphoma kinase-mediated JunB level in a cell type-specific manner.
  • Chromosomal translocation t(2;5) and the resulting fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) are detected in 50% to 70% of anaplastic large cell lymphoma (ALCL), which is a T/null cell non-Hodgkin's lymphoma showing anaplastic morphology with cell surface expression of CD30.
  • Because aberrant CD30 expression was also observed in the T-cell lymphoma derived from lineage-specific NPM-ALK transgenic mice, we tested the hypothesis that there might be a functional relationship between the two neoplastic-related proteins: NPM-ALK and CD30.
  • The NPM-ALK-repressed cells, which had low CD30 expression, were characterized with lower cell proliferation compared with cells in the control group, suggesting that altered CD30 expression may correlate to NPM-ALK-mediated tumor cell growth inhibition.
  • Combination of NPM-ALK repression and CD30 ligand leads to significantly increased tumor cell growth inhibition compared with one method alone, suggesting its potential application for ALCL-specific cancer treatment.
  • [MeSH-major] Antigens, CD30 / biosynthesis. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-jun / metabolism
  • [MeSH-minor] Cell Growth Processes / physiology. Cell Line, Tumor. Down-Regulation. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. RNA Interference. RNA, Small Interfering / genetics. Transcription, Genetic. Transcriptional Activation. Transfection

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  • (PMID = 16982741.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59318
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Proto-Oncogene Proteins c-jun; 0 / RNA, Small Interfering; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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79. Christensen JG, Zou HY, Arango ME, Li Q, Lee JH, McDonnell SR, Yamazaki S, Alton GR, Mroczkowski B, Los G: Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma. Mol Cancer Ther; 2007 Dec;6(12 Pt 1):3314-22
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  • [Title] Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma.
  • A t(2;5) chromosomal translocation resulting in expression of an oncogenic kinase fusion protein known as nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) has been implicated in the pathogenesis of anaplastic large-cell lymphoma (ALCL).
  • PF-2341066 potently inhibited cell proliferation, which was associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells (IC(50) values, approximately 30 nmol/L) but not ALK-negative lymphoma cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Lymphoma, Large-Cell, Anaplastic / pathology. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-met / antagonists & inhibitors. Pyridines / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Drug Screening Assays, Antitumor. Enzyme-Linked Immunosorbent Assay. Female. Humans. Mice. Mice, SCID. Phosphorylation. Receptor Protein-Tyrosine Kinases


80. 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.
  • Similar anaplastic lymphoma kinase (ALK) gene abnormalities as in anaplastic large cell lymphoma have been reported.
  • [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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81. Lansigan F, Cooper D, Seropian S, Foss F: Autologous and allogeneic transplantation for aggressive T-cell lymphomas: A single institution experience. J Clin Oncol; 2009 May 20;27(15_suppl):8558

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

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  • (PMID = 27960993.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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82. Joshi A, Fields P, Simo R: Anaplastic lymphoma of the cervical esophagus presenting as a tracheoesophageal fistula. Head Neck; 2008 Sep;30(9):1264-8
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  • [Title] Anaplastic lymphoma of the cervical esophagus presenting as a tracheoesophageal fistula.
  • BACKGROUND: Anaplastic kinase-1 positive lymphoma (ALK-1) is a very rare but distinct pathologic entity.
  • ALK-1 lymphoma tends to affect the bone marrow, skin, lungs, soft tissue, but very rarely the gastrointestinal tract.
  • METHODS: We report a case of ALK-1 positive lymphoma presenting as a tracheoesophageal fistula.
  • CONCLUSION: ALK-1 positive lymphoma of the upper aerodigestive involvement is extremely rare.
  • [MeSH-major] Esophageal Neoplasms / pathology. Esophageal Neoplasms / therapy. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, Large-Cell, Anaplastic / therapy. Tracheoesophageal Fistula / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biopsy, Needle. Cervical Vertebrae. Combined Modality Therapy. Diagnosis, Differential. Esophagoscopy. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Photomicrography. Risk Assessment. Salvage Therapy. Stem Cell Transplantation / methods. Tomography, X-Ray Computed. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 18228520.001).
  • [ISSN] 1097-0347
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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83. Willenbrock K, Küppers R, Renné C, Brune V, Eckerle S, Weidmann E, Bräuninger A, Hansmann ML: Common features and differences in the transcriptome of large cell anaplastic lymphoma and classical Hodgkin's lymphoma. Haematologica; 2006 May;91(5):596-604
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  • [Title] Common features and differences in the transcriptome of large cell anaplastic lymphoma and classical Hodgkin's lymphoma.
  • BACKGROUND AND OBJECTIVES: Anaplastic large cell lymphoma (ALCL) and classical Hodgkin's lymphoma (HL) are derived from different cell types, namely T cells and B cells, respectively.
  • However, both lymphomas share a similar cytological and immunohistochemical tumor cell phenotype with little resemblance to their cells of origin.
  • DESIGN AND METHODS: In this study, the transcriptional profiles of ALCL cell lines, primary ALCL tumor cells from peripheral blood and HL cell lines were compared to each other and to normal B-cell subsets, B non-Hodgkin's lymphomas (NHL) and B NHL- and Epstein-Barr virus (EBV)-transformed B-cell lines in order to establish their relationship at the transcriptional level and to identify genes with possible pathobiological impact.
  • RESULTS: HL samples clustered separately from ALCL samples, but HL and ALCL were found to be more closely related to each other than to any normal or malignant B-cell sample in the dataset.
  • Their relationship was determined to a large extent, but not exclusively, by lack of expression of B-cell antigens and by the over-expression of mRNA encoding activation markers and structural proteins.
  • INTERPRETATION AND CONCLUSIONS: At a transcriptional level HL is more closely related to Alk+ ALCL than to the B-NHL or B-cell samples investigated, although it is a B-cell derived lymphoma.
  • [MeSH-major] Gene Expression Profiling. Hodgkin Disease / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Transcription, Genetic
  • [MeSH-minor] Adult. B-Lymphocytes / metabolism. B-Lymphocytes / pathology. Cell Line, Tumor / metabolism. Cell Transformation, Neoplastic / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Leukemia / blood. Leukemia / genetics. Leukemia / metabolism. Leukemia / pathology. Lymphoma / classification. Lymphoma / genetics. Lymphoma / metabolism. Lymphoma / pathology. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. RNA, Complementary / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16670065.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Complementary; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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84. Wang P, Wu F, Ma Y, Li L, Lai R, Young LC: Functional characterization of the kinase activation loop in nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) using tandem affinity purification and liquid chromatography-mass spectrometry. J Biol Chem; 2010 Jan 1;285(1):95-103
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional characterization of the kinase activation loop in nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) using tandem affinity purification and liquid chromatography-mass spectrometry.
  • A complete loss of the 8 phosphotyrosines outside KAL was found in 3 KAL mutants, and their oncogenicity (assessed by cell viability, colony formation, and the ability to phosphorylate effector proteins) was abrogated.

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  • (PMID = 19887368.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutant Proteins; 21820-51-9 / Phosphotyrosine; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC2804230
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85. Wakata A, Cahill SM, Blumenstein M, Gunby RH, Jockusch S, Marti AA, Cimbro B, Gambacorti-Passerini C, Donella-Deana A, Pinna LA, Turro NJ, Lawrence DS: A mechanistic design principle for protein tyrosine kinase sensors: application to a validated cancer target. Org Lett; 2008 Jan 17;10(2):301-4
Hazardous Substances Data Bank. L-TYROSINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A new mechanistic principle for reporting the phosphorylation of tyrosine is described, which should prove applicable to even the most fastidious of protein tyrosine kinases, as demonstrated by the acquisition of a fluorescent sensor for the extraordinarily demanding anaplastic lymphoma kinase.

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  • (PMID = 18085786.001).
  • [ISSN] 1523-7060
  • [Journal-full-title] Organic letters
  • [ISO-abbreviation] Org. Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA079954; United States / NCRR NIH HHS / RR / RR017998; United States / NCI NIH HHS / CA / CA7994; United States / NCI NIH HHS / CA / CA079954-09; United States / NCI NIH HHS / CA / R01 CA079954-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fluorescent Dyes; 42HK56048U / Tyrosine; 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/ NIHMS263717; NLM/ PMC3057043
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86. Summers TA, Moncur JT: The small cell variant of anaplastic large cell lymphoma. Arch Pathol Lab Med; 2010 Nov;134(11):1706-10
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  • [Title] The small cell variant of anaplastic large cell lymphoma.
  • Anaplastic large cell lymphomas constitute a heterogeneous group of hematopoietic neoplasms that are characterized by immunopositivity for CD30 and the presence, in varying degrees, of large, pleomorphic "hallmark" cells.
  • Primary systemic anaplastic lymphoma kinase-positive anaplastic large cell lymphomas are a subset of this group.
  • Numerous heterogeneous histomorphologic patterns have been described in anaplastic lymphoma kinase-positive anaplastic large cell lymphomas, and all patterns tend to have a better prognosis than that found in anaplastic lymphoma kinase-negative cases.
  • We provide a short review of the small cell variant of anaplastic large cell lymphoma to facilitate the diagnosis of this difficult-to-recognize entity, which may be confused with reactive processes, commonly presents with disseminated disease, and pursues an aggressive clinical course.
  • [MeSH-major] Lymphocytes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 21043827.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30
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87. Menasce LP, Eyden B: Nasopharyngeal carcinoma mimicking large-cell anaplastic lymphoma. Histopathology; 2005 Mar;46(3):342-4
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  • [Title] Nasopharyngeal carcinoma mimicking large-cell anaplastic lymphoma.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Nasopharyngeal Neoplasms / pathology

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  • (PMID = 15720421.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mucin-1; 68238-35-7 / Keratins
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88. Gunby RH, Tartari CJ, Porchia F, Donella-Deana A, Scapozza L, Gambacorti-Passerini C: An enzyme-linked immunosorbent assay to screen for inhibitors of the oncogenic anaplastic lymphoma kinase. Haematologica; 2005 Jul;90(7):988-90
The Lens. Cited by Patents in .

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  • [Title] An enzyme-linked immunosorbent assay to screen for inhibitors of the oncogenic anaplastic lymphoma kinase.
  • The discovery of novel anti-cancer drugs targeting anaplastic lymphoma kinase (ALK), an oncogenic tyrosine kinase, raises the need for in vitro assays suitable for screening compounds for ALK inhibition.

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  • (PMID = 15996942.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Peptides; 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; H88EPA0A3N / Staurosporine
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89. Chen ST, Lee JC: An inflammatory myofibroblastic tumor in liver with ALK and RANBP2 gene rearrangement: combination of distinct morphologic, immunohistochemical, and genetic features. Hum Pathol; 2008 Dec;39(12):1854-8
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  • Rearrangement of the anaplastic lymphoma kinase gene with variable fusion partners and anaplastic lymphoma kinase expression using immunohistochemistry are noted in about half of the tumors.
  • We present a hepatic inflammatory myofibroblastic tumor from a 34-year-old man with an unusual rearrangement between the Ran binding protein 2 and anaplastic lymphoma kinase genes, as well as a peculiar round cell transformation of tumor cells and a unique nuclear membrane expression of anaplastic lymphoma kinase protein.

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  • (PMID = 18701132.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Molecular Chaperones; 0 / Nuclear Pore Complex Proteins; 0 / ran-binding protein 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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90. Milkiewicz KL, Weinberg LR, Albom MS, Angeles TS, Cheng M, Ghose AK, Roemmele RC, Theroff JP, Underiner TL, Zificsak CA, Dorsey BD: Synthesis and structure-activity relationships of 1,2,3,4-tetrahydropyrido[2,3-b]pyrazines as potent and selective inhibitors of the anaplastic lymphoma kinase. Bioorg Med Chem; 2010 Jun 15;18(12):4351-62
BindingDB. BindingDB .

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  • [Title] Synthesis and structure-activity relationships of 1,2,3,4-tetrahydropyrido[2,3-b]pyrazines as potent and selective inhibitors of the anaplastic lymphoma kinase.
  • Dysregulation of the anaplastic lymphoma kinase (ALK) is implicated in a variety of cancers.
  • Chemistry was developed to rapidly elaborate the SAR, structural elements impacting ALK inhibitory activity were exploited, and kinase selective analogs were identified that inhibit ALK with IC(50) values approximately 10 nM (enzyme) and approximately 150 nM (cell).


91. Chiarle R, Voena C, Ambrogio C, Piva R, Inghirami G: The anaplastic lymphoma kinase in the pathogenesis of cancer. Nat Rev Cancer; 2008 Jan;8(1):11-23
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The anaplastic lymphoma kinase in the pathogenesis of cancer.
  • The anaplastic lymphoma kinase (ALK) is the oncogene of most anaplastic large cell lymphomas (ALCL), driving transformation through many molecular mechanisms.
  • [MeSH-major] Lymphoma / enzymology. Lymphoma / genetics. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Humans. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, T-Cell / enzymology. Lymphoma, T-Cell / genetics. Receptor Protein-Tyrosine Kinases / metabolism. Translocation, Genetic

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  • (PMID = 18097461.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 158
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92. O'leary H, Savage KJ: The spectrum of peripheral T-cell lymphomas. Curr Opin Hematol; 2009 Jul;16(4):292-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The spectrum of peripheral T-cell lymphomas.
  • PURPOSE OF REVIEW: This review summarizes recent progress that has advanced our understanding of the pathobiology and prognosis of peripheral T-cell lymphomas including the changes introduced to the updated World Health Organization classification of lymphoid neoplasms.
  • RECENT FINDINGS: The International Peripheral T-Cell Lymphoma Project was a large collaborative project, highlighting the clinico-pathologic and geographic differences of this diverse group of diseases.
  • Peripheral T-cell lymphoma, not otherwise specified, is a biologically heterogeneous subtype, and a number of studies including investigations using molecular profiling have explored whether meaningful prognostic or biologic subgroups can be identified.
  • Angioimmunoblastic T-cell lymphoma demonstrates overlapping immunophenotypical and molecular features with normal follicular T-helper cells, giving some insight into the cell of origin.
  • Systemic anaplastic large cell lymphoma is composed of two disease groups based on the presence or absence of anaplastic lymphoma kinase overexpression.
  • Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma has a significantly better prognosis than anaplastic lymphoma kinase-negative anaplastic large cell lymphoma and molecular studies have illustrated that each entity has a distinct molecular profile.
  • Anaplastic lymphoma kinase-negative anaplastic large cell lymphoma has been recently shown to have a more favourable, but still unsatisfactory, prognosis than peripheral T-cell lymphoma, not otherwise specified, and biological and molecular distinctions confirm that they are separate entities.
  • SUMMARY: Advances are being made in understanding the unique pathobiology of the peripheral T-cell lymphoma subtypes that will help to refine diagnoses, identify potential prognostic markers, elucidate the molecular mechanisms critical in disease pathogenesis and define new therapeutic targets in the poor-risk population.
  • [MeSH-major] Lymphoma, T-Cell, Peripheral / classification. Lymphoma, T-Cell, Peripheral / pathology
  • [MeSH-minor] Antigens, Neoplasm / genetics. Cyclin A / genetics. Cyclin B / genetics. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Gene Expression Profiling. Humans. Prognosis. Proliferating Cell Nuclear Antigen / genetics. Survival Analysis. World Health Organization

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  • (PMID = 19509496.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cyclin A; 0 / Cyclin B; 0 / DNA-Binding Proteins; 0 / Proliferating Cell Nuclear Antigen; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Number-of-references] 47
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93. 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.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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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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94. Damm-Welk C, Klapper W, Oschlies I, Gesk S, Röttgers S, Bradtke J, Siebert R, Reiter A, Woessmann W: Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation. Br J Haematol; 2009 Aug;146(3):306-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation.
  • Anaplastic large cell lymphomas (ALCL) in children express anaplastic lymphoma kinase (ALK) fusion genes, most commonly NPM1-ALK.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19545284.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / MYH9 protein, human; 0 / Molecular Motor Proteins; 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; 0 / oncoprotein CLTCL-ALK; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.6.4.1 / Myosin Heavy Chains
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95. Konstantiadou I, Mastoraki A, Papanikolaou IS, Sakorafas G, Safioleas M: Surgical approach of primary splenic lymphoma: report of a case and review of the literature. Indian J Hematol Blood Transfus; 2009 Sep;25(3):120-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgical approach of primary splenic lymphoma: report of a case and review of the literature.
  • Histopathological examination confirmed the diagnosis of non-Hodgkin B-cells anaplastic lymphoma.
  • Extended range of pathological manifestations explains the variety of radiological appearances and difficulty in accurate diagnostic process of primary splenic lymphoma.

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  • (PMID = 23100989.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453420
  • [Keywords] NOTNLM ; Clinical presentation / Diagnostic approach / Primary splenic lymphoma / Surgical management
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96. Turner SD, Alexander DR: What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis? Leukemia; 2005 Jul;19(7):1128-34
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is generated as a t(2;5) chromosomal breakpoint product, typically in CD30(+) anaplastic large cell lymphomas.
  • [MeSH-major] Lymphoma / immunology. Oncogene Proteins, Fusion / immunology. Protein-Tyrosine Kinases / immunology

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  • (PMID = 15902287.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 65
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97. Pulford K, Roberton HM, Jones M: Antibody techniques used in the study of anaplastic lymphoma kinase-positive ALCL. Methods Mol Med; 2005;115:271-94
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antibody techniques used in the study of anaplastic lymphoma kinase-positive ALCL.
  • The availability of suitable reagents for routine diagnostic use has revolutionized the study of leukemia and lymphoma pathology.
  • The use of antibodies specific for anaplastic lymphoma kinase (ALK) protein has permitted the identification of the tumor entity ALK-positive from the poorly defined morphological category of anaplastic large cell lymphoma.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibodies, Neoplasm / immunology. Blotting, Western / methods. Lymphoma, Large-Cell, Anaplastic / diagnosis. Protein-Tyrosine Kinases / immunology. Receptor Protein-Tyrosine Kinases / immunology

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  • (PMID = 15998974.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 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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98. Shirinian M, Varshney G, Lorén CE, Grabbe C, Palmer RH: Drosophila Anaplastic Lymphoma Kinase regulates Dpp signalling in the developing embryonic gut. Differentiation; 2007 Jun;75(5):418-26
FlyBase. FlyBase .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drosophila Anaplastic Lymphoma Kinase regulates Dpp signalling in the developing embryonic gut.
  • The Drosophila melanogaster gene Anaplastic Lymphoma Kinase (Alk) regulates a signal transduction pathway required for founder cell specification within the visceral muscle of the developing embryonic midgut.
  • During embryonic development, the midgut visceral muscle is lined by the endodermal cell layer.
  • We propose that not only does Alk signalling regulate founder cell specification and thus fusion in the developing visceral muscle, but that Alk also regulates Dpp signalling between the visceral muscle and the endoderm.

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  • (PMID = 17286600.001).
  • [ISSN] 0301-4681
  • [Journal-full-title] Differentiation; research in biological diversity
  • [ISO-abbreviation] Differentiation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drosophila Proteins; 0 / dpp protein, Drosophila; 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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99. Ji TH, Li HL, Jiang HY, Zhao T, Yu YH: [Expression of ALK protein in large cell lymphoma with ALCL chromosome translocation in relation to prognosis]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Jun;16(3):543-6
Genetic Alliance. consumer health - Lymphoma, large-cell.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of ALK protein in large cell lymphoma with ALCL chromosome translocation in relation to prognosis].
  • The aim of this study was to investigate the expression of anaplastic lymphoma kinase (ALK) protein resulted from chromosome translocation in anaplastic large cell lymphoma (ALCL) and its relationship with the age and prognosis of patients with ALCL.
  • The tissue microarray including 30 cases of ALCL and 2 normal control tissues were established, the expression of anaplastic lymphoma kinase (ALK) protein was detected by immunohistochemistry, the statistical analysis of detected results was carried out by SPSS software.

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  • (PMID = 18549625.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] 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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100. Giuriato S, Foisseau M, Dejean E, Felsher DW, Al Saati T, Demur C, Ragab A, Kruczynski A, Schiff C, Delsol G, Meggetto F: Conditional TPM3-ALK and NPM-ALK transgenic mice develop reversible ALK-positive early B-cell lymphoma/leukemia. Blood; 2010 May 20;115(20):4061-70
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Conditional TPM3-ALK and NPM-ALK transgenic mice develop reversible ALK-positive early B-cell lymphoma/leukemia.
  • NPM-ALK (nucleophosmin-anaplastic lymphoma kinase) and TPM3-ALK (nonmuscular tropomyosin 3-anaplastic lymphoma kinase) are oncogenic tyrosine kinases implicated in the pathogenesis of human ALK-positive lymphoma.
  • Thus, our results show (1) that NPM-ALK and TPM3-ALK oncogenes are sufficient for lymphoma/leukemia development and required for tumor maintenance, hence validating ALK as potentially effective therapeutic target; and (2) for the first time, in vivo, the equal tumorigenic potential of the NPM-ALK and TPM3-ALK oncogenic tyrosine kinases.
  • [MeSH-major] Leukemia, B-Cell / pathology. Lymphoma, B-Cell / pathology. Protein-Tyrosine Kinases / genetics. Tropomyosin / genetics
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western. Cell Differentiation. Cell Proliferation. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoblotting. Immunoenzyme Techniques. Integrases / metabolism. Mice. Mice, Transgenic. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
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  • (PMID = 20223922.001).
  • [ISSN] 1528-0020
  • [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 / RNA, Messenger; 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; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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