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6. Ambrogio C, Voena C, Manazza AD, Martinengo C, Costa C, Kirchhausen T, Hirsch E, Inghirami G, Chiarle R: The anaplastic lymphoma kinase controls cell shape and growth of anaplastic large cell lymphoma through Cdc42 activation. Cancer Res; 2008 Nov 1;68(21):8899-907
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The anaplastic lymphoma kinase controls cell shape and growth of anaplastic large cell lymphoma through Cdc42 activation.
  • Anaplastic large cell lymphoma (ALCL) is a non-Hodgkin's lymphoma that originates from T cells and frequently expresses oncogenic fusion proteins derived from chromosomal translocations or inversions of the anaplastic lymphoma kinase (ALK) gene.
  • The proliferation and survival of ALCL cells are determined by the ALK activity.
  • Here we show that the kinase activity of the nucleophosmin (NPM)-ALK fusion regulated the shape of ALCL cells and F-actin filament assembly in a pattern similar to T-cell receptor-stimulated cells.
  • VAV1 increased Cdc42 activity, and in turn, Cdc42 regulated the shape and migration of ALCL cells.
  • In vitro knockdown of VAV1 or Cdc42 by short hairpin RNA, as well as pharmacologic inhibition of Cdc42 activity by secramine, resulted in a cell cycle arrest and apoptosis of ALCL cells.
  • Importantly, the concomitant inhibition of Cdc42 and NPM-ALK kinase acted synergistically to induce apoptosis of ALCL cells.
  • Finally, Cdc42 was necessary for the growth as well as for the maintenance of already established lymphomas in vivo.
  • Thus, our data open perspectives for new therapeutic strategies by revealing a mechanism of regulation of ALCL cell growth through Cdc42.

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  • (PMID = 18974134.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033; United States / NCI NIH HHS / CA / CA090773-04; United States / NIGMS NIH HHS / GM / R01-GM075252-04; United States / NIGMS NIH HHS / GM / R01 GM075252-04; United States / NIGMS NIH HHS / GM / R01 GM075252; United States / NCI NIH HHS / CA / R01 CA090773-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-vav; 0 / VAV1 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.6.5.2 / cdc42 GTP-Binding Protein
  • [Other-IDs] NLM/ NIHMS69833; NLM/ PMC2596920
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7. Gualco G, Chioato L, Weiss LM, Harrington WJ Jr, Bacchi CE: Analysis of human T-cell lymphotropic virus in CD25+ anaplastic large cell lymphoma in children. Am J Clin Pathol; 2009 Jul;132(1):28-33
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  • [Title] Analysis of human T-cell lymphotropic virus in CD25+ anaplastic large cell lymphoma in children.
  • Anaplastic large cell lymphoma (ALCL) is recognized as 2 distinct diseases: anaplastic lymphoma kinase (ALK)+ ALCL and ALK- ALCL.
  • ALK+ ALCL occurs in younger patients and has a better prognosis.
  • Human T-cell lymphotropic virus (HTLV-1) is linked to the development of adult T-cell leukemia/lymphoma (ATLL), which frequently expresses CD25.
  • CD25 is significantly expressed in childhood ALCL.
  • Some cases of adult HTLV-1-related lymphomas have characteristics of ALCL but are considered CD30+ ATLL subtypes.
  • We analyzed 33 cases of pediatric ALCL, CD25+ and CD25-, for proviral HTLV-1 DNA.
  • All cases corresponded to the common histologic ALCL type and were CD30+ in virtually all neoplastic cells.
  • ALK expression was observed in 31 (94%) of 33 cases; CD25 was positive in 27 (82%), including 1 ALK- ALCL case.
  • There was a strong positive correlation between ALK and CD25 expression.
  • ALCL in children has no relationship with HTLV-1; the frequent CD25 expression must be explained by a mechanism different from that in ATLL.

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  • (PMID = 19864230.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA112217-03; United States / NCI NIH HHS / CA / CA121935-03; United States / NCI NIH HHS / CA / R01 CA112217-03; United States / NCI NIH HHS / CA / R01 CA082274-08; United States / NCI NIH HHS / CA / R01 CA082274; United States / NCI NIH HHS / CA / R01 CA121935-03; United States / NCI NIH HHS / CA / R01 CA121935
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / IL2RA protein, human; 0 / Interleukin-2 Receptor alpha Subunit; 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/ NIHMS125676; NLM/ PMC2771325
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8. Johnston M, Lee JJ, Chottiner GS, Miller B, Tsuda T, Hussey CL, Scherson DA: Electrochemistry in ultrahigh vacuum: underpotential deposition of Al on polycrystalline W and Au from room temperature AlCl(3)/1-ethyl-3-methylimidazolium chloride melts. J Phys Chem B; 2005 Jun 9;109(22):11296-300
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Electrochemistry in ultrahigh vacuum: underpotential deposition of Al on polycrystalline W and Au from room temperature AlCl(3)/1-ethyl-3-methylimidazolium chloride melts.
  • The voltammetric characteristics of polycrystalline Au and W electrodes cleaned (thermal annealing at 1100 K) and characterized (Auger electron spectroscopy) in ultrahigh vacuum (UHV) have been examined in ultrapure AlCl(3)/1-ethyl-3-methylimidazolium chloride (EtMeImCl) melts in UHV.
  • These experiments were performed using a custom-designed transfer system that allows for the all-Al electrochemical cell to be filled with EtMeImCl in an auxiliary UHV chamber and later transferred under UHV to the main UHV chamber that houses the Auger electron spectrometer.
  • This behavior is unlike that reported in the literature for experiments performed in a glovebox, which required either extensive potential cycling in the Al bulk deposition and stripping region or excursions to potentials positive enough for chlorine evolution to ensue for Al UPD features to be clearly discerned.

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  • (PMID = 16852379.001).
  • [ISSN] 1520-6106
  • [Journal-full-title] The journal of physical chemistry. B
  • [ISO-abbreviation] J Phys Chem B
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Sandlund JT, Laver JH: Pediatric oncology: methotrexate-exploring dosing and administration in ALCL. Nat Rev Clin Oncol; 2009 Aug;6(8):440-1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric oncology: methotrexate-exploring dosing and administration in ALCL.

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  • (PMID = 19644533.001).
  • [ISSN] 1759-4782
  • [Journal-full-title] Nature reviews. Clinical oncology
  • [ISO-abbreviation] Nat Rev Clin Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA 21765; United Kingdom / Medical Research Council / /
  • [Publication-type] News; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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10. Madhavan N, Takatani T, Sherrill CD, Weck M: Macrocyclic cyclooctene-supported AlCl-salen catalysts for conjugated addition reactions: effect of linker and support structure on catalysis. Chemistry; 2009;15(5):1186-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Macrocyclic cyclooctene-supported AlCl-salen catalysts for conjugated addition reactions: effect of linker and support structure on catalysis.
  • AlCl-salen (salen=N,N'-bis(salicylidene)ethylenediamine dianion) catalysts supported onto macrocyclic oligomeric cyclooctene through linkers of varying length and flexibility have been developed to demonstrate the importance of support architecture on catalyst activity.
  • Our studies with the cyclooctene supported AlCl-salen catalysts provides significant insights for rationally designing highly efficient AlCl-salen catalysts for a diverse set of reactions.

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  • (PMID = 19101958.001).
  • [ISSN] 1521-3765
  • [Journal-full-title] Chemistry (Weinheim an der Bergstrasse, Germany)
  • [ISO-abbreviation] Chemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cross-Linking Reagents; 0 / Cyclooctanes; 0 / Ethylenediamines; 0 / Macrocyclic Compounds; 94-93-9 / disalicylaldehyde ethylenediamine; CPD4NFA903 / Aluminum
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11. Dimitrov A, Heidemann D, Kemnitz E: F/Cl-exchange on AlCl(3)-pyridine adducts: synthesis and characterization of trans-difluoro-tetrakis-pyridine-aluminum-chloride, [AlF2(Py)4]+Cl-. Inorg Chem; 2006 Dec 25;45(26):10807-14

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] F/Cl-exchange on AlCl(3)-pyridine adducts: synthesis and characterization of trans-difluoro-tetrakis-pyridine-aluminum-chloride, [AlF2(Py)4]+Cl-.

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  • (PMID = 17173440.001).
  • [ISSN] 0020-1669
  • [Journal-full-title] Inorganic chemistry
  • [ISO-abbreviation] Inorg Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Pulford K, Roberton HM, Jones M: Antibody techniques used in the study of anaplastic lymphoma kinase-positive ALCL. Methods Mol Med; 2005;115:271-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antibody techniques used in the study of anaplastic lymphoma kinase-positive ALCL.
  • The availability of suitable reagents for routine diagnostic use has revolutionized the study of leukemia and lymphoma pathology.
  • The use of antibodies specific for anaplastic lymphoma kinase (ALK) protein has permitted the identification of the tumor entity ALK-positive from the poorly defined morphological category of anaplastic large cell lymphoma.
  • This chapter describes the use of antibodies in both immunolabeling (immunocytochemical and immunofluorescence) procedures and in biochemical procedures in the study of ALK-positive ALCL.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibodies, Neoplasm / immunology. Blotting, Western / methods. Lymphoma, Large-Cell, Anaplastic / diagnosis. Protein-Tyrosine Kinases / immunology. Receptor Protein-Tyrosine Kinases / immunology

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  • (PMID = 15998974.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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13. Sarpola AT, Saukkoriipi JJ, Hietapelto VK, Jalonen JE, Jokela JT, Joensuu PH, Laasonen KE, Rämö JH: Identification of hydrolysis products of AlCl(3)*6H(2)O in the presence of sulfate by electrospray ionization time-of-flight mass spectrometry and computational methods. Phys Chem Chem Phys; 2007 Jan 21;9(3):377-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of hydrolysis products of AlCl(3)*6H(2)O in the presence of sulfate by electrospray ionization time-of-flight mass spectrometry and computational methods.

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  • (PMID = 17199154.001).
  • [ISSN] 1463-9076
  • [Journal-full-title] Physical chemistry chemical physics : PCCP
  • [ISO-abbreviation] Phys Chem Chem Phys
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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4. Luo Y, Niu F, Sun Z, Cao W, Zhang X, Guan D, Lv Z, Zhang B, Xu Y: Altered expression of Abeta metabolism-associated molecules from D-galactose/AlCl(3) induced mouse brain. Mech Ageing Dev; 2009 Apr;130(4):248-52
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altered expression of Abeta metabolism-associated molecules from D-galactose/AlCl(3) induced mouse brain.
  • Cerebral deposition of amyloid-beta peptide (Abeta) is a critical feature of Alzheimer's disease (AD).

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  • (PMID = 19150622.001).
  • [ISSN] 1872-6216
  • [Journal-full-title] Mechanisms of ageing and development
  • [ISO-abbreviation] Mech. Ageing Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Aluminum Compounds; 0 / Amyloid beta-Peptides; 0 / Chlorides; 0 / Receptors, LDL; 3CYT62D3GA / aluminum chloride; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / Bace1 protein, mouse; EC 3.4.24.11 / Neprilysin; X2RN3Q8DNE / Galactose
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15. Iwashita A, Matsuo Y, Nakamura E: AlCl(3)-mediated mono-, di-, and trihydroarylation of [60]fullerene. Angew Chem Int Ed Engl; 2007;46(19):3513-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AlCl(3)-mediated mono-, di-, and trihydroarylation of [60]fullerene.

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  • (PMID = 17385815.001).
  • [ISSN] 1433-7851
  • [Journal-full-title] Angewandte Chemie (International ed. in English)
  • [ISO-abbreviation] Angew. Chem. Int. Ed. Engl.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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21. Mann G, Gadner H: Comment on HLH in a child with anaplastic large cell lymphoma (ALCL). J Pediatr Hematol Oncol; 2008 Oct;30(10):721-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comment on HLH in a child with anaplastic large cell lymphoma (ALCL).
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / complications. Lymphoma, Large-Cell, Anaplastic / complications
  • [MeSH-minor] Antigens, CD30. Bystander Effect. Child. Cytokines / secretion. Humans. Inflammation

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  • [CommentOn] J Pediatr Hematol Oncol. 2008 Oct;30(10):785-7 [19011482.001]
  • (PMID = 19011466.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Cytokines
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22. Thakuria M, Agarwal S, Saffold OE, Jaworsky C: Fulminant cutaneous eruption in a 51-year-old man. Primary cutaneous anaplastic large cell lymphoma (C-ALCL). Arch Dermatol; 2007 Feb;143(2):255-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fulminant cutaneous eruption in a 51-year-old man. Primary cutaneous anaplastic large cell lymphoma (C-ALCL).
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Skin Neoplasms / pathology

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  • (PMID = 17310010.001).
  • [ISSN] 0003-987X
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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23. Goldman S, Coiffier B, Reiter A, Younes A, Cairo MS, International TLS Expert Panel: A medical decision tree for the prophylaxis (P) and treatment (T) of tumor lysis syndrome (TLS): An international TLS consensus panel. J Clin Oncol; 2009 May 20;27(15_suppl):e17575

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

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  • (PMID = 27963935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Kwak EL, Camidge DR, Clark J, Shapiro GI, Maki RG, Ratain MJ, Solomon B, Bang Y, Ou S, Salgia R: Clinical activity observed in a phase I dose escalation trial of an oral c-met and ALK inhibitor, PF-02341066. J Clin Oncol; 2009 May 20;27(15_suppl):3509

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor types included colorectal, pancreatic, sarcoma, ALCL and NSCLC.
  • Among 10 NSCLC pts whose tumors harbor EML4-ALK rearrangement, 1 pt has had a PR, 2 pts have achieved unconfirmed PR and 4 pts have had SD (3 have experienced reduction in tumor burden by ∼20% in measurable lesions and 1 has been treated for 28 weeks).

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  • (PMID = 27961297.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Baeza A, Nájera C, Sansano JM, Saá JM: Binolam-AlCl: a two-centre catalyst for the synthesis of enantioenriched cyanohydrin O-phosphates. Chemistry; 2005 Jun 20;11(13):3849-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Binolam-AlCl: a two-centre catalyst for the synthesis of enantioenriched cyanohydrin O-phosphates.
  • The enantioselective synthesis of cyanohydrin O-phosphates by using in situ generated bifunctional catalysts (R)- or (S)-3,3'-bis(diethylaminomethyl)-1,1'-binaphthol-aluminium chloride (binolam-AlCl) is reported.

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  • (PMID = 15776489.001).
  • [ISSN] 0947-6539
  • [Journal-full-title] Chemistry (Weinheim an der Bergstrasse, Germany)
  • [ISO-abbreviation] Chemistry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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26. Ji TH, Li HL, Jiang HY, Zhao T, Yu YH: [Expression of ALK protein in large cell lymphoma with ALCL chromosome translocation in relation to prognosis]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Jun;16(3):543-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of ALK protein in large cell lymphoma with ALCL chromosome translocation in relation to prognosis].
  • The aim of this study was to investigate the expression of anaplastic lymphoma kinase (ALK) protein resulted from chromosome translocation in anaplastic large cell lymphoma (ALCL) and its relationship with the age and prognosis of patients with ALCL.
  • The tissue microarray including 30 cases of ALCL and 2 normal control tissues were established, the expression of anaplastic lymphoma kinase (ALK) protein was detected by immunohistochemistry, the statistical analysis of detected results was carried out by SPSS software.
  • The results showed that the ALK protein was expressed negatively in 2 cases of primary skin ALCL, but in 20 out of 28 cases of systematic ALCL the ALK protein was expressed positively and mainly located in cytoplasm and/or nucleus (71.4%).
  • It is concluded that there is a high incidence of ALK expression in ALCL, especially in younger group.
  • ALK expression may be an useful and independent marker for the differential diagnosis and prognosis evaluation of ALCL.

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  • (PMID = 18549625.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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27. Kadin ME, Pinkus JL, Pinkus GS, Duran IH, Fuller CE, Onciu M, Kawaguchi H, Morris SW: Primary cutaneous ALCL with phosphorylated/activated cytoplasmic ALK and novel phenotype: EMA/MUC1+, cutaneous lymphocyte antigen negative. Am J Surg Pathol; 2008 Sep;32(9):1421-6
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  • [Title] Primary cutaneous ALCL with phosphorylated/activated cytoplasmic ALK and novel phenotype: EMA/MUC1+, cutaneous lymphocyte antigen negative.
  • Primary cutaneous anaplastic large-cell lymphoma (ALCL) ordinarily is distinguished from systemic ALCL by clinical presentation, absence of anaplastic lymphoma kinase (ALK) expression, and immunophenotype (CLA+, EMA/MUC1-).
  • We present an exceptional case of an elderly man with primary cutaneous ALCL and no systemic disease for a 13-year period.
  • Recurrent skin tumors in this patient were characterized by anaplastic, often multinucleated, cells infiltrating the lymphatics and associated with pseudoepitheliomatous hyperplasia.
  • Cutaneous lymphocyte antigen was absent and EMA/MUC1, typical of systemic ALCL, was strongly expressed by the tumor cells.
  • Remarkably, the tumor cells expressed a cytoplasmic-only variant of ALK protein, as reported in 3 previous cases of primary cutaneous ALCL.
  • Fluorescence in situ hybridization revealed lack of rearrangements of the chromosome 2 ALK gene locus usually involved by translocation t(2;5) or other chromosomal rearrangements that generate nucleophosmin-ALK or the variant ALK fusions that occur in systemic ALCL.
  • Primary cutaneous ALCL of this novel subtype should be distinguished from systemic ALCL to ensure proper clinical management.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism. Skin Neoplasms / metabolism. Skin Neoplasms / pathology

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  • (PMID = 18670345.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-69129; United States / NCRR NIH HHS / RR / P20RR018757
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / CTAGE1 protein, human; 0 / Membrane Glycoproteins; 0 / Mucin-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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28. Brazhkin VV, Lyapin AG, Popova SV, Katayama Y, Saitoh H, Utsumi W: Molecular-network-ionic structure transitions in liquid AlCl(3) and ZnCl(2) halogenides under pressure. J Phys Condens Matter; 2007 Jun 20;19(24):246104

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular-network-ionic structure transitions in liquid AlCl(3) and ZnCl(2) halogenides under pressure.
  • We present the in situ high-pressure-high-temperature x-ray diffraction study of the liquid AlCl(3) and ZnCl(2) halogenides having a quasi-molecular network structure in liquid state at normal pressure.
  • Structural study of these liquid halogenides is indicative of a rapid and strong breakdown of an intermediate-range order in a tetrahedral network of melts for the initial pressure range, 0-2.5 GPa for AlCl(3) and 0-1.8 GPa for ZnCl(2), and points to rather sharp transitions in liquids with the formation of a short-range order structure similar to ionic melt structures around 4 GPa for AlCl(3) and 3 GPa for ZnCl(2).
  • Thus, pseudo-covalent liquid halogenides like AlCl(3) and ZnCl(2) provide testimony to two phenomena under high pressures, namely, a gradual decay of structural correlations in the tetrahedral network of the melt and a sharp transition from molecular-network to ionic structure in liquid on further compression.

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  • (PMID = 21694040.001).
  • [ISSN] 0953-8984
  • [Journal-full-title] Journal of physics. Condensed matter : an Institute of Physics journal
  • [ISO-abbreviation] J Phys Condens Matter
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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29. Mencía-Gutiérrez E, Gutiérrez-Díaz E, Salamanca J, Martínez-González MA: Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL). Int J Dermatol; 2006 Jun;45(6):766-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL).
  • AIM: To report an unusual case of cutaneous presentation on the eyelid of systemic (or nodal), CD30+, anaplastic large-cell lymphoma (ALCL).
  • RESULTS: The histopathologic and immunohistochemical diagnosis was ALCL, T-cell phenotype, strongly positive for CD43 and CD30, and negative for CD3, anaplastic lymphoma kinase (ALK), and B-cell antigens.
  • CONCLUSIONS: Primary, systemic, CD30+, ALK-negative, ALCL presentations generally have a poor prognosis and tend to occur in older individuals, although the clinical outcome is highly variable and difficult to predict in individual cases.
  • Only three cases of ALCL have been described in the ocular adnexae and none was ALK-negative.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Eyelid Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Adult. Antigens, CD / analysis. Antigens, CD30 / analysis. Combined Modality Therapy. Humans. Lymphatic Metastasis. Male. Receptor Protein-Tyrosine Kinases. Treatment Outcome

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  • (PMID = 16796648.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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30. Schmitz N, Ziepert M, Nickelsen M, Wolf SP, Truemper L, Loeffler M, Ho A, Metzner B, Rosenwald A, Pfreundschuh M: Mature T-/NK-cell lymphomas: Prognostic factors and treatment outcome of patients treated on studies of the German High-Grade Lymphoma Study Group (DSHNHL). J Clin Oncol; 2009 May 20;27(15_suppl):8564

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mature T-/NK-cell lymphomas: Prognostic factors and treatment outcome of patients treated on studies of the German High-Grade Lymphoma Study Group (DSHNHL).
  • : 8564 Background: T-cell lymphomas represent a heterogeneous group of malignancies difficult to diagnose and to treat.
  • METHODS: Between 1993 and 2006 we treated 329 pts with ALK-positive ALCL (73 pts), ALK-negative ALCL (108 pts), PTCL, NOS (68 pts), AITL (28 pts), NK-/T-cell lymphoma (18 pts), and rare T-cell lymphomas on prospective studies.
  • RESULTS: The majority of pts with ALK-positive ALCL presented with IPI 0, 1 (62%) or IPI 2 (26%) and had an excellent overall survival (OS) of 89 % and event-free survival (EFS) of 75% at 3 yrs.
  • OS, EFS were significantly better for ALK-positive ALCL but did not significantly differ for pts in other histological subgroups.
  • In younger pts (ALK-positive ALCL were excluded) and good-risk disease (LDH <= N) there was a trend for better EFS after the addition of E to CHOP (EFS 63% vs. 48%, p = 0.065).
  • The MegaCHOEP protocol (Schmitz et al., CANCER 2006) failed to improve treatment results for younger pts with poor-risk disease (EFS at 3 yrs: 25.9%, 95% CI: 10.4-41.4); the prospective study comparing MegaCHOEP with CHOEP-14 was stopped for pts with T-cell lymphoma.
  • CONCLUSIONS: CHO(E)P results in excellent OS of pts with ALK-positive ALCL and selected pts with other histologies and low IPI.

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  • (PMID = 27961019.001).
  • [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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31. Bartlett N, Forero-Torres A, Rosenblatt J, Fanale M, Horning SJ, Thompson S, Sievers EL, Kennedy DA: Complete remissions with weekly dosing of SGN-35, a novel antibody-drug conjugate (ADC) targeting CD30, in a phase I dose-escalation study in patients with relapsed or refractory Hodgkin lymphoma (HL) or systemic anaplastic large cell lymphoma (sALCL). J Clin Oncol; 2009 May 20;27(15_suppl):8500

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete remissions with weekly dosing of SGN-35, a novel antibody-drug conjugate (ADC) targeting CD30, in a phase I dose-escalation study in patients with relapsed or refractory Hodgkin lymphoma (HL) or systemic anaplastic large cell lymphoma (sALCL).
  • : 8500 Background: A defining feature of HL and sALCL is CD30 expression on malignant cells.
  • The ADC SGN-35 comprises an anti-CD30 antibody conjugated to the antitubulin agent monomethyl auristatin E (MMAE).
  • SGN-35 causes cell cycle arrest and apoptosis by binding to CD30 on the tumor cell surface, internalizing, and releasing MMAE into the cell.
  • Pts with stable disease or better (Cheson 2007) after two 28-day cycles (6 doses) were eligible to continue SGN-35 treatment.

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  • (PMID = 27960851.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Blum KA, Smith M, Fung H, Zalevsky J, Combs D, Ramies DA, Younes A: Phase I study of an anti-CD30 Fc engineered humanized monoclonal antibody in Hodgkin lymphoma (HL) or anaplastic large cell lymphoma (ALCL) patients: Safety, pharmacokinetics (PK), immunogenicity, and efficacy. J Clin Oncol; 2009 May 20;27(15_suppl):8531

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

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  • (PMID = 27960926.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Brites V, Hammoutène D, Hochlaf M: Spectroscopy, metastability, and single and double ionization of AlCl. J Phys Chem A; 2008 Dec 25;112(51):13419-26

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spectroscopy, metastability, and single and double ionization of AlCl.
  • Large calculations are done to investigate the valence and inner-valence electronic states of aluminum monochloride and its cationic species AlCl+ and AlCl2+, allowing their definite assignment.
  • For the neutral molecule, our calculations show that the lifetimes of the AlCl A1pi v' > or = 10 levels are reduced to the 0.1-0.01 ps time scale because of spin-orbit induced predissociation processes and by tunneling through the potential barrier of the A state.
  • Our potential curves for the ground state of AlCl and those of the cationic and dicationic species are also used for predicting the single and double ionization spectrum of AlCl.

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  • (PMID = 19053555.001).
  • [ISSN] 1520-5215
  • [Journal-full-title] The journal of physical chemistry. A
  • [ISO-abbreviation] J Phys Chem A
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Stockklausner C, Behnisch W, Mechtersheimer G, Möller P, Kulozik AE: Long-term remission of children with relapsed and secondary anaplastic large cell non-Hodgkin lymphoma (ALCL) following treatment with pulsed dexamethasone and low dose etoposide. Pediatr Blood Cancer; 2008 Jan;50(1):126-9
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  • [Title] Long-term remission of children with relapsed and secondary anaplastic large cell non-Hodgkin lymphoma (ALCL) following treatment with pulsed dexamethasone and low dose etoposide.
  • Anaplastic large cell lymphoma (ALCL) accounts for approximately 15% of childhood NHL.
  • Relapsed ALCL represents a formidable challenge because outcome is poor despite the use of high-dose chemotherapy regimens.
  • We report two patients with relapsed T-type and 0-type ALCL who achieved long-term 3rd and 4th remissions with 4-weekly oral dexamethasone (DEX) and etoposide pulses for 2 years.
  • This regimen also induced and maintained remission in a third patient with Nijmegen breakage syndrome (NBS) with secondary T-type ALCL.
  • These patients demonstrate that low-intensity oral chemotherapy can induce long-term remissions and offer a curative perspective in refractory, relapsed and secondary ALCL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy


35. Medeiros LJ, Elenitoba-Johnson KS: Anaplastic Large Cell Lymphoma. Am J Clin Pathol; 2007 May;127(5):707-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic Large Cell Lymphoma.
  • Session 8 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop was devoted to anaplastic large cell lymphoma (ALCL).
  • Most cases submitted were anaplastic lymphoma kinase (ALK)+ ALCL highlighting unusual clinical settings, histologic variants, and variant translocation partners.
  • Cases submitted as ALK- ALCL emphasized the immunohistochemical overlap with classical Hodgkin lymphoma (eg, CD15+/CD30+).
  • It was also clear that consensus histologic and immunohistochemical criteria for the diagnosis of ALK-ALCL are lacking.
  • Many expressed the opinion that ALK-ALCL is not a distinct entity at the immunophenotypic or genetic level and is better designated as peripheral T-cell lymphoma (PTCL), unspecified.
  • Others suggested that the histologic features of ALK-ALCL are distinctive nevertheless and that this diagnosis has meaning that is lost by designating these neoplasms as PTCL, unspecified.
  • This session also included CD30+ anaplastic lymphomas involving skin in which the differential diagnosis included cutaneous ALCL and systemic ALK-ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Antigens, CD30 / analysis. Flow Cytometry. Humans. Immunophenotyping. Receptor Protein-Tyrosine Kinases. Skin Neoplasms / pathology

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  • (PMID = 17511113.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 40
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36. Rassidakis GZ, Thomaides A, Wang S, Jiang Y, Fourtouna A, Lai R, Medeiros LJ: p53 gene mutations are uncommon but p53 is commonly expressed in anaplastic large-cell lymphoma. Leukemia; 2005 Sep;19(9):1663-9
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  • [Title] p53 gene mutations are uncommon but p53 is commonly expressed in anaplastic large-cell lymphoma.
  • Anaplastic large-cell lymphoma (ALCL), as defined in the World Health Organization, is a heterogeneous category in which a subset of cases is associated with the t(2;5)(p23;q35) or variant translocations resulting in overexpression of anaplastic lymphoma kinase (ALK).
  • p53 has not been assessed in currently defined subsets of ALCL tumors.
  • In this study, we assessed ALK+ and ALK- ALCL tumors for p53 gene alterations using PCR, single-strand conformation polymorphism and direct sequencing methods.
  • We also immunohistochemically assessed ALCL tumors for p53 expression.
  • Three of 36 (8%) ALCL tumors (1/14 ALK+, 2/22 ALK-) with adequate DNA showed p53 gene mutations.
  • By contrast, p53 was overexpressed in 36 of 55 (65%) ALCL tumors (16 ALK+, 20 ALK-).
  • p21, a target of p53, was expressed in 15 of 31 (48%) ALCL tumors including seven of 15 (47%) p53-positive tumors. p21 expression in a subset of ALCL suggests the presence of functional p53 protein.
  • Apoptotic rate was significantly higher in p53-positive than p53-negative tumors (mean 2.78 vs 0.91%, P = 0.0003).
  • We conclude that the p53 gene is rarely mutated in ALK+ and ALK- ALCL tumors.
  • Nevertheless, wild-type p53 gene product is commonly overexpressed in ALCL and may be functional in a subset of these tumors.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, p53 / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Apoptosis / physiology. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Cell Proliferation. Cloning, Molecular. Cyclin-Dependent Kinase Inhibitor p21. Humans. Middle Aged. Mutation. Nuclear Proteins / biosynthesis. Nuclear Proteins / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-mdm2. Receptor Protein-Tyrosine Kinases. Sequence Analysis, DNA / methods

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  • (PMID = 15990866.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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37. Eckerle S, Brune V, Döring C, Tiacci E, Bohle V, Sundström C, Kodet R, Paulli M, Falini B, Klapper W, Chaubert AB, Willenbrock K, Metzler D, Bräuninger A, Küppers R, Hansmann ML: Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma. Leukemia; 2009 Nov;23(11):2129-38
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  • [Title] Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is a main type of T-cell lymphomas and comprises three distinct entities: systemic anaplastic lymphoma kinase (ALK) positive, systemic ALK(-) and cutaneous ALK(-) ALCL (cALCL).
  • Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK(-) ALCL and classical Hodgkin lymphoma (cHL).
  • We conducted gene expression profiling of microdissected lymphoma cells of five ALK(+) and four ALK(-) systemic ALCL, seven cALCL and sixteen cHL, and of eight subsets of normal T and NK cells.
  • The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4(+), CD8(+) or CD30(+) T-cell origin.
  • Indeed, ALCL display a down-modulation of many T-cell characteristic molecules.
  • All ALCL types show significant expression of NFkappaB target genes and upregulation of genes involved in oncogenesis (e.g. EZH2).
  • Surprisingly, few genes are differentially expressed between systemic and cALCL despite their different clinical behaviour, and between ALK(-) ALCL and cHL despite their different cellular origin.
  • ALK(+) ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK.
  • This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Hodgkin Disease / genetics. Lymphoma, Large-Cell, Anaplastic / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line. Female. Humans. Immunohistochemistry. Killer Cells, Natural / cytology. Killer Cells, Natural / physiology. Male. Microdissection. Middle Aged. NF-kappa B / metabolism. Phenotype. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / cytology. T-Lymphocytes / physiology. Young Adult

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  • (PMID = 19657361.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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38. Kempf W, Kutzner H, Cozzio A, Sander CA, Pfaltz MC, Müller B, Pfaltz M: MUM1 expression in cutaneous CD30+ lymphoproliferative disorders: a valuable tool for the distinction between lymphomatoid papulosis and primary cutaneous anaplastic large-cell lymphoma. Br J Dermatol; 2008 Jun;158(6):1280-7
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  • [Title] MUM1 expression in cutaneous CD30+ lymphoproliferative disorders: a valuable tool for the distinction between lymphomatoid papulosis and primary cutaneous anaplastic large-cell lymphoma.
  • BACKGROUND: Primary cutaneous CD30+ lymphoproliferative disorders include lymphomatoid papulosis (LyP) and primary cutaneous CD30+ anaplastic large T-cell lymphoma (ALCL).
  • Because of overlapping histological features, it is impossible to distinguish ALCL from LyP on histological grounds.
  • MUM1 (Multiple Myeloma oncogene 1) is expressed in systemic ALCL and classical Hodgkin lymphoma.
  • MUM1 expression has not been studied in detail in CD30+ lymphoproliferative disorders.
  • OBJECTIVES: To examine the expression of MUM1 in CD30+ lymphoproliferative disorders and to assess its value as a diagnostic marker.
  • METHODS: Thirty-one formalin-fixed paraffin-embedded specimens of LyP (n = 15), primary cutaneous ALCL (n = 10), secondary cutaneous infiltrates of systemic ALCL (n = 4) and secondary cutaneous Hodgkin lymphoma (n = 2) were analysed by immunohistochemistry with a monoclonal antibody against MUM1.
  • RESULTS: Positive staining for MUM1 was observed in 13 cases of LyP (87%), two cases of primary cutaneous ALCL (20%), four cases of secondary cutaneous ALCL (100%) and two cases of secondary cutaneous Hodgkin lymphoma (100%).
  • In contrast to LyP and secondary cutaneous ALCL, only two cases of primary cutaneous ALCL (20%) harboured MUM1-positive tumour cells.
  • There was a statistically significant difference in the expression of MUM1 between LyP and primary cutaneous ALCL (P = 0.002) and between primary cutaneous ALCL and secondary cutaneous ALCL (P = 0.015).
  • CONCLUSIONS: MUM1 expression is a valuable tool for the distinction of LyP and ALCL and thus represents a novel adjunctive diagnostic marker in CD30+ lymphoproliferative disorders.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Interferon Regulatory Factors / metabolism. Lymphoproliferative Disorders / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Antigens, CD30. Diagnosis, Differential. Humans. Immunohistochemistry / methods. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphomatoid Papulosis / diagnosis. Lymphomatoid Papulosis / metabolism. Multiple Myeloma / diagnosis. Multiple Myeloma / metabolism


39. Biswas K, Zhang Q, Chung I, Song JH, Androulakis J, Freeman AJ, Kanatzidis MG: Synthesis in ionic liquids: [Bi2Te2Br](AlCl4), a direct gap semiconductor with a cationic framework. J Am Chem Soc; 2010 Oct 27;132(42):14760-2
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  • The Lewis acidic ionic liquid EMIMBr-AlCl(3) (EMIM = 1-ethyl-3-methylimidazolium) allows a novel synthetic route to the semiconducting layered metal chalcogenides halide [Bi(2)Te(2)Br](AlCl(4)) and its Sb analogue.
  • [Bi(2)Te(2)Br](AlCl(4)) is a direct band gap, strongly anisotropic semiconductor and consists of cationic infinite layers of [Bi(2)Te(2)Br](+) and [AlCl(4)](-) anions inserted between the layers.

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  • (PMID = 20919739.001).
  • [ISSN] 1520-5126
  • [Journal-full-title] Journal of the American Chemical Society
  • [ISO-abbreviation] J. Am. Chem. Soc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Rudolph C, Bittner C, Feller AC, Merz H, Schlegelberger B: Cytogenetic characteristics of a murine in vitro model for the human anaplastic large cell lymphoma (ALCL). Cytogenet Genome Res; 2006;114(3-4):292-5
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  • [Title] Cytogenetic characteristics of a murine in vitro model for the human anaplastic large cell lymphoma (ALCL).
  • Anaplastic large cell lymphoma (ALCL) is an entity of non-Hodgkin lymphomas (NHL) that often occurs in young children and adolescents.
  • In the majority of cases, ALCL are of T-cell origin and contain the t(2;5)(p23;q35) leading to an NPM-ALK fusion or variant ALK translocations.
  • In addition, there is an ALK-negative subtype of ALCL.
  • The anaplastic lymphoid cell line TS1G6 established by interleukin (IL)-9 transfection of T-helper cells represents a murine model of this subtype.
  • Here, we describe the cytogenetic features of this cell line using spectral karyotyping (SKY) and single-color fluorescence in situ hybridization (FISH).
  • [MeSH-major] Chromosome Aberrations. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Animals. Chromosome Mapping. Disease Models, Animal. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping / methods. Mice. Tumor Cells, Cultured

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16954669.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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41. Rust R, Visser L, van der Leij J, Harms G, Blokzijl T, Deloulme JC, van der Vlies P, Kamps W, Kok K, Lim M, Poppema S, van den Berg A: High expression of calcium-binding proteins, S100A10, S100A11 and CALM2 in anaplastic large cell lymphoma. Br J Haematol; 2005 Dec;131(5):596-608
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of calcium-binding proteins, S100A10, S100A11 and CALM2 in anaplastic large cell lymphoma.
  • Anaplastic large cell lymphomas (ALCL) are characterised by the presence of CD30-positive large cells, which usually are of T-cell type.
  • Based on the presence or absence of translocations involving the anaplastic lymphoma kinase (ALK) locus, ALCL cases can be divided into two groups.
  • To gain more insight in the biology of ALCL, we applied serial analysis of gene expression (SAGE) on the Karpas299 cell line and identified 25 up- and 19 downregulated genes.
  • Quantitative reverse transcription polymerase chain reaction on 5 ALCL cell lines and 12 ALCL tissues confirmed the SAGE data for 13 out of 14 up- and one out of four downregulated genes.
  • Immunohistochemical staining confirmed the presence of S100A10, a calcium-binding protein, in three out of five ALK+ and all 7 ALK- ALCL cases.
  • S100A11 staining was confirmed in all ALK+ and six of seven ALK- ALCL cases.
  • Three of the upregulated genes represented calcium-binding proteins, which suggest that altered intracellular signaling might be associated with the oncogenesis of ALCL.
  • [MeSH-major] Annexin A2 / genetics. Calcium Signaling / genetics. Calmodulin / genetics. Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / genetics. S100 Proteins / genetics
  • [MeSH-minor] CD4-Positive T-Lymphocytes / metabolism. Cell Line, Tumor. Cells, Cultured. Down-Regulation. Galectin 1 / analysis. Galectin 1 / genetics. Gene Expression Profiling. Humans. Immunohistochemistry / methods. Membrane Proteins / genetics. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16351635.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A2; 0 / CALM2 protein, human; 0 / Calmodulin; 0 / Galectin 1; 0 / Membrane Proteins; 0 / S100 Proteins; 0 / S100 calcium binding protein A10; 146909-89-9 / S100A11 protein, human; 179801-28-6 / LAPTM5 protein, human
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42. Gjerdrum LM, Woetmann A, Odum N, Hother C, Henrik-Nielsen R, Gniadecki R, Ralfkiaer E: FOXP3 positive regulatory T-cells in cutaneous and systemic CD30 positive T-cell lymphoproliferations. Eur J Haematol; 2008 Jun;80(6):483-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FOXP3 positive regulatory T-cells in cutaneous and systemic CD30 positive T-cell lymphoproliferations.
  • The CD30-positive lymphoproliferations encompass a spectrum of disorders that share histological and phenotypic similarities but differ markedly in clinical behaviour.
  • In this study, skin biopsies from lymphomatoid papulosis (LyP) (n = 14), primary cutaneous anaplastic large cells lymphoma (C-ALCL) (n = 13) and systemic anaplastic large cells lymphoma (S-ALCL) with (n = 9) or without (n = 6) ALK expression were examined by immunohistology for FOXP3 expression in tumour cells and tumour infiltrating Tregs.
  • Labelling of a majority of the neoplastic cells was seen in one case of C-ALCL.
  • Another three cases (one LyP and two C-ALCL) displayed weak labelling of very occasional atypical T-cells.
  • By contrast, all biopsies contained tumour infiltrating FOXP3-positive Tregs.
  • Significant higher numbers were recorded in ALK negative S-ALCL and LyP than in C-ALCL and S-ALCL positive for ALK.
  • In conclusion, it is shown that FOXP3 expression in cutaneous and systemic CD30-positive lymphoproliferations is generally confined to tumour infiltrating Tregs.
  • These cells may have influence upon the clinical behaviour, possibly depending upon the net degree of Treg mediated immune suppression of tumour cells relative to tumour infiltrating, cytotoxic effector cells, thereby implicating the more favourable outcome of LyP compared to C-ALCL.
  • [MeSH-major] Antigens, CD30 / immunology. Cell Proliferation. Forkhead Transcription Factors / metabolism. Lymphoproliferative Disorders / metabolism. Skin / immunology. T-Lymphocytes / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Blotting, Western. Cell Line. Humans. Immunohistochemistry

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  • (PMID = 18331599.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
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43. Tamaru J, Tokuhira M, Nittsu N, Nakamura S, Ichinohasama R, Suzuki R, Mori H, Takagi T, Suzuki T, Itami J, Itoyama S, Mikata A: Hodgkin-like anaplastic large cell lymphoma (previously designated in the REAL classification) has same immunophenotypic features to classical Hodgkin lymphoma. Leuk Lymphoma; 2007 Jun;48(6):1127-38
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  • [Title] Hodgkin-like anaplastic large cell lymphoma (previously designated in the REAL classification) has same immunophenotypic features to classical Hodgkin lymphoma.
  • In the WHO classification, the majority of Hodgkin-like ALCL cases as defined by the REAL classification are considered to be CHL.
  • However, establishing a histological diagnosis for the gray zone between CHL and ALCL is often confusing.
  • Expression of PAX-5/BSAP was observed in 88% (76/87) of CHL specimens and none (0/11) of ALK-positive ALCL specimens.
  • Among specimens of Hodgkin-like ALCL and ALK-negative ALCL, expression of PAX-5/BSAP was observed in 77% (20/26) and 18% (3/17), respectively.
  • Most of the PAX-5/BSAP-positive specimens were negative for Oct.2 and/or BOB.1/OBF.1 except for four CHL specimens.
  • Our results may support the WHO classification in which most cases of Hodgkin-like ALCL are classified as CHL.
  • However, the patients with Hodgkin-like ALCL with CHL-immunophenotype (PAX-5/BSAP-positive and negative for Oct.2 and/or BOB.1) did not have a favorable outcome, with a 5-year OS rate of 58%.
  • [MeSH-major] Hodgkin Disease / diagnosis. Hodgkin Disease / pathology. Immunophenotyping. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. B-Cell-Specific Activator Protein / genetics. Biomarkers, Tumor / genetics. Diagnosis, Differential. Female. Gene Expression Regulation, Leukemic. Humans. Male. Middle Aged. Neoplasm Staging. Octamer Transcription Factor-2 / genetics. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Retrospective Studies. Survival Analysis. Trans-Activators / genetics

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  • (PMID = 17577776.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / Octamer Transcription Factor-2; 0 / PAX5 protein, human; 0 / POU2AF1 protein, human; 0 / Trans-Activators; 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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44. Lu Y, Zhao X, Wang E, Chen W, Huang Q: ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as "leukemic phase". Leuk Res; 2010 Apr;34(4):475-82
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  • [Title] ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as "leukemic phase".
  • CD30-positive anaplastic large cell lymphoma (ALCL) is a distinctive malignant large cell lymphoma of T-cell lineage, often presenting in lymph node or extranodal sites.
  • ALCL cases with extensive bone marrow and peripheral blood involvement manifested as "leukemic phase" are extremely rare and the most of those cases reported are anaplastic large cell lymphoma kinase (ALK) positive ALCL in childhood population.
  • Here we report four adult cases of ALK-negative ALCL with extensive bone marrow and peripheral blood involvement manifested as "leukemic phase".
  • Circulating large lymphoma cells varied from 20 to 80% in peripheral blood and bone marrow biopsy showed various nodular or interstitial infiltrates.
  • By reviewing the clinicopathologic data of previously reported ALCL cases with extensive bone marrow and peripheral blood involvement, there appears to be of large variations in regard to the patient's age, morphologic variants, immunophenotypic or genotypic characteristics of the disease.
  • While most cases of ALCL with peripheral blood and bone marrow involvement were ALK-positive or carrying t(2;5) translocation, rare ALK-negative cases were also present.
  • Leukemic ALCL patients usually have unfavourable prognosis, regardless of ALK expression.
  • [MeSH-major] Bone Marrow Neoplasms / secondary. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Disease Progression. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Receptor Protein-Tyrosine Kinases

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19695703.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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45. Kodama K, Hokama M, Kawaguchi K, Tanaka Y, Hongo K: Primary ALK-1-negative anaplastic large cell lymphoma of the brain: case report and review of the literature. Neuropathology; 2009 Apr;29(2):166-71
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  • [Title] Primary ALK-1-negative anaplastic large cell lymphoma of the brain: case report and review of the literature.
  • Anaplastic large cell lymphoma (ALCL) is a type of non-Hodgkin lymphoma composed of CD30-positive cells.
  • Anaplastic lymphoma kinase (ALK) -1 positive ALCL frequently involves both lymph nodes and extranodal sites.
  • While primary extranodal involvement of ALK-1 negative ALCL is rare, this case is unique in that it is a case of primary ALK-1 negative ALCL of the brain.
  • The tumor was excised and histological diagnosis of primary ALK-1-negative ALCL was made.
  • Primary ALK-1-negative ALCL in this case showed aggressive clinical behavior and fatal outcome.
  • It is of great importance to avoid any delay in reaching an accurate diagnosis, as even primary ALCL of the brain is too seldom suspected clinically.
  • [MeSH-major] Activin Receptors, Type II / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adolescent. Aged. Blotting, Southern. Brain / metabolism. Brain / pathology. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Young Adult

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  • (PMID = 18564100.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
  • [Number-of-references] 29
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46. Merkel O, Hamacher F, Laimer D, Sifft E, Trajanoski Z, Scheideler M, Egger G, Hassler MR, Thallinger C, Schmatz A, Turner SD, Greil R, Kenner L: Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK)+ and ALK- anaplastic large-cell lymphoma. Proc Natl Acad Sci U S A; 2010 Sep 14;107(37):16228-33
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  • [Title] Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK)+ and ALK- anaplastic large-cell lymphoma.
  • Aberrant anaplastic lymphoma kinase (ALK) expression is a defining feature of many human cancers and was identified first in anaplastic large-cell lymphoma (ALCL), an aggressive non-Hodgkin T-cell lymphoma.
  • We have identified a distinct profile of micro-RNAs (miRNAs) that characterize ALCL; furthermore, this profile distinguishes ALK(+) from ALK(-) subtypes, and thus points toward potential mechanisms of tumorigenesis induced by aberrant ALK.
  • Using a nucleophosmin-ALK transgenic mouse model as well as human primary ALCL tumor tissues and human ALCL-derived cell lines, we reveal a set of overlapping deregulated miRNAs that might be implicated in the development and progression of ALCL.
  • Importantly, ALK(+) and ALK(-) ALCL could be distinguished by a distinct profile of "oncomirs": Five members of the miR-17-92 cluster were expressed more highly in ALK(+) ALCL, whereas miR-155 was expressed more than 10-fold higher in ALK(-) ALCL.
  • Moreover, miR-101 was down-regulated in all ALCL model systems, but its forced expression attenuated cell proliferation only in ALK(+) and not in ALK(-) cell lines, perhaps suggesting different modes of ALK-dependent regulation of its target proteins.
  • Furthermore, inhibition of mTOR, which is targeted by miR-101, led to reduced tumor growth in engrafted ALCL mouse models.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. MicroRNAs / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Base Sequence. Cell Line, Tumor. Cell Proliferation. Gene Expression Profiling. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Mice. Mice, Transgenic. Multigene Family. Receptor Protein-Tyrosine Kinases. Sirolimus / analogs & derivatives. Sirolimus / therapeutic use. Xenograft Model Antitumor Assays

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  • (PMID = 20805506.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / V 102
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MicroRNAs; 624KN6GM2T / temsirolimus; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2941277
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47. Watanabe M, Sasaki M, Itoh K, Higashihara M, Umezawa K, Kadin ME, Abraham LJ, Watanabe T, Horie R: JunB induced by constitutive CD30-extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase signaling activates the CD30 promoter in anaplastic large cell lymphoma and reed-sternberg cells of Hodgkin lymphoma. Cancer Res; 2005 Sep 1;65(17):7628-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JunB induced by constitutive CD30-extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase signaling activates the CD30 promoter in anaplastic large cell lymphoma and reed-sternberg cells of Hodgkin lymphoma.
  • High expression of CD30 and JunB is characteristic of tumor cells in anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL).
  • Possible interactions of CD30 and JunB were examined in this study.
  • We found that the CD30 promoter in tumor cells of both nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK)-positive and NPM-ALK-negative ALCL and HL is regulated by a constitutively active CD30-extracellular signal-regulated kinase (ERK) 1/2 mitogen-activated protein kinase (MAPK).
  • Phosphorylation of ERK1/2 MAPK was confirmed in nuclei of tumor cells in both ALCL and HL.
  • CD30-ERK1/2 MAPK signals induce JunB expression, which maintains high activity of the CD30 promoter.
  • JunB induction seems to be largely independent of nuclear factor kappaB in ALCL and HL.
  • These results show a common mechanism of CD30 overexpression in ALCL and HL, although the outcome of CD30 signaling differs between NPM-ALK-positive ALCL and NPM-ALK-negative ALCL, cutaneous ALCL, and HL as we recently reported.
  • [MeSH-major] Antigens, CD30 / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. MAP Kinase Signaling System / physiology. Proto-Oncogene Proteins c-jun / biosynthesis. Reed-Sternberg Cells / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. K562 Cells. NF-kappa B / metabolism. Promoter Regions, Genetic. Protein Binding. Transcription Factor AP-1 / metabolism


48. Piva R, Agnelli L, Pellegrino E, Todoerti K, Grosso V, Tamagno I, Fornari A, Martinoglio B, Medico E, Zamò A, Facchetti F, Ponzoni M, Geissinger E, Rosenwald A, Müller-Hermelink HK, De Wolf-Peeters C, Piccaluga PP, Pileri S, Neri A, Inghirami G: Gene expression profiling uncovers molecular classifiers for the recognition of anaplastic large-cell lymphoma within peripheral T-cell neoplasms. J Clin Oncol; 2010 Mar 20;28(9):1583-90
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  • [Title] Gene expression profiling uncovers molecular classifiers for the recognition of anaplastic large-cell lymphoma within peripheral T-cell neoplasms.
  • PURPOSE: To unravel the regulatory network underlying nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) -mediated lymphomagenesis of anaplastic large-cell lymphoma (ALCL) and to discover diagnostic genomic classifiers for the recognition of patients with ALK-positive and ALK-negative ALCL among T-cell non-Hodgkin's lymphoma (T-NHL).
  • PATIENTS AND METHODS: The transcriptome of NPM-ALK-positive ALCL cell lines was characterized by silencing the expression of ALK or STAT3, a major effector of ALK oncogenic activity.
  • Gene expression profiling (GEP) was performed in a series of systemic primary T-NHL (n = 70), including a set of ALK-positive and ALK-negative ALCL (n = 36).
  • Genomic classifiers for ALK-positive and ALK-negative ALCL were generated by prediction analyses and validated by quantitative reverse-transcriptase polymerase chain reaction and/or immunohistochemistry.
  • RESULTS: In ALCL cell lines, two thirds of ALK-regulated genes were concordantly dependent on STAT3 expression.
  • GEP of systemic primary T-NHL significantly clustered ALK-positive ALCL samples in a separate subgroup, underscoring the relevance of in vitro ALK/STAT3 signatures.
  • A set of genomic classifiers for ALK-positive ALCL and for ALCL were identified by prediction analyses.
  • These gene clusters were instrumental for the distinction of ALK-negative ALCL from peripheral T-cell lymphomas not otherwise specified (PTCLs-NOS) and angioimmunoblastic lymphomas.
  • CONCLUSION: We proved that experimentally controlled GEP in ALCL cell lines represents a powerful tool to identify meaningful signaling networks for the recognition of systemic primary T-NHL.
  • The identification of a molecular signature specific for ALCL suggests that these T-NHLs may represent a unique entity discernible from other PTCLs, and that a restricted number of genes can be instrumental for clinical stratification and, possibly, therapy of T-NHL.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Expression Profiling. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, T-Cell, Peripheral / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Humans. Nuclear Proteins / genetics. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Signal Transduction

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  • (PMID = 20159827.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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49. Garner R, Li Y, Gray B, Zori R, Braylan R, Wall J, Hunger SP: Long-term disease control of refractory anaplastic large cell lymphoma with vinblastine. J Pediatr Hematol Oncol; 2009 Feb;31(2):145-7
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  • [Title] Long-term disease control of refractory anaplastic large cell lymphoma with vinblastine.
  • Anaplastic large cell lymphoma (ALCL) is a unique clinical and pathologic subtype of lymphoma characterized by the proliferation of large, highly pleomorphic CD30-positive cells.
  • Overall 70% to 80% of children with ALCL are cured with modern chemotherapy regimens, but the disease is often resistant to multiple therapies after relapse.
  • Single agent vinblastine therapy has been effective in some cases of refractory ALCL.
  • We report a case of ALCL originally diagnosed in an 8-year-old girl.
  • After relapse, the disease was refractory to multiagent chemotherapy, but has showed remarkable response to, and dependence on, single agent vinblastine treatment for almost 7 years.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / drug therapy. Vinblastine / therapeutic use

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  • (PMID = 19194204.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine
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50. 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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  • [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.
  • METHODS: In situ hybridization for EBV-encoded small RNA (EBER) and immunohistochemistry including viral latent membrane protein-1 (LMP-1) were performed on formalin-fixed, paraffin-embedded skin specimens of 26 cases of LyP and 16 cases of CD30+ ALCL involving the skin which were selected from six university hospital medical centers in South Korea.
  • RESULTS: In situ hybridization studies showed positivity of the neoplastic cells for EBER in two of 16 cases of CD30+ ALCL and in none of the cases of LyP.
  • One EBER-positive case was cutaneous CD30+ ALCL with concurrent lymph node involvement.
  • The other was CD30+ ALCL involving the skin and other organs, including lymph nodes, bone, lung, and spleen.
  • Immunostaining for LMP-1 was also positive only for the two cases of EBER-positive CD30+ ALCL.
  • CONCLUSION: LyP and primary cutaneous CD30+ ALCL are very rarely associated with EBV in South Korea.
  • [MeSH-major] Epstein-Barr Virus Infections / pathology. Herpesvirus 4, Human / growth & development. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphomatoid Papulosis / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD20 / analysis. Antigens, CD3 / analysis. Antigens, CD30 / analysis. Female. Humans. Immunohistochemistry. In Situ Hybridization. Korea. Male. Middle Aged. RNA, Viral / genetics. Viral Matrix Proteins / analysis

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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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51. Khor TS, Alessandri AJ, Jevon GP: Infant anaplastic large cell lymphoma with hemophagocytic syndrome. Pediatr Dev Pathol; 2010 Jan-Feb;13(1):72-6
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  • [Title] Infant anaplastic large cell lymphoma with hemophagocytic syndrome.
  • Anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK)-positive, is uncommon in infancy.
  • We present an unusual occurrence of infant ALCL, ALK-positive, associated with hemophagocytic syndrome.
  • To the best of our knowledge, there have been no cases of infant ALCL, ALK-positive, described that have been associated with hemophagocytic syndrome.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Antigens, CD30 / metabolism. Biomarkers, Tumor / metabolism. Chromosomes, Human, Pair 2. Failure to Thrive. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Infant. Lymph Nodes / pathology. Male. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 19863446.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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52. Gan Q, Li S, Morlet-Savary F, Wang S, Shen S, Xu H, Yang G: Photophysical properties and optical limiting property of a soluble chloroaluminum-phthalocyanine. Opt Express; 2005 Jul 11;13(14):5424-33

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A chloroaluminum-phthalocyanine (AlCl-Pc) with tetra-alpha-butoxy chains (AlCl-Pc-OC4) has been synthesized and the photophysical parameters have been determined using steady-state and time-resolved absorption as well as emission spectroscopy.
  • The optical limiting performance for 532nm-7ns laser pulses of AlCl-Pc-OC4 has been investigated in THF solution.
  • It indicates that AlCl-Pc-OC4 could be promising candidates for optical limiting material.

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  • (PMID = 19498537.001).
  • [ISSN] 1094-4087
  • [Journal-full-title] Optics express
  • [ISO-abbreviation] Opt Express
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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53. Damm-Welk C, Klapper W, Oschlies I, Gesk S, Röttgers S, Bradtke J, Siebert R, Reiter A, Woessmann W: Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation. Br J Haematol; 2009 Aug;146(3):306-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation.
  • Anaplastic large cell lymphomas (ALCL) in children express anaplastic lymphoma kinase (ALK) fusion genes, most commonly NPM1-ALK.
  • The distribution of X-ALK among 66 childhood ALCLs was analysed.
  • One ALCL was ALK-negative.
  • The remaining seven ALCL stained for ALK in the cytoplasm only: two expressed TPM3-ALK, one ATIC-ALK, one MYH9-ALK; three no TPM3-, TFG-, ATIC-, CLTC- or MYH9-ALK.
  • Almost 90% of paediatric ALK-positive ALCLs express NPM1-ALK.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19545284.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / MYH9 protein, human; 0 / Molecular Motor Proteins; 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; 0 / oncoprotein CLTCL-ALK; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.6.4.1 / Myosin Heavy Chains
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54. Chuang SS, Hsieh YC, Ye H, Hwang WS: Lymphohistiocytic anaplastic large cell lymphoma involving skin: a diagnostic challenge. Pathol Res Pract; 2009;205(4):283-7
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  • [Title] Lymphohistiocytic anaplastic large cell lymphoma involving skin: a diagnostic challenge.
  • Systemic anaplastic large cell lymphoma (ALCL) involving the skin should be differentiated from primary cutaneous CD30-positive T-cell lymphoproliferative disorders.
  • The lymphohistiocytic variant of ALCL (LH-ALCL) is rich in reactive histiocytes with relatively few neoplastic cells, which pose a diagnostic challenge.
  • We present a case of LH-ALCL involving skin mimicking granulomatous inflammation.
  • Biopsy of the cervical lymph node showed LH-ALCL with null cell phenotype.
  • Microscopically, the cutaneous lesion was located predominately around the hair follicle, with numerous reactive histiocytes and scanty medium-sized lymphoma cells expressing CD30 and anaplastic lymphoma kinase (ALK) protein.
  • Furthermore, an ALK gene rearrangement was demonstrated by locus-specific interphase fluorescent in situ hybridization, confirming cutaneous involvement with LH-ALCL.
  • LH-ALCL involving the skin is a rare event, and the numerous reactive histiocytes may mask scanty tumor cells.
  • In addition to B-and T-cell markers, (dermato) pathologists must be aware of this entity in cutaneous lymphohistiocytic proliferations and perform immunostaining for CD30 and ALK to reach a correct diagnosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Antigens, CD30 / metabolism. Gene Rearrangement. Histiocytes / pathology. Humans. In Situ Hybridization, Fluorescence. Male. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19091487.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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55. Klapper W, Böhm M, Siebert R, Lennert K: Morphological variability of lymphohistiocytic variant of anaplastic large cell lymphoma (former lymphohistiocytic lymphoma according to the Kiel classification). Virchows Arch; 2008 Jun;452(6):599-605
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  • [Title] Morphological variability of lymphohistiocytic variant of anaplastic large cell lymphoma (former lymphohistiocytic lymphoma according to the Kiel classification).
  • According to the WHO classification, anaplastic large cell lymphoma (ALCL) is a distinct T-cell lymphoma entity with a number of morphological variants.
  • The characteristic feature of lymphohistiocytic variant of ALCL according to the WHO classification is the abundance of histiocytes that exceed and mask the tumour cell population.
  • In the current, study we reanalysed a historical series of 17 lymphomas, diagnosed as lymphohistiocytic lymphoma according to the criteria of the Kiel classification, with the presence of large purple macrophages (LPM) as the decisive finding for diagnosing this lymphoma subtype.
  • We assessed the cellular composition of the tumour and correlated the results with the definition of lymphohistiocytic variant of ALCL given in the WHO classification.
  • Although all cases in our cohort matched the criteria of ALCL according to the WHO, in 30% of the cases, the total amount of macrophages did not exceed the number of CD30-positive tumour cells.
  • Our results indicate that the presence of LPM might be helpful to identify this subgroup of ALCL.
  • Because the distinction of morphological subtypes of ALCL is of clinical relevance, improved criteria for subtyping ALCL are urgently needed that might include the presence LPM as one criteria.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adolescent. Adult. Antigens, CD / analysis. Antigens, CD20 / analysis. Antigens, CD3 / analysis. Antigens, CD30 / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Child. Child, Preschool. Cohort Studies. Female. Humans. Macrophages / pathology. Male. Mitosis

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  • (PMID = 18478258.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD20; 0 / Antigens, CD3; 0 / Antigens, CD30; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human
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56. Grewal JS, Smith LB, Winegarden JD 3rd, Krauss JC, Tworek JA, Schnitzer B: Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature. Ann Hematol; 2007 Jul;86(7):499-508
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  • [Title] Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive neoplasm of T- or null cell phenotype and is recognized as a distinct clinicopathologic subtype of non-Hodgkin lymphoma (NHL) in the revised World Health Organization (WHO) classification of hematopoietic neoplasms.
  • Most cases with leukemic involvement are the small cell variant of ALCL.
  • These cases often lack the pleomorphism seen in the common variant of ALCL and may be misdiagnosed.
  • We report a series of three patients who presented with leukemic phase ALCL.
  • The patients included an 11-year-old boy, a 29-year-old man, and a 59-year-old woman.
  • The patients in our case series with leukemic phase ALCL exhibited rare clinical features.
  • The patients presented with massive extranodal disease involving cerebrospinal fluid (CSF), liver, spleen, lungs, and bone marrow.
  • Two of the patients had small cell variant and the third patient had common type ALCL.
  • The neoplastic cells in all three patients were ALK positive; however these patients died within months of diagnosis.
  • Leukemic phase ALCL is rare, and behaves in an aggressive manner.
  • Some, but not all, cases in the literature presenting with peripheral blood involvement had small cell variant ALCL, as seen in two of our cases.
  • The leukemic phase of ALCL should be considered when a T-cell leukemia with unusual morphologic features is encountered.
  • [MeSH-major] Leukemia / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 17396261.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 91
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57. Watanabe M, Ogawa Y, Itoh K, Koiwa T, Kadin ME, Watanabe T, Okayasu I, Higashihara M, Horie R: Hypomethylation of CD30 CpG islands with aberrant JunB expression drives CD30 induction in Hodgkin lymphoma and anaplastic large cell lymphoma. Lab Invest; 2008 Jan;88(1):48-57
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  • [Title] Hypomethylation of CD30 CpG islands with aberrant JunB expression drives CD30 induction in Hodgkin lymphoma and anaplastic large cell lymphoma.
  • High expression of CD30 and JunB is the hallmark of malignant cells in Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL).
  • Ligand-independent signaling by CD30 induces JunB, which activates the CD30 promoter, stabilizing CD30 expression and supporting the survival of Hodgkin-Reed-Sternberg (H-RS) and ALCL cells.
  • Here we show for the first time CpG islands encompassing 60 CpG dinucleotides, located in the core promoter, exon 1 and intron 1 of CD30 gene.
  • Analysis of the methylation status of CD30 CpG islands in H-RS, ALCL and unrelated cell lines reveals an inverse relationship between the extent of CD30 CpG methylation and CD30 expression.
  • CD30 CpG islands of H-RS and ALCL cell lines are rarely methylated.
  • Methylation of the CD30 promoter decreases CD30 induction and JunB action on the demethylated CD30 promoter enhances CD30 induction.
  • CD30 and JunB are strongly expressed in H-RS and ALCL cells, whereas they are not expressed in nonmalignant lymphocytes in which CD30 CpG islands are rarely methylated.
  • We conclude that constitutive action of aberrantly expressed JunB on hypomethylated CD30 CpG islands of lymphocytes triggers CD30 induction and initiates activation of the JunB-CD30-JunB loop, essential to the pathogenesis of HL and ALCL.
  • [MeSH-major] Antigens, CD30 / biosynthesis. CpG Islands. DNA Methylation. Hodgkin Disease / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Proto-Oncogene Proteins c-jun / metabolism
  • [MeSH-minor] Base Sequence. Blotting, Northern. Cell Line. DNA. DNA Primers. Humans. Immunohistochemistry. Molecular Sequence Data. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction


58. Costa V, Oliva T, Norton L: Successful treatment with daclizumab of refractory anaplastic lymphoma. Pediatr Blood Cancer; 2009 Dec;53(6):1130-1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment with daclizumab of refractory anaplastic lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is a relatively rare and highly malignant form of non-Hodgkin lymphoma (NHL) which accounts for 10-15% of these childhood lymphomas.
  • Current treatment protocols for ALCL in children consist of a short course of high intensity polychemotherapy.
  • Here we describe an 8-year-old female with relapsed ALCL who achieved good response with anti-CD25 monoclonal antibody daclizumab.
  • Daclizumab appears to offer a safe treatment option, but further research needs to be conducted in order to define its role in children with ALCL who do not respond to intensive chemotherapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Immunoglobulin G / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • (PMID = 19598219.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; CUJ2MVI71Y / daclizumab
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59. Nishikori M, Ohno H, Haga H, Uchiyama T: Stimulation of CD30 in anaplastic large cell lymphoma leads to production of nuclear factor-kappaB p52, which is associated with hyperphosphorylated Bcl-3. Cancer Sci; 2005 Aug;96(8):487-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stimulation of CD30 in anaplastic large cell lymphoma leads to production of nuclear factor-kappaB p52, which is associated with hyperphosphorylated Bcl-3.
  • Anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) express CD30 at high levels, but stimulation of this molecule has been reported to induce contradictory effects.
  • To elucidate the molecular mechanism of CD30-mediated apoptosis of ALCL, we compared the gene expression profiles of t(2;5)(p23;q35)-positive ALCL with those of HL altered by CD30 agonistic stimulation.
  • The results showed that BCL3, the high-level expression of which in ALCL was previously reported, was further upregulated in response to CD30 stimulation, along with several pro-apoptotic genes.
  • Bcl-3 protein was present as an intermediate phospho-form in the resting-state ALCL, becoming hyperphosphorylated (Bcl-3P) upon stimulation.
  • We next found that the stimulation promoted de novo synthesis of the nuclear factor (NF)-kappaB2/p100 precursor as well as processing to p52, and a series of immunoprecipitation and western blotting analyses consistently showed association of Bcl-3P with p52 in CD30-stimulated ALCL.
  • An electrophoretic mobility shift assay revealed the induction of kappaB binding activity of the p52 homodimer, and nuclear colocalization of Bcl-3 and p52 was demonstrated in anaplastic lymphoma kinase-positive ALCL tumor tissues by immunohistochemistry.
  • As Bcl-3 can act as an anti-repressor or transactivator or both, we propose that the (p52)2/Bcl-3P ternary complex, which is specifically induced in CD30-stimulated ALCL, can modulate expression of apoptosis-related genes regulated by NF-kappaB, thereby accounting for CD30-mediated apoptosis of ALCL.
  • [MeSH-major] Antigens, CD30 / genetics. Carcinoma / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. NF-kappa B / genetics. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Cell Line, Tumor. Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 5. Humans. NF-kappa B p52 Subunit. Phosphorylation. Transcription Factors. Translocation, Genetic


60. Rapkiewicz A, Wen H, Sen F, Das K: Cytomorphologic examination of anaplastic large cell lymphoma by fine-needle aspiration cytology. Cancer; 2007 Dec 25;111(6):499-507
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytomorphologic examination of anaplastic large cell lymphoma by fine-needle aspiration cytology.
  • BACKGROUND: The cytomorphology of anaplastic large cell lymphoma (ALCL) is distinctive yet variable.
  • To the authors' knowledge, to date only small case series have described the cytologic findings noted in patients with ALCL.
  • The current series is the largest case series presented to date to retrospectively review the cytomorpholgic findings noted in patients with ALCL, with specific attention paid to those with anaplastic lymphoma kinase (ALK)-negative ALCL.
  • METHODS: Over a 13-year period, the available Diff-Quik cytology smears and surgical excision specimens taken from patients with ALCL were evaluated.
  • Different clinical and morphologic parameters were evaluated, including ALK status.
  • ALK-negative ALCL cytology smears were found to have a high number of anaplastic cells compared with ALK-positive cases.
  • CONCLUSIONS: ALCL can be diagnosed accurately by fine-needle aspiration cytology (FNAC) alone when aided by immunocytochemistry in ALK-positive cases.
  • Ancillary studies should be anticipated such that material for cell block preparation and molecular studies is taken at the time of FNAC.
  • The results of the current study demonstrate the varied FNAC morphology of ALCL.
  • [MeSH-major] Biopsy, Fine-Needle. Lymphoma, Large-Cell, Anaplastic / pathology

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  • [Copyright] 2007 American Cancer Society
  • (PMID = 17941004.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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61. Eiden P, Liu Q, Zein El Abedin S, Endres F, Krossing I: An experimental and theoretical study of the aluminium species present in mixtures of AlCl3 with the ionic liquids [BMP]Tf2N and [EMIm]Tf2N. Chemistry; 2009;15(14):3426-34
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  • It is known that nano- or microcrystalline aluminium may be electrodeposited from mixtures of AlCl(3) and the ionic liquids 1-butyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)amide ([BMP]Tf(2)N) and 1-ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl)amide ([EMIm]Tf(2)N), and that two phases form with higher formal concentrations of AlCl(3) (at 1.6 mol L(-1) (x(Al)=0.33) and 2.5 mol L(-1) (x(Al)=0.39), respectively).
  • The addition of AlCl(3) to the two liquids first leads to complexation with [Tf(2)N](-) and then disproportionation of the initial [AlCl(x)(Tf(2)N)(y)](-) complexes give Al(Tf(2)N)(3) and [AlCl(4)](-).
  • At high concentrations of AlCl(3), the lower phase consists almost completely of Al(Tf(2)N)(3), whereas in the upper phase [AlCl(4)](-) is the dominant species.
  • Electrodeposition of aluminium in the upper phase occurs from mixed AlCl(x)(Tf(2)N)(y) species, most likely from [AlCl(2)(Tf(2)N)(2)](-) formed in small concentrations at the phase boundary between the [AlCl(4)](-) and the Al(Tf(2)N)(3) layers.
  • Moreover, the ionic liquids [BMP]AlCl(4) (m.p.
  • 74 degrees C) and [EMIm]AlCl(4) (m.p.

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  • (PMID = 19229940.001).
  • [ISSN] 1521-3765
  • [Journal-full-title] Chemistry (Weinheim an der Bergstrasse, Germany)
  • [ISO-abbreviation] Chemistry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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62. Kitamura N, Katagiri YU, Itagaki M, Miyagawa Y, Onda K, Okita H, Mori A, Fujimoto J, Kiyokawa N: The expression of granulysin in systemic anaplastic large cell lymphoma in childhood. Leuk Res; 2009 Jul;33(7):908-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of granulysin in systemic anaplastic large cell lymphoma in childhood.
  • The expression of granulysin, a cytolytic protein produced by activated T and NK cells, has been revealed to be correlated with the prognosis of some adult cancer patients.
  • By examination on various childhood lymphoma tissues, we found that granulysin level was especially high in systemic anaplastic large cell lymphoma (ALCL) cases, whereas no close correlation with the expression of CD96, a marker for activated T and NK cells, was observed.
  • We further demonstrated that both ALCL cells in biopsy specimens and cell lines established from ALCL express granulysin, indicating some correlation of granulysin with biological features of ALCL.
  • [MeSH-major] Antigens, Differentiation, T-Lymphocyte / genetics. Burkitt Lymphoma / genetics. Hodgkin Disease / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD / genetics. Antigens, CD / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Female. Flow Cytometry. Humans. Killer Cells, Natural / metabolism. Killer Cells, Natural / pathology. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured. Young Adult

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  • (PMID = 19243819.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / CD96 antigen; 0 / GNLY protein, human; 0 / RNA, Messenger
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63. Wright CW, Rumble JM, Duckett CS: CD30 activates both the canonical and alternative NF-kappaB pathways in anaplastic large cell lymphoma cells. J Biol Chem; 2007 Apr 6;282(14):10252-62
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  • [Title] CD30 activates both the canonical and alternative NF-kappaB pathways in anaplastic large cell lymphoma cells.
  • CD30 is a member of the tumor necrosis factor receptor superfamily whose expression is up-regulated on anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) cells.
  • Many different outcomes of CD30 stimulation have been reported, including cell cycle arrest, apoptosis, and activation of the prosurvival transcription factor, NF-kappaB, although this last activity is much less well defined in ALCL cells.
  • In order to better understand the signaling properties of CD30 in cancer, we established a system for the stimulation of CD30 with its physiological ligand.
  • Using this system, CD30 was stimulated on ALCL and HL cells, and the subsequent CD30 signaling properties were characterized.
  • We show that a fraction of ALCL cells rapidly underwent apoptosis following CD30 stimulation, whereas HL cells were unaffected.
  • The surviving ALCL cells exhibited robust activation of both the canonical and alternative NF-kappaB pathways as measured by nuclear translocation of RelA, p50, RelB, and p52, and this culminated in the transactivation of classical NF-kappaB-responsive genes.
  • With prolonged CD30 stimulation, ALCL cells underwent cell cycle arrest that correlated with expression of the cell cycle inhibitor p21(waf1).
  • Furthermore, p21(waf1) expression and cell cycle arrest were found to depend predominantly on the canonical NF-kappaB pathway, since it was reversed by RNA interference-mediated suppression of RelA.
  • These data reveal that in ALCL cells, in contrast to other cell types, CD30 stimulation elicits p21(waf1)-mediated arrest through the canonical but not the alternative NF-kappaB pathway.
  • [MeSH-major] Antigens, CD30 / metabolism. CD30 Ligand / metabolism. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. NF-kappa B / metabolism. Signal Transduction
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Active Transport, Cell Nucleus / genetics. Animals. CHO Cells. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Line, Tumor. Cell Nucleus / genetics. Cell Nucleus / metabolism. Cell Survival / drug effects. Cell Survival / genetics. Cricetinae. Cricetulus. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. RNA Interference / drug effects

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  • (PMID = 17261581.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM067827; United States / NIAID NIH HHS / AI / T32 AI007413-12; United States / NHLBI NIH HHS / HL / T32 HL07517
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / CD30 Ligand; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NF-kappa B; 0 / TNFSF8 protein, human
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64. Peng ZY, Ma FF, Zhu LF, Xie XM, Zhang Z: Lewis acid promoted carbon-carbon double-bond formation via organozinc reagents and carbonyl compounds. J Org Chem; 2009 Sep 4;74(17):6855-8
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  • Using cheap and readily available AlCl(3) as Lewis acid, functionalized aldehydes react with organozinc reagents to give (E)-alkenes stereoselectively in high yields.

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  • (PMID = 19658428.001).
  • [ISSN] 1520-6904
  • [Journal-full-title] The Journal of organic chemistry
  • [ISO-abbreviation] J. Org. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acids; 0 / Alcohols; 0 / Aldehydes; 0 / Bromides; 0 / Ethers; 0 / Ketones; 0 / Metals; 3FPU23BG52 / Toluene; 7440-44-0 / Carbon; 9FN79X2M3F / Lithium; I38ZP9992A / Magnesium; J41CSQ7QDS / Zinc
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65. Dalton RR, Rassidakis GZ, Atwell C, Wang S, Oyarzo MP, Medeiros LJ: Differential expression of cyclin D3 in ALK+ and ALK- anaplastic large cell lymphoma. Hum Pathol; 2005 Jul;36(7):806-11
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  • [Title] Differential expression of cyclin D3 in ALK+ and ALK- anaplastic large cell lymphoma.
  • As defined in the World Health Organization classification, anaplastic large cell lymphoma (ALCL) is a distinct type of non-Hodgkin lymphoma of T/null cell lineage, a subset of which is associated with translocations involving 2p23 resulting in expression of anaplastic lymphoma kinase (ALK).
  • In this study, we assessed cyclin D3 expression in 2 ALK+ ALCL cell lines (Karpas 299 and SU-DHL1) and 1 ALK- ALCL cell line (Mac2A) by Western blot analysis.
  • We also assessed cyclin D3 expression in 52 ALCL tumors (32 ALK+, 20 ALK-) by immunohistochemistry using tissue microarrays.
  • Both ALK+ ALCL cell lines, but not the ALK- ALCL cell line, expressed cyclin D3 and pSTAT3.
  • Cyclin D3 was expressed in 25 (78%) of 32 ALK+ ALCL tumors and in 4 (20%) of 20 ALK- ALCL tumors (P < .001, Fisher exact test ).
  • In ALK+ ALCL tumors, the mean percentage of cyclin D3-positive tumor cells was 40.6% compared with 5.1% in ALK- ALCL tumors (P < .001, Mann-Whitney U test).
  • The percentages of cyclin D3-positive and pSTAT3-positive tumor cells were positively correlated (Spearman R = 0.35, P = .036).
  • We conclude that cyclin D3 is differentially expressed in ALK+ and ALK- ALCL and that high expression levels of cyclin D3 in ALK+ ALCL may be attributable to STAT3 activation.
  • [MeSH-major] Cyclins / metabolism. Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Blotting, Western. Cell Count. Cell Line, Tumor. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cyclin D3. DNA-Binding Proteins / metabolism. Humans. Immunohistochemistry. Prognosis. Protein Array Analysis. Receptor Protein-Tyrosine Kinases. STAT3 Transcription Factor. Survival Rate. Trans-Activators / metabolism

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  • (PMID = 16084951.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND3 protein, human; 0 / Cyclin D3; 0 / Cyclins; 0 / DNA-Binding Proteins; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Trans-Activators; 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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66. Bittencourt AL, Rothers S, Boente P, Santos R: Primary cutaneous eosinophil-rich anaplastic large cell lymphoma: report of an unusual case and literature review. J Cutan Med Surg; 2008 Mar-Apr;12(2):88-92
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  • [Title] Primary cutaneous eosinophil-rich anaplastic large cell lymphoma: report of an unusual case and literature review.
  • BACKGROUND: Cutaneous, neutrophil-rich anaplastic large cell lymphoma (ALCL) is an uncommon variant of ALCL that may be confused with inflammatory dermatoses.
  • OBJECTIVE AND METHODS: We describe an eosinophil-rich variant of ALCL occurring on the left ear without systemic involvement.
  • The lesion had inflammatory characteristics, which led initially to a histological diagnosis of an inflammatory process.
  • Two months later, a second biopsy diagnosed eosinophil-rich variant of ALCL.
  • We discuss the clinicopathological findings and the differential diagnosis CONCLUSIONS: To the best of our knowledge, the occurrence of a cutaneous, eosinophil-rich variant of ALCL has not been previously reported.
  • It is important to alert pathologists to this variant of ALCL so that this possibility may be considered in the early differential diagnosis of inflammatory cutaneous conditions.
  • [MeSH-major] Ear Neoplasms / metabolism. Ear, External. Eosinophils / metabolism. Lymphoma, Primary Cutaneous Anaplastic Large Cell / metabolism. Skin Neoplasms / metabolism
  • [MeSH-minor] Aged, 80 and over. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Skin Diseases / diagnosis

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  • (PMID = 18346406.001).
  • [ISSN] 1203-4754
  • [Journal-full-title] Journal of cutaneous medicine and surgery
  • [ISO-abbreviation] J Cutan Med Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 33
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67. Sebire NJ, Webb D, Ramsay AD: Anaplastic large cell lymphoma with ALK expression and presence of the t(2;5) translocation in a 5-month-old infant. Fetal Pediatr Pathol; 2005 Jan-Feb;24(1):63-70
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  • [Title] Anaplastic large cell lymphoma with ALK expression and presence of the t(2;5) translocation in a 5-month-old infant.
  • Anaplastic large cell lymphoma (ALCL) is a well-recognized subtype of non-Hodgkin lymphoma in childhood.
  • Several series report experience with the diagnosis and management of pediatric ALCL, the average age at diagnosis being 8 to 16 years, with a reported range of 1 to 15 years.
  • We present a case of ALCL affecting a 5-month-old infant in whom the diagnosis was confirmed by the nuclear and cytoplasmic immunohistochemical expression of ALK1, in addition to the presence of classical t(2;5)(p23;q35) translocation detected using reverse transcriptase-polymerase chain reaction.
  • This is the youngest case of ALCL thus far reported and hence expands the spectrum of infantile lymphoproliferative disorders.
  • [MeSH-major] Activin Receptors, Type I / biosynthesis. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Translocation, Genetic
  • [MeSH-minor] Activin Receptors, Type II. Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 5. Humans. Infant. Male

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  • (PMID = 16175752.001).
  • [ISSN] 1551-3815
  • [Journal-full-title] Fetal and pediatric pathology
  • [ISO-abbreviation] Fetal Pediatr Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type I; EC 2.7.11.30 / Activin Receptors, Type II
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68. Sanders SD, Ruiz-Olalla A, Johnson JS: Total synthesis of (+)-virgatusin via AlCl3-catalyzed [3+2] cycloaddition. Chem Commun (Camb); 2009 Sep 14;(34):5135-7
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  • The AlCl(3)-catalyzed cycloaddition of a donor-acceptor (don-acc) cyclopropane and piperonal succinctly provides the core of virgatusin in a selective, high-yielding manner.

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  • (PMID = 20448971.001).
  • [ISSN] 1364-548X
  • [Journal-full-title] Chemical communications (Cambridge, England)
  • [ISO-abbreviation] Chem. Commun. (Camb.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aluminum Compounds; 0 / Chlorides; 0 / Furans; 0 / virgatusin; 3CYT62D3GA / aluminum chloride
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69. Zhao F, Wang C, Liu L, Zhang WX, Xi Z: Skeletal rearrangement of all-carbon spiro skeletons mediated by a Lewis acid. Chem Commun (Camb); 2009 Nov 21;(43):6569-71
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  • Mediated by AlCl(3), substituted spiro[4.5]deca-tetraenes underwent novel and selective skeletal rearrangement to generate indene derivatives in high to excellent yields.

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  • (PMID = 19865652.001).
  • [ISSN] 1364-548X
  • [Journal-full-title] Chemical communications (Cambridge, England)
  • [ISO-abbreviation] Chem. Commun. (Camb.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acids; 7440-44-0 / Carbon
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70. Rocher NM, Izgorodina EI, Rüther T, Forsyth M, Macfarlane DR, Rodopoulos T, Horne MD, Bond AM: Aluminium speciation in 1-butyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)amide/AlCl3 mixtures. Chemistry; 2009;15(14):3435-47
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  • Electrodeposition of aluminium is possible from solutions of AlCl(3) dissolved in the 1-butyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)amide (C(4)mpyrNTf(2)) ionic liquid.
  • However, electrodeposition is dependant on the AlCl(3) concentration as it only occurs at concentrations >1.6 mol L(-1).
  • At these relatively high AlCl(3) concentrations the C(4)mpyrNTf(2)/AlCl(3) mixtures exhibit biphasic behaviour.
  • Notably, at 1.6 mol L(-1) AlCl(3), aluminium can only be electrodeposited from the upper phase.
  • The complex chemistry of the C(4)mpyrNTf(2)/AlCl(3) system is described and implications of aluminium speciation in several C(4)mpyrNTf(2)/AlCl(3) mixtures, as deduced from Raman and (27)Al NMR spectroscopic data, are discussed.
  • The (27)Al NMR spectra of the C(4)mpyrNTf(2)/AlCl(3) mixtures revealed the presence of both tetrahedrally and octahedrally coordinated aluminium species.
  • Raman spectroscopy revealed that the level of uncoordinated NTf(2)(-) anions decreased with increasing AlCl(3) concentration.
  • The data indicate that the electroactive species involved are likely to be either [AlCl(3)(NTf(2))](-) or [AlCl(2)(NTf(2))(2)](-).

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  • (PMID = 19132700.001).
  • [ISSN] 1521-3765
  • [Journal-full-title] Chemistry (Weinheim an der Bergstrasse, Germany)
  • [ISO-abbreviation] Chemistry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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71. Mathas S, Kreher S, Meaburn KJ, Jöhrens K, Lamprecht B, Assaf C, Sterry W, Kadin ME, Daibata M, Joos S, Hummel M, Stein H, Janz M, Anagnostopoulos I, Schrock E, Misteli T, Dörken B: Gene deregulation and spatial genome reorganization near breakpoints prior to formation of translocations in anaplastic large cell lymphoma. Proc Natl Acad Sci U S A; 2009 Apr 7;106(14):5831-6
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  • [Title] Gene deregulation and spatial genome reorganization near breakpoints prior to formation of translocations in anaplastic large cell lymphoma.
  • We used anaplastic large cell lymphoma (ALCL) with and without the characteristic t(2;5)(p23;q35) translocation to study the mechanisms of formation of translocations and of ALCL transformation.
  • We report deregulation of several genes located near the ALCL translocation breakpoint, regardless of whether the tumor contains the t(2;5).
  • Their up-regulation promotes cell survival and repression of T cell-specific gene expression programs that are characteristic for ALCL.
  • The deregulated genes are in spatial proximity within the nuclear space of t(2;5)-negative ALCL cells, facilitating their translocation on induction of double-strand breaks.
  • Also, our data demonstrate that deregulation of breakpoint-proximal genes has a key role in ALCL.

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  • (PMID = 19321746.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOSL2 protein, human; 0 / Fos-Related Antigen-2; 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2667034
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72. Nasr MR, Laver JH, Chang M, Hutchison RE: Expression of anaplastic lymphoma kinase, tyrosine-phosphorylated STAT3, and associated factors in pediatric anaplastic large cell lymphoma: A report from the children's oncology group. Am J Clin Pathol; 2007 May;127(5):770-8
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  • [Title] Expression of anaplastic lymphoma kinase, tyrosine-phosphorylated STAT3, and associated factors in pediatric anaplastic large cell lymphoma: A report from the children's oncology group.
  • In anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK) activates (phosphorylates) signal transducer and activator of transcription 3 (STAT3) with subsequent cytoplasmic expression, in some cases, of survivin and tissue inhibitor of metalloprotease 1 (TIMP1).
  • CD56 is also a negative prognostic marker in ALCL.
  • We assayed 40 cases of predominantly ALK+ pediatric ALCL for pSTAT3, survivin, TIMP1, and CD56 using immunohistochemical analysis.
  • The patients were derived from a Pediatric Oncology Group treatment protocol that showed 72% event-free survival at 4 years for ALCL.
  • The results show that in advanced-stage pediatric ALCL, although most tumors express ALK and a majority show activated STAT3, cytoplasmic localization of survivin and TIMP1 is not frequent, nor is expression of CD56.
  • This may help, in part, explain the relatively good prognosis of pediatric ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / chemistry. Protein-Tyrosine Kinases / analysis. STAT3 Transcription Factor / analysis

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  • (PMID = 17439836.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 30969; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / STAT3 Transcription Factor; 0 / Tissue Inhibitor of Metalloproteinase-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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73. Gudgin E, Rashbass J, Pulford KJ, Erber WN: Primary and isolated anaplastic large cell lymphoma of the bone marrow. Leuk Lymphoma; 2005 Mar;46(3):461-3
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  • [Title] Primary and isolated anaplastic large cell lymphoma of the bone marrow.
  • Anaplastic large cell lymphoma (ALCL) is a T-cell lymphoma in which the majority of patients present with advanced stage III or IV disease.
  • Here we report a case of ALCL where bone marrow was the only site of disease, in a 60-year-old man with pyrexia and pancytopenia.
  • The diagnosis of ALCL was made on detection of CD30-positive anaplastic cells in the bone marrow, together with prominent hemophagocytosis.
  • Genetics confirmed the clonal nature of the disease and showed it to be anaplastic lymphoma kinase (ALK) negative.
  • Primary isolated bone marrow ALCL should be considered in the diagnosis of pancytopenia associated with hemophagocytosis.
  • [MeSH-major] Bone Marrow / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 15621840.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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74. Oyarzo MP, Medeiros LJ, Atwell C, Feretzaki M, Leventaki V, Drakos E, Amin HM, Rassidakis GZ: c-FLIP confers resistance to FAS-mediated apoptosis in anaplastic large-cell lymphoma. Blood; 2006 Mar 15;107(6):2544-7
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  • [Title] c-FLIP confers resistance to FAS-mediated apoptosis in anaplastic large-cell lymphoma.
  • We hypothesized that inhibition of the FAS-mediated apoptosis pathway by FLICE-like inhibitory protein (c-FLIP) may contribute to oncogenesis in ALK+ anaplastic large-cell lymphoma (ALCL).
  • Treatment with increasing concentrations of CH-11 (CD95/FAS agonistic antibody) had no effect on cell viability of 2 ALK+ ALCL cell lines, Karpas 299 and SU-DHL1, each expressing high levels of c-FLIP.
  • However, inhibition of endogenous c-FLIP expression by specific c-FLIP siRNA in Karpas 299 and SU-DHL1 cells treated with CH-11 resulted in FAS-mediated cell death associated with increased annexin V binding, apoptotic morphology, and cleavage of caspase-8.
  • In 26 ALK+ ALCL tumors, assessed for expression of DISC-associated proteins, CD95/FAS and c-FLIP were commonly expressed, in 23 (92%) of 25 and 21 (91%) of 23 tumors, respectively.
  • By contrast, CD95L/FASL was expressed in only 3 (12%) of 26 ALCL tumors, although it was strongly expressed by surrounding small reactive lymphocytes.
  • Our findings suggest that overexpression of c-FLIP protects ALK+ ALCL cells from death-receptor-induced apoptosis and may contribute to ALCL pathogenesis.
  • [MeSH-major] Antigens, CD95 / physiology. Apoptosis. Intracellular Signaling Peptides and Proteins / physiology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Annexin A5 / metabolism. CASP8 and FADD-Like Apoptosis Regulating Protein. Caspase 8. Caspases / metabolism. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. RNA, Small Interfering / pharmacology

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  • (PMID = 16304056.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antigens, CD95; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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75. Mathas S, Jöhrens K, Joos S, Lietz A, Hummel F, Janz M, Jundt F, Anagnostopoulos I, Bommert K, Lichter P, Stein H, Scheidereit C, Dörken B: Elevated NF-kappaB p50 complex formation and Bcl-3 expression in classical Hodgkin, anaplastic large-cell, and other peripheral T-cell lymphomas. Blood; 2005 Dec 15;106(13):4287-93
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  • [Title] Elevated NF-kappaB p50 complex formation and Bcl-3 expression in classical Hodgkin, anaplastic large-cell, and other peripheral T-cell lymphomas.
  • Transcription factor nuclear factor kappa B (NF-kappaB) plays a central role in the pathogenesis of classical Hodgkin lymphoma (cHL).
  • In anaplastic large-cell lymphomas (ALCLs), which share molecular lesions with cHL, the NF-kappaB system has not been equivalently investigated.
  • Here we describe constitutive NF-kappaB p50 homodimer [(p50)2] activity in ALCL cells in the absence of constitutive activation of the IkappaB kinase (IKK) complex.
  • Bcl-3, which is an inducer of nuclear (p50)2 and is associated with (p50)2 in ALCL and HRS cell lines, is abundantly expressed in ALCL and HRS cells.
  • Notably, a selective overexpression of Bcl-3 target genes is found in ALCL cells.
  • By immunohistochemical screening of 288 lymphoma cases, a strong Bcl-3 expression in cHL and in peripheral T-cell non-Hodgkin lymphoma (T-NHL) including ALCL was found.
  • In 3 of 6 HRS cell lines and 25% of primary ALCL, a copy number increase of the BCL3 gene locus was identified.
  • Together, these data suggest that elevated Bcl-3 expression has an important function in cHL and peripheral T-NHL, in particular ALCL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Hodgkin Disease / genetics. Hodgkin Disease / metabolism. Lymphoma, T-Cell, Peripheral / genetics. Lymphoma, T-Cell, Peripheral / metabolism. NF-kappa B p50 Subunit / metabolism. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Cell Line. Dimerization. Humans. I-kappa B Proteins / metabolism. Interleukin-9 / metabolism. Microarray Analysis. Oncogene Proteins v-rel / metabolism. Protein Binding. Transcription Factors

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  • [CommentIn] Blood. 2006 Jul 1;108(1):401-2; author reply 402-3 [16790585.001]
  • (PMID = 16123212.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / I-kappa B Proteins; 0 / Interleukin-9; 0 / NF-kappa B p50 Subunit; 0 / Oncogene Proteins v-rel; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3
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76. Querfeld C, Khan I, Mahon B, Nelson BP, Rosen ST, Evens AM: Primary cutaneous and systemic anaplastic large cell lymphoma: clinicopathologic aspects and therapeutic options. Oncology (Williston Park); 2010 Jun;24(7):574-87
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  • [Title] Primary cutaneous and systemic anaplastic large cell lymphoma: clinicopathologic aspects and therapeutic options.
  • Anaplastic large cell lymphoma (ALCL) is a biologic and clinically heterogenous subtype of T-cell lymphoma.
  • Clinically, ALCL may present as localized (primary) cutaneous disease or widespread systemic disease.
  • These two forms of ALCL are distinct entities with different clinical and biologic features.
  • Both types share similar histology, however, with cohesive sheets of large lymphoid cells expressing the Ki-1 (CD30) molecule.
  • Primary cutaneous ALCL (C-ALCL) is part of the spectrum of CD30+ lymphoproliferative diseases of the skin including lymphomatoid papulosis.
  • Using conservative measures, 5-year disease-free survival rates are > 90%.
  • The systemic ALCL type is an aggressive lymphoma that may secondarily involve the skin, in addition to other extranodal sites.
  • Further, systemic ALCL may be divided based on the expression of anaplastic lymphoma kinase (ALK) protein, which is activated most frequently through the nonrandom t(2;5) chromosome translocation, causing the fusion of the nucleophosmin (NPM) gene located at 5q35 to 2p23 encoding the receptor tyrosine kinase ALK.
  • Systemic ALK+ ALCLs have improved prognosis compared with ALK-negative ALCL, although both subtypes warrant treatment with polychemotherapy.
  • Allogeneic and, to a lesser extent, autologous stem cell transplantation play a role in relapsed disease, while the benefit of upfront transplant is not clearly defined.
  • In addition, a multitude of novel therapeutics are being studied, including anti-CD30 antibodies, histone deacetylase inhibitors, immunomodulatory drugs, proteasome inhibitors, and inhibitors of ALK and its downstream signaling pathways.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, Large-Cell, Anaplastic / therapy. Lymphoma, Primary Cutaneous Anaplastic Large Cell / pathology. Lymphoma, Primary Cutaneous Anaplastic Large Cell / therapy. Skin Neoplasms / pathology. Skin Neoplasms / therapy
  • [MeSH-minor] Antigens, CD30 / physiology. Humans. Immunophenotyping

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  • [CommentIn] Oncology (Williston Park). 2010 Jun;24(7):587, 592-3 [20669795.001]
  • [CommentIn] Oncology (Williston Park). 2010 Jun;24(7):594 [20669796.001]
  • (PMID = 20669794.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Number-of-references] 118
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77. Murphy AJ, O'Neill P, O'Brien F, Enright H, Jeffers M, Thornhill JA, Loftus BM: Anaplastic large cell lymphoma: a unique presentation with urinary bladder involvement: a case report. Int J Surg Pathol; 2005 Oct;13(4):369-73
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  • [Title] Anaplastic large cell lymphoma: a unique presentation with urinary bladder involvement: a case report.
  • Anaplastic large cell lymphoma (ALCL) is a T-cell lymphoma composed of large pleomorphic CD30-positive cells.
  • While systemic ALCL frequently involves extranodal sites, involvement of the urinary bladder is extremely rare.
  • We report a case of systemic ALCL presenting with bladder involvement.
  • Imaging revealed pelvic lymphadenopathy and a thickened bladder wall.
  • Bladder biopsies showed diffuse infiltration of the lamina propria by large pleomorphic cells, with preservation of the overlying urothelium.
  • Immunohistochemistry demonstrated cell membrane and Golgi region staining for CD30 and epithelial membrane antigen.
  • This is the first documented instance of systemic ALCL presenting with bladder symptoms.
  • [MeSH-major] Carcinoma / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Urinary Bladder Neoplasms / diagnosis
  • [MeSH-minor] Adult. Antigens, CD30 / analysis. Cell Membrane / immunology. Diagnosis, Differential. Golgi Apparatus / immunology. Humans. Immunohistochemistry. Male. Mucin-1 / analysis. Urothelium / metabolism. Urothelium / pathology

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  • (PMID = 16273198.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Mucin-1
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78. Li JF, Li GD, Gu L, Liu WP, Li FY, Liao DY, Ma ZG: [Study on activation of AKT/mTOR pathway in anaplastic large cell lymphoma]. Zhonghua Xue Ye Xue Za Zhi; 2008 Oct;29(10):649-53
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  • [Title] [Study on activation of AKT/mTOR pathway in anaplastic large cell lymphoma].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and the phosphorylation status of AKT, mammalian target of rapamycin (mTOR), 4E-binding protein 1 (4E-BP1) and ribosomal protein S6 kinase (p70S6K) and their interrelationships and clinical pathological significance in anaplastic large cell lymphoma (ALCL) patients.
  • RESULTS: Among the 81 ALCL patients, 51 (63.0%) expressed ALK, whereas the other 30 (37.0%) did not.
  • Patients with ALK(+) ALCL had a better prognosis than those with ALK-ALCL (P < 0.05).
  • Out of the 71 ALCL samples studied, p-AKT was detected in 54 (76.1%) samples and its phosphorylation was correlated with ALK expression (P < 0.05); p-mTOR was detected in 57 (80.3%) samples and its expression was correlated with both ALK and p-AKT (P < 0.05); p-4E-BP1 and p-p70S6K were detected in 64 (90.1%) and 66 (93.0%) samples respectively, and their expressions were related with p-mTOR (P < 0.05), but not with ALK or p-AKT (P > 0.05).
  • CONCLUSION: Expressions of p-AKT, p-mTOR, p-4E-BP1 and p-p70S6K are detected in ALCL, while ALK(+) cases have higher incidence than those with ALK(-) cases.
  • Phosphorylation of AKT and mTOR is correlated with ALK expression, suggesting that there is an activated pathway of AKT/mTOR in patients with ALK(+) ALCL, but the activation have no obvious prognostic significance.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Protein-Serine-Threonine Kinases / metabolism. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 19176054.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / EIF4EBP1 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Phosphoproteins; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa
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79. Benner MF, Willemze R: Bone marrow examination has limited value in the staging of patients with an anaplastic large cell lymphoma first presenting in the skin. Retrospective analysis of 107 patients. Br J Dermatol; 2008 Nov;159(5):1148-51
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  • [Title] Bone marrow examination has limited value in the staging of patients with an anaplastic large cell lymphoma first presenting in the skin. Retrospective analysis of 107 patients.
  • BACKGROUND: According to criteria of the World Health Organization-European Organization for Research and Treatment of Cancer classification for cutaneous lymphomas a diagnosis of primary cutaneous CD30-positive anaplastic large cell lymphoma (C-ALCL) should be made only when systemic localizations have been excluded by adequate staging procedures, including a bone marrow biopsy.
  • It has recently been questioned whether or not bone marrow examination should be performed routinely in indolent cutaneous lymphomas such as C-ALCL.
  • OBJECTIVES: To determine the incidence of bone marrow involvement in patients with an ALCL first presenting in the skin to find out if the current policy to advise bone marrow examination should be maintained or whether a bone marrow biopsy should be performed only in selected cases.
  • METHODS: All patients presenting with skin lesions with histological and immunophenotypical features of an ALCL were retrieved from the database of the Dutch Cutaneous Lymphoma Group.
  • Patients with a history of systemic ALCL and patients without bone marrow examination were excluded from the study.
  • The final study group included 107 patients with an ALCL first presenting in the skin, who had been staged completely.
  • RESULTS: Staging procedures showed the presence of extracutaneous disease in 20 patients, but bone marrow involvement was not detected in any of the 107 patients.
  • CONCLUSIONS: Bone marrow examination has limited value in the staging of patients with an ALCL first presenting in the skin, and should be performed only in selected cases.
  • [MeSH-major] Bone Marrow / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Skin Neoplasms / pathology

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  • (PMID = 18782320.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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80. Nguyen JT, Condron MR, Nguyen ND, De J, Medeiros LJ, Padula A: Anaplastic large cell lymphoma in leukemic phase: extraordinarily high white blood cell count. Pathol Int; 2009 May;59(5):345-53
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  • [Title] Anaplastic large cell lymphoma in leukemic phase: extraordinarily high white blood cell count.
  • Anaplastic large cell lymphoma (ALCL) is a distinct type of T/null-cell non-Hodgkin lymphoma that commonly involves nodal and extranodal sites.
  • The World Health Organization of lymphoid neoplasms recognizes two types: anaplastic lymphoma kinase (ALK) positive or ALK negative, the former as a result of abnormalities involving the ALK gene at chromosome 2p23.
  • Patients with ALCL rarely develop a leukemic phase of disease, either at the time of initial presentation or during the clinical course.
  • Described herein is a patient with ALK+ ALCL, small cell variant, associated with the t(2;5)(p23;q35), who initially presented with leukemic involvement and an extraordinarily high leukocyte count of 529 x 10(9)/L, which subsequently peaked at 587 x 10(9)/L.
  • Despite chemotherapy the patient died 2(1/2) months after diagnosis.
  • In the literature review 20 well-documented cases are identified of ALCL in leukemic phase reported previously, with a WBC ranging from 15 to 151 x 10(9)/L.
  • Leukemic phase of ALCL occurs almost exclusively in patients with ALK+ ALCL, most often associated with the small cell variant and the t(2;5)(p23;q35), similar to the present case.
  • Patients with leukemic phase ALK+ ALCL appear to have a poorer prognosis than most patients with ALK+ ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / blood. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 19432678.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 19
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81. Mussolin L, Pillon M, Bonato P, Leszl A, Franceschetto G, Di Meglio A, d'Amore ES, Sainati L, Rosolen A: Cytogenetic analysis of pediatric anaplastic large cell lymphoma. Pediatr Blood Cancer; 2010 Sep;55(3):446-51
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  • [Title] Cytogenetic analysis of pediatric anaplastic large cell lymphoma.
  • BACKGROUND: Anaplastic large cell lymphoma (ALCL) constitutes approximately 15% of pediatric and 3% of adult non-Hodgkin lymphomas.
  • Cytogenetic studies of ALCL have mostly been published as case-reports.
  • The aim of this study was to determine the cytogenetic profiles of a series of pediatric ALCL and to compare them with pediatric and adult ALCL from the literature.
  • Comparative analysis was performed on our findings and on the karyotypes of 48 pediatric and 39 adult ALCL reported in the literature.
  • RESULTS: Karyotype was obtained in 16/18 ALCL: 9 showed translocation t(2;5) and 1 an alk variant form.
  • Trisomy 7 was found in 22% (13/59) of pediatric cases with abnormal karyotype and only in 5% (2/38) of adults; monosomy of chromosome 13 in 13% (5/38) of adults and only in 2% (1/59) of pediatric patients and monosomy of chromosome 15 in 16% (6/38) of adults and in none of the pediatric ALCL.
  • CONCLUSION: Our data suggest that pediatric and adult ALCL are characterized by different numerical chromosomal abnormalities.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20658615.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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82. Dien Bard J, Gelebart P, Anand M, Zak Z, Hegazy SA, Amin HM, Lai R: IL-21 contributes to JAK3/STAT3 activation and promotes cell growth in ALK-positive anaplastic large cell lymphoma. Am J Pathol; 2009 Aug;175(2):825-34
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  • [Title] IL-21 contributes to JAK3/STAT3 activation and promotes cell growth in ALK-positive anaplastic large cell lymphoma.
  • Interleukin (IL)-21 has been reported to both stimulate cell growth and promote survival in benign lymphoid cells and several types of hematopoietic neoplasms.
  • It induces JAK3/STAT3 signaling, a biologically important cellular pathway activated in most cases of anaplastic lymphoma kinase (ALK)-expressing anaplastic large cell lymphoma (ALK(+)ALCL).
  • Therefore, we hypothesize that IL-21 may contribute to JAK3/STAT3 activation and cell growth in ALK(+)ALCL.
  • By reverse transcription-PCR, we found consistent expression of IL-21 receptor (IL-21R) in all ALK(+)ALCL cell lines and frozen tumors examined.
  • IL-21 was also consistently expressed in ALK(+)ALCL tumors, although its mRNA was detectable in only one of three cell lines tested.
  • By immunohistochemistry, we examined 10 paraffin-embedded ALK(+)ALCL tumors; all cases were positive for both IL-21 and IL-21R in these neoplastic cells.
  • IL-21 signaling is biologically significant in ALK(+)ALCL since the addition of recombinant IL-21 enhanced the activation of JAK3/STAT3 and significantly increased cell growth in ALK(+)ALCL cell lines.
  • However, small interfering RNA down-regulation of IL-21R significantly decreased both STAT3 activation and cell growth.
  • Our findings thus support the enhancement of JAK3/STAT3 activation and cell growth in ALK(+)ALCL via IL-21 signaling.
  • [MeSH-major] Interleukins / metabolism. Janus Kinase 3 / biosynthesis. Lymphoma, Large-Cell, Anaplastic / pathology. STAT3 Transcription Factor / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Protein-Tyrosine Kinases / analysis. RNA, Small Interfering / genetics. Receptor Protein-Tyrosine Kinases. Receptors, Interleukin-21 / metabolism

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  • (PMID = 19608866.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukins; 0 / JAK3 protein, human; 0 / RNA, Small Interfering; 0 / Receptors, Interleukin-21; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / interleukin-21; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3
  • [Other-IDs] NLM/ PMC2716977
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83. Kadin ME: Current management of primary cutaneous CD30+ T-cell lymphoproliferative disorders. Oncology (Williston Park); 2009 Nov 30;23(13):1158-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current management of primary cutaneous CD30+ T-cell lymphoproliferative disorders.
  • Primary cutaneous CD30+ T-cell lymphoproliferative disorders (PCLPDs) are the second most common type of cutaneous T-cell lymphoma.
  • These disorders comprise a spectrum of clinically benign lymphomatoidpapulosis (LyP) and primary cutaneous anaplastic large-cell lymphoma (ALCL).
  • The peak incidence of LyP is in the 5th decade of life, and the incidence of primary cutaneous ALCL peaks in the 6th decade, but children are also affected.
  • Both LyP and primary cutaneous ALCL have an excellent prognosis.
  • However, LyP is associated with development of malignant lymphoma (mycosis fungoides, Hodgkin lymphoma, or ALCL) in 20% of cases, and also with an increased risk of non-lymphoid cancers.
  • The diagnosis of LyP is difficult and often delayed.
  • Primary cutaneous ALCL must be distinguished from secondary skin lesions in systemic ALCL, which confer a poor prognosis.
  • Correlation of clinical findings with histopathology and immunopathology (stains for ALK kinase, epithelial membrane antigen, and cutaneous lymphocyte antigen) are important to achieve a correct diagnosis.
  • When a diagnosis of CD30+ PCLPD is established, minimal clinical staging is required.
  • Low-dose methotrexate (10-25 mg weekly) is the most effective therapy for PCLPD but is usually reserved for aggressive cases of LyP and multifocal lesions of cutaneous ALCL Many patients with LyP can be followed expectantly, with special attention to changes in character of the skin lesions or development of lymphadenopathy.
  • Patients with localized cutaneous ALCL can be treated with irradiation.
  • Extracutaneous spread of disease is an indication for multiagent chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Lymphoma, Primary Cutaneous Anaplastic Large Cell / drug therapy. Methotrexate / administration & dosage. Skin Neoplasms / drug therapy
  • [MeSH-minor] Antigens, CD30 / metabolism. Diagnosis, Differential. Humans

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  • (PMID = 20043465.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20RR018757
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 32
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84. Lones MA, Heerema NA, Le Beau MM, Perkins SL, Kadin ME, Kjeldsberg CR, Sposto R, Meadows A, Siegel S, Buckley J, Finlay J, Abromowitch M, Cairo MS, Sanger WG: Complex secondary chromosome abnormalities in advanced stage anaplastic large cell lymphoma of children and adolescents: a report from CCG-E08. Cancer Genet Cytogenet; 2006 Dec;171(2):89-96
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  • [Title] Complex secondary chromosome abnormalities in advanced stage anaplastic large cell lymphoma of children and adolescents: a report from CCG-E08.
  • Among pediatric non-Hodgkin lymphomas, one of the most distinctive types is anaplastic large cell lymphoma (ALCL).
  • Specific chromosomal abnormalities are associated with prognosis in childhood acute lymphoblastic leukemia, but chromosome abnormalities have not been evaluated for prognostic value in pediatric ALCL.
  • For Children's Cancer Group protocol CCG-E-08 Etiologic Study of Non-Hodgkin Lymphoma in Childhood, three patients were enrolled with cytogenetic analysis of ALCL and simultaneously enrolled on treatment protocol CCG-552.
  • Pathology material and karyotypes at initial diagnosis underwent central review.
  • Demographics included ages of 9, 12, and 14 years, and a male/female ratio of 1:2.
  • All patients had advanced disease (stage III).
  • Disease progressed or relapsed in two patients, and one died.
  • In two patients with progressive disease or relapse, additional chromosomal abnormalities at 1q21 and 10q24, possibly involving MCL1 and HOX11/TCL3, respectively, may have contributed to worse outcome.
  • Pediatric ALCL cases frequently have complex karyotypes and usually involve ALK/NPM translocations in this limited study.
  • Additional chromosome abnormalities may be involved in the pathogenesis of ALCL.
  • Further studies are warranted in larger cohorts of children and adolescents with ALCL.
  • [MeSH-major] Chromosome Aberrations. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology

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  • (PMID = 17116485.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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85. Ait-Tahar K, Barnardo MC, Pulford K: CD4 T-helper responses to the anaplastic lymphoma kinase (ALK) protein in patients with ALK-positive anaplastic large-cell lymphoma. Cancer Res; 2007 Mar 1;67(5):1898-901
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  • [Title] CD4 T-helper responses to the anaplastic lymphoma kinase (ALK) protein in patients with ALK-positive anaplastic large-cell lymphoma.
  • We have previously shown both humoral and CTL responses to anaplastic lymphoma kinase (ALK) in patients with ALK-positive anaplastic large-cell lymphoma (ALCL).
  • However, because CD4(+) T-helper (Th) cells also play a vital role in developing and maintaining tumor immunity, we investigated the presence of a CD4(+) Th response in ALK-positive ALCL.
  • Using an IFN-gamma ELISPOT assay, we identified two ALK-derived DRB1-restricted 24-mer promiscuous peptides, ALK1(278-301) and ALK2(233-256), as being immunogenic in six ALK-positive ALCL patients but not in two ALK-negative ALCL patients or five normal subjects.
  • A significant interleukin-4 response to the ALK peptides was detected in only one ALK-positive patient.
  • CD4(+) Th cell lines lysed ALK-positive ALCL cell lines in a MHC class II-restricted manner.
  • This first report of a CD4(+) Th response to ALK provides valuable information for developing future immunotherapeutic options for ALK-positive ALCL patients who fail to respond well to conventional therapies.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / immunology. Protein-Tyrosine Kinases / immunology. T-Lymphocytes, Helper-Inducer / immunology

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  • (PMID = 17332315.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes, T-Lymphocyte; 0 / Peptide Fragments; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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86. Fornari A, Piva R, Chiarle R, Novero D, Inghirami G: Anaplastic large cell lymphoma: one or more entities among T-cell lymphoma? Hematol Oncol; 2009 Dec;27(4):161-70
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  • [Title] Anaplastic large cell lymphoma: one or more entities among T-cell lymphoma?
  • Anaplastic large cell lymphoma (ALCL) is a subtype of peripheral T-cell lymphoma (PTCL) first described in 1985 as a lymphoid malignancy characterized by marked cellular pleomorphism, propensity to grow cohesively, tendency to invade lymph node sinuses and diffuse expression of CD30 1.
  • The discovery of the t(2;5), involving the anaplastic lymphoma kinase (ALK) gene on chromosome 2 and the nucleophosmin (NPM) gene on chromosome 5 in the majority of systemic ALCL, has soon pointed out that ALCL is a clinically and biologically heterogeneous disease.
  • While ALK-positive (ALK+) ALCL is usually characterized by onset in children and young adults and better prognosis, epidemiology, poor outcome and possibly genetic defects of ALK-negative (ALK-) ALCL suggest that this neoplasms should be considered an independent pathological entity.
  • The aim of this review is to illustrate clinical features, histology, immunophenotype, genetics and biology of ALCL and discuss possible relationship(s) among different T-non-Hodgkin lymphoma (T-NHL).
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, T-Cell, Peripheral / pathology

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19358142.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 82
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87. Willenbrock K, Küppers R, Renné C, Brune V, Eckerle S, Weidmann E, Bräuninger A, Hansmann ML: Common features and differences in the transcriptome of large cell anaplastic lymphoma and classical Hodgkin's lymphoma. Haematologica; 2006 May;91(5):596-604
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  • [Title] Common features and differences in the transcriptome of large cell anaplastic lymphoma and classical Hodgkin's lymphoma.
  • BACKGROUND AND OBJECTIVES: Anaplastic large cell lymphoma (ALCL) and classical Hodgkin's lymphoma (HL) are derived from different cell types, namely T cells and B cells, respectively.
  • However, both lymphomas share a similar cytological and immunohistochemical tumor cell phenotype with little resemblance to their cells of origin.
  • DESIGN AND METHODS: In this study, the transcriptional profiles of ALCL cell lines, primary ALCL tumor cells from peripheral blood and HL cell lines were compared to each other and to normal B-cell subsets, B non-Hodgkin's lymphomas (NHL) and B NHL- and Epstein-Barr virus (EBV)-transformed B-cell lines in order to establish their relationship at the transcriptional level and to identify genes with possible pathobiological impact.
  • RESULTS: HL samples clustered separately from ALCL samples, but HL and ALCL were found to be more closely related to each other than to any normal or malignant B-cell sample in the dataset.
  • Their relationship was determined to a large extent, but not exclusively, by lack of expression of B-cell antigens and by the over-expression of mRNA encoding activation markers and structural proteins.
  • Apart from established differences between HL and ALCL, further genes of interest could be identified that distinguish both entities from each other and from the other samples.
  • The differential expression of PRAME, DDR2, SOCS3 and CEBPD in HL and ALCL was confirmed in primary tumor tissue by immunohistochemistry and/or RT-PCR.
  • INTERPRETATION AND CONCLUSIONS: At a transcriptional level HL is more closely related to Alk+ ALCL than to the B-NHL or B-cell samples investigated, although it is a B-cell derived lymphoma.
  • The newly identified genes discriminating HL and ALCL may be pathobiologically important and may serve as possible therapeutic targets.
  • [MeSH-major] Gene Expression Profiling. Hodgkin Disease / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Transcription, Genetic
  • [MeSH-minor] Adult. B-Lymphocytes / metabolism. B-Lymphocytes / pathology. Cell Line, Tumor / metabolism. Cell Transformation, Neoplastic / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Leukemia / blood. Leukemia / genetics. Leukemia / metabolism. Leukemia / pathology. Lymphoma / classification. Lymphoma / genetics. Lymphoma / metabolism. Lymphoma / pathology. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. RNA, Complementary / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16670065.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Complementary; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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88. Shi Y, Chen G, Zhou XG, Gong LP, Yu R, Zheng YY, Xie JL, Jin Y: [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study]. Zhonghua Bing Li Xue Za Zhi; 2010 Apr;39(4):235-9
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  • [Title] [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study].
  • OBJECTIVE: To study the clinicopathologic features of 66 cases of primary systemic anaplastic large cell lymphoma (ALCL), with emphasis on the differences between ALK-positive and ALK-negative cases.
  • METHODS: The clinical data of 66 cases of ALCL was analyzed.
  • Immunohistochemical study for CD30, ALK protein, epithelial membrane antigen, CD2, CD3, granzyme B and TIA-1 was carried out.
  • The differences between ALK-positive and ALK-negative cases were statistically analyzed.
  • RESULTS: There were 48 cases of ALK-positive ALCL and 18 cases of ALK-negative ALCL.
  • The patients with ALK-positive ALCL were younger than those with ALK-negative ALCL (P < 0.05), with the median age being 18 years and 36 years, respectively.
  • Fever, especially hyperpyrexia, was more commonly observed in ALK-positive ALCL patients than in ALK-negative ALCL patients (33 cases versus 4 cases, P < 0.05).
  • The overall survival rate and median duration of survival in patients with ALK-positive ALCL were higher and longer than those in patients with ALK-negative ALCL (80% versus 71%; 21 months versus 12.5 months, P > 0.05).
  • There were however no significant differences in histology between ALK-positive ALCL and ALK-negative ALCL.
  • "Hallmark" cells were seen in most of the ALCL cases.
  • Most ALK-positive cases belonged to the common variant (35 cases).
  • Small cell variant and sarcomatoid subtype were found only in few cases (3 cases and 2 cases, respectively).On the other hand, common variant (17 cases) constituted the majority of ALK-negative ALCL.
  • Immunohistochemical study showed that ALK-positive ALCL always expressed CD30 and epithelial membrane antigen.
  • ALK-positive ALCL more often expressed epithelial membrane antigen (100% versus 72%; P < 0.05) but less so for T-cell markers (including CD2, CD3, CD43 and CD45RO).
  • Cytotoxic molecules were more commonly expressed in ALK-positive ALCL (P > 0.05).
  • FISH showed that in ALK-positive ALCL, 1 case had normal ALK gene, 1 had deletion and multicopy and 2 had deletion.
  • On the other hand, 1 case of ALK-negative ALCL had normal ALK gene.
  • CONCLUSIONS: While there are no significant morphologic differences between ALK-positive ALCL and ALK-negative ALCL, the clinical features, immunophenotypes and genetic features of both groups vary.
  • These differences are helpful in guiding the differential diagnosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antigens, CD30 / metabolism. Child. Child, Preschool. Diagnosis, Differential. Female. Follow-Up Studies. Gene Deletion. Humans. Male. Malignant Hyperthermia / etiology. Middle Aged. Mucin-1 / metabolism. Neoplasm Recurrence, Local. Receptor Protein-Tyrosine Kinases. Survival Rate. Young Adult

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  • (PMID = 20654121.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Mucin-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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89. Rassidakis GZ, Feretzaki M, Atwell C, Grammatikakis I, Lin Q, Lai R, Claret FX, Medeiros LJ, Amin HM: Inhibition of Akt increases p27Kip1 levels and induces cell cycle arrest in anaplastic large cell lymphoma. Blood; 2005 Jan 15;105(2):827-9
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  • [Title] Inhibition of Akt increases p27Kip1 levels and induces cell cycle arrest in anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is a highly proliferative neoplasm that frequently carries the t(2;5)(p23;q35) and aberrantly expresses nucleophosmin-anaplastic lymphoma kinase (NPM-ALK).
  • As the cyclin-dependent kinase (CDK) inhibitor p27(Kip1) (p27) is usually not expressed in ALCL, we hypothesized that activated Akt (pAkt) phosphorylates p27 resulting in increased p27 proteolysis and cell cycle progression.
  • Here we demonstrate that inhibition of pAkt activity in ALCL decreases p27 phosphorylation and degradation, resulting in increased p27 levels and cell cycle arrest.
  • Using immunohistochemistry, pAkt was detected in 24 (57%) of 42 ALCL tumors, including 8 (44%) of 18 ALK-positive tumors and 16 (67%) of 24 ALK-negative tumors, and was inversely correlated with p27 levels.
  • The mean percentage of p27-positive tumor cells was 5% in the pAkt-positive group compared with 26% in the pAkt-negative group (P = .0076).
  • These findings implicate that Akt activation promotes cell cycle progression through inactivation of p27 in ALCL.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins / antagonists & inhibitors. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Cell Division / physiology. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p27. Cytoplasm / metabolism. Down-Regulation. Humans. Proto-Oncogene Proteins c-akt

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  • (PMID = 15374880.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090853
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS8253; NLM/ PMC1382060
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90. Benner MF, Jansen PM, Meijer CJ, Willemze R: Diagnostic and prognostic evaluation of phenotypic markers TRAF1, MUM1, BCL2 and CD15 in cutaneous CD30-positive lymphoproliferative disorders. Br J Dermatol; 2009 Jul;161(1):121-7

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  • [Title] Diagnostic and prognostic evaluation of phenotypic markers TRAF1, MUM1, BCL2 and CD15 in cutaneous CD30-positive lymphoproliferative disorders.
  • BACKGROUND: CD30 is expressed in various types of cutaneous lymphomas, including lymphomatoid papulosis (LyP), primary cutaneous anaplastic large cell lymphoma (C-ALCL), some cases of mycosis fungoides showing large cell transformation (MF-TR) and skin localizations of systemic anaplastic lymphoma kinase (ALK)-positive or ALK-negative ALCL.
  • OBJECTIVE: To evaluate the diagnostic and prognostic significance of these markers in a large group of cutaneous CD30-positive lymphoproliferations.
  • METHODS: An immunohistochemical study on the expression of TRAF1, MUM1, BCL2 and CD15 was performed on skin biopsies from 28 patients with C-ALCL, 39 patients with LyP, 11 patients with CD30-positive MF-TR, two with ALK-positive ALCL and six with ALK-negative ALCL.
  • RESULTS: TRAF1 was expressed in roughly 70-80% and MUM1 was expressed in 70-100% of all the groups of cutaneous CD30-positive lymphoproliferations.
  • Highest levels of BCL2 were expressed in MF-TR (73%), in contrast to 21% in C-ALCL and 36% in LyP.
  • Highest levels of CD15 were expressed in C-ALCL (43%), compared with 18% in LyP and 9% in MF-TR.
  • CONCLUSIONS: The results of the present study suggest that TRAF1, MUM1, BCL2 and CD15 cannot be considered as useful diagnostic or prognostic marker in cutaneous CD30-positive lymphoproliferations.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoproliferative Disorders / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD15 / analysis. Antigens, CD30 / analysis. Biopsy. Child. Female. Humans. Immunohistochemistry / methods. Interferon Regulatory Factors / analysis. Lymphoma, Primary Cutaneous Anaplastic Large Cell / chemistry. Lymphoma, Primary Cutaneous Anaplastic Large Cell / diagnosis. Lymphoma, Primary Cutaneous Anaplastic Large Cell / immunology. Lymphomatoid Papulosis / diagnosis. Lymphomatoid Papulosis / immunology. Lymphomatoid Papulosis / metabolism. Male. Middle Aged. Mycosis Fungoides / chemistry. Mycosis Fungoides / immunology. Mycosis Fungoides / pathology. Proto-Oncogene Proteins c-bcl-2 / analysis. TNF Receptor-Associated Factor 1 / analysis. Young Adult

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  • (PMID = 19416236.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD15; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TNF Receptor-Associated Factor 1; 0 / interferon regulatory factor-4
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91. Hirsch B, Hummel M, Bentink S, Fouladi F, Spang R, Zollinger R, Stein H, Dürkop H: CD30-induced signaling is absent in Hodgkin's cells but present in anaplastic large cell lymphoma cells. Am J Pathol; 2008 Feb;172(2):510-20
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  • [Title] CD30-induced signaling is absent in Hodgkin's cells but present in anaplastic large cell lymphoma cells.
  • High CD30 expression in classical Hodgkin's lymphoma and anaplastic large cell lymphoma (ALCL) suggests an important pathogenic role of this cytokine receptor.
  • To test this hypothesis, we investigated CD30 signaling in Hodgkin's and ALCL cell lines by different approaches:.
  • 1) CD30 stimulation, 2) CD30 down-regulation, and 3) a combination of both.
  • We demonstrate that Hodgkin's cells are virtually CD30 unresponsive.
  • Neither CD30 stimulation nor CD30 silencing of Hodgkin's cells had any significant effect.
  • In contrast, CD30 stimulation of ALCL cells activated nuclear transcription factor-kappaB (NF-kappaB), induced major transcriptional changes, and decreased proliferation.
  • These effects could be abrogated by down-regulation of CD30.
  • Stimulation of CD30 in ALCL cells, stably transfected with a dominant-negative NF-kappaB inhibitor, induced pronounced caspase activation and massive apoptosis.
  • Our data indicate that 1) CD30 signaling is not effective in Hodgkin's cell lines but is effective in ALCL cell lines, 2) CD30 is probably not significantly involved in the pathogenesis of classical Hodgkin's lymphoma, and 3) CD30 stimulation triggers two competing effects in ALCL cells, namely activation of caspases and NF-kappaB-mediated survival.
  • These data suggest that CD30-targeted therapy in ALCL should be combined with NF-kappaB inhibitors to induce effective cell killing.
  • [MeSH-major] Antigens, CD30 / metabolism. Gene Expression Regulation, Neoplastic. Hodgkin Disease / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Apoptosis / physiology. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation. Electrophoretic Mobility Shift Assay. Enzyme Activation / physiology. Flow Cytometry. Gene Expression. Gene Expression Profiling. Humans. Immunoblotting. NF-kappa B / metabolism. Oligonucleotide Array Sequence Analysis. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 18187570.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / NF-kappa B; 0 / RNA, Small Interfering; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC2312360
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92. Staber PB, Noehammer C, Dürkop H, Schauer S, Kenner L, Linkesch W, Hoefler G: mRNA expression patterns indicate CD30 mediated activation of different apoptosis pathways in anaplastic large cell lymphoma but not in Hodgkin's lymphoma. Leuk Res; 2006 Mar;30(3):343-8
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  • [Title] mRNA expression patterns indicate CD30 mediated activation of different apoptosis pathways in anaplastic large cell lymphoma but not in Hodgkin's lymphoma.
  • CD30, a member of the TNFR superfamily is overexpressed in highly proliferating tumors such as anaplastic large cell lymphoma (ALCL) and Hodgkin's lymphoma (HL).
  • CD30 stimulation leads to apoptosis and growth arrest in cultured ALCL, but not in Hodgkin-Reed-Sternberg cells.
  • To identify changes in the transcriptional program responsible for these opposing effects, we performed gene expression analysis in CD30-stimulated ALCL (Karpas 299) and HL (KM-H2) cell lines using cDNA microarrays.
  • Hierarchical clustering was applied to the whole dataset and separated the cell lines clearly with respect to their origin.
  • In HL, there were only minor CD30-specific alterations, whereas ALCL unequivocally showed a pronounced CD30-specific transcriptional response.
  • Ninety-three genes (6.6% of total) were deregulated by more than a factor of two after CD30 stimulation in ALCL cells.
  • The majority of genes identified are involved in cell cycle regulation and apoptosis. mRNA expression patterns further indicate that in contrast to HL, CD30 stimulation in ALCL induces cell death via the CD95-CD95 ligand (CD95L) pathway and the TNF-R1/TNF-R2 crosstalk.
  • These data provide a detailed view on the transcriptional changes upon CD30 stimulation and may explain the observed functional differences of HL and ALCL.
  • [MeSH-major] Antigens, CD30. Apoptosis / genetics. Cell Cycle / genetics. Gene Expression Regulation, Leukemic. Lymphoma, Large B-Cell, Diffuse / genetics. Signal Transduction
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Profiling. Hodgkin Disease / genetics. Hodgkin Disease / metabolism. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 16198418.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD30
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93. Clarke LE, Bayerl MG, Bruggeman RD, Mauger D, Ioffreda MD, Abou-Elella A, Helm KF: Death receptor apoptosis signaling mediated by FADD in CD30-positive lymphoproliferative disorders involving the skin. Am J Surg Pathol; 2005 Apr;29(4):452-9
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  • [Title] Death receptor apoptosis signaling mediated by FADD in CD30-positive lymphoproliferative disorders involving the skin.
  • BACKGROUND: The CD30-positive lymphoproliferative disorders lymphomatoid papulosis (LyP), primary cutaneous anaplastic large cell lymphoma (C-ALCL), and systemic anaplastic large cell lymphoma (S-ALCL) are lesions that overlap clinically, histopathologically, and immunophenotypically.
  • In particular, lesions of LyP regress spontaneously while those of S-ALCL persist and often progress.
  • METHODS: Dual immunohistochemistry for CD30 and activated forms of FADD and caspase 3 was performed on cutaneous biopsy specimens from 27 patients with CD30-positive lymphoproliferative disorders involving the skin.
  • The patients included 18 with primary cutaneous CD30-positive LPDs (15 with LyP and 3 with C-ALCL) and 9 with S-ALCL.
  • RESULTS: The proportion of CD30-positive cells expressing activated FADD was significantly different between primary cutaneous CD30-positive lymphoproliferative disorders and S-ALCL (36.4% vs. 14.5%, P = 0.0083).
  • Expression of cleaved caspase 3 was also significantly different between primary cutaneous lesions and S-ALCL (9.2% vs. 1.9%, P = 0.048).
  • CONCLUSIONS: Although a larger number of cases should be studied to validate these results, these data provide evidence that differences in signaling through the death-receptor apoptosis pathway mediated by FADD may be responsible for the varying biologic behaviors of CD30-positive lymphoproliferative disorders involving the skin.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Antigens, CD30 / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphomatoid Papulosis / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 15767797.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / FADD protein, human; 0 / Fas-Associated Death Domain Protein; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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94. Gorgidze LA, Vorob'ev IA: [A morphometric analysis of the nuclei and nucleoli in tumor cells in lymphogranulomatosis, diffuse large B-cell lymphoma and anaplastic large cell lymphoma]. Ter Arkh; 2009;81(2):71-5
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  • [Title] [A morphometric analysis of the nuclei and nucleoli in tumor cells in lymphogranulomatosis, diffuse large B-cell lymphoma and anaplastic large cell lymphoma].
  • AIM: To make a comparative morphometric analysis of the nuclei and nucleoli of tumor cells in lymphogranulomatosis (LGM), diffuse large B-cell lymphoma (DLBCL) and anaplastic large cell lymphoma (ALCL) for differential diagnosis of these lymphomas.
  • RESULTS: Mean area of tumor cell nuclei in LGM was 97.25 +/- 68.77 mcm2, in DLBCL and ALCL--55.89 +/- 20.13 mcm2 and 70.31 +/- 34.64 mcm2, respectively.
  • Hodgkin's and Berezovsky-Rid-Sternberg cell bucleoli area was the largest (11.44 +/- 7.83 mcm2).
  • Mean area of the nucleoli in DLBCL was 3.05 +/- 1.58, in ALCL--5.53 +/- 4.94 mcm2.
  • CONCLUSION: Nucleoli in Hodgkin 's cells are significantly larger than those in the tumor cells in ALCL and DLBCL and the nucleoli with the area more than 12 mcm2 can be used in differential diagnosis between LGM and DLBCL but not between LGM and ALCL.
  • [MeSH-major] Cell Nucleolus / pathology. Cell Nucleus / pathology. Hodgkin Disease / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Humans


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

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

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  • (PMID = 27960935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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96. Rust R, Harms G, Blokzijl T, Boot M, Diepstra A, Kluiver J, Visser L, Peh SC, Lim M, Kamps WA, Poppema S, van den Berg A: High expression of Mcl-1 in ALK positive and negative anaplastic large cell lymphoma. J Clin Pathol; 2005 May;58(5):520-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of Mcl-1 in ALK positive and negative anaplastic large cell lymphoma.
  • AIM: To gain more insight into the genes involved in the aetiology and pathogenesis of anaplastic large cell lymphoma (ALCL).
  • METHODS: Serial analysis of gene expression (SAGE) was undertaken on the CD4+ALK+ (anaplastic lymphoma kinase positive) ALCL derived cell line Karpas299 and as comparison on CD4+ T cells.
  • Quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry were performed on five ALCL derived cell lines and 32 tissue samples to confirm the SAGE data.
  • RESULTS: High expression of Mcl-1 was seen in the Karpas299 cell line, whereas the two other antiapoptotic Bcl-2 family members, Bcl-2 and Bcl-X(L), were not detected in the SAGE library.
  • Quantitative RT-PCR confirmed the high expression of Mcl-1 mRNA and low expression of Bcl-2 and Bcl-X(L) in Karpas299 and in four other ALCL cell lines.
  • All 23 ALK+ and nine ALK- ALCL cases were positive for Mcl-1.
  • Bcl-2 and Bcl-X(L) were expressed infrequently in ALK+ ALCL cases, but were present in a higher proportion of ALK- ALCL cases.
  • CONCLUSION: The consistent high expression of Mcl-1 in ALK+ and ALK- ALCL suggests that Mcl-1 is the main antiapoptotic protein in this disease.
  • The high frequency of Mcl-1, Bcl-2, and Bcl-X(L) positive ALCL cases in the ALK- group compared with the ALK+ group indicates that ALK induced STAT3 activation is not the main regulatory pathway in ALCL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Neoplasm Proteins / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Apoptosis / genetics. CD4-Positive T-Lymphocytes / physiology. Cell Line, Tumor. Genes, bcl-2 / genetics. Humans. Immunohistochemistry / methods. Myeloid Cell Leukemia Sequence 1 Protein. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction / methods. bcl-X Protein

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  • (PMID = 15858125.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / bcl-X 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
  • [Other-IDs] NLM/ PMC1770666
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97. Marschalkó M, Eros N, Holló P, Hársing J, Bottlik G, Bátai A, Csukly Z, Masszi T, Szentirmai Z, Fodor J, Kárpáti S, Matolcsy A, Csomor J: Secondary ALK negative anaplastic large cell lymphoma in a patient with lymphomatoid papulosis of 40 years duration. Am J Dermatopathol; 2010 Oct;32(7):708-12
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary ALK negative anaplastic large cell lymphoma in a patient with lymphomatoid papulosis of 40 years duration.
  • At age 44, regional lymph node manifestation of anaplastic lymphoma kinase (ALK) anaplastic large cell lymphoma (ALCL) developed.
  • Four years later, systemic relapse was detected which was refractory to therapy.
  • Histology and immunohistochemistry showed congruent characteristics of multiple skin and lymph node biopsies: diffuse mixed infiltrate with large, anaplastic CD30 cells.
  • Immunophenotype and microscopic morphology suggested a common origin of the different manifestations-however, this could not be proven due to lack of T-cell receptor (TCR) gamma gene rearrangement in most of the samples.
  • The diagnosis of ALK-negative systemic ALCL with cutaneous symptoms was set up at the second flare up, however, the possibility of primary cutaneous ALCL was not excluded steadily.
  • Lymphomatoid papulosis, primary cutaneous ALCL, and systemic ALK ALCL are 3 different entities but the separation of them cannot be solved without distinctive diagnostic tools.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphomatoid Papulosis / pathology. Neoplasms, Second Primary / pathology. Skin Neoplasms / pathology

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  • (PMID = 20644462.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [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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98. Kadin ME: Pathobiology of CD30+ cutaneous T-cell lymphomas. J Cutan Pathol; 2006 Feb;33 Suppl 1:10-7
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  • [Title] Pathobiology of CD30+ cutaneous T-cell lymphomas.
  • CD30+ cutaneous lymphoproliferative disorders include lymphomatoid papulosis (LyP) and anaplastic large cell lymphoma (ALCL).
  • LyP is associated with development of lymphoma in nearly 20% of patients.
  • Herein is reviewed the clonal relationship of LyP to malignant lymphoma, the concept of a common stem cell for LyP and associated lymphomas, and the role of genetic instability in lymphomagenesis.
  • The possible role of the CD30+ cell as a regulatory T-cell is introduced and a model for progression of LyP to ALCL is illustrated.
  • [MeSH-major] Antigens, CD30 / metabolism. Lymphoma, T-Cell, Cutaneous / pathology. Skin Neoplasms / pathology

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  • (PMID = 16412208.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50-CA93683
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
  • [Number-of-references] 43
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99. Nagajothi N, Dham SK, Gelfand Y, Sanmugarajah J: Treatment of AIDS-associated anaplastic large-cell lymphoma with dose-adjusted EPOCH chemotherapy. J Natl Med Assoc; 2007 Jul;99(7):799-801
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  • [Title] Treatment of AIDS-associated anaplastic large-cell lymphoma with dose-adjusted EPOCH chemotherapy.
  • Anaplastic large-cell lymphoma (ALCL) has rarely been described in patients with acquired immunodeficiency syndrome (AIDS).
  • Reports of treatment of ALCL in the setting of AIDS are rare as well.
  • Dose-adjusted EPOCH (DA-EPOCH; etoposide, prednisone, vincristine, cyclophosphamide and doxorubicin) has been shown to be well tolerated and effective in the treatment of AIDS-related aggressive B-cell lymphomas.
  • Treatment of AIDS-associated ALCL with DA-EPOCH has not been reported.
  • This report describes two patients with AIDS-associated ALCL treated with DA-EPOCH chemotherapy.
  • Both patients presented with advanced disease.
  • She had an excellent response with rapid improvement of cutaneous disease and lymphadenopathy starting three days after the first cycle.
  • Our experience suggests that DA-EPOCH is an effective treatment for AIDS-associated ALCL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols. Lymphoma, AIDS-Related / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy

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  • (PMID = 17668647.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; EPOCH protocol
  • [Other-IDs] NLM/ PMC2574342
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100. Balachandran I, Walker JW Jr, Broman J: Fine needle aspiration cytology of ALK1(-), CD30+ anaplastic large cell lymphoma post renal transplantation: a case report and literature review. Diagn Cytopathol; 2010 Mar;38(3):213-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fine needle aspiration cytology of ALK1(-), CD30+ anaplastic large cell lymphoma post renal transplantation: a case report and literature review.
  • Epstein-Barr virus (EBV) related non-Hodgkin's lymphomas of B-cell type is more common than those of T-cell origin.
  • CD30 positive Anaplastic Large Cell Lymphoma (ALCL) is a Non-Hodgkin's lymphoma (B or T cell type) that accounts for a small percentage of PTLD's.
  • ALCL of T-cell type are a spectrum of disease ranging from primary cutaneous to systemic nodal ALCL.
  • The systemic nodal ALCL is further subdivided into anaplastic lymphoma kinase-1 (ALK-1) positive or negative.
  • We present an unusual manifestation of ALK-1 negative CD30 positive ALCL in a post renal transplant patient in FNA cytology with all supportive adjuvant studies and differential diagnoses and review the cytology literature on this topic.
  • [MeSH-major] Antigens, CD30 / analysis. Kidney Transplantation / adverse effects. Lymphoma, Large-Cell, Anaplastic / pathology. Mediastinal Neoplasms / pathology. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Carcinoma / diagnosis. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Humans. Immunocompromised Host. Immunohistochemistry. Male. Melanoma / diagnosis. Postoperative Complications. Prednisone / therapeutic use. Receptor Protein-Tyrosine Kinases. Remission Induction. Seminoma / diagnosis. Seminoma / secondary. Testicular Neoplasms / diagnosis. Vincristine / therapeutic use

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  • (PMID = 19774614.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
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