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1. Wu F, Wang P, Zhang J, Young LC, Lai R, Li L: Studies of phosphoproteomic changes induced by nucleophosmin-anaplastic lymphoma kinase (ALK) highlight deregulation of tumor necrosis factor (TNF)/Fas/TNF-related apoptosis-induced ligand signaling pathway in ALK-positive anaplastic large cell lymphoma. Mol Cell Proteomics; 2010 Jul;9(7):1616-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Studies of phosphoproteomic changes induced by nucleophosmin-anaplastic lymphoma kinase (ALK) highlight deregulation of tumor necrosis factor (TNF)/Fas/TNF-related apoptosis-induced ligand signaling pathway in ALK-positive anaplastic large cell lymphoma.
  • The oncogenic fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), found exclusively in a subset of ALK-positive anaplastic large cell lymphoma, promotes tumorigenesis by exerting its constitutively active tyrosine kinase activity.
  • Thus, characterization of the NPM-ALK-induced changes in the phosphoproteome will likely provide insights into the biology of this oncoprotein.
  • GP293 cells transfected with either NPM-ALK or an NPM-ALK mutant with decreased tyrosine kinase activity (negative control) were used.
  • We identified 506 phosphoproteins detectable in NPM-ALK-expressing cells but not in the negative control.
  • Bioinformatics analysis revealed that these phosphoproteins carry a wide diversity of biological functions, some of which have not been described in association with NPM-ALK, such as the tumor necrosis factor (TNF)/Fas/tumor necrosis factor-related apoptosis-induced ligand (TRAIL) signaling pathway and the ubiquitin proteasome degradation pathway.
  • In particular, modulations of the TNF/Fas/TRAIL pathway by NPM-ALK were supported by our antibody microarray data.
  • Further validation of the TNF/Fas/TRAIL pathway was performed in ALK(+) anaplastic large cell lymphoma (ALCL) cell lines with knockdown of NPM-ALK using short interference RNA, resulting in the loss of the tyrosine phosphorylation of tumor necrosis factor receptor-associated protein 1 (TRAP1) and receptor-interacting protein 1, two crucial TNF signaling molecules.
  • Functional analyses revealed that knockdown of TRAP1 facilitated cell death induced by TRAIL or doxorubicin in ALK(+) ALCL cells.
  • This suggests that down-regulation of TRAP1 in combination with TRAIL or doxorubicin might be a potential novel therapeutic strategy for ALK(+) ALCL.
  • These findings demonstrated that our strategy allowed the identification of novel proteins downstream of NPM-ALK that contribute to the maintenance of neoplastic phenotype and holds great potential for future studies of cellular tyrosine kinases in normal states and diseases.


2. Quintanilla-Martinez L, Pittaluga S, Miething C, Klier M, Rudelius M, Davies-Hill T, Anastasov N, Martinez A, Vivero A, Duyster J, Jaffe ES, Fend F, Raffeld M: NPM-ALK-dependent expression of the transcription factor CCAAT/enhancer binding protein beta in ALK-positive anaplastic large cell lymphoma. Blood; 2006 Sep 15;108(6):2029-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM-ALK-dependent expression of the transcription factor CCAAT/enhancer binding protein beta in ALK-positive anaplastic large cell lymphoma.
  • Although C/EBPbeta has important functions in B- and T-cell differentiation, its expression has not been well studied in lymphoid tissues.
  • We, therefore, analyzed its expression by immunohistochemistry and Western blot in normal lymphoid tissues and in 248 well-characterized lymphomas and lymphoma cell lines.
  • Nonneoplastic lymphoid tissues and most B-cell, T-cell, and Hodgkin lymphomas lacked detectable levels of C/EBPbeta.
  • In contrast, most (40 of 45; 88%) cases of ALK-positive anaplastic large cell lymphoma (ALCL) strongly expressed C/EBPbeta.
  • Western blot analysis confirmed C/EBPbeta expression in the ALK-positive ALCLs and demonstrated elevated levels of the LIP isoform, which has been associated with increased proliferation and aggressiveness in carcinomas.
  • Transfection of Ba/F3 and 32D cells with NPM-ALK and a kinase-inhibitable modified NPM-ALK resulted in the induction of C/EBPbeta and demonstrated dependence on NPM-ALK kinase activity.
  • In conclusion, we report the constitutive expression of C/EBPbeta in ALK-positive ALCL and show its relationship to NPM-ALK.
  • We suggest that C/EBPbeta is likely to play an important role in the pathogenesis and unique phenotype of this lymphoma.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / genetics. CCAAT-Enhancer-Binding Protein-beta / metabolism. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Cell Line, Tumor. Gene Expression. Humans. Immunohistochemistry. Lymphoid Tissue / metabolism. Receptor Protein-Tyrosine Kinases. Transfection

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  • (PMID = 16709933.001).
  • [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 / CCAAT-Enhancer-Binding Protein-beta; 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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3. Bordon V, De Paepe P, Dhooge C, Vandecruys E, Benoit Y, Laureys G: Successful treatment with allogeneic bone marrow transplantation of an early relapse of ALK-positive anaplastic large cell lymphoma. Haematologica; 2005 Mar;90(3):ECR19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment with allogeneic bone marrow transplantation of an early relapse of ALK-positive anaplastic large cell lymphoma.
  • [MeSH-major] Bone Marrow Transplantation. Lymphoma, Large-Cell, Anaplastic / therapy


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4. 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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5. Li C, Takino H, Eimoto T, Ishida T, Inagaki A, Ueda R, Suzuki R, Yoshino T, Nakagawa A, Nakamura S, Inagaki H: Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma. Mod Pathol; 2007 Jun;20(6):648-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma.
  • In anaplastic large-cell lymphomas positive for anaplastic lymphoma kinase (ALK) protein, the ALK gene is most commonly fused to the NPM gene, and less commonly to TPM3, TFG, ATIC, and other rare genes.
  • Although this lymphoma is generally associated with a favorable clinical outcome, 25% of the patients die of the disease within 5 years.
  • (1) a sensitive reverse transcription-polymerase chain reaction (RT-PCR) assay for various X-ALK fusion genes, (2) a 5' rapid amplification of cDNA ends (RACE) assay to identify unknown fusion partners, and (3) a real-time RT-PCR assay to quantify the amount of the NPM-ALK fusion transcript.
  • In 26 cases of ALK(+) anaplastic large-cell lymphoma, the RT-PCR assay showed that the ALK was fused to NPM in 21 cases, to TPM3 in three, and to TFG in one.
  • The 5' RACE assay detected ATIC-ALK fusion in the remaining case.
  • The real-time quantitative RT-PCR assay showed that the NPM-ALK transcript was over expressed in four of 20 quantifiable cases.
  • Patients with NPM-ALK overexpression showed a significantly unfavorable overall survival compared with those with a low expression of this transcript.
  • The RT-PCR and 5' RACE assays developed here may be useful for identification of known and unknown gene partners fused to the ALK gene.
  • Overexpression of the NPM-ALK fusion transcript may be associated with a poor prognosis of the patients with ALK(+) anaplastic large-cell lymphomas.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Protein-Tyrosine Kinases / biosynthesis

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  • (PMID = 17464320.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Fixatives; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; 1HG84L3525 / Formaldehyde; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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6. Sung CO, Ko YH, Park S, Kim K, Kim W: Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma. J Korean Med Sci; 2005 Dec;20(6):952-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma.
  • To verify the spectrum of CD99-expressing lymphoid malignancy, an immunohistochemical study for CD99 was carried out in 182 cases of non-Hodgkin's lymphoma, including 21 lymphoblastic lymphomas, 11 small lymphocytic lymphomas, 9 mantle cell lymphomas, 12 follicular lymphomas, 37 diffuse large B cell lymphomas, 18 Burkitt's lymphomas, 28 NK/T-cell lymphomas, 8 angioimmunoblastic T-cell lymphomas, 23 peripheral T-cell lymphomas, unspecified, and 15 systemic anaplastic large cell lymphomas.
  • CD99 was positive in all T-lymphoblastic lymphomas and in 60% of B-lymphoblastic lymphomas.
  • Majority of T and NK cell lymphomas were negative for CD99, except anaplastic large cell lymphomas (ALCLs).
  • Seven of 10 (70%) ALK positive ALCLs expressed CD99, whereas only 1 of 5 (20%) ALK negative ALCLs were positive.
  • Of the mature B-cell lymphomas, 5.4% (2/37) of diffuse large B cell lymphomas and 11.1% (2/18) of Burkitt's lymphomas expressed CD99.
  • In conclusion, CD99 is infrequently expressed in mature B and T cell lymphomas, except ALK-positive ALCL.
  • High expression of CD99 in ALK-positive ALCL is unexpected finding and its biologic and clinical significances have yet to be clarified.
  • [MeSH-major] Antigens, CD / metabolism. Cell Adhesion Molecules / metabolism. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Non-Hodgkin / immunology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16361803.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 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/ PMC2779325
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7. Wang C, Zhang WM, Zhang ZH, Li BZ: [ALK-positive anaplastic large cell lymphoma with obvious nodular growth pattern: report of a case]. Zhonghua Bing Li Xue Za Zhi; 2010 Nov;39(11):779-80
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  • [Title] [ALK-positive anaplastic large cell lymphoma with obvious nodular growth pattern: report of a case].
  • [MeSH-major] Lymph Nodes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Receptor Protein-Tyrosine Kinases / metabolism

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  • (PMID = 21215175.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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8. Niitsu N, Kohri M, Hayama M, Tamaru J, Miura I: ALK-positive anaplastic large cell lymphoma with dic(2;4)(p23;q33). Leuk Res; 2009 Jun;33(6):e23-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ALK-positive anaplastic large cell lymphoma with dic(2;4)(p23;q33).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 4. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / metabolism. Translocation, Genetic

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  • (PMID = 19036440.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [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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9. Liu T, He M, Carlson DL, Hedvat C, Teruya-Feldstein J: ALK-positive anaplastic large cell lymphoma in a patient with chronic lymphocytic leukemia. Int J Surg Pathol; 2010 Oct;18(5):424-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ALK-positive anaplastic large cell lymphoma in a patient with chronic lymphocytic leukemia.
  • This article reports the case of a 59-year-old patient with an 8-year history of chronic lymphocytic leukemia (CLL), prostate carcinoma, and squamous cell carcinoma who developed an ALK-positive anaplastic large cell lymphoma (ALCL).
  • Lymph node and bone marrow biopsies showed 2 distinct morphologic populations: (a) the CLL component showing a diffuse monomorphous infiltrate of small lymphocytes with the typical immunophenotype showing positive CD20, CD5, CD23, and κ light chain restriction and (b) the ALCL component showing large anaplastic pleomorphic cells positive for CD30, CD45, ALK, CD45Ro, CD4, and vimentin.
  • Polymerase chain reaction performed on the lymph node for immunoglobulin heavy chain and T-cell receptor γ and β showed gene rearrangements after macrodissection of morphologically distinct populations, indicating confirmed genetically distinct populations.
  • This case represents the rare occurrence of an ALK-positive ALCL developing in a patient with CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasms, Multiple Primary. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 18794171.001).
  • [ISSN] 1940-2465
  • [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 / DNA, 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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10. Youssif C, Goldenbogen J, Hamoudi R, Carreras J, Viskaduraki M, Cui YX, Bacon CM, Burke GA, Turner SD: Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: a Children's Cancer and Leukaemia Group Study. Genes Chromosomes Cancer; 2009 Nov;48(11):1018-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: a Children's Cancer and Leukaemia Group Study.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) is a T-cell malignancy in which ALK expression is a consequence of the t(2;5) or a variant translocation involving Chromosome 2.
  • Although the t(2;5) product nucleophosmin-ALK has been extensively studied for its transforming properties, very little is known regarding cooperative genetic mutations that may contribute to lymphomagenesis and may predict survival outcome, specifically in a purely pediatric population.
  • We collected biopsy material from 15 UK-resident children with ALK-expressing ALCL.
  • A range of genomic imbalances exist in ALK-expressing ALCL of a pediatric origin, with a greater number associated with poorer overall survival.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19691112.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / DDB1 protein, human; 0 / DNA-Binding Proteins; 0 / HOXB1 homeodomain protein; 0 / Homeodomain Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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11. Matsubara K, Tanaka T, Taki T, Nakagawa A, Nigami H, Tamura A, Fukaya T: [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature]. Rinsho Ketsueki; 2008 May;49(5):325-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature].
  • We report a 10-year-old girl with ATIC-anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • Pathological findings showed that staining of ALK was restricted to the cytoplasm of ALCL cells.
  • ATIC-ALK chimeric transcripts were detected by reverse transcriptase polymerase chain reaction.
  • The patient was assigned to the standard risk group proposed by the international multicenter study for pediatric ALCL, ALCL99.
  • To date, 7 genes have been identified as a fusion partner of ALK, with the highest frequency in nucleophosmin (NPM).
  • Little is known about the clinical implications of subtypes of ALCL harboring each of the 7 fusion genes, especially those of variant fusion genes other than NPM-ALK.
  • In this paper, we review 9 patients with ATIC-ALK-positive ALCL in the literature in addition to discussing our patient.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Oncogene Proteins, Fusion / analysis

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  • (PMID = 18572809.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 18
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12. Bohling SD, Jenson SD, Crockett DK, Schumacher JA, Elenitoba-Johnson KS, Lim MS: Analysis of gene expression profile of TPM3-ALK positive anaplastic large cell lymphoma reveals overlapping and unique patterns with that of NPM-ALK positive anaplastic large cell lymphoma. Leuk Res; 2008 Mar;32(3):383-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of gene expression profile of TPM3-ALK positive anaplastic large cell lymphoma reveals overlapping and unique patterns with that of NPM-ALK positive anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) comprises a group of non-Hodgkin lymphomas characterized by the expression of the CD30/Ki-1 antigen.
  • A subset of ALCL is characterized by chromosomal translocations involving the anaplastic lymphoma kinase (ALK) gene on chromosome 2.
  • While the most common translocation is the t(2;5)(p23;q35) involving the nucleophosmin (NPM) gene on chromosome 5, up to 12 other translocations partners of the ALK gene have been identified.
  • One of these is the t(1;2)(q25;p23) which results in the formation of the chimeric protein TPM3-ALK.
  • While several of the signaling pathways induced by NPM-ALK have been elucidated, those involved in ALCLs harboring TPM3-ALK are largely unknown.
  • In order to investigate the expression profiles of ALCLs carrying the NPM-ALK and TPM3-ALK fusions, we carried out cDNA microarray analysis of two ALCL tissue samples, one expressing the NPM-ALK fusion protein and the other the TPM3-ALK fusion protein.
  • Our results show a significant overlap of genes deregulated in the NPM-ALK and TPM-ALK positive lymphomas.
  • These deregulated genes are involved in diverse cellular functions, such as cell cycle regulation, apoptosis, proliferation, and adhesion.
  • More importantly, many genes that were not previously associated with ALK positive lymphomas were identified.
  • Our results demonstrate the overlapping and unique transcriptional patterns associated with the NPM-ALK and TPM3-ALK fusions in ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Tropomyosin / genetics

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  • (PMID = 17720243.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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13. Andorsky DJ, Yamada R, Steward K, De Vos S, Said J, Timmerman J: Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells. J Clin Oncol; 2009 May 20;27(15_suppl):8526

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

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  • (PMID = 27960901.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Shi X, Franko B, Frantz C, Amin HM, Lai R: JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells. Br J Haematol; 2006 Oct;135(1):26-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells.
  • As STAT3 activation is pathogenetically important in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ ALCL), we investigated whether JSI-124 can mediate significant inhibitory effects in this cell type.
  • In two ALK+ ALCL cell lines (Karpas 299 and SU-DHL-1), JSI-124 significantly reduced the number of viable cells to 50% of that of negative controls at a dose of 5-10 micromol/l at 24 h and 1-1.25 micromol/l at 48 h.
  • Interestingly, JSI-124 also dramatically decreased the protein levels of JAK3 and nucleophosmin (NPM)-ALK, and these effects were reversible by MG132.
  • Our data support that JSI-124 is a potentially useful therapeutic agent for ALK+ ALCL.
  • In addition to its role as a tyrosine kinase inhibitor, JSI-124 appears to be involved in regulating proteosome degradation for proteins such as JAK3 and NPM-ALK.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Triterpenes / pharmacology

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  • (PMID = 16939498.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / JAK3 protein, human; 0 / Triterpenes; 2222-07-3 / cucurbitacin I; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 3
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15. Daneshbod Y, Oryan A, Khojasteh HN, Rasekhi A, Ahmadi N, Mohammadianpanah M: Primary ALK-positive anaplastic large cell lymphoma of the breast: a case report and review of the literature. J Pediatr Hematol Oncol; 2010 Mar;32(2):e75-8
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  • [Title] Primary ALK-positive anaplastic large cell lymphoma of the breast: a case report and review of the literature.
  • BACKGROUND: Non-Hodgkin lymphomas of the breast are uncommon, which represent less than 1% of all breast malignancies and predominantly are of B-cell origin.
  • OBSERVATION: In this report, a rare case of anaplastic lymphoma kinase (ALK)-positive anaplastic large T-cell lymphoma in the breast of a 16-year-old female without breast implant is described.
  • The immunohistochemical profile showed positivity for CD30 and ALK and confirmed the diagnosis of ALK-positive anaplastic large T-cell lymphoma of the breast.
  • CONCLUSION: Anaplastic large T-cell lymphoma of the breast is rare, and can clinically mimic inflammatory breast carcinoma in adolescence.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / analysis

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  • (PMID = 20168249.001).
  • [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; 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] 33
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16. Alsop S, Sanger WG, Elenitoba-Johnson KS, Lim MS: Chronic myeloid leukemia as a secondary malignancy after ALK-positive anaplastic large cell lymphoma. Hum Pathol; 2007 Oct;38(10):1576-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myeloid leukemia as a secondary malignancy after ALK-positive anaplastic large cell lymphoma.
  • The development of Philadelphia chromosome-positive chronic myelogenous leukemia (CML) in the adolescent population is very rare.
  • CML occurring as a secondary malignancy in individuals treated for anaplastic large cell lymphoma (ALCL) is also rare.
  • We present the case of a 16-year-old adolescent boy who developed a right orbital mass that was diagnosed as ALCL with the t(2;5)(p23;q25) chromosomal aberration.
  • Four years after receiving treatment for ALCL, he presented with a swollen leg and a white cell count of 431,000.
  • We present the histopathologic, molecular, and cytogenetic findings of this patient's initial presentation with systemic ALCL as well as his secondary presentation with CML 4 years later.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Neoplasms, Second Primary / pathology. Protein-Tyrosine Kinases / metabolism


17. Damm-Welk C, Busch K, Burkhardt B, Schieferstein J, Viehmann S, Oschlies I, Klapper W, Zimmermann M, Harbott J, Reiter A, Woessmann W: Prognostic significance of circulating tumor cells in bone marrow or peripheral blood as detected by qualitative and quantitative PCR in pediatric NPM-ALK-positive anaplastic large-cell lymphoma. Blood; 2007 Jul 15;110(2):670-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of circulating tumor cells in bone marrow or peripheral blood as detected by qualitative and quantitative PCR in pediatric NPM-ALK-positive anaplastic large-cell lymphoma.
  • Clinical and histopathological characteristics have limited prognostic value for children with anaplastic large-cell lymphoma (ALCL).
  • We evaluated the presence, extent, and prognostic impact of circulating tumor cells in bone marrow (BM) and peripheral blood (PB) of children and adolescents with NPM-ALK-positive ALCL at diagnosis using qualitative and quantitative polymerase chain reaction (PCR) for NPM-ALK.
  • Numbers of NPM-ALK transcripts were normalized to 10(4) copies ABL (NCNs).
  • BM was positive for NPM-ALK in 47.5% of patients, and positivity was significantly correlated with clinical stage, mediastinal or visceral involvement, microscopic BM involvement, and histologic subtype.
  • BM PCR was associated with the cumulative incidence of relapses (CI-Rs): CI-R was 50% +/- 10% for 38 PCR-positive and 15% +/- 7% for 42 PCR-negative patients (P < .001).
  • Sixteen patients with more than 10 NCNs NPM-ALK in BM had a CI-R of 71% +/- 14% compared with a CI-R of 18% +/- 6% for 59 patients with 10 or fewer NCNs (P < .001).
  • [MeSH-major] Bone Marrow Cells / physiology. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 17392503.001).
  • [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 / DNA Primers; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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18. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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 in our case series with leukemic phase ALCL exhibited rare clinical features.
  • 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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19. Castillo J, Milani C, Pantanowitz L: HIV-associated anaplastic large cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19563

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIV-associated anaplastic large cell lymphoma.
  • : e19563 Background: Anaplastic large cell lymphoma (ALCL) is a CD30+ T-cell lymphoma that is generally unrelated to EBV in the non-HIV setting.
  • Based upon anaplastic lymphoma kinase (ALK) expression, the new WHO classification provisionally distinguishes between ALK+ (favorable) and ALK- (unfavorable) ALCL.
  • The characteristics of ALCL, such as ALK expression and EBV coinfection, in individuals with HIV infection have not been adequately evaluated.
  • The aim of this study was to investigate these features in HIV-associated ALCL cases.
  • METHODS: A MEDLINE search for all cases of HIV-associated non-cutaneous ALCL was undertaken.
  • Data regarding patient age, gender, HIV status (CD4 count, viral load, opportunistic infections), HAART, lymphoma features (B symptoms, stage, sites of involvement, immunophenotype, ALK expression, molecular studies), EBV coinfection, therapy and outcome (survival, cause of death) were extracted and analyzed.
  • ALCL was extranodal in 22 cases (96%) affecting most commonly lung, soft tissue and liver.
  • T-cell receptor gene rearrangement was present in all cases, CD30 was positive in 22 (96%), and the vast majority (90%) were ALK-negative.
  • Therapy for ALCL was documented in 15 (67%) cases; 64% received CHOP.
  • Death was caused by either lymphoma progression (42%) or infection (58%).
  • CONCLUSIONS: HIV-associated non-cutaneous ALCL appears to affect younger individuals and is associated with EBV infection in a subset of cases.
  • Apart from marked immunosuppression, the poor prognosis of HIV-associated ALCL appears to be related to the absence of ALK expression, advanced stage at presentation with prominent extranodal disease, inadequate therapy including HAART, and poor response to CHOP.
  • Further research is needed to better understand and treat this unique HIV-associated lymphoma.

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  • (PMID = 27961064.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Patel P, Godwin J, Velankar M, Alkan S: Nodal ALK positive anaplastic large cell lymphoma of the axilla with spontaneous regression. Leuk Lymphoma; 2007 Jun;48(6):1250-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nodal ALK positive anaplastic large cell lymphoma of the axilla with spontaneous regression.
  • [MeSH-major] Axilla. Lymph Nodes / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Neoplasm Regression, Spontaneous. Protein-Tyrosine Kinases / genetics

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  • (PMID = 17577798.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [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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21. Krishnan C, Moline S, Anders K, Warnke RA: Intravascular ALK-positive anaplastic large-cell lymphoma mimicking inflammatory breast carcinoma. J Clin Oncol; 2009 May 20;27(15):2563-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intravascular ALK-positive anaplastic large-cell lymphoma mimicking inflammatory breast carcinoma.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adult. Antigens, CD30 / biosynthesis. Biomarkers, Tumor / metabolism. Cellulitis / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Inflammation / pathology. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19364961.001).
  • [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] 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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22. Han Y, Amin HM, Frantz C, Franko B, Lee J, Lin Q, Lai R: Restoration of shp1 expression by 5-AZA-2'-deoxycytidine is associated with downregulation of JAK3/STAT3 signaling in ALK-positive anaplastic large cell lymphoma. Leukemia; 2006 Sep;20(9):1602-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Restoration of shp1 expression by 5-AZA-2'-deoxycytidine is associated with downregulation of JAK3/STAT3 signaling in ALK-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALK+ ALCL) is characterized by constitutive activation of the Janus kinase (JAK)3/signal transducers and activators of transcription 3 (STAT3) signaling pathway.
  • SHP1, a tyrosine phosphatase that negatively regulates JAK/STAT, is frequently absent in ALK+ ALCL owing to gene methylation.
  • To test the hypothesis that loss of SHP1 contributes to JAK3/STAT3 activation in ALK+ ALCL cells, we induced SHP1 expression using 5-aza-2'-deoxycytidine (5-AZA), an inhibitor of DNA methyltransferase, in ALK+ ALCL cell lines, and correlated with changes in the JAK3/STAT3 pathway.
  • 5-AZA induced no significant increase in apoptosis but it sensitized ALCL cells to doxorubicin-induced apoptosis.
  • Our findings support the concept that loss of SHP1 contributes to the constitutive activation of JAK3/STAT3 in ALK+ ALCL cells.
  • [MeSH-major] Azacitidine / analogs & derivatives. Down-Regulation / drug effects. Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / metabolism. STAT3 Transcription Factor / metabolism. Signal Transduction
  • [MeSH-minor] Apoptosis / drug effects. Base Sequence. Blotting, Western. Cell Cycle. Cell Line. DNA Primers. Doxorubicin / pharmacology. Humans. Janus Kinase 3. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Receptor Protein-Tyrosine Kinases

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  • (PMID = 16871283.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Intracellular Signaling Peptides and Proteins; 0 / JAK3 protein, human; 0 / STAT3 Transcription Factor; 776B62CQ27 / decitabine; 80168379AG / Doxorubicin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.48 / Protein Tyrosine Phosphatases; M801H13NRU / Azacitidine
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23. Hwang YY, Liang RH: An update in management of noncutaneous T-cell lymphomas. Adv Hematol; 2010;2010:424786

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An update in management of noncutaneous T-cell lymphomas.
  • T-cell lymphoma is a heterogeneous group of diseases.
  • Except for ALK positive anaplastic large cell lymphoma, T-cell lymphoma responds to conventional chemotherapy unfavourably, and most patients carry poor prognosis.
  • In recent years, efforts have been made to improve the outcome of T-cell lymphoma patients.
  • Novel agents, high-dose therapy, and allogeneic stem cell transplantation are studied, and various results are reported in literature.
  • This paper looks into the prognostication and treatment approach of different entities of noncutaneous T-cell lymphoma and would focus on the latest updates in its management.

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  • (PMID = 21188274.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3003949
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24. Lamant L, Pileri S, Sabattini E, Brugières L, Jaffe ES, Delsol G: Cutaneous presentation of ALK-positive anaplastic large cell lymphoma following insect bites: evidence for an association in five cases. Haematologica; 2010 Mar;95(3):449-55
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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 of ALK-positive anaplastic large cell lymphoma following insect bites: evidence for an association in five cases.
  • BACKGROUND: Skin involvement is frequent in ALK-positive anaplastic large cell lymphomas.
  • DESIGN AND METHODS: We retrospectively investigated five cases of ALK-positive anaplastic large cell lymphoma who presented with skin lesions occurring after an insect bite.
  • Biopsies were immunostained with antibodies against CD30, ALK, T- and B-cell antigens.
  • In four cases the correct diagnosis was delayed due to misinterpretation of the findings as a reactive infiltrate in the skin (n=2) or lymph nodes (n=2); all cases subsequently showed small numbers of cells with nuclear and cytoplasmic staining for ALK.
  • The final diagnoses were lymphohistiocytic variant (n=3) and composite common/small cell type (n=2) anaplastic large cell lymphoma.
  • CONCLUSIONS: In these cases the sequence of events between the insect bites and the occurrence of both skin lesions and satellite lymphadenopathy suggest a direct relationship between the bite and the presentation with anaplastic large cell lymphoma.
  • The subsequent release of cytokines at the site of the bite could act as a 'second hit', eliciting activation of the latter cells, which would then express the oncogenic NPM-ALK protein and undergo uncontrolled proliferation.

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  • (PMID = 19951975.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [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] Italy
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2833075
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25. Driss M, Abbes I, Mrad K, Sassi S, Oubich F, Barsaoui S, Romdhane KB: Primary CD30/ALK-1 positive anaplastic large cell lymphoma of the skeletal muscle in a child. Pathologica; 2009 Apr;101(2):97-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary CD30/ALK-1 positive anaplastic large cell lymphoma of the skeletal muscle in a child.
  • Anaplastic large cell lymphoma (ALCL) represents approximately 10 to 30% of all childhood non-Hodgkin lymphomas.
  • Biopsy of the lesion showed large anaplastic cells with voluminous and abundant cytoplasm as well as folded nuclei.
  • The tumour cells were positive for CD30, CD3, EMA and ALK-1.
  • This case emphasizes the occurrence of anaplastic large cell lymphoma in the soft tissue and the favourable outcome of ALK-positive anaplastic large cell lymphoma.
  • [MeSH-major] Activin Receptors, Type II / biosynthesis. Antigens, CD30 / biosynthesis. Lymphoma, Large-Cell, Anaplastic / pathology. Muscle Neoplasms / pathology. Muscle, Skeletal / pathology

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  • (PMID = 19886557.001).
  • [ISSN] 0031-2983
  • [Journal-full-title] Pathologica
  • [ISO-abbreviation] Pathologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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26. Kelleher FC, McDermott R: The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene. Eur J Cancer; 2010 Sep;46(13):2357-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene.
  • The anaplastic lymphoma kinase gene (ALK) is a gene on chromosome 2p23 that has expression restricted to the brain, testis and small intestine but is not expressed in normal lymphoid tissue.
  • This gene was originally established as being implicated in the pathogenesis of rare diseases including inflammatory myofibroblastic tumour (IMT) and ALK-positive anaplastic large cell lymphoma, which is a subtype of non-Hodgkin's lymphoma.
  • Recently the number of diseases in which ALK is implicated in their pathogenesis has increased.
  • In 2007, an inversion of chromosome 2 involving ALK and a fusion partner gene in a subset of non-small cell lung cancer was discovered.
  • In 2008, publications emerged implicating ALK in familial and sporadic cases of neuroblastoma, a childhood cancer of the sympatho-adrenal system.
  • Chromosomal abnormalities involving ALK are translocations, amplifications or mutations.
  • Chromosomal translocations are the longest recognised ALK genetic abnormality.
  • When translocations occur a fusion gene is created between ALK and a gene partner.
  • This has been described in ALK-positive anaplastic large cell lymphoma in which ALK is fused to NPM (nucleolar protein gene) and in non-small cell lung cancer where ALK is fused to EML4 (Echinoderm microtubule-associated protein 4).
  • The most frequently described partner genes in inflammatory myofibroblastic tumour are tropomyosin 3/4 (TMP3/4), however in IMTs a diversity of ALK fusion partners have been found, with the ability to homodimerise a common characteristic.
  • Point mutations and amplification of the ALK gene occur in the childhood cancer neuroblastoma.
  • Therapeutic targeting of ALK fusion genes using tyrosine kinase inhibition, vaccination using an ALK specific antigen and treatment using viral vectors for RNAi are emerging potential therapeutic possibilities.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / therapy. Drug Synergism. Gene Amplification. Humans. Lung Neoplasms / genetics. Lung Neoplasms / therapy. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Mutation / genetics. Neuroblastoma / genetics. Neuroblastoma / therapy. Pyrimidines / therapeutic use. Pyrroles / therapeutic use. Receptor Protein-Tyrosine Kinases. Receptor, IGF Type 1 / antagonists & inhibitors

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20451371.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GSK 1838705A; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase
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27. Damm-Welk C, Schieferstein J, Schwalm S, Reiter A, Woessmann W: Flow cytometric detection of circulating tumour cells in nucleophosmin/anaplastic lymphoma kinase-positive anaplastic large cell lymphoma: comparison with quantitative polymerase chain reaction. Br J Haematol; 2007 Aug;138(4):459-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flow cytometric detection of circulating tumour cells in nucleophosmin/anaplastic lymphoma kinase-positive anaplastic large cell lymphoma: comparison with quantitative polymerase chain reaction.
  • Quantification of occult circulating tumour cells in blood or bone marrow (BM) enables the identification of patients with a high risk for relapse in nucleophosmin/anaplastic lymphoma kinase (NPM-ALK)-positive anaplastic large cell lymphoma (ALCL).
  • We have developed a flow cytometric (FCM) assay to quantify the rare ALK- and CD30-positive ALCL cells.
  • When ALCL cells were admixed with normal peripheral blood or BM, ALK- and CD30-positive cells could be detected above background level at an added concentration of 10(-5) for all three cell lines tested.
  • Sensitivity and costs of the assay were compared with quantitative real-time polymerase chain reaction (PCR) for NPM-ALK.
  • The results of the FCM assay and quantitative PCR for NPM-ALK correlated.
  • Both methods were compared on BM or blood samples from 11 ALCL patients.
  • FCM using antibodies against ALK and CD30 can sensitively and specifically detect the circulating ALCL cells in BM or blood.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Neoplastic Cells, Circulating / pathology

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  • (PMID = 17608768.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / Nuclear Proteins; 0 / RNA, Messenger; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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28. de Leval L, Bisig B, Thielen C, Boniver J, Gaulard P: Molecular classification of T-cell lymphomas. Crit Rev Oncol Hematol; 2009 Nov;72(2):125-43

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular classification of T-cell lymphomas.
  • T-cell neoplasms encompass a heterogeneous group of relatively rare disease entities.
  • This review, focused on lymphoblastic tumors (T-ALL/LBL) and nodal-based peripheral T-cell lymphomas (PTCL), summarizes recent advances in the molecular characterization of these diseases.
  • Angioimmunoblastic T-cell lymphoma (AITL), one of the most common PTCL entities, comprises neoplastic cells with a molecular signature similar to normal follicular helper T cells, and this cellular derivation might account for several of the peculiar aspects of this disease.
  • Except in ALK-positive anaplastic large cell lymphoma, defined by ALK gene fusions, chromosomal translocations are otherwise rare in PTCLs, but some recurrent rearrangements might be associated with distinct lymphoma subtypes.
  • [MeSH-major] Biomarkers, Tumor / genetics. Lymphoma, T-Cell / classification. Lymphoma, T-Cell / genetics

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  • (PMID = 19233683.001).
  • [ISSN] 1879-0461
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 111
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29. Savage KJ: Aggressive peripheral T-cell lymphomas (specified and unspecified types). Hematology Am Soc Hematol Educ Program; 2005;:267-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive peripheral T-cell lymphomas (specified and unspecified types).
  • Peripheral T-cell lymphomas (PTCLs) are a biologically diverse and uncommon group of diseases.
  • Compared to their B-cell counterparts, PTCLs remain largely unexplored and the optimal treatment ill-defined due to disease rarity and biological heterogeneity.
  • For the majority of PTCL subtypes, prognosis is poor with a 5-year overall survival of approximately 30% in most series.The notable exception is ALK-positive anaplastic large-cell lymphoma (ALK-pos ALCL), which has a superior outcome.

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  • [ErratumIn] Hematology Am Soc Hematol Educ Program. 2006;()
  • (PMID = 16304391.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Gustafson S, Medeiros LJ, Kalhor N, Bueso-Ramos CE: Anaplastic large cell lymphoma: another entity in the differential diagnosis of small round blue cell tumors. Ann Diagn Pathol; 2009 Dec;13(6):413-27
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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: another entity in the differential diagnosis of small round blue cell tumors.
  • We saw in consultation a biopsy specimen from a 6-year old girl with anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • Immunohistochemical workup with a large panel of antibodies at another institution showed immunoreactivity for NB84 and neuron specific enolase (dim).
  • Antibodies specific for CD3, CD20, and CD45/LCA were negative; CD30 or ALK were not assessed.
  • At the time of our review, we considered the possibility of ALCL.
  • Immunohistochemical analysis for CD30 showed bright, uniform expression and ALK was positive in a nuclear and cytoplasmic pattern, confirming the diagnosis of ALK+ ALCL.
  • The purpose of this review is to discuss ALK+ ALCL and many of the other entities included under the rubric of small round blue cell tumor, with a focus on tumors that occur in children.
  • [MeSH-major] Lymphoma / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasms, Complex and Mixed / pathology. Neuroblastoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Rhabdomyosarcoma / pathology. Sarcoma, Ewing / pathology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Child. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Immunohistochemistry. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases


31. Drakos E, Atsaves V, Schlette E, Li J, Papanastasi I, Rassidakis GZ, Medeiros LJ: The therapeutic potential of p53 reactivation by nutlin-3a in ALK+ anaplastic large cell lymphoma with wild-type or mutated p53. Leukemia; 2009 Dec;23(12):2290-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The therapeutic potential of p53 reactivation by nutlin-3a in ALK+ anaplastic large cell lymphoma with wild-type or mutated p53.
  • p53 is expressed frequently, but is rarely mutated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) tumours.
  • We show that nutlin-3a activates p53 in ALK+ ALCL cells carrying a wild type (wt) or mutated but partially functional p53 gene resulting in p53-dependent cell-cycle arrest and apoptosis.
  • Cell-cycle arrest was associated with upregulation of the cyclin-dependent kinase inhibitor p21.
  • Nutlin-3a-induced apoptotic cell death was accompanied by Bax and Puma upregulation, downregulation of Bcl-xl, survivin, and caspase-3 cleavage, and this was reduced when p53-dependent transactivation activity was inhibited by pifithrin-alpha, or when pifithrin-mu was used to inhibit direct p53 targeting of mitochondria.
  • Nutlin-3a sensitized the activation of the extrinsic apoptotic pathway in wt-p53 ALK+ ALCL cells, in part, through upregulation of DR-5 and downregulation of c-Flip(S/L), and was synergistic with TRAIL in cell death induction.
  • In addition, nutlin-3a treatment enhanced doxorubicin cytotoxicity against ALK+ ALCL cells harbouring mt p53, and this was associated with p73 upregulation.
  • These data suggest that disruption of the p53-mdm2 interaction by nutlin-3a offers a novel therapeutic approach for ALK+ ALCL patients.
  • [MeSH-major] Imidazoles / pharmacology. Lymphoma, Large-Cell, Anaplastic / drug therapy. Mutation. Piperazines / pharmacology. Tumor Suppressor Protein p53 / drug effects
  • [MeSH-minor] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. Cell Cycle. Cell Line, Tumor. Doxorubicin / pharmacology. Drug Synergism. Humans. TNF-Related Apoptosis-Inducing Ligand / pharmacology


32. Monaco S, Tsao L, Murty VV, Nandula SV, Donovan V, Oesterheld J, Bhagat G, Alobeid B: Pediatric ALK+ anaplastic large cell lymphoma with t(3;8)(q26.2;q24) translocation and c-myc rearrangement terminating in a leukemic phase. Am J Hematol; 2007 Jan;82(1):59-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric ALK+ anaplastic large cell lymphoma with t(3;8)(q26.2;q24) translocation and c-myc rearrangement terminating in a leukemic phase.
  • Pediatric ALK-positive anaplastic large cell lymphoma (ALK+ ALCL) is usually associated with a favorable prognosis.
  • ALK+ ALCL associated with a leukemic phase is uncommon, but has been associated with an aggressive clinical course and unfavorable prognosis.
  • Overexpression of c-myc has been shown to be a consistent finding in ALK+, but not ALK-negative ALCL (ALK- ALCL), and the c-myc gene is considered a downstream target of deregulated ALK signaling.
  • We describe a pediatric ALK+ ALCL with a leukemic phase at relapse.
  • Lymphoma cells showed aberrant ALK expression and c-myc overexpression.
  • The findings in this case demonstrate the association of peripheral blood leukemic involvement and aggressive clinical course, and suggest that other factors, such as c-myc rearrangement, may be responsible for the aggressive clinical behavior in ALK+ ALCL.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Gene Rearrangement. Leukemia / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins c-myc / genetics. Translocation, Genetic

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  • (PMID = 16955462.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc; 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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33. Ait-Tahar K, Damm-Welk C, Burkhardt B, Zimmermann M, Klapper W, Reiter A, Pulford K, Woessmann W: Correlation of the autoantibody response to the ALK oncoantigen in pediatric anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor dissemination and relapse risk. Blood; 2010 Apr 22;115(16):3314-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation of the autoantibody response to the ALK oncoantigen in pediatric anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor dissemination and relapse risk.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) constitutes an ideal model disease to study tumor-specific immune responses.
  • All the tumor cells express oncogenic ALK resulting from a chromosomal translocation involved in lymphomagenesis.
  • Although antibodies and T-cell responses to ALK have previously been detected in ALK-positive ALCL patients, their prognostic significance is unknown.
  • We investigated a large cohort of uniformly treated ALK-positive pediatric ALCL patients to ascertain whether the titers of preexisting ALK autoantibodies correlated with clinical and histologic characteristics, tumor dissemination, and patient outcome.
  • ALK autoantibodies were analyzed in pretherapeutic serum samples from 95 patients enrolled into 2 therapy studies between 1996 and 2007.
  • ALK autoantibodies were detected in 87/95 patients.
  • Our results provide the first clinical evidence that a robust preexisting immune response to an oncoantigen resulting from an oncogenic chromosomal translocation inhibits lymphoma dissemination and decreases the risk of relapse.
  • [MeSH-major] Autoantibodies / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasm Recurrence, Local / immunology. Protein-Tyrosine Kinases / immunology

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  • (PMID = 20185586.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Autoantigens; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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34. Reimer P, Hentrich M: [Peripheral T-cell lymphoma: diagnosis and treatment]. Dtsch Med Wochenschr; 2006 Mar 31;131(13):685-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Peripheral T-cell lymphoma: diagnosis and treatment].
  • Peripheral T/NK-cell lymphomas (PTCL) comprise a heterogeneous group of rare diseases accounting for approximately 10-15% of all non-Hodgkin"s lymphomas.
  • Compared to B-cell lymphomas, PTCL more frequently involve extranodal sites and have a worse prognosis.
  • Because of their usually indolent course, primary cutaneous T/NK-cell lymphomas should be distinguished from the other PTCL.
  • The International Prognostic Index, established for aggressive B-cell lymphomas, has also proved relevant for PTCL.
  • Apart from (ALK-positive) anaplastic large cell lymphoma it thus gives poorer results than those obtained in patients with aggressive B-cell lymphomas.
  • Data for high-dosage therapy with autologous stem cell transplantation (autoSCT) for relapsing and refractory PTCL are similar to those reported for aggressive B-cell lymphomas.
  • Allogeneic stem cell transplantation following reduced conditioning regimens has also given promising results in patients with relapse.
  • [MeSH-major] Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / therapy
  • [MeSH-minor] Humans. Stem Cell Transplantation. Survival Analysis. Transplantation, Homologous

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  • [CommentIn] Dtsch Med Wochenschr. 2006 Aug 25;131(34-35):1884; author reply 1884 [16915558.001]
  • (PMID = 16555177.001).
  • [ISSN] 0012-0472
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 56
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35. Corradini P, Tarella C, Zallio F, Dodero A, Zanni M, Valagussa P, Gianni AM, Rambaldi A, Barbui T, Cortelazzo S: Long-term follow-up of patients with peripheral T-cell lymphomas treated up-front with high-dose chemotherapy followed by autologous stem cell transplantation. Leukemia; 2006 Sep;20(9):1533-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term follow-up of patients with peripheral T-cell lymphomas treated up-front with high-dose chemotherapy followed by autologous stem cell transplantation.
  • We report the results of two prospective phase II studies investigating the role of high-dose sequential chemotherapy, followed by autologous stem cell transplantation (ASCT) in 62 patients with advanced stage peripheral T-cell lymphomas (PTCLs) at diagnosis.
  • Conditioning regimen consisted of mitoxantrone (60 mg/m2) and melphalan (180 mg/m2) or carmustine, etoposide, Ara-C and melphalan followed by peripheral blood stem cell autografting.
  • OS and EFS were significantly better in patients with anaplastic lymphoma-kinase (ALK)-positive anaplastic large-cell lymphoma (ALCL), as compared with the remaining PTCL.
  • In conclusion, our findings indicate (1) up-front high-dose therapy and ASCT are feasible, but could induce a high rate of long-term CR only in patients with ALK-positive ALCL and (2) the achievement of CR before autografting is a strong predictor of better survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, T-Cell / drug therapy. Lymphoma, T-Cell / surgery. Stem Cell Transplantation

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  • (PMID = 16871285.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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36. Momose S, Tamaru J, Kishi H, Mikata I, Mori M, Toyozumi Y, Itoyama S: Hyperactivated STAT3 in ALK-positive diffuse large B-cell lymphoma with clathrin-ALK fusion. Hum Pathol; 2009 Jan;40(1):75-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hyperactivated STAT3 in ALK-positive diffuse large B-cell lymphoma with clathrin-ALK fusion.
  • Anaplastic lymphoma kinase (ALK)-positive large B-cell lymphoma is a rare subtype of diffuse large B-cell lymphoma (DLBCL).
  • Although a few cases of ALK-positive large B-cell lymphoma harbor nucleophosmin-ALK chromosomal translocation similar to ALK-positive anaplastic large cell lymphoma, most reported cases are characterized by t(2;17)(p23;q23) involving the clathrin gene.
  • Here, we report 2 cases of ALK-positive DLBCL.
  • The 2 cases presented similar morphologic features and immunohistochemical characteristics, that is, positivity for ALK, IgA, CD138, and MUM1; weak positivity for CD30 and CD79a; and negativity for CD20.
  • The clathrin-ALK transcript was identified by reverse transcription-polymerase chain reaction, and the sequence was determined by direct sequencing.
  • Recently, the essential role of STAT3 activation as well as STAT 5 activation in nucleophosmin-ALK fusion protein-mediated lymphomagenesis was reported.
  • However, differential effects of ALK-fusion variant proteins on proliferation, transformation, and invasion properties were reported.
  • Thus, we evaluated the phosphorylation status of STAT 3 and STAT 5, and found highly hyperphosphorylated STAT 3 on tyrosine 705 but not STAT 5 in our 2 cases of ALK-positive DLBCL with clathrin-ALK fusion.
  • Furthermore, STAT 5A expression was not detected in either of the ALK-positive DLBCL cases, although 11 of the 36 ALK-negative DLBCL cases revealed STAT 5A expression.
  • However, there were no significant associations between expression of survivin or BCL-X(L) and ALK positivity among the diffuse large B-cell lymphomas.
  • In summary, similar signaling transduction mechanism involving STAT proteins seems to underlie DLBCL harboring the clathrin-ALK or nucleophosmin-ALK fusion gene.
  • [MeSH-major] Clathrin / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Adult. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Cytarabine / administration & dosage. Doxorubicin / therapeutic use. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Prednisone / therapeutic use. Receptor Protein-Tyrosine Kinases. Recurrence. Remission Induction. Stem Cell Transplantation. Time Factors. Treatment Outcome. Vincristine / therapeutic use

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  • (PMID = 18755494.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Clathrin; 0 / Oncogene Proteins, Fusion; 0 / STAT3 Transcription Factor; 04079A1RDZ / Cytarabine; 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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37. Beltran B, Castillo J, Salas R, Quiñones P, Morales D, Hurtado F, Riva L, Winer E: ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature. J Hematol Oncol; 2009;2:11
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature.
  • BACKGROUND: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma (ALK-DLBCL) is a rare lymphoma with several clinicopathological differences from ALK-positive anaplastic large cell lymphoma (ALCL).
  • The latest WHO classification of lymphomas recognizes ALK-DLBCL as a separate entity.
  • By immunohistochemistry, cases were positive for cytoplasmic ALK, MUM1, CD45, and EMA; they marked negative for CD3, CD30 and CD20.
  • CONCLUSION: ALK-DLBCL is a distinct variant of DLBCL with plasmacytic differentiation, which is characterized by a bimodal age incidence curve, primarily nodal involvement, plasmablastic morphology, lack of expression of CD20, aggressive behavior and poor response to standard therapies, although some cases can have prolonged survival as the cases reported in this study.
  • ALK-DLBCL does not seem associated to immunosuppression or the presence of EBV or HHV8.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 19250532.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 39
  • [Other-IDs] NLM/ PMC2651189
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38. Vega F, Medeiros LJ, Leventaki V, Atwell C, Cho-Vega JH, Tian L, Claret FX, Rassidakis GZ: Activation of mammalian target of rapamycin signaling pathway contributes to tumor cell survival in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma. Cancer Res; 2006 Jul 1;66(13):6589-97
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  • [Title] Activation of mammalian target of rapamycin signaling pathway contributes to tumor cell survival in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) frequently carries the t(2;5)(p23;q35) resulting in aberrant expression of chimeric nucleophosmin-ALK.
  • Previously, nucleophosmin-ALK has been shown to activate phosphatidylinositol 3-kinase (PI3K) and its downstream effector, the serine/threonine kinase AKT.
  • In this study, we hypothesized that the mammalian target of rapamycin (mTOR) pathway, which functions downstream of AKT, mediates the oncogenic effects of activated PI3K/AKT in ALK+ ALCL.
  • Here, we provide evidence that mTOR signaling phosphoproteins, including mTOR, eukaryotic initiation factor 4E-binding protein-1, p70S6K, and ribosomal protein S6, are highly phosphorylated in ALK+ ALCL cell lines and tumors.
  • We also show that inhibition of mTOR with rapamycin, as well as silencing mTOR gene product expression using mTOR-specific small interfering RNA, decreased phosphorylation of mTOR signaling proteins and induced cell cycle arrest and apoptosis in ALK+ ALCL cells.
  • Cell cycle arrest was associated with modulation of G(1)-S-phase regulators, including the cyclin-dependent kinase inhibitors p21(waf1) and p27(kip1).
  • These findings suggest that the mTOR pathway contributes to nucleophosmin-ALK/PI3K/AKT-mediated tumorigenesis and that inhibition of mTOR represents a potential therapeutic strategy in ALK+ ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Kinases / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / physiology. Chromones / pharmacology. Down-Regulation. Enzyme Activation. Humans. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. Receptor Protein-Tyrosine Kinases. Signal Transduction. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Transfection

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  • (PMID = 16818631.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090853
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromones; 0 / Morpholines; 0 / RNA, Small Interfering; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS443817; NLM/ PMC4839264
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39. Rudzki Z, Rucińska M, Jurczak W, Skotnicki AB, Maramorosz-Kurianowicz M, Mruk A, Piróg K, Utych G, Bodzioch P, Srebro-Stariczyk M, Włodarska I, Stachura J: ALK-positive diffuse large B-cell lymphoma: two more cases and a brief literature review. Pol J Pathol; 2005;56(1):37-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ALK-positive diffuse large B-cell lymphoma: two more cases and a brief literature review.
  • Anaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma (DLBCL) is a rare, recently defined tumor distinct in many aspects from ALK-positive anaplastic large cell lymphoma (ALCL).
  • We present two additional cases of ALK+DLBCL recently diagnosed in our department and a review of literature.
  • A 48-year old man presented with a large upper neck mass growing slowly over 18 months.
  • Histologically the tumor was diagnosed as an ALK-positive diffuse large B-cell lymphoma. with plasmablastic features.
  • Large, frequently intrasinusoidal tumor cells expressed CD138, EMA, weakly IgA and kappa, but were negative for other B-cell markers, T-cell markers and CD30.
  • The ALK staining was cytoplasmic with the increased intensity in the Golgi area.
  • At the diagnosis the patient manifested with the stage IIIB.
  • The patient died of massive bleeding from his decomposing tumor 3 months after the diagnosis.
  • The tumor showed immunoblastic/anaplastic morphology, with some Reed-Sternberg-like cells positive for ALK.
  • ALK immunostaining was cytoplasmic, weak in a routine immunostain, enhanced with double (proteinase + pressure cooker) antigen retrieval.
  • FISH was consistent with the t(2;5)/nucleophosmin(NPM)-ALK rearrangement.
  • ALK-positive DLBCL affects mostly middle-aged men, shows generally poor but stage-dependent prognosis (at least 60% mortality rate), presents typically as a lymph node-based disseminated disease, and very rarely involves the bone marrow.
  • Genetic studies showed that the majority of ALK+DLBCL cases are characterized by the clathrin (CLTC)-ALK fusion and in a few cases the NPM-ALK rearrangement has been found.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 15921012.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 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
  • [Number-of-references] 17
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40. Anastasov N, Bonzheim I, Rudelius M, Klier M, Dau T, Angermeier D, Duyster J, Pittaluga S, Fend F, Raffeld M, Quintanilla-Martinez L: C/EBPβ expression in ALK-positive anaplastic large cell lymphomas is required for cell proliferation and is induced by the STAT3 signaling pathway. Haematologica; 2010 May;95(5):760-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] C/EBPβ expression in ALK-positive anaplastic large cell lymphomas is required for cell proliferation and is induced by the STAT3 signaling pathway.
  • BACKGROUND: Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma is characterized by the t(2;5) chromosomal translocation, resulting in the expression of a fusion protein formed of nucleophosmin (NPM) and ALK.
  • Recently, we reported the abnormal expression of the transcription factor CCAAT/enhancer binding protein-beta (C/EBPbeta) in ALK-positive anaplastic large cell lymphomas, and demonstrated its dependence on NPM-ALK activity.
  • DESIGN AND METHODS: In this study, the role of C/EBPbeta in proliferation and survival of ALK-positive anaplastic large cell lymphomas was investigated, as well as the mechanism of its expression and activity.
  • RESULTS: Interference with C/EBPbeta expression resulted in a dramatic decrease in cell proliferation in ALK-positive anaplastic large cell lymphomas, with a mild induction of apoptosis after 6 days.
  • Down-regulation of STAT3 resulted in a marked decrease in C/EBPbeta mRNA and protein levels with impairment in cell proliferation and viability, underscoring the important role of these two proteins in ALK-mediated oncogenesis.
  • CONCLUSIONS: These findings reveal the convergence of STAT3 and ERK1/2 signaling pathways activated by NPM-ALK in mediating the regulation of C/EBPbeta expression, a transcription factor central to NPM-ALK transformation.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / biosynthesis. Cell Proliferation. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / enzymology. Receptor Protein-Tyrosine Kinases / biosynthesis. STAT3 Transcription Factor / physiology. Signal Transduction
  • [MeSH-minor] Animals. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cell Survival / genetics. Down-Regulation / genetics. Humans. Mice


41. Ait-Tahar K, Cerundolo V, Banham AH, Hatton C, Blanchard T, Kusec R, Becker M, Smith GL, Pulford K: B and CTL responses to the ALK protein in patients with ALK-positive ALCL. Int J Cancer; 2006 Feb 1;118(3):688-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B and CTL responses to the ALK protein in patients with ALK-positive ALCL.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) has a good prognosis compared to ALK-negative ALCL, possibly as a result of the immune recognition of the ALK proteins.
  • The aim of our study was to investigate the presence of both a B and cytotoxic T cell (CTL) response to ALK in ALK-positive ALCL.
  • We confirmed the presence of an antibody response to ALK in all 9 ALK-positive ALCL patients investigated.
  • An ELISpot assay was used to detect a gamma-interferon (IFN) T cell response after short term culture of mononuclear blood cells with 2 ALK-derived HLA-A*0201 restricted peptides: ALKa and ALKb.
  • A significant gamma-IFN response was identified in all 7 HLA-A*0201-positive ALK-positive ALCL patients but not in ALK-negative ALCL patients (n = 2) or normal subjects (n = 6).
  • CTL lines (>95% CD8-positive) raised from 2 ALK-positive ALCL patients lysed ALK-positive ALCL derived cell lines in a MHC-Class I restricted manner.
  • This is the first report of both a B cell and CTL response to ALK in patients with ALK-positive ALCL.
  • The use of modified vaccinia virus Ankara (MVA) to express ALK is also described.
  • Our findings are of potential prognostic value and open up therapeutic options for those ALK-positive patients who do not respond to conventional treatment.
  • [MeSH-major] Epitopes, B-Lymphocyte / immunology. Epitopes, T-Lymphocyte / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Protein-Tyrosine Kinases / immunology. Protein-Tyrosine Kinases / metabolism. T-Lymphocytes, Cytotoxic / immunology

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16114011.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes, B-Lymphocyte; 0 / Epitopes, T-Lymphocyte; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Peptide Fragments; 82115-62-6 / Interferon-gamma; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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42. Delsol G: [Molecular abnormalities in lymphomas]. Bull Cancer; 2010 Nov;97(11):1347-64
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  • In the present review, molecular abnormalities observed in the most frequent B, T or NK cell lymphomas are discussed.
  • In the broad spectrum of diffuse large B-cell lymphomas microarray analysis shows mostly two subgroups of tumors, one with gene expression signature corresponding to germinal center B-cell-like (GCB: CD10+, BCL6 [B-Cell Lymphoma 6]+, centerine+, MUM1-) and a subgroup expressing an activated B-cell-like signature (ABC: CD10-, BCL6-, centerine-, MUM1+).
  • Among other B-cell lymphomas with well characterized molecular abnormalies are follicular lymphoma (BCL2 deregulation), MALT lymphoma (Mucosa Associated Lymphoid Tissue) [API2-MALT1 (mucosa-associated-lymphoid-tissue-lymphoma-translocation-gene1) fusion protein or deregulation BCL10, MALT1, FOXP1.
  • MALT1 transcription factors], mantle cell lymphoma (cycline D1 [CCND1] overexpression) and Burkitt lymphoma (c-Myc expression).
  • Except for ALK (anaplastic lymphoma kinase)-positive anaplastic large cell lymphoma, well characterized molecular anomalies are rare in lymphomas developed from T or NK cells.
  • Peripheral T cell lymphomas not otherwise specified are a heterogeneous group of tumors with frequent but not recurrent molecular abnormalities.
  • In angio-immunoblastic T-cell lymphomas molecular abnormalities are found in follicular helper T-cell (TFH) that express some distinctive markers such as CD10, PD-1, CXCR5 and the CXCL13 chemokine.
  • ALK-positive anaplastic large cell lymphoma is a paradigme of T-cell lymphoma since it is associated with an X-ALK oncogenic fusion protein due to a translocation involving ALK gene at 2p23.
  • ALK tyrosine kinase activates downstream pathways (Stat3/5b, Src kinases, PLCγ, PI3 kinase) implicated in lymphomagenesis, proliferation and protection against apoptosis.
  • Specific ALK inhibitors are currently in clinical evaluation.
  • Helicobacter pylori in MALT lymphoma) in lymphomagenesis.
  • [MeSH-major] Gene Amplification / genetics. Genes, Tumor Suppressor. Lymphoma / genetics. Mutation / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Gene Deletion. Gene Expression Regulation, Neoplastic / genetics. Genetic Techniques. Humans. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / metabolism. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell / metabolism. Neoplasm Proteins / metabolism

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  • (PMID = 21084243.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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43. Matsushita H, Nakamura N, Asai S, Yabe M, Hayama N, Kondo Y, Urano T, Miyachi H: A leukemic change as an initial manifestation of the common variant type of ALK-positive anaplastic large cell lymphoma in a patient with lung adenocarcinoma. Intern Med; 2008;47(23):2057-62
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  • [Title] A leukemic change as an initial manifestation of the common variant type of ALK-positive anaplastic large cell lymphoma in a patient with lung adenocarcinoma.
  • We report an 81-year-old man who had leukemic presentation of ALK-positive anaplastic large cell lymphoma (ALCL) as an initial manifestation.
  • The peripheral blood smear and bone marrow aspiration revealed the infiltration of atypical large cells with horseshoe-shaped or lobulated nuclei.
  • The detection of CD30 expression and the t (2;5) (p23;q35) translocation in these cells was confirmatory of a diagnosis of common variant ALK-positive ALCL in a leukemic phase.
  • An adequate, prompt diagnosis is necessary for this rare disease status in oncologic emergency to improve the disease management.
  • [MeSH-major] Adenocarcinoma / diagnosis. Genetic Variation / genetics. Lung Neoplasms / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis
  • [MeSH-minor] Aged, 80 and over. Antigens, CD30 / genetics. Diagnosis, Differential. Humans. Male

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  • (PMID = 19043261.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Number-of-references] 20
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44. Sjostrom C, Seiler C, Crockett DK, Tripp SR, Elenitoba Johnson KS, Lim MS: Global proteome profiling of NPM/ALK-positive anaplastic large cell lymphoma. Exp Hematol; 2007 Aug;35(8):1240-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Global proteome profiling of NPM/ALK-positive anaplastic large cell lymphoma.
  • OBJECTIVE: Constitutive overexpression of nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) is a key oncogenic event in anaplastic large cell lymphomas (ALCL) that carry the t(2;5)(p23;q35) translocation.
  • Global proteomic analysis of NPM/ALK-positive ALCL would improve understanding of the disease pathogenesis and yield new candidate targets for novel treatment and diagnostic strategies.
  • MATERIALS AND METHODS: To comprehensively determine the inventory of proteins from NPM/ALK-positive ALCL SUDHL-1 cells, the membrane, cytoplasm, and nuclear subcellular fractions were resolved by one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS).
  • Extensive annotation and systematic examination of the literature for information on 209 representative proteins indicated that 19.9% were reported to be expressed in T cells and 44.7% were reported to have important function in cancers, while only 4.3% were reported to be involved in ALCL pathogenesis.
  • CONCLUSION: We present an extensive catalog of proteins expressed by NPM/ALK-positive ALCL.
  • This study illustrates the potential for novel pathogenetic discovery in NPM/ALK-positive ALCL and the utility of combining cellular subfractionation, 1D SDS-PAGE, and LC-MS/MS for the comprehensive protein analysis of lymphoma.
  • [MeSH-major] Gene Expression Profiling. Lymphoma, Large B-Cell, Diffuse / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proteome
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. Humans. Molecular Sequence Data. Neoplasm Proteins / genetics

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  • (PMID = 17560012.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proteome; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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45. Lim ZY, Grace R, Salisbury JR, Creamer D, Jayaprakasam A, Ho AY, Devereux S, Mufti GJ, Pagliuca A: Cardiac presentation of ALK positive anaplastic large cell lymphoma. Eur J Haematol; 2005 Dec;75(6):511-4
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  • [Title] Cardiac presentation of ALK positive anaplastic large cell lymphoma.
  • Cardiac involvement as an initial presentation of malignant lymphoma is a rare occurrence.
  • Transcutaneous cardiac biopsy was non-diagnostic, therefore an open cardiac biopsy was performed from which a provisional diagnosis of a cardiac inflammatory pseudotumour was made.
  • Histological and immunophenotypic review of the initial cardiac biopsy revealed features consistent with a diagnosis of CD30, ALK1 positive anaplastic large cell lymphoma (ALCL).
  • Despite intensive treatment with combination chemotherapy, there was significant progression of disease, and he died 11 months after diagnosis.
  • The overall prognosis of cardiac lymphoma remains poor, which may be due to the often late presentation of the tumour.
  • To our knowledge, this is the first reported case of a cardiac ALK positive ALCL.
  • Although rare, cardiac presentation of ALCL should be added to the list of differential diagnoses of cardiac lymphomas.
  • [MeSH-major] Activin Receptors, Type I. Heart Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 16313264.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 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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46. Vassallo J, Lamant L, Brugieres L, Gaillard F, Campo E, Brousset P, Delsol G: ALK-positive anaplastic large cell lymphoma mimicking nodular sclerosis Hodgkin's lymphoma: report of 10 cases. Am J Surg Pathol; 2006 Feb;30(2):223-9
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  • [Title] ALK-positive anaplastic large cell lymphoma mimicking nodular sclerosis Hodgkin's lymphoma: report of 10 cases.
  • Anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) are recognized as biologically distinct entities.
  • In the last 10 years, we have collected 380 cases of ALK-positive ALCL of which 10 cases were originally diagnosed as nodular sclerosis classic HL (NSHL) on conventional histopathological examination.
  • After immunostaining, these cases proved to be ALK-positive ALCL mimicking HL (so-called Hodgkin-like ALCL).
  • These cases account for 2.6% of our cases of ALK-positive ALCL (10 of 380 cases).
  • Neoplastic cells were positive for CD30 (10 of 10 cases), ALK protein (10 of 10 cases), epithelial membrane antigen (EMA) (9 of 9 cases), CD43 (6 of 9 cases), and perforin (8 of 8 cases), but negative for CD15 (10 of 10 cases), CD20 (10 of 10 cases), Pax5/BSAP (6 of 6 cases), and EBV (8 of 8 cases).
  • Although rare, Hodgkin-like ALCL may mimic NSHL, and it is advisable to include EMA in the first line panel and to ask for ALK staining in EMA-positive, CD15-negative lesions with morphologic features suggestive of NSHL.
  • [MeSH-major] Biomarkers, Tumor / analysis. Hodgkin Disease / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged, 80 and over. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Receptor Protein-Tyrosine Kinases. Sclerosis / pathology

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  • (PMID = 16434897.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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47. Bakshi NA, Ross CW, Finn WG, Valdez R, Ruiz R, Koujok K, Schnitzer B: ALK-positive anaplastic large cell lymphoma with primary bone involvement in children. Am J Clin Pathol; 2006 Jan;125(1):57-63
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  • [Title] ALK-positive anaplastic large cell lymphoma with primary bone involvement in children.
  • We describe the clinical, radiologic, and pathologic features of primary bone anaplastic large cell lymphoma (ALCL) in 3 boys.
  • Differential diagnoses included osteomyelitis and small round cell tumors of childhood, particularly Ewing sarcoma.
  • Preoperatively, ALCL was not a diagnostic consideration in any case.
  • Two cases showed classic large pleomorphic cells; 1 showed a composite pattern with a distinct small cell component and the more typical large cell type.
  • Neoplastic cells in all cases showed strong CD30 and anaplastic lymphoma kinase expression with relatively weak epithelial membrane antigen positivity.
  • Two patients were disease-free at last follow-up (15 months and 11 years); 1 patient died of disseminated disease within a year of diagnosis.
  • ALCL should be considered a diagnostic possibility when evaluating neoplastic bone lesions in children.
  • Although expression of NSE in ALCL has not been emphasized in the literature, it is worth noting because it may pose a diagnostic pitfall.
  • [MeSH-major] Bone Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / analysis

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  • (PMID = 16482992.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase; 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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48. 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.
  • IL-21R expression is not linked to nucleophosmin-ALK since forced expression of nucleophosmin-ALK and small interfering RNA down-regulation of nucleophosmin-ALK did not significantly change the expression of either IL-21R or IL-21.
  • 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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49. Singh RR, Cho-Vega JH, Davuluri Y, Ma S, Kasbidi F, Milito C, Lennon PA, Drakos E, Medeiros LJ, Luthra R, Vega F: Sonic hedgehog signaling pathway is activated in ALK-positive anaplastic large cell lymphoma. Cancer Res; 2009 Mar 15;69(6):2550-8
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  • [Title] Sonic hedgehog signaling pathway is activated in ALK-positive anaplastic large cell lymphoma.
  • Deregulation of the sonic hedgehog (SHH) signaling pathway has been implicated in several cancers but has not been explored in T-cell lymphomas.
  • Here, we report that the SHH/GLI1 signaling pathway is activated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • We show that SHH, but not its transcriptional effector GLI1, is amplified in ALK+ ALCL tumors and cell lines, and that SHH and GLI1 proteins are highly expressed in ALK+ ALCL tumors and cell lines.
  • We also show that inhibition of SHH/GLI1 signaling with cyclopamine-KAAD, as well as silencing GLI1 gene expression by small interfering (si)RNA, decreased cell viability and clonogenicity of ALK+ ALCL cells.
  • Transfection of wild-type or mutant NPM-ALK into 293T cells showed that only wild-type NPM-ALK increased GLI1 protein levels and activated SHH/GLI1 signaling as shown by increase of CCND2 mRNA levels.
  • Inhibition of ALK tyrosine kinase and phosphatidylinositol 3-kinase (PI3K)/AKT or forced expression of pAKT down-regulated or up-regulated SHH/GLI1 signaling, respectively.
  • In conclusion, the SHH/GLI1 signaling pathway is activated in ALK+ ALCL.
  • SHH/GLI1 activation is the result of SHH gene amplification and is further mediated by NPM-ALK through activation of PI3K/AKT and stabilization of GLI1 protein.
  • There is a positive synergistic effect between the SHH/GLI1 and PI3K/AKT pathways that contributes to the lymphomagenic effect of NPM-ALK.
  • [MeSH-major] Hedgehog Proteins / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism
  • [MeSH-minor] Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / physiology. Enzyme Activation. Gene Amplification. Humans. Immunohistochemistry. Jurkat Cells. Phosphatidylinositol 3-Kinases / metabolism. Protein-Tyrosine Kinases / biosynthesis. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction. Transcription Factors / antagonists & inhibitors. Transcription Factors / biosynthesis. Transcription Factors / genetics. Transcription Factors / metabolism. Transcription, Genetic. Transfection

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  • (PMID = 19244133.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / SHH protein, human; 0 / Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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50. Cluzeau T, Pécuchet N, Mounier N, Vignot S: [Implications of ALK (anaplastic lymphoma kinase) in oncohematology]. Bull Cancer; 2010 Aug;97(8):991-6
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  • [Title] [Implications of ALK (anaplastic lymphoma kinase) in oncohematology].
  • [Transliterated title] Implications d'ALK (anaplastic lymphoma kinase) en oncohématologie.
  • The anaplastic lymphoma kinase gene (ALK) code for a receptor tyrosine-kinase.
  • The fusion proteins from the ALK gene have been identified in oncohaematology malignancies including ALK positive anaplastic lymphoma large cell and non small cells lung cancer with EML4-ALK fusion gene.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / enzymology. Lung Neoplasms / enzymology. Lymphoma, Large-Cell, Anaplastic / enzymology. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 20483705.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Nucleoplasmins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 27
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51. Savage KJ, Harris NL, Vose JM, Ullrich F, Jaffe ES, Connors JM, Rimsza L, Pileri SA, Chhanabhai M, Gascoyne RD, Armitage JO, Weisenburger DD, International Peripheral T-Cell Lymphoma Project: ALK- anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project. Blood; 2008 Jun 15;111(12):5496-504
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  • [Title] ALK- anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project.
  • The International Peripheral T-Cell Lymphoma Project is a collaborative effort designed to gain better understanding of peripheral T-cell and natural killer (NK)/T-cell lymphomas (PTCLs).
  • Of the 1314 eligible patients, 181 had anaplastic large-cell lymphoma (ALCL; 13.8%) on consensus review: One hundred fifty-nine had systemic ALCL (12.1%) and 22 had primary cutaneous ALCL (1.7%).
  • Patients with anaplastic lymphoma kinase-positive (ALK(+)) ALCL had a superior outcome compared with those with ALK(-) ALCL (5-year failure-free survival [FFS], 60% vs 36%; P = .015; 5-year overall survival [OS], 70% vs 49%; P = .016).
  • However, contrary to prior reports, the 5-year FFS (36% vs 20%; P = .012) and OS (49% vs 32%; P = .032) were superior for ALK(-) ALCL compared with PTCL, not otherwise specified (PTCL-NOS).
  • Patients with primary cutaneous ALCL had a very favorable 5-year OS (90%), but with a propensity to relapse (5-year FFS, 55%).
  • In summary, ALK(-) ALCL should continue to be separated from both ALK(+) ALCL and PTCL-NOS.
  • Although the prognosis of ALK(-) ALCL appears to be better than that for PTCL-NOS, it is still unsatisfactory and better therapies are needed.
  • Primary cutaneous ALCL is associated with an indolent course.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / mortality. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, T-Cell, Peripheral / mortality. Lymphoma, T-Cell, Peripheral / pathology. Protein-Tyrosine Kinases / immunology
  • [MeSH-minor] Adult. Asia. Diagnosis, Differential. Europe. Female. Follow-Up Studies. Humans. Immunophenotyping. International Cooperation. Male. Middle Aged. North America. Prognosis. Receptor Protein-Tyrosine Kinases. Recurrence. Retrospective Studies. Skin Neoplasms / immunology. Skin Neoplasms / mortality. Skin Neoplasms / pathology. Skin Neoplasms / therapy. Survival Analysis. Treatment Outcome

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  • (PMID = 18385450.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Investigator] Savage K; Connors J; Gascoyne R; Chhanabhai M; Wilson W; Jaffe E; Armitage J; Vose J; Weisenburger D; Anderson J; Ullrich F; Bast M; Hochberg E; Harris N; Levine A; Nathwani B; Miller T; Rimsza L; Montserrat E; Lopez-Guillermo A; Campo E; Cuadros M; Alvarez Ferreira J; Martinez Delgado B; Holte H; Delabie J; Rüdiger T; Müller-Hermelink K; Reimer P; Adam P; Wilhelm M; Schmitz N; Nerl C; Lister A; Norton A; MacLennan KA; Zinzani PL; Pileri S; Federico M; Bellei M; Coiffier B; Berger F; Tanin I; Wannakrairot P; Au W; Liang R; Loong F; Rajan S; Sng I; Tobinai K; Matsuno Y; Morishima Y; Nakamura S; Seto M; Tanimoto M; Yoshino T; Suzumiya J; Ohshima K; Kim WS; Ko YH
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52. 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).
  • The most common translocation, the t(2;5)(p23;q35), results in expression of nucleophosmin (NPM)-ALK.
  • NPM-ALK has been shown to activate signal transducer and activator of transcription (STAT) 3, a transcriptional regulator of cyclin D3.
  • 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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53. Yaakup H, Sagap I, Fadilah SA: Primary oesophageal Ki (CD30)-positive ALK+ anaplastic large cell lymphoma of T-cell phenotype. Singapore Med J; 2008 Oct;49(10):e289-92
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  • [Title] Primary oesophageal Ki (CD30)-positive ALK+ anaplastic large cell lymphoma of T-cell phenotype.
  • Primary oesophageal lymphoma is a very rare entity, with fewer than 30 reported cases worldwide.
  • Most of the oesophageal lymphomas are diffuse large B-cell type, with only one reported case of anaplastic large cell lymphoma (ALCL) of T-cell phenotype.
  • We describe the first case of primary oesophageal Ki (CD30)-positive ALK+ALCL of T-cell phenotype in a 34-year-old immunocompetent woman, who presented with a two-year history of dysphagia.
  • She was treated with chemotherapy and endoscopic oesophageal dilations and stenting, resulting in complete remission of the lymphoma and resolution of the dysphagia.
  • She then underwent autologous peripheral blood haematopoietic stem cell transplantation and remained disease-free two years after the diagnosis.
  • [MeSH-major] Antigens, CD30 / biosynthesis. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Adult. Disease-Free Survival. Endoscopy / methods. Female. Hematopoietic Stem Cell Transplantation / methods. Humans. Phenotype. Receptor Protein-Tyrosine Kinases. Remission Induction. T-Lymphocytes / metabolism. Tomography, X-Ray Computed / methods. Treatment Outcome

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  • (PMID = 18946602.001).
  • [ISSN] 0037-5675
  • [Journal-full-title] Singapore medical journal
  • [ISO-abbreviation] Singapore Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
  • [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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54. Shi P, Lai R, Lin Q, Iqbal AS, Young LC, Kwak LW, Ford RJ, Amin HM: IGF-IR tyrosine kinase interacts with NPM-ALK oncogene to induce survival of T-cell ALK+ anaplastic large-cell lymphoma cells. Blood; 2009 Jul 9;114(2):360-70
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  • [Title] IGF-IR tyrosine kinase interacts with NPM-ALK oncogene to induce survival of T-cell ALK+ anaplastic large-cell lymphoma cells.
  • Although it promotes the growth of stimulated hematopoietic cells, a direct role of IGF-IR in malignant lymphoma has not been identified.
  • Anaplastic lymphoma kinase-positive anaplastic large-cell lymphoma (ALK(+) ALCL) is a unique type of T-cell lymphoma.
  • Approximately 85% of ALK(+) ALCL cases harbor the translocation t(2;5)(p23;q35), which generates the chimeric oncogene NPM-ALK.
  • In the present study, we explored a possible role of IGF-IR in ALK(+) ALCL.
  • Our results demonstrate that IGF-IR and IGF-I are widely expressed in ALK(+) ALCL cell lines and primary tumors.
  • Importantly, we identified novel reciprocal functional interactions between IGF-IR and NPM-ALK.
  • Antagonism of IGF-IR decreased the viability, induced apoptosis and cell-cycle arrest, and decreased proliferation and colony formation of ALK(+) ALCL cell lines.
  • These effects could be explained by alterations of cell survival regulatory proteins downstream of IGF-IR signaling.
  • Our findings improve current understanding of the biology of IGF-IR and NPM-ALK and have significant therapeutic implications as they identify IGF-IR signaling as a potential therapeutic target in ALK(+) ALCL and possibly other types of malignant lymphoma.

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  • (PMID = 19423729.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395; United States / NCI NIH HHS / CA / CA114395
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; 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 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2714211
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55. Tamiolakis D, Papadopoulos N, Venizelos J, Kakagia D, Nikolaidou S, Bolioti S, Kouskoukis C: ALK-positive neutrophil-rich variant of anaplastic large cell lymphoma diagnosed after head trauma. Onkologie; 2005 Jun;28(6-7):356-8
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  • [Title] ALK-positive neutrophil-rich variant of anaplastic large cell lymphoma diagnosed after head trauma.
  • BACKGROUND: Anaplastic lymphoma kinase (ALK) expression has not been described in neutrophil-rich anaplastic large cell lymphoma (NR-ALCL).
  • CASE REPORT: A 12-year old female with a 4-weeks history of a non-resolving bump over the forehead resulting from injury, was diagnosed of stage IE cutaneous T-cell lymphoma, and radiation was employed.
  • A fine-needle aspiration of the hand mass was performed, and a diagnosis of CD30+/ALK+ NR-ALCL, was rendered.
  • METHODS: We studied the morphological characteristics of CD30+/ALK+ NR-ALCL using histological methods.
  • A panel of antibodies were used to establish diagnosis and subtyping.
  • CONCLUSIONS: ALK-ALCL arising in the skin represents a single disease with a broad spectrum of morphology; clinicians and pathologists should be aware of this neutrophil-rich (NR) variant with aggressive clinical presentation.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / blood. Lymphoma, Large B-Cell, Diffuse / pathology. Neutrophils / pathology. Protein-Tyrosine Kinases / blood. Skin Neoplasms / blood. Skin Neoplasms / pathology

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  • (PMID = 15933425.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [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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56. 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
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  • [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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57. Thompson MA, Stumph J, Henrickson SE, Rosenwald A, Wang Q, Olson S, Brandt SJ, Roberts J, Zhang X, Shyr Y, Kinney MC: Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas. Hum Pathol; 2005 May;36(5):494-504
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  • [Title] Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive large T- or null-cell lymphoma.
  • Most ALCLs arising in children and young adults express a constitutively active receptor tyrosine kinase, anaplastic lymphoma kinase (ALK).
  • Anaplastic large cell lymphomas lacking ALK are clinically heterogeneous and their pathogenesis is unknown.
  • This study is the first complementary DNA (cDNA) microarray analysis using RNA extracted from tumor tissue (7 ALK+ ALCLs and 7 ALK- ALCLs) to identify genes differentially expressed or shared between the ALK+ and ALK- tumors.
  • Unsupervised hierarchical clustering using the top 11 most statistically significant discriminator cDNAs correctly grouped all ALK+ and ALK- tumors.
  • Hierarchical clustering analysis using the 44 cDNAs with the greatest differential expression between ALK+ and ALK- RNAs grouped 6 of 7 ALK+ ALCLs together and 1 ALK+ ALCL with the ALK- group.
  • In general, ALK+ tumors overexpress genes encoding signal transduction molecules (SYK , LYN , CDC37) and underexpress transcription factor genes (including HOXC6 and HOX A3 ) compared with the ALK- group.
  • Cyclin D3 was overexpressed in the ALK+ group and the cell cycle inhibitor p19INK4D was decreased in the ALK- group, suggesting different mechanisms of promoting G 1 /S transition.
  • Genes highly expressed in both ALK- and ALK+ ALCLs included kinases (LCK, protein kinase C, vav2, and NKIAMRE) and antiapoptotic molecules, suggesting possible common pathogenetic mechanisms as well.
  • [MeSH-major] Gene Expression. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Child. Cyclin D3. Cyclin-Dependent Kinase Inhibitor p19. Cyclins / genetics. Cyclins / metabolism. Female. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15948116.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM007753
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND3 protein, human; 0 / CDKN2D protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin D3; 0 / Cyclin-Dependent Kinase Inhibitor p19; 0 / Cyclins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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58. Ma L, Katz Y, Sharan KP, Schwarting R, Kim AS: Epstein-Barr virus positive anaplastic large cell lymphoma: myth or reality? Int J Clin Exp Pathol; 2010;4(1):100-10
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  • [Title] Epstein-Barr virus positive anaplastic large cell lymphoma: myth or reality?
  • The World Health Organization (WHO) Classification of Tumours of Haematopoietic and Lymphoid Tissue, 2008 edition, states that anaplastic large cell lymphoma (ALCL) is "consistently negative for Epstein-Barr virus (EBV)".
  • The statement made by the WHO has led to the widespread belief that EBV can have no pathogenic role in ALCL.
  • Herein we report a case of an immunocompetent 35-year-old male who presented with hemophagocytic syndrome secondary to lymphoma for which diagnostic material consisted solely of a bone marrow biopsy.
  • The biopsy demonstrated large anaplastic cells which were uniformly positive for surface CD3, CD30 (strong membranous and Golgi expression), CD45, TIA-1 and Granzyme B but negative for ALK-1.
  • In-situ hybridization was strongly positive for EBER in the large neoplastic cells.
  • The uniformity of CD30 expression and positivity for cytotoxic markers on the anaplastic tumor cells raised the diagnostic possibility of an EBV-associated ALCL, ALK-.
  • Discussion of this case as well as a retrospective review of 64 cases of reported of EBV+ ALCL are presented.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Herpesvirus 4, Human / isolation & purification. Lymphoma, Large-Cell, Anaplastic / virology. Tumor Virus Infections / complications

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  • (PMID = 21228932.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC3016108
  • [Keywords] NOTNLM ; ALK / Epstein-Barr virus / anaplastic large cell lymphoma
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59. 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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60. Siordia-Reyes AG, Ferman-Cano F, Rodríguez-Velasco A: [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case]. Gac Med Mex; 2005 Nov-Dec;141(6):531-4
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  • [Title] [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case].
  • [Transliterated title] Linfoma anaplásico de células grandes ALK-1 positivo, primario de pulmón. Informe de un caso pediátrico.
  • Ki-1 anaplastic large cell non-Hodgkin lymphoma is a well recognized clinical entity.
  • Anaplastic large cell lymphoma is more common among young people, in whom the prognosis is more favorable.
  • Primary anaplastic large cell lymphoma of the lung is a rare clinical entity.
  • Its clinical expression is similar to a high grade malignant lymphoma, and in most cases the diagnosis is made in advanced stages.
  • We present a pediatric case with ALK-1 positive anaplastic large cell lymphoma of the lung.
  • [MeSH-major] Lung Neoplasms / chemistry. Lymphoma, Large B-Cell, Diffuse / chemistry. Membrane Proteins / analysis

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  • (PMID = 16381509.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
  • [Number-of-references] 16
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61. Li JF, Li GD, Liu WP, Wang Y, Cheng JR, Chen Y, Yang H, Tang HL, Bai YQ, Lin DG, DU LH, Peng FX, Yang YH, Zhao C: [Expression of anaplastic lymphoma kinase and survivin proteins in anaplastic large cell lymphoma and its significance]. Zhonghua Bing Li Xue Za Zhi; 2006 Apr;35(4):213-7
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  • [Title] [Expression of anaplastic lymphoma kinase and survivin proteins in anaplastic large cell lymphoma and its significance].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and survivin proteins in anaplastic large cell lymphoma (ALCL) and there clinical significance.
  • Immunohistochemical staining for ALK and survivin proteins was performed using LSAB method.
  • RESULTS: ALK protein was positive in 51 cases (63%) and negative in 30 cases (37%) of the 81 cases of ALCL studied.
  • The prognosis of patients with ALK protein expression was better than those without ALK expression (P < 0.05).
  • As for survivin protein, there were various degrees of expression in all the 77 ALCL cases studied.
  • The expression of survivin protein did not correlate with that of ALK protein (P > 0.05).
  • In cases with ALK protein expression, the prognosis was less favorable if there was also high co-expression of survivin protein (P < 0.05).
  • In ALK protein negative cases, prognosis did not significantly correlate with the expression of survivin protein (P > 0.05).
  • In addition, multivariate analysis confirmed the prognosis value of ALK protein expression, survivin protein expression and constitutional symptoms.
  • CONCLUSION: Survivin protein expression can serve as an independent prognostic predictor of unfavorable clinical outcome in patients with ALCL, especially when ALK protein is positive.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16776978.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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62. Rekhi B, Sridhar E, Viswanathan S, Shet TM, Jambhekar NA: ALK+ anaplastic large cell lymphoma with cohesive, perivascular arrangements on cytology, mimicking a soft tissue sarcoma: a report of 2 cases. Acta Cytol; 2010 Jan-Feb;54(1):75-8
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  • [Title] ALK+ anaplastic large cell lymphoma with cohesive, perivascular arrangements on cytology, mimicking a soft tissue sarcoma: a report of 2 cases.
  • BACKGROUND: An accurate recognition of a lymphoma at an extranodal site is essential to avoid unnecessary excisions.
  • Fine needle aspiration cytology (FNAC) has been recognized as a useful tool in the primary diagnosis of soft tissue tumors.
  • An anaplastic large cell lymphoma (ALCL), occurring in soft tissues, poses a diagnostic challenge.
  • We present the cytomorphology of 2 cases of anaplastic lymphoma kinase (ALK)+ ALCL that displayed a perivascular arrangement, thereby mimicking a sarcoma.
  • Differential diagnoses included a rhabdomyosarcoma and a lymphoma.
  • On biopsy and immunohistochemistry, tumor cells were positive for vimentin, LCA, EMA, CD30 and ALK.
  • CONCLUSION: ALCL should be considered in the differential diagnosis of pediatric soft tissue tumors, especially in cases with multifocal involvement.
  • [MeSH-major] Biopsy, Fine-Needle. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Adolescent. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Receptor Protein-Tyrosine Kinases. Sarcoma / pathology

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  • (PMID = 20306994.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [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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63. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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64. Yamamoto R, Nishikori M, Tashima M, Sakai T, Ichinohe T, Takaori-Kondo A, Ohmori K, Uchiyama T: B7-H1 expression is regulated by MEK/ERK signaling pathway in anaplastic large cell lymphoma and Hodgkin lymphoma. Cancer Sci; 2009 Nov;100(11):2093-100
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  • [Title] B7-H1 expression is regulated by MEK/ERK signaling pathway in anaplastic large cell lymphoma and Hodgkin lymphoma.
  • We examined B7-H1 expression in anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) and found that it was constitutively expressed in both clinical samples and cell lines.
  • In anaplastic lymphoma kinase-positive (ALK(+)) ALCL cells, B7-H1 expression was suppressed by the blocking of extracellular signal-regulated kinase (ERK) signaling and upregulated by the augmentation of ERK activity by phorbol 13-myristate 12-acetate stimulation, suggesting that B7-H1 expression is regulated by ERK signaling pathway in ALCL.
  • ERK is one of the downstream mediators of nucleophosmin (NPM)/ALK signaling in ALK(+)ALCL, and pharmacological inhibition of ALK was shown to dephosphorylate ERK and down-regulate B7-H1.
  • The involvement of NPM/ALK in B7-H1 expression was also demonstrated by introducing the construct into human non-ALCL lymphoid cell lines, which resulted in B7-H1 expression.
  • These results suggest that B7-H1 expression is controlled by common ERK signaling pathways in ALCL and HL cells.
  • [MeSH-major] Antigens, CD / analysis. Extracellular Signal-Regulated MAP Kinases / physiology. Hodgkin Disease / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. MAP Kinase Signaling System / physiology. Mitogen-Activated Protein Kinase Kinases / physiology
  • [MeSH-minor] Antigens, CD274. Cell Line, Tumor. Humans. Protein-Tyrosine Kinases / physiology. STAT3 Transcription Factor / physiology

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  • (PMID = 19703193.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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65. 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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66. 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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67. Vinogradova IuE, Lutsenko IN, Kaplanskaia IB, Vorob'ev IA, Samoĭlova RS, Gorgidze LA, Ryzhikova NA, Valiev TT, Giliazitdinova EA, Dzhulakian UL, Egorova EK, Zvonkov EE, Krasil'nikova BB, Magomedova AU, Margolin OV, Mar'in DS, Kremenetskaia AM, Kravchenko SK, Vorob'ev AI: [Efficacy of therapy of different variants of anaplastic large T-cell lymphomas]. Ter Arkh; 2008;80(7):33-7
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  • [Title] [Efficacy of therapy of different variants of anaplastic large T-cell lymphomas].
  • AIM: To compare efficacy of NHL-BFM-90 and CHOP-like courses in the treatment of anaplastic large cell lymphoma (ALCL).
  • MATERIAL AND METHODS: Twenty-two patients with ALCL participated in the study.
  • The diagnosis was made basing on the findings of clinical, device, morphological, immunohistochemical and molecular-genetic examinations with application of a panel of monoclonal antibodies to CD30, ALK, CD3, CD4, CDS, CD7, CD34, CD15, CD68, CD20, CD45RO, CD45RA, Ki-67.
  • 14 cases of 22 were negative by kinase of anaplastic lymphocytes (ALK-) and 8 were positive (ALK+).
  • Mean age of ALK-ALCL patients was 39.6 +/- 4.1 years, of ALK+ALCL patients - 23.4 +/- 2.6 years.
  • All 14 patients treated according to NHL-BFM-90 had ALCL stages III-IV with B-symptoms.
  • Of 8 ALCL patients treated initially according to other schemes, a complete remission was achieved in 4 patients (2 had stage II).
  • CONCLUSION: ALCL occurs more frequently in young and middle-aged patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • (PMID = 18763592.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 3.5.1.1 / Asparaginase; Q573I9DVLP / Leucovorin; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; BEACOPP protocol; CHOP protocol; MACOP-B protocol; PVDA protocol
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68. Lagarrigue F, Dupuis-Coronas S, Ramel D, Delsol G, Tronchère H, Payrastre B, Gaits-Iacovoni F: Matrix metalloproteinase-9 is upregulated in nucleophosmin-anaplastic lymphoma kinase-positive anaplastic lymphomas and activated at the cell surface by the chaperone heat shock protein 90 to promote cell invasion. Cancer Res; 2010 Sep 1;70(17):6978-87
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  • [Title] Matrix metalloproteinase-9 is upregulated in nucleophosmin-anaplastic lymphoma kinase-positive anaplastic lymphomas and activated at the cell surface by the chaperone heat shock protein 90 to promote cell invasion.
  • Many anaplastic large cell lymphomas (ALCL) express the chimeric oncogene NPM-ALK, which drives malignant transformation and invasion.
  • In this study, we show that NPM-ALK expression increases matrix metalloproteinase-9 (MMP-9) expression.
  • Accordingly, we found that 100% of a large panel of ALK(+) ALCL biopsies examined were also MMP-9(+), in contrast to only 36.3% of ALK(-) tumors.
  • The MMP inhibitor GM6001 and MMP-9 blocking antibodies abolished the invasiveness of NPM-ALK(+) cells.
  • Interestingly, the hyaluronan receptor CD44 acted as a docking surface for MMP-9 and the chaperone heat shock protein 90 on the cell surface, where MMP-9 was cleaved and activated.
  • Taken together, our observations strengthen the concept that chaperones have a major extracellular role in the regulation of protein activation status, and reveal new factors that are crucial for spreading and invasion of ALK(+) ALCL.
  • They also point out new factors crucial for ALK(+) ALCL.
  • [MeSH-major] HSP90 Heat-Shock Proteins / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Matrix Metalloproteinase 9 / biosynthesis. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Antigens, CD44 / metabolism. Cell Line, Tumor. Cell Membrane / metabolism. Dipeptides / pharmacology. Enzyme Activation. Enzyme Precursors / metabolism. Humans. Matrix Metalloproteinase Inhibitors. Neoplasm Invasiveness. Up-Regulation. rac1 GTP-Binding Protein / metabolism

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  • (PMID = 20699364.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / CD44 protein, human; 0 / Dipeptides; 0 / Enzyme Precursors; 0 / HSP90 Heat-Shock Proteins; 0 / Matrix Metalloproteinase Inhibitors; 0 / N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide; 0 / RAC1 protein, human; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.4.24.- / pro-matrix metalloproteinase 9; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.5.2 / rac1 GTP-Binding Protein
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69. Tan BT, Seo K, Warnke RA, Arber DA: The frequency of immunoglobulin heavy chain gene and T-cell receptor gamma-chain gene rearrangements and Epstein-Barr virus in ALK+ and ALK- anaplastic large cell lymphoma and other peripheral T-cell lymphomas. J Mol Diagn; 2008 Nov;10(6):502-12
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  • [Title] The frequency of immunoglobulin heavy chain gene and T-cell receptor gamma-chain gene rearrangements and Epstein-Barr virus in ALK+ and ALK- anaplastic large cell lymphoma and other peripheral T-cell lymphomas.
  • We previously identified a relatively high frequency of B-cell proliferations along with simultaneous T-cell receptor gamma-chain gene (TRG) and immunoglobulin heavy chain gene (IGH) rearrangements in a series of angioimmunoblastic T-cell lymphoma and peripheral T-cell lymphoma, unspecified.
  • Here, we report on a series of 74 peripheral T-cell lymphoma (PTCL) cases composed entirely of specific PTCL subtypes, including 28 cases of ALK+ anaplastic large-cell lymphoma (ALCL), 35 cases of ALK- ALCL, and 11 cases that represent other specific PTCL subtypes.
  • We performed IGH and TRG gene rearrangement studies and in situ hybridization for Epstein-Barr virus (EBV) to determine the frequency of IGH clonality and to investigate the relationship between EBV, clonality, and associated B-cell proliferations.
  • Using BIOMED-2 PCR assays, we detected TRG clones in 64 of 74 (86%) cases and IGH clones in 6 of 74 (8%) cases, with all IGH-positive cases exhibiting a concurrent TRG clone.
  • Despite the detection of occasional IGH clones, there was no correlation between IGH clonality and EBV, and B-cell proliferations were not identified in any of the cases.
  • These findings suggest that other factors contribute to IGH clonality and demonstrate that, in the absence of an associated B-cell proliferation, IGH clonality occurs infrequently (8%) in specific PTCL subtypes.
  • [MeSH-major] Gene Rearrangement. Genes, T-Cell Receptor gamma. Herpesvirus 4, Human / immunology. Immunoglobulin Heavy Chains / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, T-Cell, Peripheral / genetics. Protein-Tyrosine Kinases / metabolism. Receptors, Antigen, T-Cell, gamma-delta / genetics

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  • (PMID = 18832464.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2570633
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70. 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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71. 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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72. Buxton D, Bacchi CE, Gualco G, Weiss LM, Zuppan CW, Rowsell EH, Huang Q, Wang J: Frequent expression of CD99 in anaplastic large cell lymphoma: a clinicopathologic and immunohistochemical study of 160 cases. Am J Clin Pathol; 2009 Apr;131(4):574-9
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  • [Title] Frequent expression of CD99 in anaplastic large cell lymphoma: a clinicopathologic and immunohistochemical study of 160 cases.
  • By using conventional paraffin immunoperoxidase staining and tissue microarrays, we retrospectively investigated CD99 expression in a series of 160 anaplastic large cell lymphoma (ALCL) cases.
  • Of the 160 cases, 103 (64.4%) were positive for CD99.
  • CD99 expression was present in 96 (64.4%) of 149 of the common type, 4 (80%) of 5 of the small cell variant, and 3 (50%) of 6 of the lymphohistiocytic variant cases.
  • CD99 expression was slightly more frequent in anaplastic large cell lymphoma kinase (ALK)+ cases compared with ALK- cases (43/54 [80%] vs 44/81 [54%]).
  • With 2 exceptions, ALK+ ALCL was seen only in patients younger than 41 years.
  • We conclude that CD99 is frequently expressed in ALCL, with a slightly increased frequency in the younger age ALK+ cases.
  • Nodal and extranodal ALCL should be considered in the differential diagnosis when a CD99+ neoplasm is encountered.
  • [MeSH-major] Antigens, CD / biosynthesis. Biomarkers, Tumor / analysis. Cell Adhesion Molecules / biosynthesis. Lymphoma, Large-Cell, Anaplastic / metabolism

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  • (PMID = 19289593.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 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. Bubała H, Małdyk J, Włodarska I, Sońta-Jakimczyk D, Szczepański T: ALK-positive diffuse large B-cell lymphoma. Pediatr Blood Cancer; 2006 May 1;46(5):649-53
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  • [Title] ALK-positive diffuse large B-cell lymphoma.
  • Anaplastic lymphoma kinase (ALK) positive diffuse large B-cell lymphoma (DLBCL) is a rare subtype of non-Hodgkins lymphoma.
  • We present a 9-year-old boy, in whom diagnosis of DLBCL has been established in addition to congenital multiple enchondromatosis.
  • Immunohistopathological evaluation of tumor biopsy established the final diagnosis of ALK + DLBCL.
  • The clathrin gene (CLTC)-ALK fusion underlying aberrant expression of ALK in the present case was demonstrated by interphase fluorescence in situ hybridization (FISH) using break-apart rearrangement probes for ALK and CLTC.
  • Analysis of the disease course in our patient and review of other cases reported previously show that ALK + DLBCL can be an aggressive malignancy that can be cured with conventional chemotherapy protocols only at stage of localized disease.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 15852431.001).
  • [ISSN] 1545-5009
  • [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] 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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74. Yang J, Zhang F, Fang H, Ye Z, Lin S, Han A: Clinicopathologic features of primary lymphoma in soft tissue. Leuk Lymphoma; 2010 Nov;51(11):2039-46
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  • [Title] Clinicopathologic features of primary lymphoma in soft tissue.
  • By reviewing 3725 lymphomas diagnosed in our institution from 1999 to 2010, we found eight cases (0.21%) of primary lymphoma in soft tissue with comprehensive histologic and immunohistochemical studies.
  • Of the eight cases of primary lymphoma in soft tissue, two patients were male and six were female.
  • Six cases were diffuse large B-cell lymphoma (DLBCL), subclassified as three DLBCL non-germinal center B-cell phenotype, one DLBCL germinal center B-cell phenotype, and two (Epstein-Barr Virus) EBV-positive DLBCL of the elderly; one case was anaplastic large cell lymphoma, ALK-positive; and one case was peripheral T cell lymphoma, not otherwise specified.
  • One patient who refused further therapy died of the disease at 2 months after diagnosis.
  • [MeSH-major] Lymphoma / pathology. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Immunophenotyping. Male. Middle Aged. Retrospective Studies. Young Adult

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  • (PMID = 20929318.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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75. Lai R, Rassidakis GZ, Lin Q, Atwell C, Medeiros LJ, Amin HM: Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma. Hum Pathol; 2005 Sep;36(9):939-44
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  • [Title] Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma.
  • In previous studies of anaplastic large cell lymphoma (ALCL), we showed that inhibition of Jak3 down-regulates activated/phosphorylated Stat3 (pStat3), decreases anaplastic lymphoma kinase (ALK) enzymatic activity, and induces cell-cycle arrest and apoptosis in ALK-positive ALCL.
  • These findings implicate Jak3 as playing a significant role in the pathogenesis of ALK-positive ALCL; most likely via Stat3 and ALK activation.
  • To assess this possibility, we used immunohistochemical staining to evaluate the frequency of expression of Jak3 and its activated/phosphorylated form (pJak3) in 48 systemic ALCL tumors included in a tissue microarray. pJak3 was detected in 17 (81%) of 21 ALK-positive tumors, compared with 3 (11%) of 27 ALK-negative tumors (P < .0001, Fisher exact test).
  • pStat3 was present in 12 (86%) of 14 ALK-positive tumors and in 10 (40%) of 25 ALK-negative tumors assessed (P = .0078).
  • Of 12 ALK-positive/pStat3-positive tumors, 8 (67%) expressed pJak3, but none of 10 ALK-negative/pStat3-positive tumors expressed pJak3.
  • We conclude that Jak3 activation is predominantly restricted to ALK-positive ALCL tumors.
  • Most likely, Jak3 collaborates with ALK in activating Stat3, leading to cell survival, cell-cycle progression, and tumor growth.
  • In contrast, the mechanism of Stat3 activation in ALK-negative ALCL tumors appears to be independent of Jak3.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16153455.001).
  • [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 / JAK3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3
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76. Vose J, Armitage J, Weisenburger D, International T-Cell Lymphoma Project: International peripheral T-cell and natural killer/T-cell lymphoma study: pathology findings and clinical outcomes. J Clin Oncol; 2008 Sep 1;26(25):4124-30
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  • [Title] International peripheral T-cell and natural killer/T-cell lymphoma study: pathology findings and clinical outcomes.
  • PURPOSE: Peripheral T-cell lymphoma (PTCL) and natural killer/T-cell lymphoma (NKTCL) are rare and heterogeneous forms of non-Hodgkin's lymphoma (NHL) that, in general, are associated with a poor clinical outcome.
  • RESULTS: A diagnosis of PTCL or NKTCL was confirmed in 1,153 (87.8%) of the cases.
  • The most common subtypes were PTCL not otherwise specified (NOS; 25.9%), angioimmunoblastic type (18.5%), NKTCL (10.4%), and adult T-cell leukemia/lymphoma (ATLL; 9.6%).
  • Misclassification occurred in 10.4% of the cases including Hodgkin's lymphoma (3%), B-cell lymphoma (1.4%), unclassifiable lymphoma (2.8%), or a diagnosis other than lymphoma (2.3%).
  • The use of an anthracycline-containing regimen was not associated with an improved outcome in PTCL-NOS or angioimmunoblastic type, but was associated with an improved outcome in anaplastic large-cell lymphoma, ALK positive.
  • However, expert hematopathology review is important for accurate diagnosis.
  • The clinical outcome for patients with most of these lymphoma subtypes is poor with standard therapies, and novel agents and new modalities are needed to improve survival.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / mortality. T-Lymphocytes / pathology

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  • (PMID = 18626005.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Investigator] Savage K; Connors J; Gascoyne R; Chhanabhai M; Wilson W; Jaffe E; Armitage J; Vose J; Weisenburger D; Anderson J; Ullrich F; Bast M; Hochberg E; Harris N; Levine A; Nathwani B; Miller T; Rimsza L; Montserrat E; Lopez-Guillermo A; Campo E; Cuadros M; Alvarez Ferreira J; Martinez Delgado B; Holte H; Delabie J; Rüdiger T; Müller-Hermelink K; Reimer P; Adam P; Wilhelm M; Schmitz N; Nerl C; Lister A; Norton A; MacLennan KA; Luigi Zinzani P; Pileri S; Federico M; Bellei M; Coiffier B; Berger F; Tanin I; Wannakrairot P; Au W; Liang R; Loong F; Rajan S; Sng I; Tobinai K; Matsuno Y; Morishima Y; Nakamura S; Seto M; Tanimoto M; Yoshino T; Suzumiya J; Ohshima K; Kim WS; Ko YH
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77. Salaverria I, Beà S, Lopez-Guillermo A, Lespinet V, Pinyol M, Burkhardt B, Lamant L, Zettl A, Horsman D, Gascoyne R, Ott G, Siebert R, Delsol G, Campo E: Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas. Br J Haematol; 2008 Mar;140(5):516-26
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  • [Title] Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is a T/null-cell neoplasm characterized by chromosomal translocations involving the anaplastic lymphoma kinase (ALK) gene (ALK).
  • Tumours with similar morphology and phenotype but negative for ALK have been also recognized.
  • We have examined 74 ALCL, 43 ALK-positive and 31 ALK-negative, cases by comparative genomic hybridization (CGH), and locus-specific alterations for TP53 and ATM were examined by fluorescence in situ hybridization and real-time quantitative polymerase chain reaction.
  • Chromosomal imbalances were detected in 25 (58%) ALK-positive and 20 (65%) ALK-negative ALCL.
  • ALK-positive ALCL with NPM-ALK or other ALK variant translocations showed a similar profile of secondary genetic alterations.
  • Gains of 17p and 17q24-qter and losses of 4q13-q21, and 11q14 were associated with ALK-positive cases (P = 0.05), whereas gains of 1q and 6p21 were more frequent in ALK-negative tumours (P = 0.03).
  • ALCL-negative tumours had a significantly worse prognosis than ALK-positive.
  • In conclusion, ALK-positive and negative ALCL have different secondary genomic aberrations, suggesting they correspond to different genetic entities.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromosome Aberrations. Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 18275429.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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78. Huang W, Li X, Yao X, Lu Y, Li B, Sheng W, Lu H, Jin A, Zhou X: Expression of ALK protein, mRNA and fusion transcripts in anaplastic large cell lymphoma. Exp Mol Pathol; 2009 Apr;86(2):121-6
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  • [Title] Expression of ALK protein, mRNA and fusion transcripts in anaplastic large cell lymphoma.
  • Systemic anaplastic large cell lymphoma (ALCL) can be divided into two subgroups, anaplastic lymphoma kinase (ALK)-positive and ALK-negative, based on the expression of ALK protein.
  • Expression of this protein is due to genetic alterations of ALK at 2p23.
  • Overall, observations on ALK protein, ALK mRNA, ALK-associated genetic alterations and their relationships, to one another are not often reported in the literature.
  • In this study, we investigated the expression of ALK protein, mRNA and fusion transcripts involving ALK and their relationships in ALCL and analyzed formalin-fixed, paraffin-embedded tissues.
  • Forty-five human cases were analyzed with immunohistochemistry for the ALK protein and RT-PCR for ALK mRNA and seven kinds of ALK involved fusion transcripts.
  • Our results showed that the expression of ALK protein, ALK mRNA and ALK fusion transcripts were significantly related to one another (P<0.01).
  • Consistent with the expression of ALK protein, patients presenting with ALK mRNA or ALK involved fusion transcripts were significantly younger than those lacking ALK gene alteration (P<0.01).
  • This study demonstrates expression of both ALK protein and ALK mRNA are positively correlated with expression of ALK-associated fusion transcripts.
  • Combined detection of ALK protein, ALK mRNA and ALK fusion transcripts can complement each other to aid in the diagnosis of ALCL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19135051.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 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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79. Van Roosbroeck K, Cools J, Dierickx D, Thomas J, Vandenberghe P, Stul M, Delabie J, De Wolf-Peeters C, Marynen P, Wlodarska I: ALK-positive large B-cell lymphomas with cryptic SEC31A-ALK and NPM1-ALK fusions. Haematologica; 2010 Mar;95(3):509-13
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  • [Title] ALK-positive large B-cell lymphomas with cryptic SEC31A-ALK and NPM1-ALK fusions.
  • We report 2 ALK-positive large B-cell lymphoma cases showing granular cytoplasmic and cytoplasmic/nuclear ALK immunostaining in which cryptic ALK rearrangements were identified by fluorescent in situ hybridization and molecular analysis.
  • In the first case, the ALK-involving t(2;3)(p23;q27) masked the cryptic SEC31A-ALK fusion generated by an insertion of the 5' end of SEC31A (4q21) upstream of the 3' end of ALK.
  • This rearrangement was associated with loss of the 5' end of ALK and duplication of SEC31A-ALK on der(20).
  • In the second case with complex rearrangements of both chromosomes 2, a submicroscopic NPM1-ALK fusion created by insertion of the 3' end of ALK into the NPM1 locus was evidenced.
  • Further studies of SEC31A-ALK showed that this variant fusion transforms IL3-dependent Ba/F3 cells to growth factor independence, and that the ALK inhibitor TAE-684 reduces cell proliferation and kinase activity of SEC31A-ALK and its downstream effectors ERK1/2, AKT, STAT3 and STAT5.
  • [MeSH-major] Gene Rearrangement. Lymphoma, Large B-Cell, Diffuse / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Vesicular Transport Proteins / genetics

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  • (PMID = 20207848.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / SEC31A protein, human; 0 / Vesicular Transport Proteins; 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
  • [Other-IDs] NLM/ PMC2833084
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80. Lee HW, Kim K, Kim W, Ko YH: ALK-positive diffuse large B-cell lymphoma: report of three cases. Hematol Oncol; 2008 Jun;26(2):108-13
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of three cases.
  • Diffuse large B-cell lymphoma positive for anaplastic lymphoma kinase (ALK(+) DLBCL) is a rare variant of diffuse large B-cell lymphoma, with characteristic morphological, immunohistochemical and cytogenetic features.
  • Only 34 cases of ALK-positive diffuse large B-cell lymphoma have so far been reported in the literature.
  • We examined three new cases, which showed similar characteristics to previously reported cases, but with peculiar nuclear-membrane staining for ALK protein in one patient and a 5'-ALK gene deletion in another.
  • The tumour cells showed immunoblastic/plasmablastic histology and were positive for ALK and Oct2, but negative for CD3, CD20, CD79a, CD30 and PAX5.
  • The staining pattern of ALK protein was cytoplasmic in two patients and associated with the nuclear membrane in one patient.
  • Fluorescence in situ hybridization (FISH) analysis using the ALK break-apart probe revealed ALK gene rearrangements in all three patients, with a 5'-ALK gene deletion in one patient.
  • These three cases suggest that different types of cytogenetic aberrations may involve the ALK gene in ALK-positive diffuse large B-cell lymphoma leading to peculiar immunohistochemical staining patterns.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / therapy. Protein-Tyrosine Kinases / biosynthesis. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Cell Nucleus / metabolism. Chromosome Aberrations. Cytogenetics. Female. Gene Deletion. Humans. Immunohistochemistry. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Receptor Protein-Tyrosine Kinases. Treatment Outcome

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  • (PMID = 18220322.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [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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81. Kapur S, Tiemann M, Menke MA, Schubert C, Parwaresch R: The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases. Indian J Med Res; 2005 Jan;121(1):46-54
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  • [Title] The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases.
  • BACKGROUND AND OBJECTIVES: Molecular events that precede transformations from lymphomatoid palulosis (LyP) to mycosis fungoides (MF) or to cutaneous anaplastic large cell lymphoma (ALCL) in the CD 30(+) cutaneous lymphoproliferative diseases (LPDs) are not known.
  • Expression of the anaplastic lymphoma kinase (ALK) gene product has also been described as an important prognostic indicator in ALCL.
  • ALK positive systemic nodal ALCL are associated with a good prognosis.
  • However, primary cutaneous ALCL that are ALK negative have a better overall survival.
  • The current study was done to see if mutated p(53) gene or ALK reactivity were poor prognostic indicators in those patients with CD 30(+) cutaneous LPD who showed progression of the disease.
  • METHODS: Mutations of the p(53) gene and expression of the ALK gene product were analysed in 36 patients (23 of LyP and 13 of CD30(+) cutaneous ALCL).
  • Transformation occurred in 5 patients (4 from LyP to ALCL and 1 from MF to ALCL) and clinical progression in 4 patients with ALCL.
  • ALK gene products were not detected in any of the biopsy specimens of LyP and primary cutaneous ALCL.
  • INTERPRETATION AND CONCLUSION: Although 9 of 36 patients with cutaneous CD30(+) LPDs had progression of their disease, neither mutations of the p(53) gene nor ALK immunoreactivity were found in any of these biopsies.

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  • (PMID = 15713979.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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82. Thornber K, Colomba A, Ceccato L, Delsol G, Payrastre B, Gaits-Iacovoni F: Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas. Oncogene; 2009 Jul 23;28(29):2690-6
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  • [Title] Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas.
  • The chimera nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), the tyrosine kinase activity of which is constitutively upregulated, is the causative agent of 75% of the anaplastic large-cell lymphomas (ALCLs).
  • We have demonstrated that NPM-ALK induces the production of reactive oxygen species (ROS) by a pathway involving the arachidonic acid-metabolizing enzymes of the lipoxygenase (LOX) family.
  • The use of the LOX inhibitor nordihydroguaiaretic acid (NDGA) and of the anti-oxidant N-acetylcysteine (NAC) demonstrated that ROS are important in maintaining the ALK kinase active.
  • Consistent with this, NDGA treatment resulted in the inhibition of key pathways, such as Akt, signal transducer and activator of transcription factor 3 (STAT3) and extracellular signal-regulated kinase (ERK), which are involved in NPM-ALK antiapoptotic and pro-mitogenic functions.
  • Interestingly, 5-LOX, an isoform involved in many cancers, was found to be activated in NPM-ALK(+) cells.
  • Together, these data point to the ROS/LOX pathway as a potential new target for therapy in NPM-ALK-positive tumors.
  • [MeSH-major] Arachidonate 5-Lipoxygenase / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Humans. Lipoxygenase Inhibitors / pharmacology. Masoprocol / analysis

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  • (PMID = 19503098.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipoxygenase Inhibitors; 0 / Reactive Oxygen Species; 7BO8G1BYQU / Masoprocol; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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83. Mencía-Gutiérrez E, Gutiérrez-Díaz E, Salamanca J, Martínez-González MA: Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL). Int J Dermatol; 2006 Jun;45(6):766-9
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  • [Title] Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL).
  • AIM: To report an unusual case of cutaneous presentation on the eyelid of systemic (or nodal), CD30+, anaplastic large-cell lymphoma (ALCL).
  • RESULTS: The histopathologic and immunohistochemical diagnosis was ALCL, T-cell phenotype, strongly positive for CD43 and CD30, and negative for CD3, anaplastic lymphoma kinase (ALK), and B-cell antigens.
  • 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

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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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84. Kameoka J, Ichinohasama R, Inoue H, Yamamoto J, Yokoyama H, Tomiya Y, Yamada M, Ishizawa K, Harigae H, Sawai T, Sasaki T: CD26, together with cell surface adenosine deaminase, is selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma. Leuk Lymphoma; 2006 Oct;47(10):2181-8
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  • [Title] CD26, together with cell surface adenosine deaminase, is selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma.
  • CD26/dipeptidyl peptidase IV is a cell surface antigen with multiple biological functions.
  • Although its involvement in tumor biology has been suggested, the significance of its expression in malignant lymphoma has not been clarified in detail.
  • This study examined the expression of CD26 and cell surface adenosine deaminase (ADA) in 42 cases of Hodgkin's lymphoma (HL) and T-cell lymphoma by immunohistochemistry on frozen sections.
  • CD26 was expressed in three of 14 cases of HL, in four of eight cases of anaplastic large cell lymphoma (ALCL), in two of nine cases of peripheral T-cell lymphoma, in one of six cases of lymphoblastic lymphoma and in none of three cases of adult T-cell lymphoma/leukemia.
  • Expression of cell surface ADA was fully correlated with the expression of CD26 and expression of CD26/ADA in ALCL and HL was also completely correlated with the expression of p80 and epithelial membrane antigen.
  • Of 10 CD26-positive patients, seven had fever and elevated CRP at initial diagnosis and over a median follow-up of 61 months (range, 7 - 152 months) only three survived.
  • This study suggested that CD26 is selectively expressed on ALK-positive, but not on ALK-negative, ALCL and HL.
  • This is also the first report to demonstrate that ADA is coexpressed with CD26 on the cell surface of malignant neoplasms in vivo.
  • [MeSH-major] Adenosine Deaminase / biosynthesis. Cell Membrane / enzymology. Dipeptidyl Peptidase 4 / biosynthesis. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / biosynthesis

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  • (PMID = 17071493.001).
  • [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 / Antigens, CD3; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.5.4.4 / Adenosine Deaminase
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85. Georgakis GV, Li Y, Rassidakis GZ, Medeiros LJ, Younes A: The HSP90 inhibitor 17-AAG synergizes with doxorubicin and U0126 in anaplastic large cell lymphoma irrespective of ALK expression. Exp Hematol; 2006 Dec;34(12):1670-9
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  • [Title] The HSP90 inhibitor 17-AAG synergizes with doxorubicin and U0126 in anaplastic large cell lymphoma irrespective of ALK expression.
  • OBJECTIVE: Heat shock protein 90 (HSP90) chaperones and maintains the molecular integrity of a variety of signal transduction proteins, including the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) oncogenic protein, a genetic abnormality that is frequently observed in anaplastic large cell lymphoma (ALCL) cells.
  • Here we demonstrate that HSP90 is overexpressed in primary and cultured ALK-positive and ALK-negative ALCL cells, and we evaluate the potential role of the small molecule inhibitor of HSP90, 17-allylamino-17-demethoxygeldanamycin (17-AAG) in treating ALCL.
  • Apoptosis and cell-cycle arrest were determined by Annexin-V/propidium iodide and propidium iodide staining, respectively, and fluorescein-activated cell sorting analysis.
  • RESULTS: Treatment of cultured ALCL cells with 17-AAG induced cell-cycle arrest and apoptosis, irrespective of ALK expression.
  • At the molecular level, 17-AAG induced degradation of ALK and Akt proteins, dephosphorylated extracellular signal-regulated kinase, and degraded the cell-cycle regulatory protein cyclin D1 and its cyclin-dependent kinases, CDK4 and CDK6, but had a differential effect on p27 and p53 proteins.
  • Inhibition of extracellular signal-regulated kinase phosphorylation by the mitogen activated protein kinase inhibitor U0126 induced cell death in all ALCL cell lines, and sublethal concentration 17-AAG showed synergistic antiproliferative effects when combined with U0126 or doxorubicin.
  • CONCLUSION: Our data demonstrate that targeting HSP90 function by 17-AAG may offer a novel therapeutic strategy for ALCL, either as single-agent activity or by combining 17-AAG with conventional or targeted therapeutic schemes.
  • [MeSH-major] Benzoquinones / pharmacology. Butadienes / pharmacology. Doxorubicin / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / pharmacology. Lymphoma, Large-Cell, Anaplastic / metabolism. Nitriles / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis / drug effects. Caspase 3 / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D. Cyclin-Dependent Kinase 4 / drug effects. Cyclin-Dependent Kinase 4 / metabolism. Cyclin-Dependent Kinase 6 / drug effects. Cyclin-Dependent Kinase 6 / metabolism. Cyclins / drug effects. Cyclins / metabolism. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Drug Synergism. Extracellular Signal-Regulated MAP Kinases / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. G0 Phase / drug effects. G1 Phase / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / drug effects. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / drug effects. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphorylation. Receptor Protein-Tyrosine Kinases. Time Factors

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  • (PMID = 17157164.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Butadienes; 0 / Cyclin D; 0 / Cyclins; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Nitriles; 0 / U 0126; 4GY0AVT3L4 / tanespimycin; 80168379AG / Doxorubicin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.22.- / Caspase 3
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86. 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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  • [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.
  • Reverse transcription polymerase chain reaction detected NPM1-ALK in 58 tumours, all showing nuclear and cytoplasmic ALK staining.
  • 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.
  • There was complete concordance between ALK staining pattern and the presence of a typical/variant ALK fusion partner.
  • [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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87. Zhang Q, Wang HY, Bhutani G, Liu X, Paessler M, Tobias JW, Baldwin D, Swaminathan K, Milone MC, Wasik MA: Lack of TNFalpha expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15843-8
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  • [Title] Lack of TNFalpha expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis.
  • Here we report that T-cell lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express the TNFalpha and frequently display DNA methylation of the TNFalpha gene promoter.
  • While only a subset of the ALK+ TCL-derived cell lines showed a high degree of the promoter methylation, all 6 showed low to nondetectable expression of the TNFalpha mRNA, and none expressed the TNFalpha protein.
  • All 14 ALK+ TCL tissue samples examined displayed some degree of the TNFalpha promoter methylation, which was the most prominent in the distal portion of the the promoter.
  • Notably, the ALK+ TCL cell lines uniformly expressed the type 1 TNFalpha receptor (TNF-R1) protein known to transduce the TNFalpha-induced pro-apoptotic signals.
  • Moreover, exogenous TNFalpha inhibited growth of the ALK+ TCL cell lines in a dose-dependent manner and induced activation of the members of the cell apoptotic pathway: Caspase 8 and caspase 3.
  • These findings provide additional rationale for the therapeutic inhibition of DNA methyltransferases in ALK+ TCL.
  • They also suggest that treatment with TNFalpha may be highly effective in this type of lymphoma.

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  • (PMID = 19717436.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089194; United States / NCI NIH HHS / CA / R01 CA096856; United States / NCI NIH HHS / CA / R01-CA89194; United States / NCI NIH HHS / CA / R01-CA96856
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2747206
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88. Zhang D, Denley RC, Filippa DA, Teruya-Feldstein J: ALK-positive diffuse large B-cell lymphoma with the t(2;17)(p23;q23). Appl Immunohistochem Mol Morphol; 2009 Mar;17(2):172-7
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  • [Title] ALK-positive diffuse large B-cell lymphoma with the t(2;17)(p23;q23).
  • Diffuse large B-cell lymphoma (DLBCL) with plasmablastic features associated with t(2;17)(p23;q23) and characteristic granular cytoplasmic anaplastic lymphoma kinase-1 (ALK1) protein expression is a rare lymphoma subtype.
  • Lymph node biopsy showed large atypical cells with prominent plasmablastic differentiation, abundant amphophilic cytoplasm, and prominent central nucleoli.
  • Paraffin immunohistochemistry showed finely granular cytoplasmic ALK1 expression, positive CD138, IgA, p63 (VS38), focal positive epithelial membrane antigen and CD4, and lambda light chain restriction whereas negative CD20 and CD30 staining.
  • While reports show detection of the unique CLTC-ALK fusion by either reverse transcription-polymerase chain reaction or fluorescence in situ hybridization, our case represents the second case in the literature to detect the t(2;17)(p23;q23) translocation by multiplex karyotyping (multiplex fluorescence in situ hybridization) and the usefulness of this technique to detect hidden translocations not seen by G-banding.
  • Differential diagnoses of neoplasms with plasmablastic differentiation and a comprehensive molecular/cytogenetic literature review of ALK+DLBCL is discussed.

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  • (PMID = 19521280.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [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 II
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89. Fernandez-Vidal A, Mazars A, Gautier EF, Prévost G, Payrastre B, Manenti S: Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation. Cell Cycle; 2009 May 1;8(9):1373-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation.
  • Here, we demonstrate that the expression of the dual specificity phosphatase CDC25A, a key regulator of cell cycle progression, is deregulated in Ba/F3 cells expressing the oncogenic protein NPM/ALK and in human cell lines derived from NPM/ALK-positive anaplastic large cell lymphomas (ALCL).
  • Importantly, pharmacological inhibition of CDC25 dramatically inhibits the proliferation of NPM/ALK-expressing cells, while moderately affecting the proliferation of control Ba/F3 cells.
  • RNA interference-mediated downregulation of CDC25A confirmed that NPM/ALK-expressing cells are highly dependent on this protein for their proliferation.
  • Altogether, our data point to the functional link between hematopoietic oncogenic tyrosine kinases and the G(1) cell cycle regulator CDC25A, and we propose that this protein may be a potential therapeutic target in ALCL and other hematological malignancies.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / pathology. Oncogenes. Protein-Tyrosine Kinases / metabolism. Up-Regulation. cdc25 Phosphatases / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. Oncogene Proteins, Fusion / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction

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  • (PMID = 19305144.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.16 / Cdc25a protein, mouse; EC 3.1.3.48 / CDC25A protein, human; EC 3.1.3.48 / cdc25 Phosphatases
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90. 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

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


92. Gonin J, Kadiri H, Bensaci S, Le Tourneau A, Molina TJ, Diebold J, Abdellouche DJ, Audouin J: Primary mediastinal anaplastic alk-1-positive large-cell lymphoma of T/NK-cell type expressing CD20. Virchows Arch; 2007 Mar;450(3):355-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary mediastinal anaplastic alk-1-positive large-cell lymphoma of T/NK-cell type expressing CD20.
  • We describe an unusual case of ALK-1-positive primary mediastinal lymphoma with the morphology of an anaplastic large-cell lymphoma (ALCL) of T/NK cell type but expressing CD20.
  • This tumour had T/NK morphology and immunophenotype, as demonstrated by its expression of CD30, EMA, ALK-1, CD7 and TiA-1 and the lack of expression of B-cell markers other than CD20.
  • The significance of such a co-expression of a B cell-associated antigen in a case of ALCL of T/NK cell type is discussed.
  • [MeSH-major] Activin Receptors, Type II / metabolism. Antigens, CD20 / metabolism. Killer Cells, Natural / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Mediastinal Neoplasms / pathology. T-Lymphocytes / pathology

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  • (PMID = 17252228.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Biomarkers, Tumor; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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93. Li HL, Jiang HY, Ji TH, Chu HJ, Liu F, Chen XY, Wang X, Zhang G, Zhao T: [Nuclear microarray combined with fluorescence in situ hybridization for detecting ALK gene translocation in paraffin-embedded anaplastic large cell lymphoma and its significance]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Apr;28(4):572-5
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  • [Title] [Nuclear microarray combined with fluorescence in situ hybridization for detecting ALK gene translocation in paraffin-embedded anaplastic large cell lymphoma and its significance].
  • OBJECTIVE: To compare the efficacy of nuclear microarray combined with fluorescence in situ hybridization (FISH) and immunohistochemistry in detecting ALK gene translocation and ALK fusion protein in anaplastic large cell lymphoma (ALCL).
  • METHODS: ALK gene translocation and ALK fusion protein in 17 paraffin-embedded ALCL specimens were detected using nuclear microarray combined with FISH and immunohistochemical straining, respectively.
  • RESULTS: The expression of ALK fusion protein was detected immunohistochemically with ALK antibody in 8 of the 17 specimens of systemic ALCL, including 4 with both nuclear and cytoplasmic positivity and 4 with only cytoplasmic positivity.
  • Dual-color FISH identified 6 positive specimens, including the 4 specimens with both nuclear and cytoplasmic positivity as identified immunohistochemically, and 2 with immunohistochemical cytoplasmic positivity.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics. Translocation, Genetic

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  • (PMID = 18495593.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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94. Iqbal J, Weisenburger DD, Greiner TC, Vose JM, McKeithan T, Kucuk C, Geng H, Deffenbacher K, Smith L, Dybkaer K, Nakamura S, Seto M, Delabie J, Berger F, Loong F, Au WY, Ko YH, Sng I, Armitage JO, Chan WC, International Peripheral T-Cell Lymphoma Project: Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma. Blood; 2010 Feb 4;115(5):1026-36
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  • [Title] Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma.
  • Peripheral T-cell lymphoma (PTCL) is often challenging to diagnose and classify.
  • Gene expression profiling was performed on 144 cases of PTCL and natural killer cell lymphoma and robust molecular classifiers were constructed for angioimmunoblastic T-cell lymphoma (AITL), anaplastic lymphoma kinase-positive (ALK(+)) anaplastic large-cell lymphoma (ALCL), and adult T-cell leukemia/lymphoma.
  • Many of the pathologic features and substantial components of the molecular signature of AITL are contributed by the follicular dendritic cells, B-cell, and other stromal components.
  • The expression of Th17-associated molecules in ALK(+) ALCL was noted and may represent aberrant activation of Th17-cell differentiation by abnormal cytokine secretion.
  • Adult T-cell leukemia/lymphoma has a homogeneous molecular signature demonstrating high expression of human T-lymphotropic virus type 1-induced genes.

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  • (PMID = 19965671.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE19069
  • [Grant] United States / NCI NIH HHS / CA / U01 CA114778; United States / NCI NIH HHS / CA / CA36727; United States / NCRR NIH HHS / RR / P20 RR016469; United States / NCI NIH HHS / CA / 5U01/CA114778; United States / NCI NIH HHS / CA / P30 CA036727
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2817630
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95. Reichard KK, McKenna RW, Kroft SH: ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature. Mod Pathol; 2007 Mar;20(3):310-9
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] ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature.
  • We report detailed clinical and pathologic features of four cases of anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma (ALK-DLBCL), a rare entity with only 29 currently reported cases.
  • By immunohistochemistry and/or flow cytometry, they expressed cytoplasmic ALK-1, CD138, VS38 (3/3), monoclonal cytoplasmic light chain, CD45, EMA, CD4, and CD57 (2/3), and were negative for CD3, CD30, CD56, and TIA-1.
  • [MeSH-major] Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 17277765.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 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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