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1. Attili VS, Reddy CO: An interesting case of lung mass. J Lab Physicians; 2009 Jan;1(1):25-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An interesting case of lung mass.
  • Anaplastic large cell lymphoma of lung.
  • Although lung involvement in cases of lymphoma is observed in as high as 40% of cases, in autopsy series, the exact clinical incidence is not known.
  • One of the largest lymphoma groups reported it to be around 25%.
  • However, primary pulmonary lymphomas have been extremely rare (0.4%), and whenever present they are of (Mucosa Associate Lymphoid tissue) MALT type, with occasional diffuse large cell lymphomas.
  • The anaplastic variant is extremely uncommon.
  • Here we report the case of anaplastic primary nonHodgkin's lymphoma of lung and review the literature.

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  • (PMID = 21938246.001).
  • [ISSN] 0974-2727
  • [Journal-full-title] Journal of laboratory physicians
  • [ISO-abbreviation] J Lab Physicians
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3167963
  • [Keywords] NOTNLM ; Primary pulmonary lymphoma / immuno histo chemistry / treatment
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2. Cluzeau T, Pécuchet N, Mounier N, Vignot S: [Implications of ALK (anaplastic lymphoma kinase) in oncohematology]. Bull Cancer; 2010 Aug;97(8):991-6
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] [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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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors.
  • We have established an automated platform for examining the sensitivity to various molecularly targeted inhibitors across a large panel of human tumor-derived cell lines to identify additional genotype-correlated responses that may be clinically relevant.
  • Among the inhibitors tested in a panel of 602 cell lines derived from a variety of human cancers, we found that a selective inhibitor of the anaplastic lymphoma kinase (ALK) potently suppressed growth of a small subset of tumor cells.
  • This subset included lines derived from anaplastic large cell lymphomas, non-small-cell lung cancers, and neuroblastomas.
  • ALK is a receptor tyrosine kinase that was first identified as part of a protein fusion derived from a chromosomal translocation detected in the majority of anaplastic large cell lymphoma patients, and has recently been implicated as an oncogene in a small fraction of non-small-cell lung cancers and neuroblastomas.
  • Significantly, sensitivity in these cell lines was well correlated with specific ALK genomic rearrangements, including chromosomal translocations and gene amplification.
  • Moreover, in such cell lines, ALK kinase inhibition can lead to potent suppression of downstream survival signaling and an apoptotic response.
  • These findings suggest that a subset of lung cancers, lymphomas, and neuroblastomas that harbor genomic ALK alterations may be clinically responsive to pharmacologic ALK inhibition.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzimidazoles / therapeutic use. Cell Line, Tumor. Cytogenetic Analysis. Drug Evaluation, Preclinical. Gene Amplification / physiology. Genomic Instability / drug effects. Humans. Mutation. Protein Kinase Inhibitors / therapeutic use. Pyridones / therapeutic use. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 18451166.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA115830; United States / NCI NIH HHS / CA / R01 CA115830
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BMS 536924; 0 / Benzimidazoles; 0 / NVP-TAE684; 0 / Protein Kinase Inhibitors; 0 / Pyridones; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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4. Lowe EJ, Sposto R, Perkins SL, Gross TG, Finlay J, Zwick D, Abromowitch M, Children's Cancer Group Study 5941: Intensive chemotherapy for systemic anaplastic large cell lymphoma in children and adolescents: final results of Children's Cancer Group Study 5941. Pediatr Blood Cancer; 2009 Mar;52(3):335-9
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

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  • [Title] Intensive chemotherapy for systemic anaplastic large cell lymphoma in children and adolescents: final results of Children's Cancer Group Study 5941.
  • BACKGROUND: Anaplastic large cell lymphoma (ALCL) is characterized by advanced disease at presentation (70-80% of pediatric cases) and accounts for 10-15% of all childhood lymphomas.
  • METHODS: CCG-5941 used a compressed aggressive multiagent T-cell lineage chemotherapy regimen consisting of a 3-week induction therapy (vincristine, prednisone, cyclophosphamide, daunomycin, asparaginase) followed by a 3-week consolidation period (vincristine, prednisone, etoposide, 6-thioguanine, cytarabine, asparaginase, methotrexate) followed by six courses of maintenance chemotherapy at 7-week intervals (cyclophosphamide, 6-thioguanine, vincristine, prednisone, doxorubicin, asparaginase, methotrexate etoposide, cytarabine).
  • Extranodal disease was common (mediastinum 35%, skin 15%, lung 14%, bone 12%, bone marrow 13%, liver 6%, and other viscera 17%).
  • Relapse occurred early with 17 (81%) relapses occurring within 2 years of diagnosis and 12 (57%) while receiving therapy.

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  • (PMID = 18985718.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA098543-06
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS123401; NLM/ PMC2769495
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5. Matsushita H, Nakamura N, Asai S, Yabe M, Hayama N, Kondo Y, Urano T, Miyachi H: A leukemic change as an initial manifestation of the common variant type of ALK-positive anaplastic large cell lymphoma in a patient with lung adenocarcinoma. Intern Med; 2008;47(23):2057-62
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] A leukemic change as an initial manifestation of the common variant type of ALK-positive anaplastic large cell lymphoma in a patient with lung adenocarcinoma.
  • We report an 81-year-old man who had leukemic presentation of ALK-positive anaplastic large cell lymphoma (ALCL) as an initial manifestation.
  • He had been well after chemotherapy and irradiation for the advanced lung adenocarcinoma, but suddenly suffered from severe lactic acidosis and hypotension.
  • The peripheral blood smear and bone marrow aspiration revealed the infiltration of atypical large cells with horseshoe-shaped or lobulated nuclei.
  • The detection of CD30 expression and the t (2;5) (p23;q35) translocation in these cells was confirmatory of a diagnosis of common variant ALK-positive ALCL in a leukemic phase.
  • An adequate, prompt diagnosis is necessary for this rare disease status in oncologic emergency to improve the disease management.
  • [MeSH-major] Adenocarcinoma / diagnosis. Genetic Variation / genetics. Lung Neoplasms / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis
  • [MeSH-minor] Aged, 80 and over. Antigens, CD30 / genetics. Diagnosis, Differential. Humans. Male

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  • (PMID = 19043261.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Number-of-references] 20
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6. Palmer RH, Vernersson E, Grabbe C, Hallberg B: Anaplastic lymphoma kinase: signalling in development and disease. Biochem J; 2009 Jun 15;420(3):345-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase: signalling in development and disease.
  • The ALK (anaplastic lymphoma kinase) RTK was originally identified as a member of the insulin receptor subfamily of RTKs that acquires transforming capability when truncated and fused to NPM (nucleophosmin) in the t(2;5) chromosomal rearrangement associated with ALCL (anaplastic large cell lymphoma).
  • Recent reports of the EML4 (echinoderm microtubule-associated protein like 4)-ALK oncoprotein in NSCLC (non-small cell lung cancer), together with the identification of activating point mutations in neuroblastoma, have highlighted ALK as a significant player and target for drug development in cancer.
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / pathology. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Models, Biological. Neuroblastoma / genetics. Neuroblastoma / metabolism. Neuroblastoma / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Receptor Protein-Tyrosine Kinases

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 19459784.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 237
  • [Other-IDs] NLM/ PMC2708929
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7. Le Deley MC, Reiter A, Williams D, Delsol G, Oschlies I, McCarthy K, Zimmermann M, Brugières L, European Intergroup for Childhood Non-Hodgkin Lymphoma: Prognostic factors in childhood anaplastic large cell lymphoma: results of a large European intergroup study. Blood; 2008 Feb 1;111(3):1560-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors in childhood anaplastic large cell lymphoma: results of a large European intergroup study.
  • To study prognostic factors of progression/relapse, data concerning 225 children enrolled between 1987 and 1997 in Berlin-Frankfurt-Münster, Société Française d'Oncologie Pédiatrique and United Kingdom Children's Cancer Study Group prospective studies for the treatment of anaplastic large cell lymphoma (ALCL) were merged.
  • In the multivariate analysis, 3 factors remained significant: mediastinal involvement (relative risk [RR] = 2.1 [1.2-3.5]), visceral involvement defined as lung, liver, or spleen involvement (RR = 2.1 [1.3-3.6]), and skin lesions (RR = 1.9 [1.1-3.2]).
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / epidemiology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 17957029.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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8. Siordia-Reyes AG, Ferman-Cano F, Rodríguez-Velasco A: [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case]. Gac Med Mex; 2005 Nov-Dec;141(6):531-4
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  • [Title] [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case].
  • Ki-1 anaplastic large cell non-Hodgkin lymphoma is a well recognized clinical entity.
  • In the extranodal disease, which occurs in approximately half of the cases, the skin is the most common site; bone marrow, lung and central nervous system are generally not involved.
  • Anaplastic large cell lymphoma is more common among young people, in whom the prognosis is more favorable.
  • Primary anaplastic large cell lymphoma of the lung is a rare clinical entity.
  • Its clinical expression is similar to a high grade malignant lymphoma, and in most cases the diagnosis is made in advanced stages.
  • We present a pediatric case with ALK-1 positive anaplastic large cell lymphoma of the lung.
  • [MeSH-major] Lung Neoplasms / chemistry. Lymphoma, Large B-Cell, Diffuse / chemistry. Membrane Proteins / analysis

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  • (PMID = 16381509.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
  • [Number-of-references] 16
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9. Yang HB, Li J, Shen T: Primary anaplastic large cell lymphoma of the lung. Report of two cases and literature review. Acta Haematol; 2007;118(3):188-91
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  • [Title] Primary anaplastic large cell lymphoma of the lung. Report of two cases and literature review.
  • To our knowledge, only eleven cases of primary anaplastic large cell lymphoma (ALCL) of the lung have previously been reported.
  • CD30-positive ALCL was demonstrated by histopathological studies of the lung tissue.
  • Primary pulmonary lymphoma is a great challenge for pneumologists since the clinical presentations and radiological findings are nonspecific.
  • Appropriate invasive biopsy is necessary for early diagnosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / pathology

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  • [Copyright] 2007 S. Karger AG, Basel
  • (PMID = 17934256.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD30; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  • [Number-of-references] 15
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10. 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


11. Sevilla DW, Choi JK, Gong JZ: Mediastinal adenopathy, lung infiltrates, and hemophagocytosis: unusual manifestation of pediatric anaplastic large cell lymphoma: report of two cases. Am J Clin Pathol; 2007 Mar;127(3):458-64
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  • [Title] Mediastinal adenopathy, lung infiltrates, and hemophagocytosis: unusual manifestation of pediatric anaplastic large cell lymphoma: report of two cases.
  • To date, only 1 report describes an anaplastic large cell lymphoma (ALCL) associated with hemophagocytosis in the pediatric population.
  • Both patients had fever, cytopenia, decreased fibrinogen level, mediastinal or hilar adenopathy, minimal to no peripheral adenopathy, and lung infiltrates.
  • Definitive diagnosis required lymph node biopsies that showed CD30+, anaplastic lymphoma kinase-l+ ALCL.
  • Both tumors responded to standard lymphoma chemotherapy.
  • These findings are similar to the first reported case and indicate that pediatric ALCL can manifest with an unusual constellation of symptoms consisting of hemophagocytosis, mediastinal or hilar adenopathy, and lung infiltrates.
  • [MeSH-major] Lung Diseases / pathology. Lymphatic Diseases / pathology. Lymphohistiocytosis, Hemophagocytic / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Activin Receptors, Type II / genetics. Antigens, CD30 / analysis. Antigens, CD8 / analysis. Child. Child, Preschool. Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 5. Diagnosis, Differential. Fatal Outcome. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Mediastinum. Translocation, Genetic

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  • (PMID = 17276937.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antigens, CD8; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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12. Le Deley MC, Rosolen A, Williams DM, Horibe K, Wrobel G, Attarbaschi A, Zsiros J, Uyttebroeck A, Marky IM, Lamant L, Woessmann W, Pillon M, Hobson R, Mauguen A, Reiter A, Brugières L: Vinblastine in children and adolescents with high-risk anaplastic large-cell lymphoma: results of the randomized ALCL99-vinblastine trial. J Clin Oncol; 2010 Sep 1;28(25):3987-93
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  • [Title] Vinblastine in children and adolescents with high-risk anaplastic large-cell lymphoma: results of the randomized ALCL99-vinblastine trial.
  • PURPOSE: The impact of adding vinblastine to a 4-month chemotherapy regimen, based on the Non-Hodgkin's Lymphoma Berlin-Frankfurt-Münster 90 protocol, in childhood high-risk anaplastic large-cell lymphoma (ALCL) was assessed.
  • PATIENTS AND METHODS: Children and adolescents with high-risk ALCL, defined by mediastinal, lung, liver, spleen, or skin involvement, were eligible for the trial.
  • [MeSH-minor] Adolescent. Child. Disease-Free Survival. Humans. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • [CommentIn] J Clin Oncol. 2011 Feb 1;29(4):e90-1; author reply e92-3 [21172896.001]
  • (PMID = 20679620.001).
  • [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
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine
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13. Palumbo G, Grana CM, Cocca F, De Santis R, Del Principe D, Baio SM, Mei R, Paganelli G: Pretargeted antibody-guided radioimmunotherapy in a child affected by resistant anaplastic large cell lymphoma. Eur J Haematol; 2007 Sep;79(3):258-62
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  • [Title] Pretargeted antibody-guided radioimmunotherapy in a child affected by resistant anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is characterized by preferential paracortical and intrasinusoidal lymph node involvement by large anaplastic tumor cells expressing the CD30 antigen.
  • In these cases, the highly aggressive clinical course of ALCL, associated with systemic symptoms and extranodal involvement, has been treated with different approaches in various cooperative trials, including conventional chemotherapy and human stem cell transplantation (HSCT).
  • More recently, radioimmunotherapy has been studied with encouraging results in cancer patients, including non-Hodgkin's lymphoma.
  • [MeSH-major] Antibodies, Neoplasm / therapeutic use. Lymphoma, Large-Cell, Anaplastic / radionuclide imaging. Radioimmunotherapy / methods
  • [MeSH-minor] Child. Female. Hematopoietic Stem Cell Transplantation. Humans. Lung Neoplasms / secondary. Salvage Therapy / methods

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  • (PMID = 17655697.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm
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14. 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.
  • ALCL was extranodal in 22 cases (96%) affecting most commonly lung, soft tissue and liver.
  • 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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15. Cerimagić Z, Guska S, Banjanović B: A case of T/null anaplastic large cell lymphoma arising in lung. Bosn J Basic Med Sci; 2006 Aug;6(3):34-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of T/null anaplastic large cell lymphoma arising in lung.
  • Anaplastic large cell lymphoma (ALCL) is a rare non-Hodgkin, T-cell lymphoma, representing only 2-3% of all lymphoid neoplasm's in adults according to World Health Organization (WHO).
  • CD30 antigen-positive, large neoplastic cells characterize ALCL.
  • The neoplastic cells were large and had clear cytoplasm, large vesicular nuclei, and prominent nucleoli.
  • The progression of Hodgkin lymphoma to aggressive non-Hodgkin lymphoma (ALCL in this case) is well known entity.
  • After the diagnosis was established, our patient immediately had been referred to the Department of Hematology in order to get appropriate chemotherapy, necessary in such cases.


16. Kim YC, Yang WI, Lee MG, Kim SN, Cho KH, Lee SJ, Lee MW, Koh JK: Epstein-Barr virus in CD30 anaplastic large cell lymphoma involving the skin and lymphomatoid papulosis in South Korea. Int J Dermatol; 2006 Nov;45(11):1312-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epstein-Barr virus in CD30 anaplastic large cell lymphoma involving the skin and lymphomatoid papulosis in South Korea.
  • AIM: To elucidate the possible association of EBV with CD30+ anaplastic large cell lymphoma (ALCL) involving the skin and lymphomatoid papulosis (LyP) in South Korea.
  • The other was CD30+ ALCL involving the skin and other organs, including lymph nodes, bone, lung, and spleen.
  • [MeSH-major] Epstein-Barr Virus Infections / pathology. Herpesvirus 4, Human / growth & development. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphomatoid Papulosis / pathology

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  • (PMID = 17076712.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, CD3; 0 / Antigens, CD30; 0 / EBV-associated membrane antigen, Epstein-Barr virus; 0 / Epstein-Barr virus encoded RNA 1; 0 / Epstein-Barr virus encoded RNA 2; 0 / RNA, Viral; 0 / Viral Matrix Proteins
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17. Kelleher FC, McDermott R: The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene. Eur J Cancer; 2010 Sep;46(13):2357-68
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  • [Title] The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene.
  • The anaplastic lymphoma kinase gene (ALK) is a gene on chromosome 2p23 that has expression restricted to the brain, testis and small intestine but is not expressed in normal lymphoid tissue.
  • This gene was originally established as being implicated in the pathogenesis of rare diseases including inflammatory myofibroblastic tumour (IMT) and ALK-positive anaplastic large cell lymphoma, which is a subtype of non-Hodgkin's lymphoma.
  • In 2007, an inversion of chromosome 2 involving ALK and a fusion partner gene in a subset of non-small cell lung cancer was discovered.
  • This has been described in ALK-positive anaplastic large cell lymphoma in which ALK is fused to NPM (nucleolar protein gene) and in non-small cell lung cancer where ALK is fused to EML4 (Echinoderm microtubule-associated protein 4).
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / therapy. Drug Synergism. Gene Amplification. Humans. Lung Neoplasms / genetics. Lung Neoplasms / therapy. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Mutation / genetics. Neuroblastoma / genetics. Neuroblastoma / therapy. Pyrimidines / therapeutic use. Pyrroles / therapeutic use. Receptor Protein-Tyrosine Kinases. Receptor, IGF Type 1 / antagonists & inhibitors

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20451371.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GSK 1838705A; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase
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18. Zhou X, Sun C, Wang J, Mao J, Guo H: Rapid fatal pulmonary complications in a Chinese patient after bortezomib treatment for ALK-negative anaplastic large-cell lymphoma. Clin Lymphoma Myeloma Leuk; 2010 Apr;10(2):152-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid fatal pulmonary complications in a Chinese patient after bortezomib treatment for ALK-negative anaplastic large-cell lymphoma.
  • Herein, we present a case of rapid fatal pulmonary complications in a patient with ALK-negative anaplastic large-cell lymphoma after receiving a treatment with bortezomib.
  • [MeSH-minor] Aged. Asian Continental Ancestry Group. Bortezomib. Enzyme Inhibitors / therapeutic use. Fatal Outcome. Hematologic Neoplasms / chemically induced. Hematologic Neoplasms / enzymology. Humans. Lung / enzymology. Lung / metabolism. Lymphoma, Large B-Cell, Diffuse / chemically induced. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large-Cell, Anaplastic / chemically induced. Lymphoma, Large-Cell, Anaplastic / enzymology. Male

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  • (PMID = 20371451.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
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19. 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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20. 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.
  • The breadth of inhibitors combined with the recent discoveries of the involvement of ALK in lung, breast and colorectal cancers has kept the field advancing at a rapid pace.

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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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21. Settleman J: Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK). Semin Oncol; 2009 Apr;36(2 Suppl 1):S36-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK).
  • The potential broader significance of this relationship has been further highlighted in preclinical studies using tumor-derived cell lines as a model system that can faithfully recapitulate the association of specific genotypes with drug sensitivity, suggesting the utility of cancer cell lines to identify novel candidate biomarkers for predicting clinically responsive patient subsets for newly developed anticancer agents.
  • The case of the anaplastic lymphoma kinase (ALK) nicely exemplifies this, and cell line profiling has revealed that ALK mutations present in a subset of anaplastic large cell lymphomas (ALCLs), non-small cell lung cancers (NSCLCs), and neuroblastomas appear to sensitize cancer cells to treatment with selective ALK kinase inhibitors.

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  • (PMID = 19393834.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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22. Sano F, Tasaka T, Nishimura H, Akiyama T, Kubo Y, Matsuhashi Y, Wada H, Sugihara T, Sadahira Y: Small cell variant of anaplastic large cell lymphoma diagnosed by a novel chromosomal abnormality t(2;5;3)(p23;q35;p21) of bone marrow cells. Pathol Int; 2008 Aug;58(8):494-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small cell variant of anaplastic large cell lymphoma diagnosed by a novel chromosomal abnormality t(2;5;3)(p23;q35;p21) of bone marrow cells.
  • Because of the rarity and the morphological variations, small cell variant of anaplastic large cell lymphoma (ALCL) represents a diagnostic challenge.
  • Herein is reported a case of leukemic type of small cell variant of ALCL, in which the diagnosis was established by a cytogenetic analysis.
  • The initial differential diagnosis on bone marrow trephine biopsy sections included viral infection and peripheral T-cell lymphoma unspecified.
  • But a cytogenetic study on bone marrow cells indicated a novel complex translocation, t(2;5;3)(p23;q35;p21), which led to confirmation of anaplastic lymphoma kinase (ALK)-positive pleomorphic small to medium-sized cells scattered in bone marrow cells, on immunohistochemistry.
  • The patient achieved complete remission after four courses of combination chemotherapy, and received autologous peripheral stem cell transplantation (auto-PBSCT) after two additional courses of combination chemotherapy, but relapsed 2 months after auto-PBSCT in the bilateral lung.
  • Allogeneic stem cell transplantation led to a second remission.
  • This case demonstrates the diagnostic importance of cytogenetic study for malignant lymphoma involving bone marrow.
  • [MeSH-major] Bone Marrow Cells / pathology. Chromosomes, Human, 1-3 / genetics. Chromosomes, Human, Pair 5 / genetics. Lymphoma, Large-Cell, Anaplastic / diagnosis. Translocation, Genetic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Chromosome Banding. Diagnosis, Differential. Female. Humans. Lymphoma, T-Cell, Peripheral / diagnosis. Protein-Tyrosine Kinases / immunology. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Remission Induction. Spectral Karyotyping. Virus Diseases / diagnosis

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  • (PMID = 18705769.001).
  • [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 / 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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23. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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24. 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.
  • These observations have sparked the development of small molecule kinase inhibitors, the most advanced of which is currently in clinical testing and which has shown promising preliminary activity in the subset of lung cancer patients whose tumours harbour activated ALK.

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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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25. 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


26. Barthwal MS, Deoskar RB, Falleiro JJ, Singh P: Endobronchial non-Hodgkin's lymphoma. Indian J Chest Dis Allied Sci; 2005 Apr-Jun;47(2):117-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endobronchial non-Hodgkin's lymphoma.
  • A 23-year-old male presented with clinical and radiological features of left lung collapse.
  • Needle aspiration and endobronchial biopsy from the mass revealed it to be a case of anaplastic large cell lymphoma, a subtype of non-Hodgkin's lymphoma.
  • This report documents the rare presentation of non-Hodgkin's lymphoma as an endobronchial mass.
  • [MeSH-major] Bronchial Neoplasms / diagnosis. Bronchial Neoplasms / drug therapy. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / drug therapy

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  • (PMID = 15832956.001).
  • [ISSN] 0377-9343
  • [Journal-full-title] The Indian journal of chest diseases & allied sciences
  • [ISO-abbreviation] Indian J Chest Dis Allied Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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27. Li BZ, Zhou XY, Ye HT, Yang WT, Fan YZ, Lu HF, Shi DR: [Abnormal expression of bcl-10 protein in extranodal marginal zone B cell lymphoma of mucosa-associated lymphoid tissue lymphoma type]. Zhonghua Bing Li Xue Za Zhi; 2007 Dec;36(12):819-24

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Abnormal expression of bcl-10 protein in extranodal marginal zone B cell lymphoma of mucosa-associated lymphoid tissue lymphoma type].
  • OBJECTIVE: To evaluate the diagnostic role of nuclear expression of bcl-10 protein in extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) type.
  • METHODS: One hundred and forty cases of MALT lymphoma were collected from Cancer Hospital of Fudan University (including 38 cases from stomach, 35 cases from ocular adnexa, 16 cases from intestine, 15 cases from skin, 15 cases from salivary gland, 14 cases from lung, 3 cases from thyroid and 4 cases from other sites).
  • Ten cases of reactive follicular hyperplasia of tonsil, 5 cases of reactive lymphoid hyperplasia of orbit and 143 cases of non-Hodgkin's lymphoma other than MALT lymphoma (including 20 cases of NK/T cell lymphoma, 20 cases of follicular lymphomas, 20 cases of anaplastic large cell lymphomas, 20 cases of nodal diffuse large cell B-cell lymphoma (DLBCL), 10 cases of gastric diffuse large B-cell lymphoma, 13 cases of nodal marginal zone B-cell lymphoma, 12 cases of mantle cell lymphoma, 11 cases of splenic marginal zone B-cell lymphoma, 6 cases of angioimmunoblastic T-cell lymphoma, 6 cases of peripheral T-cell lymphoma, not otherwise specified, 3 cases of small lymphocytic lymphoma, 1 case of lymphoplasmacytic lymphoma and 1 case of plasmacytoma were used as controls.
  • In some cases of lymphoma, bcl-10 was expressed in tumor cells but not in reactive lymphoid cells.
  • On the other hand, 92.1% (129/140) of MALT lymphoma were bcl-10 positive.
  • The staining was most intense in MALT lymphoma of ocular adnexa.
  • Cytoplasmic expression of bcl-10 is seen in many different kinds of non-Hodgkin's lymphoma and reactive lymphoid conditions.
  • In some cases of lymphoma, bcl-10 is expressed in tumor cells but not in reactive lymphoid cells, suggesting a possible role of abnormal bcl-10 expression in tumorgenesis.
  • Nuclear expression of bcl-10 is seen mainly in MALT lymphoma, especially when occurring in ocular adnexa and lung.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Gene Expression Regulation, Neoplastic. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / pathology
  • [MeSH-minor] Antigens, CD20 / immunology. Cell Nucleus / genetics. Cytoplasm / genetics. Humans. Lymphocytes / pathology. Palatine Tonsil / pathology. Pseudolymphoma / genetics

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  • (PMID = 18346354.001).
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD20; 0 / BCL10 protein, human
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28. Tian XL, Feng RE, Shi JH, Duan MH, Wang JL, Liu HR, Cai BQ, Gao JM, Xu WB, Zhu YJ: [Primary pulmonary lymphoma: analysis of 18 cases]. Zhonghua Jie He He Hu Xi Za Zhi; 2008 Jun;31(6):401-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary pulmonary lymphoma: analysis of 18 cases].
  • OBJECTIVE: To study the clinical characteristics, pathology, diagnosis and treatment of primary pulmonary lymphoma.
  • METHODS: Eighteen cases of primary pulmonary lymphoma diagnosed from Jan 1989 to Feb 2007 were retrospectively analyzed.
  • Fifteen cases were diagnosed by surgical lung biopsy; 1 by percutaneous needle lung biopsy (1/6), 1 by percutaneous needle lung biopsy and bronchoscopic examination at the same time, the other 1 by bronchoscopic examination (1/10).
  • Histological diagnosis showed that 2 cases were Hodgkin lymphoma, 9 mucosa-associated lymphoid tissue lymphoma, 1 follicular lymphoma, 2 diffuse large B cell lymphoma 2 anaplastic large cell lymphoma, 2 non-Hodgkin lymphoma whichcould not be classified because the slides were from other hospitals.
  • CONCLUSIONS: The clinical manifestations of primary pulmonary lymphoma are nonspecific.
  • Surgical lung biopsy is necessary for early diagnosis.
  • [MeSH-major] Lung Neoplasms / diagnosis. Lung Neoplasms / pathology. Lymphoma / diagnosis. Lymphoma / pathology

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  • (PMID = 19031796.001).
  • [ISSN] 1001-0939
  • [Journal-full-title] Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
  • [ISO-abbreviation] Zhonghua Jie He He Hu Xi Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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29. Weiss J, Sos ML, Seidel D, Peifer M, Zander T, Heuckmann JM, Ullrich RT, Menon R, Maier S, Soltermann A, Moch H, Wagener P, Fischer F, Heynck S, Koker M, Schöttle J, Leenders F, Gabler F, Dabow I, Querings S, Heukamp LC, Balke-Want H, Ansén S, Rauh D, Baessmann I, Altmüller J, Wainer Z, Conron M, Wright G, Russell P, Solomon B, Brambilla E, Brambilla C, Lorimier P, Sollberg S, Brustugun OT, Engel-Riedel W, Ludwig C, Petersen I, Sänger J, Clement J, Groen H, Timens W, Sietsma H, Thunnissen E, Smit E, Heideman D, Cappuzzo F, Ligorio C, Damiani S, Hallek M, Beroukhim R, Pao W, Klebl B, Baumann M, Buettner R, Ernestus K, Stoelben E, Wolf J, Nürnberg P, Perner S, Thomas RK: Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer. Sci Transl Med; 2010 Dec 15;2(62):62ra93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer.
  • Lung cancer remains one of the leading causes of cancer-related death in developed countries.
  • Although lung adenocarcinomas with EGFR mutations or EML4-ALK fusions respond to treatment by epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) inhibition, respectively, squamous cell lung cancer currently lacks therapeutically exploitable genetic alterations.
  • We conducted a systematic search in a set of 232 lung cancer specimens for genetic alterations that were therapeutically amenable and then performed high-resolution gene copy number analyses.
  • We identified frequent and focal fibroblast growth factor receptor 1 (FGFR1) amplification in squamous cell lung cancer (n = 155), but not in other lung cancer subtypes, and, by fluorescence in situ hybridization, confirmed the presence of FGFR1 amplifications in an independent cohort of squamous cell lung cancer samples (22% of cases).
  • Using cell-based screening with the FGFR inhibitor PD173074 in a large (n = 83) panel of lung cancer cell lines, we demonstrated that this compound inhibited growth and induced apoptosis specifically in those lung cancer cells carrying amplified FGFR1.
  • We validated the FGFR1 dependence of FGFR1-amplified cell lines by FGFR1 knockdown and by ectopic expression of an FGFR1-resistant allele (FGFR1(V561M)), which rescued FGFR1-amplified cells from PD173074-mediated cytotoxicity.
  • Thus, focal FGFR1 amplification is common in squamous cell lung cancer and associated with tumor growth and survival, suggesting that FGFR inhibitors may be a viable therapeutic option in this cohort of patients.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Receptor, Fibroblast Growth Factor, Type 1 / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Apoptosis / genetics. Apoptosis / physiology. Blotting, Western. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line. Enzyme Inhibitors / therapeutic use. Gene Expression Regulation, Neoplastic / genetics. Humans. Male. Mice. Mice, Nude. Pyrimidines / therapeutic use. RNA Interference. Xenograft Model Antitumor Assays

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  • [CommentIn] Sci Transl Med. 2010 Dec 15;2(62):62ps56 [21160076.001]
  • [CommentIn] Nat Rev Drug Discov. 2011 Feb;10(2):98-9 [21283102.001]
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  • (PMID = 21160078.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE25016
  • [Grant] United States / NCI NIH HHS / CA / K08 CA097980; United States / NCI NIH HHS / CA / P01 CA129243; United States / NCI NIH HHS / CA / R01 CA121210
  • [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 / Enzyme Inhibitors; 0 / PD 173074; 0 / Pyrimidines; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; Adenocarcinoma of lung
  • [Other-IDs] NLM/ NIHMS569992; NLM/ PMC3990281
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30. Lin E, Li L, Guan Y, Soriano R, Rivers CS, Mohan S, Pandita A, Tang J, Modrusan Z: Exon array profiling detects EML4-ALK fusion in breast, colorectal, and non-small cell lung cancers. Mol Cancer Res; 2009 Sep;7(9):1466-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exon array profiling detects EML4-ALK fusion in breast, colorectal, and non-small cell lung cancers.
  • The echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion gene has been identified as an oncogene in a subset of non-small cell lung cancers (NSCLC).
  • Screening of a large collection of patient tumor samples showed the presence of EML4-ALK fusion in 2.4% of breast (5 of 209), 2.4% of colorectal (2 of 83), and in 11.3% of NSCLC (12 of 106).
  • EML4-ALK translocation was also confirmed by fluorescence in situ hybridization assay, which revealed its substantial heterogeneity in both primary tumors and tumor-derived cell lines.
  • To elucidate the functional significance of EML4-ALK, we examined the growth of cell lines harboring the fusion following EML4 and ALK silencing by small interfering RNA.
  • Significant growth inhibition was observed in some but not all cell lines, suggesting their variable dependence on ALK-mediated cell survival signaling.
  • [MeSH-major] Breast Neoplasms / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Colorectal Neoplasms / genetics. Exons. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Cell Survival / physiology. Chromosome Breakpoints. Female. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Oligonucleotide Array Sequence Analysis / methods. RNA Interference. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19737969.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Small Interfering
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31. Katano H, Sato Y, Hoshino S, Tachikawa N, Oka S, Morishita Y, Ishida T, Watanabe T, Rom WN, Mori S, Sata T, Weiden MD, Hoshino Y: Integration of HIV-1 caused STAT3-associated B cell lymphoma in an AIDS patient. Microbes Infect; 2007 Nov-Dec;9(14-15):1581-9
LANL HIV Databases. LANL HIV Databases .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integration of HIV-1 caused STAT3-associated B cell lymphoma in an AIDS patient.
  • High expression of STAT3 has also been implicated in cancer and lymphoma.
  • Here, we show a case of B cell lymphoma in which a defective human immunodeficiency virus 1 (HIV-1) integrated upstream of the first STAT3 coding exon.
  • The lymphoma cells with anaplastic large cell morphology formed multiple nodular lesions in the lung of an acquired immunodeficiency syndrome (AIDS) patient with Kaposi's sarcoma.
  • Immunohistochemistry showed increased expression of STAT3 in the nuclei of lymphoma cells.
  • Transfection of STAT3 resulted in transient cell proliferation in primary B cells in vitro.
  • Although this is a very rare case of HIV-1-integrated lymphoma, these data suggest that up-regulation of STAT3 caused by HIV-1 integration resulted in the development of B cell lymphoma in this special case.

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  • (PMID = 18024124.001).
  • [ISSN] 1286-4579
  • [Journal-full-title] Microbes and infection
  • [ISO-abbreviation] Microbes Infect.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000096; United States / NIDA NIH HHS / DA / R21 DA022162-02; United States / NCRR NIH HHS / RR / MO1 RR00096; United States / NIDA NIH HHS / DA / R21 DA022162-01; United States / NIDA NIH HHS / DA / DA022162; United States / NIDA NIH HHS / DA / DA022162-01; United States / NHLBI NIH HHS / HL / HL 59832; United States / NHLBI NIH HHS / HL / R01 HL059832; United States / NIDA NIH HHS / DA / DA022162-02; United States / NIDA NIH HHS / DA / R21 DA022162; United States / NHLBI NIH HHS / HL / HL57879; United States / NHLBI NIH HHS / HL / R01 HL057879
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / STAT3 Transcription Factor
  • [Other-IDs] NLM/ NIHMS36353; NLM/ PMC2200298
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32. Neal JW, Sequist LV: Exciting new targets in lung cancer therapy: ALK, IGF-1R, HDAC, and Hh. Curr Treat Options Oncol; 2010 Jun;11(1-2):36-44
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] Exciting new targets in lung cancer therapy: ALK, IGF-1R, HDAC, and Hh.
  • The anaplastic lymphoma kinase (ALK) inhibitor crizotinib will become an integral addition to the treatment of patients with non-small cell lung cancer (NSCLC) harboring genetic ALK translocations.
  • The histone deacetylation (HDAC) inhibitor vorinostat did not demonstrate an improvement in overall survival (OS) compared with placebo in a large randomized trial, but other agents in this class may have greater selectivity and efficacy.
  • Inhibitors of the hedgehog (Hh) signaling pathways have some early clinical promise in both NSCLC and small cell lung cancer (SCLC), and larger studies using these agents are eagerly anticipated.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hedgehog Proteins / antagonists & inhibitors. Histone Deacetylases / chemistry. Lung Neoplasms / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, IGF Type 1 / antagonists & inhibitors

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  • (PMID = 20676809.001).
  • [ISSN] 1534-6277
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / Histone Deacetylase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.5.1.98 / Histone Deacetylases
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33. Inamura K, Takeuchi K, Togashi Y, Nomura K, Ninomiya H, Okui M, Satoh Y, Okumura S, Nakagawa K, Soda M, Choi YL, Niki T, Mano H, Ishikawa Y: EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers. J Thorac Oncol; 2008 Jan;3(1):13-7
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] EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers.
  • INTRODUCTION: Very recently, we have found a novel fusion product between the echinoderm microtubule-associated protein-like4 (EML4) and the anaplastic lymphoma kinase (ALK) in non-small cell lung cancers (NSCLCs).
  • Herein, we present results of a first large scale study of EML4-ALK fusion in lung cancers.
  • METHODS: Using reverse transcription-polymerase chain reaction for EML4-ALK fusion mRNA, we investigated 149 lung adenocarcinomas, 48 squamous cell carcinomas, 3 large-cell neuroendocrine carcinomas, and 21 small-cell carcinomas.
  • CONCLUSIONS: In the present first investigation of EML4-ALK fusion in a large study of lung cancers (5/221), we found an interesting histotype-genotype relationship.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adenocarcinoma / pathology. Carcinoma, Neuroendocrine / pathology. Carcinoma, Squamous Cell / pathology. Cell Cycle Proteins / genetics. Chromosome Inversion. Chromosomes, Human, Pair 2. DNA Mutational Analysis. Female. Humans. Immunohistochemistry. Male. Microtubule-Associated Proteins / genetics. Protein-Tyrosine Kinases / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Survival Analysis

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  • (PMID = 18166835.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / EML4-ALK fusion protein, human; 0 / Microtubule-Associated Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, 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; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases
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34. Takahashi T, Sonobe M, Kobayashi M, Yoshizawa A, Menju T, Nakayama E, Mino N, Iwakiri S, Sato K, Miyahara R, Okubo K, Manabe T, Date H: Clinicopathologic features of non-small-cell lung cancer with EML4-ALK fusion gene. Ann Surg Oncol; 2010 Mar;17(3):889-97
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] Clinicopathologic features of non-small-cell lung cancer with EML4-ALK fusion gene.
  • BACKGROUND: A fusion gene between echinoderm microtubule-associated protein-like 4 (EML4) and the anaplastic lymphoma kinase (ALK) has recently been identified in nonsmall-cell lung cancers (NSCLCs).
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Mutation / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Aged. Carcinoma, Large Cell / genetics. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Proto-Oncogene Proteins / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics. Reverse Transcriptase Polymerase Chain Reaction. ras Proteins / genetics


35. Rodig SJ, Mino-Kenudson M, Dacic S, Yeap BY, Shaw A, Barletta JA, Stubbs H, Law K, Lindeman N, Mark E, Janne PA, Lynch T, Johnson BE, Iafrate AJ, Chirieac LR: Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population. Clin Cancer Res; 2009 Aug 15;15(16):5216-23
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] Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population.
  • PURPOSE: The anaplastic large cell kinase gene (ALK) is rearranged in approximately 5% of lung adenocarcinomas within the Asian population.
  • We evaluated the incidence and the characteristics of ALK-rearranged lung adenocarcinomas within the western population and the optimal diagnostic modality to detect ALK rearrangements in routine clinical practice.
  • EXPERIMENTAL DESIGN: We tested 358 lung adenocarcinomas from three institutions for ALK rearrangements by fluorescent in situ hybridization (FISH) and immunohistochemistry with and without tyramide amplification.
  • RESULTS: We identified 20 (5.6%) lung adenocarcinomas with ALK rearrangements within our cohort of western patients.
  • CONCLUSIONS: Lung adenocarcinomas with ALK rearrangements are uncommon in the western population and represent a distinct entity of carcinomas with unique characteristics.
  • For suspected cases, dual diagnostic testing, with FISH and immunohistochemistry, should be considered to accurately identify lung adenocarcinomas with ALK rearrangement.

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  • (PMID = 19671850.001).
  • [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 / CA136851-02; United States / PHS HHS / / R01-135257; United States / PHS HHS / / R01-136851; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R01 CA136851-02; United States / NCI NIH HHS / CA / R01 CA136851; United States / NCI NIH HHS / CA / 2P50 CA090578-06
  • [Publication-type] 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/ NIHMS198972; NLM/ PMC2865649
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36. Ambrosini V, Quarta C, Zinzani PL, Nanni C, Fini M, Torricelli P, Giavaresi G, D'Errico-Grigioni A, Malvi D, Franchi R, Fanti S: 18[F]FDG small animal PET study of sorafenib efficacy in lymphoma preclinical models. Q J Nucl Med Mol Imaging; 2010 Dec;54(6):689-97
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  • [Title] 18[F]FDG small animal PET study of sorafenib efficacy in lymphoma preclinical models.
  • On-going studies are investigating the efficacy of Sorafenib in other solid tumours such as melanoma and non-small cells lung carcinoma and pre-clinical models showed the efficacy of treatment with Sorafenib in murine models of renal cells carcinoma, breast cancer, colon carcinoma and melanoma.
  • To our knowledge, Sorafenib has never been employed in human lymphoma.
  • The aim of the present study was to assess the efficacy of Sorafenib in murine models of human anaplastic large cells lymphoma (ALCL) and Hodgkin lymphoma (HD).
  • Caspase-3 production showed a dose-dependent trend reaching significantly higher values for 0.046 mg/L and 0.465 mg/L drug concentrations in both cell lines.
  • CONCLUSION: Sorafenib showed a good cytotoxic effect in vitro especially on human HD cell line, but these findings were not confirmed in vivo.
  • [MeSH-major] Benzenesulfonates / therapeutic use. Fluorodeoxyglucose F18. Lymphoma / drug therapy. Lymphoma / radionuclide imaging. Positron-Emission Tomography / veterinary. Pyridines / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Drug Evaluation, Preclinical / methods. Drug Evaluation, Preclinical / veterinary. Humans. Mice. Niacinamide / analogs & derivatives. Phenylurea Compounds. Prognosis. Radiopharmaceuticals. Treatment Outcome

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  • (PMID = 20639808.001).
  • [ISSN] 1824-4785
  • [Journal-full-title] The quarterly journal of nuclear medicine and molecular imaging : official publication of the Italian Association of Nuclear Medicine (AIMN) [and] the International Association of Radiopharmacology (IAR), [and] Section of the Society of Radiopharmaceutical Chemistry and Biology
  • [ISO-abbreviation] Q J Nucl Med Mol Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
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37. Rikova K, Guo A, Zeng Q, Possemato A, Yu J, Haack H, Nardone J, Lee K, Reeves C, Li Y, Hu Y, Tan Z, Stokes M, Sullivan L, Mitchell J, Wetzel R, Macneill J, Ren JM, Yuan J, Bakalarski CE, Villen J, Kornhauser JM, Smith B, Li D, Zhou X, Gygi SP, Gu TL, Polakiewicz RD, Rush J, Comb MJ: Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. Cell; 2007 Dec 14;131(6):1190-203
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  • [Title] Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer.
  • Here we present the first large-scale survey of tyrosine kinase activity in lung cancer.
  • Using a phosphoproteomic approach, we characterize tyrosine kinase signaling across 41 non-small cell lung cancer (NSCLC) cell lines and over 150 NSCLC tumors.
  • By focusing on activated cell circuitry, the approach outlined here provides insight into cancer biology not available at the chromosomal and transcriptional levels and can be applied broadly across all human cancers.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Phosphotyrosine / metabolism. Protein-Tyrosine Kinases / metabolism. Signal Transduction / genetics
  • [MeSH-minor] Cell Line, Tumor. Enzyme Activation. Gene Fusion. Humans. Models, Biological. Molecular Sequence Data. Phosphorylation. Receptor Protein-Tyrosine Kinases. Receptor, Platelet-Derived Growth Factor alpha / metabolism


38. Jokoji R, Yamasaki T, Minami S, Komuta K, Sakamaki Y, Takeuchi K, Tsujimoto M: Combination of morphological feature analysis and immunohistochemistry is useful for screening of EML4-ALK-positive lung adenocarcinoma. J Clin Pathol; 2010 Dec;63(12):1066-70
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  • [Title] Combination of morphological feature analysis and immunohistochemistry is useful for screening of EML4-ALK-positive lung adenocarcinoma.
  • BACKGROUND: A subset of lung cancers harbours the fusion gene echinoderm microtubule-associated protein-like-4-anaplastic lymphoma kinase (EML4-ALK).
  • Recently, immunohistochemistry for ALK has shown sensitivity for the detection of EML4-ALK-positive lung adenocarcinoma almost equal to that of the fluorescence in situ hybridisation (FISH) assay.
  • AIMS: To study the clinicopathological features of EML4-ALK-positive lung adenocarcinoma in a large number of surgically resected samples using immunohistochemistry, in order to establish a useful screening method for EML4-ALK-positive lung adenocarcinoma.
  • METHODS: Immunohistochemistry for ALK was used to screen for EML4-ALK-positive lung adenocarcinomas in 254 cases of surgically resected samples.
  • RESULTS: EML4-ALK-positive cases were detected in 3.1% of lung adenocarcinomas (8/254).
  • EML4-ALK-positive lung adenocarcinomas showed significant associations with intra- and/or extra-cytoplasmic mucin (p=0.0001), and cribriform pattern with excessive extracytoplasmic mucin (p<0.0001).
  • Signet-ring cell appearance alone lacked significance (p=0.149).
  • CONCLUSION: EML4-ALK-positive lung adenocarcinoma has a tendency to express a characteristic morphological pattern.
  • The combined use of morphological feature analysis and immunohistochemistry may be a useful and cost effective screening method for EML4-ALK lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Early Detection of Cancer / methods. Lung Neoplasms / pathology. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Cytoplasm / enzymology. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Proteins / metabolism

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  • (PMID = 20935334.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion
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39. Mino-Kenudson M, Chirieac LR, Law K, Hornick JL, Lindeman N, Mark EJ, Cohen DW, Johnson BE, Jänne PA, Iafrate AJ, Rodig SJ: A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry. Clin Cancer Res; 2010 Mar 1;16(5):1561-71
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  • [Title] A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry.
  • PURPOSE: Approximately 5% of lung adenocarcinomas harbor an EML4-ALK gene fusion and define a unique tumor group that may be responsive to targeted therapy.
  • However ALK-rearranged lung adenocarcinomas are difficult to detect by either standard fluorescence in situ hybridization or immunohistochemistry (IHC) assays.
  • In the present study, we used novel antibodies to compare ALK protein expression in genetically defined lung cancers and anaplastic large cell lymphomas.
  • RESULTS: ALK protein is invariably and exclusively expressed in ALK-rearranged lung adenocarcinomas but at much lower levels than in the prototypic ALK-rearranged tumor, anaplastic large cell lymphoma, and as a result, is often not detected by conventional IHC.
  • We further validate a novel IHC that shows excellent sensitivity and specificity (100% and 99%, respectively) for the detection of ALK-rearranged lung adenocarcinomas in biopsy specimens, with excellent interobserver agreement between pathologists (kappa statistic, 0.94).
  • CONCLUSIONS: Low levels of ALK protein expression is a characteristic feature of ALK-rearranged lung adenocarcinomas.
  • However, a novel, highly sensitive IHC assay reliably detects lung adenocarcinomas with ALK rearrangements and obviates the need for fluorescence in situ hybridization analysis for the majority of cases, and therefore could be routinely applicable in clinical practice to detect lung cancers that may be responsive to ALK inhibitors.

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  • (PMID = 20179225.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / CA090578; United States / NCI NIH HHS / CA / CA136851-01A1; United States / NCI NIH HHS / CA / R01 CA136851-01A1; United States / NCI NIH HHS / CA / R01CA136851; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / R01 CA114465; United States / NCI NIH HHS / CA / R01 CA136851
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ NIHMS170973; NLM/ PMC2831135
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40. Rodig SJ, Shapiro GI: Crizotinib, a small-molecule dual inhibitor of the c-Met and ALK receptor tyrosine kinases. Curr Opin Investig Drugs; 2010 Dec;11(12):1477-90
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  • Crizotinib (PF-02341066), under development by Pfizer, is an orally bioavailable, ATP-competitive, small-molecule inhibitor of the receptor tyrosine kinases (RTKs) c-Met (also known as hepatocyte growth factor receptor) and anaplastic lymphoma kinase (ALK), for the potential treatment of cancers dependent on these oncogenic kinases for growth and survival.
  • In preclinical tumor xenograft studies, crizotinib inhibited the growth and survival of cell lines dependent upon c-Met or ALK enzymatic activity.
  • Crizotinib has been particularly effective against anaplastic large cell lymphoma and non-small cell lung cancer (NSCLC) cell lines that harbor ALK translocations resulting in expression of oncogenic ALK fusion proteins.
  • At the time of publication, an ongoing phase III clinical trial is comparing crizotinib with standard second-line chemotherapy in previously treated patients with NSCLC harboring ALK rearrangement, and a phase III trial comparing crizotinib with standard chemotherapy in the first-line setting in non-squamous lung cancer is planned.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-met / antagonists & inhibitors. Pyrazoles / therapeutic use. Pyridines / therapeutic use. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Clinical Trials as Topic. Drug Approval. Drug Evaluation, Preclinical. Humans

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  • (PMID = 21154129.001).
  • [ISSN] 2040-3429
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Pyrazoles; 0 / Pyridines; 53AH36668S / crizotinib; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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41. Mossé YP, Wood A, Maris JM: Inhibition of ALK signaling for cancer therapy. Clin Cancer Res; 2009 Sep 15;15(18):5609-14
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  • A variety of human malignancies have anaplastic lymphoma kinase (ALK) translocations, amplifications, or oncogenic mutations, including anaplastic large cell lymphoma, inflammatory myofibroblastic tumors, non-small cell lung cancer, and neuroblastoma.

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  • (PMID = 19737948.001).
  • [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 / PHS HHS / / K08-111733; United States / NCI NIH HHS / CA / R01-CA124709; United States / NCI NIH HHS / CA / R01-CA78454
  • [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] 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] 57
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42. Armstrong F, Lamant L, Hieblot C, Delsol G, Touriol C: TPM3-ALK expression induces changes in cytoskeleton organisation and confers higher metastatic capacities than other ALK fusion proteins. Eur J Cancer; 2007 Mar;43(4):640-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Translocations of the anaplastic lymphoma kinase (ALK) gene result in the production of a number of oncogenic ALK fusion proteins implicated in tumour development.
  • In the present study, we have investigated the metastatic potential of various X-ALK expressing cell lines using an experimental lung metastasis assay.
  • We have shown that TPM3-ALK expression bestows higher metastatic capacities than other X-ALK fusion proteins and in addition, that TPM3-ALK fusion protein expression specifically induces changes in cell morphology and cytoskeleton organisation.
  • Together the specific actions of TPM3-ALK on the cytoskeleton organisation offer an interesting hypothesis with respect to the higher cell motility and metastatic potential of this fusion protein.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics. Tropomyosin / genetics
  • [MeSH-minor] Animals. Blotting, Western. Cytoskeleton / metabolism. Humans. Immunohistochemistry. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Mice. Mice, Nude. NIH 3T3 Cells. Receptor Protein-Tyrosine Kinases. Transfection

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  • (PMID = 17276053.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TPM3 protein, human; 0 / Tropomyosin; 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. Cannizzo E, Sohani AR, Ferry JA, Hochberg EP, Kluk MJ, Dorn ME, Sadowski C, Bucci JJ, Ackerman AM, Longtine JA, Carulli G, Preffer FI: Carcinoma and multiple lymphomas in one patient: establishing the diagnoses and analyzing risk factors. J Hematop; 2009;2(3):163-70
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  • We report the case of a patient who showed the sequential occurrence of four different lymphoid neoplasms together with a squamous cell carcinoma of the lung.
  • A 62-year-old man with adenopathy was admitted to the hospital, and lymph node biopsy was positive for low-grade follicular lymphoma.
  • Two years later, a PET-CT scan showed a left hilar mass in the lung; biopsy showed a squamous cell carcinoma.
  • Simultaneously, he was diagnosed with diffuse large B cell lymphoma in a neck lymph node; after chemo- and radiotherapy, he achieved a complete response.
  • A restaging PET-CT scan 2 years later revealed a retroperitoneal nodule, and biopsy again showed a low-grade follicular lymphoma, while a biopsy of a cutaneous scalp lesion showed a CD30-positive peripheral T cell lymphoma.
  • After some months, a liver biopsy and a right cervical lymph node biopsy showed a CD30-positive peripheral T cell lymphoma consistent with anaplastic lymphoma kinase-negative anaplastic large cell lymphoma.
  • Flow cytometry and cytogenetic and molecular genetic analysis performed at diagnosis and during the patient's follow-up confirmed the presence of two clonally distinct B cell lymphomas, while the two T cell neoplasms were confirmed to be clonally related.

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  • (PMID = 20309424.001).
  • [ISSN] 1865-5785
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2766444
  • [Keywords] NOTNLM ; Anaplastic large cell lymphoma / Cytogenetics / Diffuse large B cell lymphoma / Follicular lymphoma / Multiple malignancies / Risk factors
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44. Gan MF, Lu HS, Zhang JW, Yu XR: [Interdigitating dendritic cell sarcoma/tumor: a study of 3 cases]. Zhonghua Bing Li Xue Za Zhi; 2008 Oct;37(10):676-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Interdigitating dendritic cell sarcoma/tumor: a study of 3 cases].
  • OBJECTIVE: To study the pathologic features, diagnosis and differential diagnosis of interdigitating dendritic cell sarcoma (IDCS).
  • The site of occurrence included lung, spleen (with lymph node metastasis) and lymph node.
  • They were oval to spindle in shape and contained pale eosinophilic cytoplasm, oval and sometimes grooved nuclei, small distinct nucleoli and ill-defined cell borders.
  • CONCLUSIONS: IDCS is a rare type of histiocytic and dendritic cell malignancy with distinctive morphologic findings.
  • It needs to be distinguished from follicular dendritic cell sarcoma, inflammatory pseudotumor, Langerhans' cell histiocytosis, malignant melanoma, undifferentiated carcinoma and anaplastic large cell lymphoma.
  • Immunohistochemical staining for S-100 protein is helpful in confirming the diagnosis.
  • [MeSH-major] Dendritic Cell Sarcoma, Follicular / pathology. Dendritic Cell Sarcoma, Interdigitating / pathology. Lymph Nodes / pathology. Lymphatic Metastasis / pathology. S100 Proteins / immunology
  • [MeSH-minor] Adolescent. Carcinoma / pathology. Dendritic Cells / pathology. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19094486.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / S100 Proteins
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45. Lucioni M, Capello D, Riboni R, Ippoliti G, Campana C, Bandiera L, Arcaini L, Rossi D, Cerri M, Dionigi P, Lazzarino M, Magrini U, Viganò M, Gaidano G, Paulli M: B-cell posttransplant lymphoproliferative disorders in heart and/or lungs recipients: clinical and molecular-histogenetic study of 17 cases from a single institution. Transplantation; 2006 Oct 27;82(8):1013-23
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  • [Title] B-cell posttransplant lymphoproliferative disorders in heart and/or lungs recipients: clinical and molecular-histogenetic study of 17 cases from a single institution.
  • This study details the clinicopathological and molecular features of 17 B-cell PTLDs observed in a single center series of 988 heart and/or lung transplant recipients.
  • METHODS: Cases were classified according to World Health Organization lymphoma classification and tested for Epstein-Barr Virus (EBV), clonality, histogenetic phenotypic (CD10, Bcl-6, MUM1, CD138), and genotypic (immunoglobulin and BCL-6 genes somatic hypermutation) markers.
  • RESULTS: This series of 17 PTLDs included: two B-cell monoclonal polymorphic PTLDs and 15 B-cell monomorphic PTLDs (13 diffuse large B-cell lymphomas [DLBCL] and 2 Burkitt lymphomas [BL]).
  • CONCLUSIONS: Correlation between morphology, histogenesis, and EBV status demonstrated a high degree of homogeneity in the two GC-related groups, mostly including EBV-negative cases with BL and DLBCL-centroblastic features; the third group, consisting of post GC EBV-positive cases, was histologically less homogeneous, as it included polymorphic PTLDs and DLBCL with immunoblastic and anaplastic features.
  • [MeSH-major] B-Lymphocytes / cytology. Heart Transplantation / adverse effects. Lung Transplantation / adverse effects. Lymphoproliferative Disorders / diagnosis. Lymphoproliferative Disorders / etiology

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  • (PMID = 17060848.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Variable Region
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46. Campo E, Chott A, Kinney MC, Leoncini L, Meijer CJ, Papadimitriou CS, Piris MA, Stein H, Swerdlow SH: Update on extranodal lymphomas. Conclusions of the Workshop held by the EAHP and the SH in Thessaloniki, Greece. Histopathology; 2006 Apr;48(5):481-504
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  • Classification and proper treatment of extranodal lymphoma is hindered by the diversity of lymphoma types and the relative rarity of many of these tumour types.
  • In order to review controversial issues in extranodal lymphoma diagnosis, a joint Workshop of the European Haematopathology Association (EAHP) and the Society for Hematopathology (SH) was held, where 99 selected cases were reviewed and discussed.
  • This Workshop summary is focused on the most controversial aspect of cutaneous B-cell lymphoma, other extranodal B-cell lymphomas, plasmablastic lymphoma and anaplastic large-cell lymphoma in extranodal sites, and makes practical recommendations about diagnosis and therapeutic approaches.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, T-Cell / pathology
  • [MeSH-minor] Diagnosis, Differential. Gastrointestinal Tract / pathology. Humans. Lung / pathology. Salivary Glands / pathology. Skin / pathology

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  • (PMID = 16623775.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 145
  • [Other-IDs] NLM/ PMC1448691
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47. Sozzi G, Martelli MP, Conte D, Modena P, Pettirossi V, Pileri SA, Falini B: The EML4-ALK transcript but not the fusion protein can be expressed in reactive and neoplastic lymphoid tissues. Haematologica; 2009 Sep;94(9):1307-11
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  • ALK+ anaplastic large cell lymphoma and a rare subset of ALK+ diffuse large B-cell lymphoma.
  • Recently, rearrangements involving ALK and the echinoderm microtubule associated protein-like 4 (EML4) gene were described as a specific genetic alteration in about 6% of non-small cell lung cancer (NSCLC).
  • EML4-ALK transcripts were detected in 3/51 (5.9%) of reactive lymphoid tissues and 12/58 (20.7%) of lymphomas of different categories, including follicular lymphoma, diffuse large B-cell lymphoma and Hodgkin's disease.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma / metabolism. Oncogene Proteins, Fusion / biosynthesis
  • [MeSH-minor] Animals. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Mice. NIH 3T3 Cells

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  • (PMID = 19734424.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC2738726
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48. Palanisamy N, Ateeq B, Kalyana-Sundaram S, Pflueger D, Ramnarayanan K, Shankar S, Han B, Cao Q, Cao X, Suleman K, Kumar-Sinha C, Dhanasekaran SM, Chen YB, Esgueva R, Banerjee S, LaFargue CJ, Siddiqui J, Demichelis F, Moeller P, Bismar TA, Kuefer R, Fullen DR, Johnson TM, Greenson JK, Giordano TJ, Tan P, Tomlins SA, Varambally S, Rubin MA, Maher CA, Chinnaiyan AM: Rearrangements of the RAF kinase pathway in prostate cancer, gastric cancer and melanoma. Nat Med; 2010 Jul;16(7):793-8
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  • Recently, rare targetable gene fusions involving the anaplastic lymphoma receptor tyrosine kinase (ALK) gene, have been identified in 1-5% of lung cancers, suggesting that similar rare gene fusions may occur in other common epithelial cancers, including prostate cancer.
  • Screening a large cohort of patients, we found that, although rare, recurrent rearrangements in the RAF pathway tend to occur in advanced prostate cancers, gastric cancers and melanoma.

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  • (PMID = 20526349.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / U54 DA21519-01A1; United States / NCI NIH HHS / CA / R01 CA125612-01; United States / NCI NIH HHS / CA / R01 CA132874; United States / NCI NIH HHS / CA / U01 CA111275-01; United States / NCI NIH HHS / CA / P50 CA069568-06A19001; United States / NCI NIH HHS / CA / CA069568-06A19001; United States / NCI NIH HHS / CA / R01 CA125612-01A1; United States / NCI NIH HHS / CA / P50CA69568; United States / NCI NIH HHS / CA / R01 CA125612; Canada / Canadian Institutes of Health Research / / ; United States / NCI NIH HHS / CA / P50 CA069568-06A10016; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / R01CA132874; United States / NCI NIH HHS / CA / CA069568-06A10016; United States / NIDA NIH HHS / DA / U54 DA021519; United States / NCI NIH HHS / CA / P50 CA069568; United States / NCI NIH HHS / CA / U01 CA111275
  • [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 / ESRP1 protein, human; 0 / Membrane Transport Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Proteins; 0 / SLC45a3 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
  • [Other-IDs] NLM/ NIHMS212353; NLM/ PMC2903732
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49. Zhang L, Wu G: Complete atelectasis of the left lung from anaplastic large-cell lymphoma. ScientificWorldJournal; 2010;10:1332-3
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  • [Title] Complete atelectasis of the left lung from anaplastic large-cell lymphoma.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / complications. Pulmonary Atelectasis / etiology

  • Genetic Alliance. consumer health - Anaplastic Large Cell Lymphoma.
  • Genetic Alliance. consumer health - Lymphoma, large-cell.
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  • (PMID = 20623092.001).
  • [ISSN] 1537-744X
  • [Journal-full-title] TheScientificWorldJournal
  • [ISO-abbreviation] ScientificWorldJournal
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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50. Yang SL, Song H, Tang YM: [Primary anaplastic large cell lymphoma originated from lung in a case]. Zhonghua Er Ke Za Zhi; 2007 Dec;45(12):949
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] [Primary anaplastic large cell lymphoma originated from lung in a case].
  • [MeSH-major] Lung Neoplasms / congenital. Lymphoma, Large-Cell, Anaplastic / physiopathology

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  • (PMID = 18339290.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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51. Allory Y, Merabet Z, Copie-Bergman C, Lange F, Yiou R, Gaulard P: Sarcomatoid variant of anaplastic large cell lymphoma mimics ALK-1-positive inflammatory myofibroblastic tumor in bladder. Am J Surg Pathol; 2005 Jun;29(6):838-9; author reply 839
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] Sarcomatoid variant of anaplastic large cell lymphoma mimics ALK-1-positive inflammatory myofibroblastic tumor in bladder.
  • [MeSH-major] Activin Receptors, Type I / immunology. Biomarkers, Tumor / immunology. Lung Neoplasms / immunology. Lymphoma, Large B-Cell, Diffuse / immunology. Urinary Bladder Neoplasms / immunology


52. Fernandez FG, Denlinger CE, Crabtree TD: Primary non-Hodgkin's lymphoma of the trachea. J Thorac Oncol; 2010 Mar;5(3):403-4
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary non-Hodgkin's lymphoma of the trachea.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Tracheal Neoplasms / pathology

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  • (PMID = 20186028.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Case Reports; 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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