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1. Prochazka V, Faber E, Raida L, Vondrakova J, Kucerova L, Jarosova M, Indrak K, Papajik T: Prolonged survival of patients with peripheral T-cell lymphoma after first-line intensive sequential chemotherapy with autologous stem cell transplantation. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub; 2009 Mar;153(1):63-6
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  • [Title] Prolonged survival of patients with peripheral T-cell lymphoma after first-line intensive sequential chemotherapy with autologous stem cell transplantation.
  • BACKGROUND: Nodal peripheral T-cell lymphomas (PTCLs) are infrequent subtypes of non-Hodgkin's lymphomas.
  • The WHO classification recognizes three subgroups of nodal PTCL: peripheral T-cell lymphoma not otherwise specified (PTCL, NOS), anaplastic large cell lymphoma (ALCL) and angioimmunoblastic lymphoma (AIL).
  • Optimal first-line chemotherapy is not established and the role of high-dose therapy with autologous stem cell support is still controversial.
  • Consolidation was provided with myeloablative conditioning (BEAM 200) and autologous stem cell support.
  • Eighty-four patients with aggressive high-risk lymphoma were treated with the sequential protocol from 2000 to 2007 in our institution.
  • Here we report our experience with 18 patients with nodal PTCL (10 PTCL, NOS; 3 ALCL, ALKnegative; 2 ALCL, ALK-positive; 2 ALCL, unknown ALK status; 1 AIL).
  • After a median follow-up of 25.7 months, nine patients relapsed or progressed (6 PTCL, NOS; 2 ALCL ALK-positive; 1 ALCL ALK-negative; median 14.1 months) and four patients died (lymphoma progression).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Lymphoma, T-Cell, Peripheral / mortality. Lymphoma, T-Cell, Peripheral / therapy

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  • (PMID = 19365529.001).
  • [ISSN] 1213-8118
  • [Journal-full-title] Biomedical papers of the Medical Faculty of the University Palacký, Olomouc, Czechoslovakia
  • [ISO-abbreviation] Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
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2. 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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3. 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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  • [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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4. Schmitz N, Trümper L, Ziepert M, Nickelsen M, Ho AD, Metzner B, Peter N, Loeffler M, Rosenwald A, Pfreundschuh M: Treatment and prognosis of mature T-cell and NK-cell lymphoma: an analysis of patients with T-cell lymphoma treated in studies of the German High-Grade Non-Hodgkin Lymphoma Study Group. Blood; 2010 Nov 4;116(18):3418-25
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  • [Title] Treatment and prognosis of mature T-cell and NK-cell lymphoma: an analysis of patients with T-cell lymphoma treated in studies of the German High-Grade Non-Hodgkin Lymphoma Study Group.
  • To evaluate outcome and prognosis of patients with T-cell lymphoma we analyzed 343 patients treated within trials of the German High-Grade Non-Hodgkin Lymphoma Study Group (DSHNHL).
  • Two hundred eighty-nine patients belonged to 1 of the 4 major T-cell lymphoma subtypes: anaplastic large cell lymphoma (ALCL), anaplastic large cell lymphoma kinase (ALK)-positive (n = 78); ALCL, ALK-negative (n = 113); peripheral T-cell lymphoma, unspecified (PTCLU; n = 70); and angioimmunoblastic T-cell lymphoma (AITL; n = 28).
  • Three-year event-free survival (EFS) and overall survival were 75.8% and 89.8% (ALK-positive ALCL), 50.0% and 67.5% (AITL), 45.7% and 62.1% (ALK-negative ALCL), and 41.1% and 53.9% (PTCLU), respectively.
  • Patients with ALK-negative ALCL, PTCLU, or AITL presenting with IPI > 1 have a poor prognosis and should be considered candidates for novel treatment strategies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Cohort Studies. Cyclophosphamide / administration & dosage. Cyclophosphamide / therapeutic use. Doxorubicin / administration & dosage. Doxorubicin / therapeutic use. Female. Humans. Killer Cells, Natural / pathology. Lymphoma, Extranodal NK-T-Cell / diagnosis. Lymphoma, Extranodal NK-T-Cell / drug therapy. Lymphoma, Extranodal NK-T-Cell / pathology. Male. Middle Aged. Prednisone / administration & dosage. Prednisone / therapeutic use. Prognosis. Treatment Outcome. Vincristine / administration & dosage. Vincristine / therapeutic use. Young Adult


5. Savopoulos CG, Tsesmeli NE, Kaiafa GD, Zantidis AT, Bobos MT, Hatzitolios AI, Papavramidis ST, Kostopoulos IS: Primary pancreatic anaplastic large cell lymphoma, ALK negative: a case report. World J Gastroenterol; 2005 Oct 21;11(39):6221-4
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  • [Title] Primary pancreatic anaplastic large cell lymphoma, ALK negative: a case report.
  • We present the fourth case of a primary pancreatic anaplastic large cell lymphoma (ALCL), ALK-.
  • Duodenal and surgical biopsies identified an ALCL of T-cell lineage, ALK-.
  • Our case is the first one indicating that primary pancreatic lymphoma should be suspected in a patient with pancreatic mass and elevated serum LDH and beta(2) microglobulin.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Pancreatic Neoplasms / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16273656.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [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
  • [Number-of-references] 12
  • [Other-IDs] NLM/ PMC4436646
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6. 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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7. Khor TS, Alessandri AJ, Jevon GP: Infant anaplastic large cell lymphoma with hemophagocytic syndrome. Pediatr Dev Pathol; 2010 Jan-Feb;13(1):72-6
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  • [Title] Infant anaplastic large cell lymphoma with hemophagocytic syndrome.
  • Anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK)-positive, is uncommon in infancy.
  • We present an unusual occurrence of infant ALCL, ALK-positive, associated with hemophagocytic syndrome.
  • To the best of our knowledge, there have been no cases of infant ALCL, ALK-positive, described that have been associated with hemophagocytic syndrome.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 19863446.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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8. Aitova LG, Vinogradova IuE, Kaplanskaia IB, Lutsenko IN, Zvonkov EE, Momotiuk KS, Kravchenko SK, Kremenetskaia AM, Vorob'ev AI: [High-dose polychemotherapy of patients with poor-prognosis anaplastic T.0-large cell ALK+ lymphosarcoma]. Ter Arkh; 2009;81(7):53-7
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  • [Title] [High-dose polychemotherapy of patients with poor-prognosis anaplastic T.0-large cell ALK+ lymphosarcoma].
  • AIM: To evaluate efficacy of the protocol NHL BFM-90 in the treatment of adult anaplastic large cell lymphosarcoma (ALCL) ALK+ and validity of addition of transplantation of autologous stem hemopoietic cells (ASHC) into first line treatment.
  • MATERIAL AND METHODS: We treated 13 patients with stage III-IV ALCL ALK+.
  • The diagnosis was made using morphological, histological, immunohistochemical methods with application of monoclonal antibodies to CD30, ALK, CD3, CD4, CD8, CD7, CD34, CD15, CD68, CD20, CD45RO, CD45RA.
  • CONCLUSION: ALCL ALK+ is characterized by an aggressive clinical course (11 of 13 patients had stage III-IV), high rate of extranodal lesions.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 19708574.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [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. Macák J, Falková I, Smardová J, Kren L: [Lymphoma of the small intestine]. Cesk Patol; 2010 Jan;46(1):20-4
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  • [Title] [Lymphoma of the small intestine].
  • A series of eight small intestine lymphomas comprised two cases of follicular lymphoma (FL), one anaplastic large cell lymphoma (ALCL) ALK negative, and five cases of diffuse large B-cell lymphoma.
  • Immunohistochemistry revealed that the diffuse large B-cell lymphomas were of the non-germinal center type (non GC-DLBCL).
  • In one case of follicular lymphoma, microscopic foci of tumor were found in the intestinal mucosa which spread far from the primary nodule and probably beyond the resection border.
  • It is difficult to ascertain whether this phenomenon represents colonization of pre-existing non-neoplastic follicles by lymphoma or spreading of the tumor within the same tissue.
  • In this case, surgical removal of the lymphoma is problematic.
  • [MeSH-major] Intestinal Neoplasms / pathology. Intestine, Small. Lymphoma, Follicular / pathology. Lymphoma, Large B-Cell, Diffuse / pathology

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  • (PMID = 21280278.001).
  • [ISSN] 1210-7875
  • [Journal-full-title] Československá patologie
  • [ISO-abbreviation] Cesk Patol
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
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10. Ziarkiewicz-Wróblewska B, Górnicka B, Gierej B, Suleiman W, Nowacka-Cieciura E, Durlik M, Bogdańska M, Wasiutyński A, Pileri SA: Hodgkin-like lymphoma, simulating anaplastic large cell lymphoma in the patient after renal transplantation--unusual case report and literature review. Pol J Pathol; 2008;59(1):63-9
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  • [Title] Hodgkin-like lymphoma, simulating anaplastic large cell lymphoma in the patient after renal transplantation--unusual case report and literature review.
  • We report the atypical case of posttransplant lymphoproliferative disorder (PTLD) diagnosed in 55-year men 9 years after renal transplantation.
  • It was evaluated only by bone marrow biopsy, which showed its total involvement with malignant lymphoma.
  • It was composed of two populations of lymphoid cells: large RS-like cells and small to medium ones, with slightly angular nuclei without visible nucleoli.
  • Both cellpopulations did not show positive reaction for typical B cell markers (CD20, CD79a).
  • Large RS-like cells were positive with CD30 and EBV-LMP.
  • However, negative reaction with CD15 and positive reactions with UCHL1 and EMA were not consistent with classical type of Hodgkin lymphoma.
  • Morphological picture and immunophenotype had suggested anaplastic T cell lymphoma.
  • Because of negative reaction with ALK1, initial diagnosis was ALCL ALK-negative.
  • Then, additional stains with BOB1 and Oct2 were performed, which were positive.
  • Taking it into account the diagnosis was changed; finally Hodgkin-like B lymphoma was diagnosed.
  • 2. Negative reactions with typical immunohistochemical markers for lymphocytes of B cell line do not exclude the possibility of B-cell proliferation.
  • [MeSH-major] Hodgkin Disease / diagnosis. Kidney Transplantation / adverse effects. Lymphoma, Large-Cell, Anaplastic / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antiviral Agents / therapeutic use. Biomarkers, Tumor / metabolism. Bone Marrow / metabolism. Bone Marrow / pathology. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Epstein-Barr Virus Infections / complications. Epstein-Barr Virus Infections / pathology. Ganciclovir / therapeutic use. Humans. Immunosuppression. Male. Middle Aged. Postoperative Complications. Prednisone / therapeutic use. Treatment Outcome. Vincristine / therapeutic use


11. Vera L, Reategui R, Beltran B, Morales D, Capellino A, Desposorio C, Castillo J: The clinicopathological spectrum of HIV-associated lymphoma: Eleven-year-experience in a general hospital in Peru. J Clin Oncol; 2009 May 20;27(15_suppl):e19561

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinicopathological spectrum of HIV-associated lymphoma: Eleven-year-experience in a general hospital in Peru.
  • METHODS: This is a retrospective review of the clinical records of patients with diagnosis of HIV in our institution from March 1997 to March 2008.
  • RESULTS: Forty-eight patients with HIV-associated lymphoma were identified.
  • Forty-four cases (92%) were diagnosed with non-Hodgkin lymphoma (NHL) and 4 cases (8%) with Hodgkin lymphoma (HL).
  • From the 44 NHL cases, 40 cases (91%) were of B-cell origin; 23 cases (57.5%) had diffuse large B-cell, 9 cases (22.5%) had Burkitt, 3 cases (7.5%) had plasmablastic, 2 cases (5%) had primary CNS, 2 cases (5%) had MALT and 1 case (2.5%) had primary effusion lymphoma.
  • The remaining 4 cases (9%) were of T-cell origin; 3 cases (75%) had peripheral T-cell lymphoma NOS and 1 case (25%) was ALK-negative anaplastic large cell lymphoma.
  • Only 16 patients (33%) were receiving HAART previously the diagnosis of NHL and 33 patients (68%) received any oncology treatment.

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  • (PMID = 27961062.001).
  • [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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12. 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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13. Kwak EL, Camidge DR, Clark J, Shapiro GI, Maki RG, Ratain MJ, Solomon B, Bang Y, Ou S, Salgia R: Clinical activity observed in a phase I dose escalation trial of an oral c-met and ALK inhibitor, PF-02341066. J Clin Oncol; 2009 May 20;27(15_suppl):3509

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical activity observed in a phase I dose escalation trial of an oral c-met and ALK inhibitor, PF-02341066.
  • : 3509 Background: PF-02341066 (PF) is a selective, ATP-competitive, small molecule oral inhibitor of the c-Met/HGFR and ALK receptor tyrosine kinases that has not previously been tested in humans.
  • Tumor types included colorectal, pancreatic, sarcoma, ALCL and NSCLC.
  • Ten pts have entered an enriched RP2D cohort of pts with tumors harboring c-Met amplification/gene mutation or ALK fusion genes.
  • There has been 1 confirmed PR in a sarcoma pt with ALK rearrangement (inflammatory myofibroblastic tumor).
  • Among 10 NSCLC pts whose tumors harbor EML4-ALK rearrangement, 1 pt has had a PR, 2 pts have achieved unconfirmed PR and 4 pts have had SD (3 have experienced reduction in tumor burden by ∼20% in measurable lesions and 1 has been treated for 28 weeks).
  • Treatment with PF-02341066 resulted in promising clinical activity against tumors carrying activating ALK gene rearrangements.
  • Further study of PF in pts with ALK-dependent tumors is warranted.

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  • (PMID = 27961297.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. 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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15. Schmitz N, Ziepert M, Nickelsen M, Wolf SP, Truemper L, Loeffler M, Ho A, Metzner B, Rosenwald A, Pfreundschuh M: Mature T-/NK-cell lymphomas: Prognostic factors and treatment outcome of patients treated on studies of the German High-Grade Lymphoma Study Group (DSHNHL). J Clin Oncol; 2009 May 20;27(15_suppl):8564

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

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  • (PMID = 27961019.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Oki M, Isozaki M, Nakamura N, Kikuchi A, Tsuchiya T, Arbogast P, Ogawa Y, Ando K: A multivariate analysis for the survival of nodal peripheral T-cell lymphoma (PTCL). J Clin Oncol; 2009 May 20;27(15_suppl):e19521

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

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  • (PMID = 27960935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Lansigan F, Cooper D, Seropian S, Foss F: Autologous and allogeneic transplantation for aggressive T-cell lymphomas: A single institution experience. J Clin Oncol; 2009 May 20;27(15_suppl):8558

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous and allogeneic transplantation for aggressive T-cell lymphomas: A single institution experience.
  • : 8558 Aggressive T-cell lymphomas (ATCL) represent 10-15% of non-Hodgkin lymphoma and have a worse prognosis than aggressive B-cell lymphomas.
  • Both autologous (Auto) and allogeneic (Allo) stem cell transplantation have been used as consolidation in first remission and at relapse, but the role of transplantation has not been clearly defined.
  • The Allo group consisted of 4 PTCLu, 3 angioimmunoblastic(AITL), 2 panniculitis-like, 2 cutaneous(CTCL) with large cell transformation, 2 NK-cell, 2 anaplastic large cell(ALCL), 1 hepatosplenic, 1 enteropathic, and 1 refractory CTCL.
  • The Auto group consisted of 6 PTCLu, 12 ALCL (5 Alk+, 5 Alk-, 2 Alk unk), 4 AITL, 1 CTCL with transformation, and 1 T-lymphoblastic lymphoma.
  • Median time from diagnosis to Allo or Auto was 18 and 8mo, respectively.

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  • (PMID = 27960993.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. 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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19. 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.


20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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21. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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22. Shi X, Franko B, Frantz C, Amin HM, Lai R: JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells. Br J Haematol; 2006 Oct;135(1):26-32
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  • [Title] JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells.
  • As STAT3 activation is pathogenetically important in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ ALCL), we investigated whether JSI-124 can mediate significant inhibitory effects in this cell type.
  • In two ALK+ ALCL cell lines (Karpas 299 and SU-DHL-1), JSI-124 significantly reduced the number of viable cells to 50% of that of negative controls at a dose of 5-10 micromol/l at 24 h and 1-1.25 micromol/l at 48 h.
  • JSI-124 decreased the phosphorylated-STAT3 and -Janus kinase-3 (JAK3) levels in a dose-dependent fashion, and these changes were coupled with significant decreases in several STAT3 downstream targets, including mcl-1, bcl-2, bcl-xL and cyclin D3.
  • 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
  • [MeSH-minor] Blotting, Western. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Janus Kinase 3. Signal Transduction / drug effects. Tumor Cells, Cultured

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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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23. 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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24. 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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  • [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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25. 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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  • [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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26. 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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27. 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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  • [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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28. 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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29. 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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  • [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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30. 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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  • [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.
  • Nutlin-3a is a recently developed small molecule that targets Mdm2, a critical negative regulator of p53, and disrupts the p53-Mdm2 interaction resulting in p53 stabilization and activation.
  • 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


31. Marschalkó M, Eros N, Holló P, Hársing J, Bottlik G, Bátai A, Csukly Z, Masszi T, Szentirmai Z, Fodor J, Kárpáti S, Matolcsy A, Csomor J: Secondary ALK negative anaplastic large cell lymphoma in a patient with lymphomatoid papulosis of 40 years duration. Am J Dermatopathol; 2010 Oct;32(7):708-12
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  • [Title] Secondary ALK negative anaplastic large cell lymphoma in a patient with lymphomatoid papulosis of 40 years duration.
  • At age 44, regional lymph node manifestation of anaplastic lymphoma kinase (ALK) anaplastic large cell lymphoma (ALCL) developed.
  • Histology and immunohistochemistry showed congruent characteristics of multiple skin and lymph node biopsies: diffuse mixed infiltrate with large, anaplastic CD30 cells.
  • Immunophenotype and microscopic morphology suggested a common origin of the different manifestations-however, this could not be proven due to lack of T-cell receptor (TCR) gamma gene rearrangement in most of the samples.
  • The diagnosis of ALK-negative systemic ALCL with cutaneous symptoms was set up at the second flare up, however, the possibility of primary cutaneous ALCL was not excluded steadily.
  • Lymphomatoid papulosis, primary cutaneous ALCL, and systemic ALK ALCL are 3 different entities but the separation of them cannot be solved without distinctive diagnostic tools.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphomatoid Papulosis / pathology. Neoplasms, Second Primary / pathology. Skin Neoplasms / pathology

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  • (PMID = 20644462.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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32. Medeiros LJ, Elenitoba-Johnson KS: Anaplastic Large Cell Lymphoma. Am J Clin Pathol; 2007 May;127(5):707-22
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  • [Title] Anaplastic Large Cell Lymphoma.
  • Session 8 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop was devoted to anaplastic large cell lymphoma (ALCL).
  • Most cases submitted were anaplastic lymphoma kinase (ALK)+ ALCL highlighting unusual clinical settings, histologic variants, and variant translocation partners.
  • Cases submitted as ALK- ALCL emphasized the immunohistochemical overlap with classical Hodgkin lymphoma (eg, CD15+/CD30+).
  • It was also clear that consensus histologic and immunohistochemical criteria for the diagnosis of ALK-ALCL are lacking.
  • Many expressed the opinion that ALK-ALCL is not a distinct entity at the immunophenotypic or genetic level and is better designated as peripheral T-cell lymphoma (PTCL), unspecified.
  • Others suggested that the histologic features of ALK-ALCL are distinctive nevertheless and that this diagnosis has meaning that is lost by designating these neoplasms as PTCL, unspecified.
  • This session also included CD30+ anaplastic lymphomas involving skin in which the differential diagnosis included cutaneous ALCL and systemic ALK-ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / analysis

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  • (PMID = 17511113.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 40
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33. Bard JD, Gelebart P, Anand M, Amin HM, Lai R: Aberrant expression of IL-22 receptor 1 and autocrine IL-22 stimulation contribute to tumorigenicity in ALK+ anaplastic large cell lymphoma. Leukemia; 2008 Aug;22(8):1595-603
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  • [Title] Aberrant expression of IL-22 receptor 1 and autocrine IL-22 stimulation contribute to tumorigenicity in ALK+ anaplastic large cell lymphoma.
  • One of the characteristic features of anaplastic lymphoma kinase (ALK)(+), anaplastic large cell lymphoma (ALK(+)ALCL) is the constitutive activation of signal transducers and activators of transcription-3 (STAT3), a defect believed to be important for the pathogenesis of these tumors.
  • In this report, we describe the existence of an autocrine stimulatory loop involving interleukin-22 (IL-22) that contributes to STAT3 activation and tumorigenicity of ALK(+)ALCL.
  • The IL-22 receptor, a heterodimer composed of IL-22R1 and IL-10R2, was expressed in all ALK(+)ALCL cell lines and tumors examined.
  • The expression of IL-22R1 in ALK(+)ALCL is aberrant, as this protein is absent in benign lymphocytes.
  • Although ALK(+)ALCL cells produce endogenous IL-22, addition of recombinant IL-22 to ALK(+)ALCL cell lines significantly increased STAT3 activation, cell proliferation and colony formation in soft agar.
  • Nucleophosmin (NPM)-ALK, the characteristic fusion gene oncoprotein expressed in ALK(+)ALCL, directly contributes to the aberrant expression of IL-22R1, as transfection of NPM-ALK in Jurkat cells-induced IL-22R1 expression and IL-22-mediated STAT3 activation.
  • To conclude, for the first time, we demonstrate the importance of the IL-22 autocrine pathway in a lymphoid malignancy, and reveal yet another novel function of NPM-ALK.

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  • (PMID = 18509351.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395; United States / NCI NIH HHS / CA / CA114395
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Interleukins; 0 / RNA, Small Interfering; 0 / Receptors, Interleukin; 0 / STAT3 Transcription Factor; 0 / interleukin-22; 0 / interleukin-22 receptor
  • [Other-IDs] NLM/ NIHMS400234; NLM/ PMC3429118
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34. Han Y, Amin HM, Franko B, Frantz C, Shi X, Lai R: Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma. Blood; 2006 Oct 15;108(8):2796-803
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  • [Title] Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma.
  • Previous studies showed that most cases of ALK(+) anaplastic large-cell lymphoma (ALK(+)ALCL) do not express SHP1, a tyrosine phosphatase and an important negative regulator for cellular signaling pathways such as that of JAK/STAT.
  • To fully assess the biologic significance of loss of SHP1 in ALK(+)ALCL, we transfected SHP1 plasmids into 2 SHP1(-), ALK(+)ALCL cell lines, Karpas 299 and SU-DHL-1.
  • Expression of SHP1 in these 2 cell lines also resulted in marked decreases in the protein levels of JAK3 and NPM-ALK, and these effects were reversible by proteosome inhibitor MG132.
  • Conversely, when SHP1 expression in SUP-M2 (a SHP1(+) ALK(+)ALCL cell line) was inhibited using siRNA, pSTAT3, pJAK3, JAK3, and NPM-ALK were all up-regulated.
  • Coimmunoprecipitation studies showed that SHP1 was physically associated with JAK3 and NPM-ALK.
  • SHP1 expression in Karpas 299 and SU-DHL-1 led to significant G(1) cell cycle arrest but not apoptosis.
  • To conclude, loss of SHP1 contributes to the pathogenesis of ALK(+)ALCL by 2 mechanisms:.
  • (1) it leaves the tyrosine phosphorylation and activation of JAK3/STAT3 unchecked and (2) it decreases proteosome degradation of JAK3 and NPM-ALK.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / metabolism. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Apoptosis. Base Sequence. Cell Cycle. Cell Line, Tumor. Gene Expression. Humans. Janus Kinase 3. Proteasome Endopeptidase Complex / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 6. RNA, Neoplasm / genetics. RNA, Small Interfering / genetics. Signal Transduction. Transfection

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  • (PMID = 16825495.001).
  • [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 / Intracellular Signaling Peptides and Proteins; 0 / JAK3 protein, human; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 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 2.7.10.2 / 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; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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35. 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.
  • Type I insulin-like growth factor receptor (IGF-IR) tyrosine kinase plays important roles in the pathogenesis of several malignancies.
  • 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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36. Li C, Takino H, Eimoto T, Ishida T, Inagaki A, Ueda R, Suzuki R, Yoshino T, Nakagawa A, Nakamura S, Inagaki H: Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma. Mod Pathol; 2007 Jun;20(6):648-55
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  • [Title] Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma.
  • In anaplastic large-cell lymphomas positive for anaplastic lymphoma kinase (ALK) protein, the ALK gene is most commonly fused to the NPM gene, and less commonly to TPM3, TFG, ATIC, and other rare genes.
  • Although this lymphoma is generally associated with a favorable clinical outcome, 25% of the patients die of the disease within 5 years.
  • (1) a sensitive reverse transcription-polymerase chain reaction (RT-PCR) assay for various X-ALK fusion genes, (2) a 5' rapid amplification of cDNA ends (RACE) assay to identify unknown fusion partners, and (3) a real-time RT-PCR assay to quantify the amount of the NPM-ALK fusion transcript.
  • In 26 cases of ALK(+) anaplastic large-cell lymphoma, the RT-PCR assay showed that the ALK was fused to NPM in 21 cases, to TPM3 in three, and to TFG in one.
  • The 5' RACE assay detected ATIC-ALK fusion in the remaining case.
  • The real-time quantitative RT-PCR assay showed that the NPM-ALK transcript was over expressed in four of 20 quantifiable cases.
  • Patients with NPM-ALK overexpression showed a significantly unfavorable overall survival compared with those with a low expression of this transcript.
  • The RT-PCR and 5' RACE assays developed here may be useful for identification of known and unknown gene partners fused to the ALK gene.
  • Overexpression of the NPM-ALK fusion transcript may be associated with a poor prognosis of the patients with ALK(+) anaplastic large-cell lymphomas.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Protein-Tyrosine Kinases / biosynthesis

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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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37. Ji TH, Li HL, Jiang HY, Zhao T, Yu YH: [Expression of ALK protein in large cell lymphoma with ALCL chromosome translocation in relation to prognosis]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Jun;16(3):543-6
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  • [Title] [Expression of ALK protein in large cell lymphoma with ALCL chromosome translocation in relation to prognosis].
  • The aim of this study was to investigate the expression of anaplastic lymphoma kinase (ALK) protein resulted from chromosome translocation in anaplastic large cell lymphoma (ALCL) and its relationship with the age and prognosis of patients with ALCL.
  • The tissue microarray including 30 cases of ALCL and 2 normal control tissues were established, the expression of anaplastic lymphoma kinase (ALK) protein was detected by immunohistochemistry, the statistical analysis of detected results was carried out by SPSS software.
  • The results showed that the ALK protein was expressed negatively in 2 cases of primary skin ALCL, but in 20 out of 28 cases of systematic ALCL the ALK protein was expressed positively and mainly located in cytoplasm and/or nucleus (71.4%).
  • Clinically, the patients with ALK expression were younger than those without ALK expression (p < 0.05).
  • The prognosis of patients with ALK expression was better than those without ALK expression (p < 0.05).
  • It is concluded that there is a high incidence of ALK expression in ALCL, especially in younger group.
  • ALK expression may be an useful and independent marker for the differential diagnosis and prognosis evaluation of ALCL.

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  • (PMID = 18549625.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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38. 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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39. 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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40. Lamant L, de Reyniès A, Duplantier MM, Rickman DS, Sabourdy F, Giuriato S, Brugières L, Gaulard P, Espinos E, Delsol G: Gene-expression profiling of systemic anaplastic large-cell lymphoma reveals differences based on ALK status and two distinct morphologic ALK+ subtypes. Blood; 2007 Mar 1;109(5):2156-64
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  • [Title] Gene-expression profiling of systemic anaplastic large-cell lymphoma reveals differences based on ALK status and two distinct morphologic ALK+ subtypes.
  • With the use of microarray gene-expression profiling, we analyzed a homogeneous series of 32 patients with systemic anaplastic large-cell lymphoma (ALCL) and 5 ALCL cell lines.
  • Unsupervised analysis classified ALCL in 2 clusters, corresponding essentially to morphologic subgroups (ie, common type vs small cell and "mixed" variants) and clinical variables.
  • Patients with a morphologic variant of ALCL had advanced-stage disease.
  • Supervised analysis showed that ALK+ALCL and ALK- ALCL have different gene-expression profiles, further confirming that they are different entities.
  • Among the most significantly differentially expressed genes between ALK+ and ALK- samples, we found BCL6, PTPN12, CEBPB, and SERPINA1 genes to be overexpressed in ALK+ ALCL.
  • The molecular signature of ALK- ALCL included overexpression of CCR7, CNTFR, IL22, and IL21 genes but did not provide any obvious clues to the molecular mechanism underlying this tumor subtype.
  • Once confirmed on a larger number of patients, the results of the present study could be used for clinical and therapeutic management of patients at the time of diagnosis.
  • [MeSH-major] Cell Shape. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Cell Line, Tumor. Humans. Immunohistochemistry. RNA, Messenger / genetics. Receptor Protein-Tyrosine Kinases. Tissue Array Analysis


41. Duplantier MM, Lamant L, Sabourdy F, de Reynies A, Delsol G, Espinos E: Serpin A1 is overexpressed in ALK+ anaplastic large cell lymphoma and its expression correlates with extranodal dissemination. Leukemia; 2006 Oct;20(10):1848-54
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  • [Title] Serpin A1 is overexpressed in ALK+ anaplastic large cell lymphoma and its expression correlates with extranodal dissemination.
  • Anaplastic large cell lymphoma (ALCL) is a distinct subtype of non-Hodgkin's lymphoma.
  • Most of ALCLs (85%) carry a chromosomal translocation involving different partners in the 5' portion, and the anaplastic lymphoma kinase (ALK) receptor kinase domain in the 3' portion.
  • These translocations induce the ectopic expression of X-ALK proteins, thought to be involved in lymphomagenesis, through the dysregulation of cell proliferation and apoptotic pathways.
  • In the present study, based on several ALK+ and ALK- ALCL cell lines and biopsy specimens, we showed that serpin A1, a secretory glycoprotein, was overexpressed in ALK+ ALCL cell lines and ALK+ tumors at both the transcriptional and translational levels.
  • The crucial role of NPM-ALK in the regulation of serpin A1 expression was further demonstrated by using both ectopic expression and downregulation, by RNA interference, of the NPM-ALK oncogene.
  • In addition, in ALK+ tumors, serpin A1 expression appeared to be correlated with the clinical status of the patients as the serpin A1 mRNA level was higher in patients presenting with extranodal dissemination.
  • These data, together with the pattern of expression of serpin A1 we observed in ALK+ tumors, suggest that serpin A1 has an invasion-promoting effect in ALK+ ALCL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. alpha 1-Antitrypsin / genetics
  • [MeSH-minor] Adult. Biopsy. Cell Line, Tumor. Child. Humans. Lymph Nodes / pathology. Neoplasm Invasiveness. Protein Biosynthesis. Protein-Tyrosine Kinases / genetics. RNA, Messenger / analysis. Receptor Protein-Tyrosine Kinases. Transcription, Genetic. Translocation, Genetic

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  • (PMID = 16900211.001).
  • [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 / RNA, Messenger; 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin; 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. Grewal JS, Smith LB, Winegarden JD 3rd, Krauss JC, Tworek JA, Schnitzer B: Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature. Ann Hematol; 2007 Jul;86(7):499-508
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  • [Title] Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive neoplasm of T- or null cell phenotype and is recognized as a distinct clinicopathologic subtype of non-Hodgkin lymphoma (NHL) in the revised World Health Organization (WHO) classification of hematopoietic neoplasms.
  • Most cases with leukemic involvement are the small cell variant of ALCL.
  • These cases often lack the pleomorphism seen in the common variant of ALCL and may be misdiagnosed.
  • We report a series of three patients who presented with leukemic phase ALCL.
  • The patients 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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43. 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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44. Nelson M, Horsman DE, Weisenburger DD, Gascoyne RD, Dave BJ, Loberiza FR, Ludkovski O, Savage KJ, Armitage JO, Sanger WG: Cytogenetic abnormalities and clinical correlations in peripheral T-cell lymphoma. Br J Haematol; 2008 May;141(4):461-9
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  • [Title] Cytogenetic abnormalities and clinical correlations in peripheral T-cell lymphoma.
  • Cytogenetic correlations among most types of peripheral T-cell lymphoma (PTCL) have not been very informative to date.
  • This study aimed to identify recurrent chromosomal abnormalities in angioimmunoblastic T-cell lymphoma (AITL), ALK-negative anaplastic large cell lymphoma (ALK-ALCL) and peripheral T-cell lymphoma, unspecified (PTCL-US), and to evaluate their prognostic value.
  • In ALK(-) ALCL, gains of 1q (50%) and 3p (30%), and losses of 16pter (50%), 6q13q21 (30%), 15 (30%), 16qter (30%) and 17p13 (30%) were frequent findings.
  • However, cases with complex karyotypes, most frequently observed in ALK(-) ALCL and PTCL-US, had a significantly shorter OS.
  • [MeSH-major] Chromosome Aberrations. Lymphoma, T-Cell, Peripheral / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Follow-Up Studies. Humans. Immunoblastic Lymphadenopathy / genetics. Karyotyping. Lymphoma, Large-Cell, Anaplastic / genetics. Male. Middle Aged. Prognosis. Survival Analysis

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  • (PMID = 18341637.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
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45. 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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46. Youssif C, Goldenbogen J, Hamoudi R, Carreras J, Viskaduraki M, Cui YX, Bacon CM, Burke GA, Turner SD: Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: a Children's Cancer and Leukaemia Group Study. Genes Chromosomes Cancer; 2009 Nov;48(11):1018-26
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  • [Title] Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: a Children's Cancer and Leukaemia Group Study.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) is a T-cell malignancy in which ALK expression is a consequence of the t(2;5) or a variant translocation involving Chromosome 2.
  • 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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47. 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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48. Wan W, Albom MS, Lu L, Quail MR, Becknell NC, Weinberg LR, Reddy DR, Holskin BP, Angeles TS, Underiner TL, Meyer SL, Hudkins RL, Dorsey BD, Ator MA, Ruggeri BA, Cheng M: Anaplastic lymphoma kinase activity is essential for the proliferation and survival of anaplastic large-cell lymphoma cells. Blood; 2006 Feb 15;107(4):1617-23
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  • [Title] Anaplastic lymphoma kinase activity is essential for the proliferation and survival of anaplastic large-cell lymphoma cells.
  • The roles of aberrant expression of constitutively active ALK chimeric proteins in the pathogenesis of anaplastic large-cell lymphoma (ALCL) have been well defined; nevertheless, the notion that ALK is a molecular target for the therapeutic modulation of ALK+ ALCL has not been validated thus far.
  • Select fused pyrrolocarbazole (FP)-derived small molecules with ALK inhibitory activity were used as pharmacologic tools to evaluate whether functional ALK is essential for the proliferation and survival of ALK+ ALCL cells in culture.
  • These compounds inhibited interleukin 3 (IL-3)-independent proliferation of BaF3/NPM-ALK cells in an ALK inhibition-dependent manner and significantly blocked colony formation in agar of mouse embryonic fibroblast (MEF) cells harboring NPM-ALK.
  • Inhibition of NPM-ALK phosphorylation in the ALK+ ALCL-derived cell lines resulted in significant inhibition of cell proliferation and induction of apoptotic-cell death, while having marginal effects on the proliferation and survival of K562, an ALK- leukemia cell line.
  • ALK inhibition resulted in cell-cycle G1 arrest and inactivation of ERK1/2, STAT3, and AKT signaling pathways.
  • Potent and selective ALK inhibitors may have therapeutic application for ALK+ ALCL and possibly other solid and hematologic tumors in which ALK activation is implicated in their pathogenesis.
  • [MeSH-major] Cell Division / physiology. Cell Survival / physiology. Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Apoptosis. Carbazoles / pharmacology. Caspases / metabolism. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Indazoles / pharmacology. Phenylurea Compounds / pharmacology. Receptor Protein-Tyrosine Kinases


49. Qiu L, Lai R, Lin Q, Lau E, Thomazy DM, Calame D, Ford RJ, Kwak LW, Kirken RA, Amin HM: Autocrine release of interleukin-9 promotes Jak3-dependent survival of ALK+ anaplastic large-cell lymphoma cells. Blood; 2006 Oct 1;108(7):2407-15
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  • [Title] Autocrine release of interleukin-9 promotes Jak3-dependent survival of ALK+ anaplastic large-cell lymphoma cells.
  • The aberrant fusion protein NPM-ALK plays an important pathogenetic role in ALK+ anaplastic large-cell lymphoma (ALCL).
  • We previously demonstrated that Jak3 potentiates the activity of NPM-ALK.
  • NPM-ALK was previously shown to promote widespread lymphomas in IL-9 transgenic mice by unknown mechanisms.
  • We hypothesized that IL-9 plays an important role in ALK+ ALCL via Jak3 activation.
  • Our studies demonstrate the expression of IL-9Ralpha and IL-9 in 3 ALK+ ALCL-cell lines and 75% and 83% of primary tumors, respectively.
  • IL-9 was detected in serum-free culture medium harvested from ALK+ ALCL-cell lines, supporting autocrine release of IL-9.
  • Treatment of these cells with an anti-IL-9-neutralizing antibody decreased pJak3 and its kinase activity, along with pStat3 and ALK kinase activity.
  • These effects were associated with decreased cell proliferation and colony formation in soft agar and cell-cycle arrest.
  • Evidence suggests that cell-cycle arrest can be attributed to up-regulation of p21 and down-regulation of Pim-1.
  • Our results illustrate that IL-9/Jak3 signaling plays a significant role in the pathogenesis of ALK+ ALCL and that it represents a potential therapeutic target for treating patients with ALK+ ALCL.

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  • (PMID = 16763206.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395; United States / NIAID NIH HHS / AI / AI053566; United States / NCI NIH HHS / CA / K08CA114395; United States / NCRR NIH HHS / RR / SG12RR008124
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-9; 0 / JAK3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Jak3 protein, mouse; EC 2.7.10.2 / Janus Kinase 3
  • [Other-IDs] NLM/ PMC1895569
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50. Oyarzo MP, Drakos E, Atwell C, Amin HM, Medeiros LJ, Rassidakis GZ: Intrinsic apoptotic pathway in anaplastic large cell lymphoma. Hum Pathol; 2006 Jul;37(7):874-82
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  • [Title] Intrinsic apoptotic pathway in anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) includes a subset of tumors that has abnormalities of chromosome 2p23, resulting in overexpression of anaplastic lymphoma kinase (ALK).
  • Previous studies have reported differences in apoptotic rate and expression levels of apoptosis regulatory proteins between ALK+ and ALK- ALCL.
  • In this study, we assessed for expression of the intrinsic apoptotic pathway proteins cytochrome c, apoptosis protease-activating factor 1, and procaspase 9 in 2 ALK+ ALCL cell lines and 42 ALCL tumors (17 ALK+, 25 ALK-).
  • We used the Karpas 299 and SU-DHL-1 cell lines, and the inhibitors Z-LEHD-FMK (specific for caspase 9) and Boc-D-FMK (general caspase inhibitor) to investigate the role of caspase 9 activation in chemotherapy-induced apoptotic cell death.
  • Both caspase inhibitors rescued a substantial fraction of Karpas 299 and SU-DHL-1 cells from drug-induced cell death.
  • In ALCL tumors, expression of cytochrome c, apoptosis protease-activating factor 1, and procaspase 9 was also assessed and correlated with apoptotic rate and activated caspase 3 levels.
  • Cytochrome c was expressed in all 13 (100%) ALK+ and 18 (95%) of 19 ALK- ALCL tumors.
  • Apoptosis protease-activating factor 1 was detected in 14 (88%) of 16 ALK+ and 19 (79%) of 24 ALK- ALCL tumors.
  • Procaspase 9 was expressed in 5 (30%) of 17 ALK+ and 2 (8%) of 25 ALK- ALCL tumors (P = .09).
  • In the entire study group (ALK+ and ALK- ALCL), procaspase 9 expression levels significantly correlated with apoptotic rate (P = .02) and activated caspase 3 levels (P = .05).
  • This correlation could not be shown in the ALK+ or ALK- ALCL subgroups, presumably because of the small sample size.
  • In conclusion, chemotherapy-induced cell death in ALK+ ALCL cells involves the intrinsic apoptotic pathway, and apoptosome function may be an important determinant of apoptosis in ALCL tumors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Apoptosis Regulatory Proteins / drug effects. Apoptosis Regulatory Proteins / metabolism. Blotting, Western. Caspase 3. Caspase 9. Caspases / biosynthesis. Caspases / drug effects. Caspases / metabolism. Cell Line, Tumor. Cytochromes c / biosynthesis. Disease-Free Survival. Doxorubicin / pharmacology. Enzyme Activation / drug effects. Enzyme Activation / physiology. Enzyme Inhibitors / pharmacology. Etoposide / pharmacology. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Receptor Protein-Tyrosine Kinases

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  • (PMID = 16784988.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Enzyme Inhibitors; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 9007-43-6 / Cytochromes c; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
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51. 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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52. 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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  • [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


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

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  • (PMID = 16304056.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antigens, CD95; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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54. 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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55. 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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56. Miranda RN, Lin L, Talwalkar SS, Manning JT, Medeiros LJ: Anaplastic large cell lymphoma involving the breast: a clinicopathologic study of 6 cases and review of the literature. Arch Pathol Lab Med; 2009 Sep;133(9):1383-90
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  • [Title] Anaplastic large cell lymphoma involving the breast: a clinicopathologic study of 6 cases and review of the literature.
  • CONTEXT: Lymphomas involving the breast are rare, and most cases are of B-cell lineage; T-cell neoplasms represent less than 10% of all breast lymphomas.
  • OBJECTIVE: To define the clinicopathologic spectrum of anaplastic large cell lymphomas (ALCLs) involving the breast.
  • DESIGN: Six cases of ALCL involving the breast were identified at a single institution during 21 years.
  • There were 4 anaplastic lymphoma kinase- negative (ALK(-)) ALCL cases; 3 of these neoplasms developed around breast implants.
  • Two patients with ALK(-) ALCL had a history of cutaneous ALCL.
  • There were 2 ALK(+) ALCLs; both patients had stage IV disease.
  • Histologically, all neoplasms were composed of large anaplastic cells that were uniformly CD30(+) and expressed markers of T-cell lineage.
  • Four patients with adequate follow-up are alive, with a mean of 4.1 years (range, 1.5-9 years) after diagnosis of the breast tumor.
  • Included in this group are 2 patients with ALK(-) ALCL associated with breast implants who were alive 4 years and 9 years after diagnosis.
  • CONCLUSIONS: Including the 6 cases we describe, a total of 21 cases of ALCL involving the breast are reported.
  • Fifteen cases, all ALK(-), were associated with breast implants, suggesting a possible pathogenetic relationship, and associated with an excellent prognosis.
  • Patients with cutaneous ALCL can subsequently develop ALK(-) ALCL involving the breast, and these tumors can be associated with breast implants.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adult. Aged. Antigens, CD30 / metabolism. Biomarkers, Tumor / metabolism. Breast Implantation. Combined Modality Therapy. DNA, Neoplasm / analysis. Fatal Outcome. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Humans. Middle Aged. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Young Adult

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  • (PMID = 19722744.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 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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57. Li JF, Li GD, Gu L, Liu WP, Li FY, Liao DY, Ma ZG: [Study on activation of AKT/mTOR pathway in anaplastic large cell lymphoma]. Zhonghua Xue Ye Xue Za Zhi; 2008 Oct;29(10):649-53
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  • [Title] [Study on activation of AKT/mTOR pathway in anaplastic large cell lymphoma].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and the phosphorylation status of AKT, mammalian target of rapamycin (mTOR), 4E-binding protein 1 (4E-BP1) and ribosomal protein S6 kinase (p70S6K) and their interrelationships and clinical pathological significance in anaplastic large cell lymphoma (ALCL) patients.
  • METHODS: Immunohistochemical and EnVision methods were used to detect the expression of ALK, p-AKT, p-mTOR, p-4E-BP1 and p-p70S6K.
  • RESULTS: Among the 81 ALCL patients, 51 (63.0%) expressed ALK, whereas the other 30 (37.0%) did not.
  • Patients with ALK(+) ALCL had a better prognosis than those with ALK-ALCL (P < 0.05).
  • Out of the 71 ALCL samples studied, p-AKT was detected in 54 (76.1%) samples and its phosphorylation was correlated with ALK expression (P < 0.05); p-mTOR was detected in 57 (80.3%) samples and its expression was correlated with both ALK and p-AKT (P < 0.05); p-4E-BP1 and p-p70S6K were detected in 64 (90.1%) and 66 (93.0%) samples respectively, and their expressions were related with p-mTOR (P < 0.05), but not with ALK or p-AKT (P > 0.05).
  • COX Proportional Hazard Model analysis showed that both the expression of ALK and the B symptoms affected the prognosis (P < 0.05), moreover, the former had greater impact than the later.
  • CONCLUSION: Expressions of p-AKT, p-mTOR, p-4E-BP1 and p-p70S6K are detected in ALCL, while ALK(+) cases have higher incidence than those with ALK(-) cases.
  • Phosphorylation of AKT and mTOR is correlated with ALK expression, suggesting that there is an activated pathway of AKT/mTOR in patients with ALK(+) ALCL, but the activation have no obvious prognostic significance.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Protein-Serine-Threonine Kinases / metabolism. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 19176054.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / EIF4EBP1 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Phosphoproteins; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa
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58. 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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59. Merkel O, Hamacher F, Laimer D, Sifft E, Trajanoski Z, Scheideler M, Egger G, Hassler MR, Thallinger C, Schmatz A, Turner SD, Greil R, Kenner L: Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK)+ and ALK- anaplastic large-cell lymphoma. Proc Natl Acad Sci U S A; 2010 Sep 14;107(37):16228-33
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  • [Title] Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK)+ and ALK- anaplastic large-cell lymphoma.
  • Aberrant anaplastic lymphoma kinase (ALK) expression is a defining feature of many human cancers and was identified first in anaplastic large-cell lymphoma (ALCL), an aggressive non-Hodgkin T-cell lymphoma.
  • Since that time, many studies have set out to identify the mechanisms used by aberrant ALK toward tumorigenesis.
  • We have identified a distinct profile of micro-RNAs (miRNAs) that characterize ALCL; furthermore, this profile distinguishes ALK(+) from ALK(-) subtypes, and thus points toward potential mechanisms of tumorigenesis induced by aberrant ALK.
  • Using a nucleophosmin-ALK transgenic mouse model as well as human primary ALCL tumor tissues and human ALCL-derived cell lines, we reveal a set of overlapping deregulated miRNAs that might be implicated in the development and progression of ALCL.
  • Importantly, ALK(+) and ALK(-) ALCL could be distinguished by a distinct profile of "oncomirs": Five members of the miR-17-92 cluster were expressed more highly in ALK(+) ALCL, whereas miR-155 was expressed more than 10-fold higher in ALK(-) ALCL.
  • Moreover, miR-101 was down-regulated in all ALCL model systems, but its forced expression attenuated cell proliferation only in ALK(+) and not in ALK(-) cell lines, perhaps suggesting different modes of ALK-dependent regulation of its target proteins.
  • Furthermore, inhibition of mTOR, which is targeted by miR-101, led to reduced tumor growth in engrafted ALCL mouse models.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. MicroRNAs / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Base Sequence. Cell Line, Tumor. Cell Proliferation. Gene Expression Profiling. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Mice. Mice, Transgenic. Multigene Family. Receptor Protein-Tyrosine Kinases. Sirolimus / analogs & derivatives. Sirolimus / therapeutic use. Xenograft Model Antitumor Assays

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  • (PMID = 20805506.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / V 102
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MicroRNAs; 624KN6GM2T / temsirolimus; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2941277
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60. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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61. 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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62. 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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63. Nguyen JT, Condron MR, Nguyen ND, De J, Medeiros LJ, Padula A: Anaplastic large cell lymphoma in leukemic phase: extraordinarily high white blood cell count. Pathol Int; 2009 May;59(5):345-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic large cell lymphoma in leukemic phase: extraordinarily high white blood cell count.
  • Anaplastic large cell lymphoma (ALCL) is a distinct type of T/null-cell non-Hodgkin lymphoma that commonly involves nodal and extranodal sites.
  • The World Health Organization of lymphoid neoplasms recognizes two types: anaplastic lymphoma kinase (ALK) positive or ALK negative, the former as a result of abnormalities involving the ALK gene at chromosome 2p23.
  • Patients with ALCL rarely develop a leukemic phase of disease, either at the time of initial presentation or during the clinical course.
  • Described herein is a patient with ALK+ ALCL, small cell variant, associated with the t(2;5)(p23;q35), who initially presented with leukemic involvement and an extraordinarily high leukocyte count of 529 x 10(9)/L, which subsequently peaked at 587 x 10(9)/L.
  • Despite chemotherapy the patient died 2(1/2) months after diagnosis.
  • In the literature review 20 well-documented cases are identified of ALCL in leukemic phase reported previously, with a WBC ranging from 15 to 151 x 10(9)/L.
  • Leukemic phase of ALCL occurs almost exclusively in patients with ALK+ ALCL, most often associated with the small cell variant and the t(2;5)(p23;q35), similar to the present case.
  • Patients with leukemic phase ALK+ ALCL appear to have a poorer prognosis than most patients with ALK+ ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / blood. Lymphoma, Large-Cell, Anaplastic / pathology

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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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64. Galietta A, Gunby RH, Redaelli S, Stano P, Carniti C, Bachi A, Tucker PW, Tartari CJ, Huang CJ, Colombo E, Pulford K, Puttini M, Piazza RG, Ruchatz H, Villa A, Donella-Deana A, Marin O, Perrotti D, Gambacorti-Passerini C: NPM/ALK binds and phosphorylates the RNA/DNA-binding protein PSF in anaplastic large-cell lymphoma. Blood; 2007 Oct 1;110(7):2600-9
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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 binds and phosphorylates the RNA/DNA-binding protein PSF in anaplastic large-cell lymphoma.
  • The oncogenic fusion tyrosine kinase nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) induces cellular transformation in anaplastic large-cell lymphomas (ALCLs) carrying the t(2;5) chromosomal translocation.
  • Protein-protein interactions involving NPM/ALK are important for the activation of downstream signaling pathways.
  • This study was aimed at identifying novel NPM/ALK-binding proteins that might contribute to its oncogenic transformation.
  • Using a proteomic approach, several RNA/DNA-binding proteins were found to coimmunoprecipitate with NPM/ALK, including the multifunctional polypyrimidine tract binding proteinassociated splicing factor (PSF).
  • The interaction between NPM/ALK and PSF was dependent on an active ALK kinase domain and PSF was found to be tyrosine-phosphorylated in NPM/ALK-expressing cell lines and in primary ALK(+) ALCL samples.
  • Furthermore, PSF was shown to be a direct substrate of purified ALK kinase domain in vitro, and PSF Tyr293 was identified as the site of phosphorylation.
  • Y293F PSF was not phosphorylated by NPM/ALK and was not delocalized in NPM/ALK(+) cells.
  • The expression of ALK fusion proteins induced delocalization of PSF from the nucleus to the cytoplasm and forced overexpression of PSF-inhibited proliferation and induced apoptosis in cells expressing NPM/ALK.
  • These results identify PSF as a novel NPM/ALK-binding protein and substrate, and suggest that PSF function may be perturbed in NPM/ALK-transformed cells.

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  • (PMID = 17537995.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092318; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / CA92318
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / PTB-associated splicing factor; 0 / RNA-Binding Proteins; 21820-51-9 / Phosphotyrosine; 63231-63-0 / RNA; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC1988934
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65. Hwang YY, Liang RH: An update in management of noncutaneous T-cell lymphomas. Adv Hematol; 2010;2010:424786

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  • [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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66. 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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67. Lu L, Ghose AK, Quail MR, Albom MS, Durkin JT, Holskin BP, Angeles TS, Meyer SL, Ruggeri BA, Cheng M: ALK mutants in the kinase domain exhibit altered kinase activity and differential sensitivity to small molecule ALK inhibitors. Biochemistry; 2009 Apr 28;48(16):3600-9
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  • [Title] ALK mutants in the kinase domain exhibit altered kinase activity and differential sensitivity to small molecule ALK inhibitors.
  • Abnormal expression of constitutively active anaplastic lymphoma kinase (ALK) chimeric proteins in the pathogenesis of anaplastic large-cell lymphoma (ALCL) is well established.
  • Recent studies with small molecule kinase inhibitors have provided solid proof-of-concept validation that inhibition of ALK is sufficient to attenuate the growth and proliferation of ALK (+) ALCL cells.
  • In this study, several missense mutants of ALK in the phosphate anchor and gatekeeper regions were generated and their kinase activity was measured.
  • NPM-ALK L182M, L182V, and L256M mutants displayed kinase activity in cells comparable to or higher than that of NPM-ALK wild type (WT) and rendered BaF3 cells into IL-3-independent growth, while NPM-ALK L182R, L256R, L256V, L256P, and L256Q displayed much weaker or little kinase activity in cells.
  • Similar kinase activities were obtained with corresponding GST-ALK mutants with in vitro kinase assays.
  • With regard to inhibitor response, NPM-ALK L182M and L182V exhibited sensitivity to a fused pyrrolocarbazole (FP)-derived ALK inhibitor comparable to that of NPM-ALK WT but were dramatically less sensitive to a diaminopyrimidine (DAP)-derived ALK inhibitor.
  • On the other hand, NPM-ALK L256M exhibited >30-fold lower sensitivity to both FP-derived and DAP-derived ALK inhibitors.
  • The growth inhibition and cytotoxicity of BaF3/NPM-ALK mutant cells induced by ALK inhibitors were consistent with inhibition of cellular NPM-ALK autophosphorylation.
  • In a mouse survival model, treatment with the orally bioavailable DAP-ALK inhibitor substantially extended the survival of the mice inoculated with BaF3/NPM-ALK WT cells but not those inoculated with BaF3/NPM-ALK L256M cells.
  • Binding of ALK inhibitors to ALK WT and mutants was analyzed using ALK homology models.
  • In summary, several potential active ALK mutants were identified, and our data indicate that some of these mutants are resistant to select small molecule ALK inhibitors.
  • Further characterization of these mutants may help to identify and develop potent ALK inhibitors active against both WT and resistant mutants of ALK.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line. Humans. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / metabolism. Mice. Molecular Sequence Data. Molecular Structure. Neoplasm Transplantation. Receptor Protein-Tyrosine Kinases. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Sequence Alignment. Survival Rate

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  • (PMID = 19249873.001).
  • [ISSN] 1520-4995
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Fusion Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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68. 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.
  • In the case of HL, B7-H1 expression was shown to be dependent on the ERK and p38 mitogen-activated protein kinase (MAPK) signaling pathways.
  • 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


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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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. Asano N, Suzuki R, Ohshima K, Kagami Y, Ishida F, Yoshino T, Ogawa H, Morishima Y, Nakamura S: Linkage of expression of chemokine receptors (CXCR3 and CCR4) and cytotoxic molecules in peripheral T cell lymphoma, not otherwise specified and ALK-negative anaplastic large cell lymphoma. Int J Hematol; 2010 Apr;91(3):426-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Linkage of expression of chemokine receptors (CXCR3 and CCR4) and cytotoxic molecules in peripheral T cell lymphoma, not otherwise specified and ALK-negative anaplastic large cell lymphoma.
  • Peripheral T cell lymphoma not otherwise specified (PTCL-N) and ALK-negative anaplastic large cell lymphoma (ALCL) are heterogeneous categories with poor diagnostic reproducibility.
  • To clarify the biologic features of these categories, we investigated the expression of two chemokine receptors, type 1 (Th1/Tc1)-associated CXCR3 and type 2 (Th2/Tc2)-associated CCR4 in 110 PTCL-N and 35 ALK-negative ALCL cases, as well as the expression of cytotoxic molecules (CM).
  • CXCR3 and CCR4 were expressed in 69 (63%) and 37 (34%) of PTCL-N, and in 12 (34%) and 6 (17%) of ALK-negative ALCL, respectively.
  • In PTCL-N, type 1 pattern (CXCR3(+)CCR4(-)) was dominant (52%), whereas in ALK-negative ALCL, 54% were negative for both (P < 0.0001).
  • CM was expressed in 38% of PTCL-N and 51% of ALK-negative ALCL.
  • CM-positive PTCL-N consisted mostly of type 1 disease, which shows type 1 phenotype.
  • In contrast, type 2 pattern (CXCR3(-)CCR4(+)) was recognized in the CM-negative group only.
  • Among type 1 disease, CM-positive cases had a higher female ratio and more aggressive clinical features than CM-negative cases and a poorer prognosis (P = 0.006).
  • In both PTCL-N and ALK-negative ALCL, CM-positive type 1 disease had an extremely poor prognosis.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, T-Cell / metabolism. Receptors, CCR4 / metabolism. Receptors, CXCR3 / metabolism

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  • (PMID = 20217288.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CCR4 protein, human; 0 / CXCR3 protein, human; 0 / Receptors, CCR4; 0 / Receptors, CXCR3
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71. 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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72. 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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73. Kruczynski A, Mayer P, Marchand A, Vispé S, Fournier E, Annereau JP, Brel V, Barret JM, Delsol G, Imbert T, Fahy J, Bailly C: Antitumor activity of pyridoisoquinoline derivatives F91873 and F91874, novel multikinase inhibitors with activity against the anaplastic lymphoma kinase. Anticancer Drugs; 2009 Jun;20(5):364-72
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  • [Title] Antitumor activity of pyridoisoquinoline derivatives F91873 and F91874, novel multikinase inhibitors with activity against the anaplastic lymphoma kinase.
  • The anaplastic lymphoma kinase (ALK) is a validated target for the therapy of different malignancies.
  • Aberrant expression of constitutively active ALK chimeric proteins has been implicated in the pathogenesis of anaplastic large-cell lymphoma (ALCL) and has been detected in other cancers such as inflammatory myofibroblastic tumors, diffuse large B-cell lymphomas, certain non-small-cell lung cancers, rhabdomyosarcomas, neuroblastomas and glioblastomas.
  • In the course of a screening program aimed at identifying kinase inhibitors with novel scaffolds, the two pyridoisoquinoline derivatives F91873 and F91874, were identified as multikinase inhibitors with activity against ALK in a biochemical screen.
  • F91873 and F91874 also inhibited nucleophosmin-ALK and signal transducer and activator of transcription 3 phosphorylation in the ALCL cell line COST with the same potency.
  • Both F91873 and F91874 behaved as ATP noncompetitive inhibitors and inhibited cell proliferation of the ALK(+) ALCL cell lines COST, PIO, and Karpas299 ALCL.
  • This growth inhibition effect was associated with a G1-phase cell cycle arrest.
  • Furthermore, administration of F91874 to severe combined immunodeficient mice bearing COST tumor xenografts resulted in a significant antitumor efficacy at 15 mg/kg/day, illustrating the potential utility of such compounds in the treatment of ALK-related pathologies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinolizines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. Female. G1 Phase / drug effects. Lung Neoplasms / enzymology. Lung Neoplasms / pathology. Mice. Mice, Inbred ICR. Mice, SCID. Ovarian Neoplasms / enzymology. Ovarian Neoplasms / pathology. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases. Recombinant Fusion Proteins / antagonists & inhibitors. Xenograft Model Antitumor Assays

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  • (PMID = 19322071.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / F 91873; 0 / F 91874; 0 / Protein Kinase Inhibitors; 0 / Quinolizines; 0 / Recombinant Fusion Proteins; 0 / Thiazoles; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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74. Osoegawa A, Nosaki K, Miyamoto H, Kometani T, Hirai F, Ondo K, Seto T, Sugio K, Choi YL, Soda M, Mano H, Ichinose Y: Incidentally proven pulmonary "ALKoma". Intern Med; 2010;49(6):603-6
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  • [Title] Incidentally proven pulmonary "ALKoma".
  • Genetic alterations of echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) inversion were recently found in lung cancer.
  • Biopsy from her supraclavicular lymph nodes was performed to differentiate the diagnosis between lymphoma and lung cancer.
  • On the other hand, the commercially available chromosomal fluorescent in situ hybridization (FISH) analysis showed split signals of ALK, which was confirmed to be the EML4-ALK inversion.
  • The commercial-based ALK FISH is useful for screening pulmonary ALKoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / genetics. Cell Cycle Proteins / genetics. Chromosome Inversion / genetics. Lung Neoplasms / diagnosis. Lung Neoplasms / genetics. Microtubule-Associated Proteins / genetics. Protein-Tyrosine Kinases / genetics. Serine Endopeptidases / genetics
  • [MeSH-minor] Adult. Biopsy. Diagnosis, Differential. Female. Humans. In Situ Hybridization, Fluorescence. Lymph Nodes / pathology. Lymphoma / diagnosis. Lymphoma / pathology. Receptor Protein-Tyrosine Kinases

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  • (PMID = 20228600.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Microtubule-Associated Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases
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75. 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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76. 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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77. 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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  • [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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78. Drakos E, Leventaki V, Schlette EJ, Jones D, Lin P, Medeiros LJ, Rassidakis GZ: c-Jun expression and activation are restricted to CD30+ lymphoproliferative disorders. Am J Surg Pathol; 2007 Mar;31(3):447-53
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  • Cellular Jun (c-Jun), a member of the JUN family, is an activator protein-1 transcription factor involved in cell differentiation, proliferation, and apoptosis that can be activated by phosphorylation at serine-73 and -63 residues.
  • Using tissue microarrays and immunohistochemistry, we investigated c-Jun expression and serine-73 phosphorylation in 112 CD30 lymphomas and 232 CD30 lymphomas of B- or T-cell lineage, and 24 cases of lymphomatoid papulosis. c-Jun was expressed exclusively by CD30 lymphoproliferative disorders including 41/41 (100%) classical Hodgkin lymphoma (cHL), 20/23 (87%) anaplastic lymphoma kinase (ALK)+ anaplastic large cell lymphoma (ALCL), 18/26 (69%) ALK- ALCL, 5/9 (56%) primary cutaneous ALCL, 4/11 (36%) CD30 diffuse large B-cell lymphoma (DLBCL), and 11/24 (46%) cases of lymphomatoid papulosis.
  • The percentage of c-Jun-positive tumor cells was highest in cHL and ALCL (P=0.002).
  • In contrast, all CD30 lymphomas, including nodular lymphocyte predominant HL and CD30 non-Hodgkin lymphomas of B- or T-cell lineage were negative for c-Jun.
  • Serine-73 phosphorylated c-Jun (p-c-Jun), the activated form of c-Jun, was expressed more frequently and at a higher level in cHL and ALK+ ALCL than other CD30 tumors.
  • The percentage of p-c-Jun-positive tumor cells correlated significantly with the percentage of total c-Jun-positive cells (P<0.0001), suggesting that activated c-Jun positively regulates total c-Jun levels in CD30 lymphomas through a well-established positive feedback loop.
  • [MeSH-major] Antigens, CD30 / metabolism. Hodgkin Disease / pathology. Lymphoma, Non-Hodgkin / pathology. Lymphomatoid Papulosis / pathology. Proto-Oncogene Proteins c-jun / metabolism. Transcriptional Activation
  • [MeSH-minor] Biomarkers, Tumor / biosynthesis. Cell Count. Cell Line, Tumor. Cell Nucleus / metabolism. Cell Nucleus / pathology. Humans. Phosphorylation. Serine / metabolism. Tissue Array Analysis


79. 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.
  • Studies for EBV and HHV-8 were negative.
  • 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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80. Thompson MA, Stumph J, Henrickson SE, Rosenwald A, Wang Q, Olson S, Brandt SJ, Roberts J, Zhang X, Shyr Y, Kinney MC: Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas. Hum Pathol; 2005 May;36(5):494-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive large T- or null-cell lymphoma.
  • Most ALCLs arising in children and young adults express a constitutively active receptor tyrosine kinase, anaplastic lymphoma kinase (ALK).
  • Anaplastic large cell lymphomas lacking ALK are clinically heterogeneous and their pathogenesis is unknown.
  • 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


81. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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82. de Leval L, Gaulard P: Pathobiology and molecular profiling of peripheral T-cell lymphomas. Hematology Am Soc Hematol Educ Program; 2008;:272-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathobiology and molecular profiling of peripheral T-cell lymphomas.
  • Peripheral T-cell lymphomas (PTCLs) are a heterogeneous group of rare diseases, usually manifesting clinical aggressiveness.
  • Angioimmunoblastic T-cell lymphoma (AITL) comprises CD4+ CXCL13+ neoplastic cells displaying overlapping immunophenotypical and molecular features with normal follicular helper T cells.
  • ALK+ anaplastic large cell lymphoma (ALCL), defined by ALK gene translocation with various gene partners, is composed of CD30+ ALK+ cells with a cytotoxic phenotype and usually carries a good prognosis.
  • ALK- ALCL, now considered as a distinct disease entity, is morphologically and immunophenotypically similar to ALK+ ALCL, except for ALK expression, but has distinctive molecular features.

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  • (PMID = 19074096.001).
  • [ISSN] 1520-4391
  • [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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83. 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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84. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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85. 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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86. Willenbrock K, Küppers R, Renné C, Brune V, Eckerle S, Weidmann E, Bräuninger A, Hansmann ML: Common features and differences in the transcriptome of large cell anaplastic lymphoma and classical Hodgkin's lymphoma. Haematologica; 2006 May;91(5):596-604
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  • [Title] Common features and differences in the transcriptome of large cell anaplastic lymphoma and classical Hodgkin's lymphoma.
  • BACKGROUND AND OBJECTIVES: Anaplastic large cell lymphoma (ALCL) and classical Hodgkin's lymphoma (HL) are derived from different cell types, namely T cells and B cells, respectively.
  • However, both lymphomas share a similar cytological and immunohistochemical tumor cell phenotype with little resemblance to their cells of origin.
  • DESIGN AND METHODS: In this study, the transcriptional profiles of ALCL cell lines, primary ALCL tumor cells from peripheral blood and HL cell lines were compared to each other and to normal B-cell subsets, B non-Hodgkin's lymphomas (NHL) and B NHL- and Epstein-Barr virus (EBV)-transformed B-cell lines in order to establish their relationship at the transcriptional level and to identify genes with possible pathobiological impact.
  • RESULTS: HL samples clustered separately from ALCL samples, but HL and ALCL were found to be more closely related to each other than to any normal or malignant B-cell sample in the dataset.
  • Their relationship was determined to a large extent, but not exclusively, by lack of expression of B-cell antigens and by the over-expression of mRNA encoding activation markers and structural proteins.
  • Apart from established differences between HL and ALCL, further genes of interest could be identified that distinguish both entities from each other and from the other samples.
  • The differential expression of PRAME, DDR2, SOCS3 and CEBPD in HL and ALCL was confirmed in primary tumor tissue by immunohistochemistry and/or RT-PCR.
  • INTERPRETATION AND CONCLUSIONS: At a transcriptional level HL is more closely related to Alk+ ALCL than to the B-NHL or B-cell samples investigated, although it is a B-cell derived lymphoma.
  • The newly identified genes discriminating HL and ALCL may be pathobiologically important and may serve as possible therapeutic targets.
  • [MeSH-major] Gene Expression Profiling. Hodgkin Disease / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Transcription, Genetic
  • [MeSH-minor] Adult. B-Lymphocytes / metabolism. B-Lymphocytes / pathology. Cell Line, Tumor / metabolism. Cell Transformation, Neoplastic / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Leukemia / blood. Leukemia / genetics. Leukemia / metabolism. Leukemia / pathology. Lymphoma / classification. Lymphoma / genetics. Lymphoma / metabolism. Lymphoma / pathology. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. RNA, Complementary / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16670065.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Complementary; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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87. 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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88. 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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89. 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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90. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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91. Mencía-Gutiérrez E, Gutiérrez-Díaz E, Salamanca J, Martínez-González MA: Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL). Int J Dermatol; 2006 Jun;45(6):766-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL).
  • AIM: To report an unusual case of cutaneous presentation on the eyelid of systemic (or nodal), CD30+, anaplastic large-cell lymphoma (ALCL).
  • RESULTS: The histopathologic and immunohistochemical diagnosis was ALCL, T-cell phenotype, strongly positive for CD43 and CD30, and negative for CD3, anaplastic lymphoma kinase (ALK), and B-cell antigens.
  • CONCLUSIONS: Primary, systemic, CD30+, ALK-negative, ALCL presentations generally have a poor prognosis and tend to occur in older individuals, although the clinical outcome is highly variable and difficult to predict in individual cases.
  • Only three cases of ALCL have been described in the ocular adnexae and none was ALK-negative.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Eyelid Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / analysis

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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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92. 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.
  • Peripheral blood and bone marrow evaluation revealed a myeloproliferative disorder.
  • 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


93. 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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  • [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 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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94. 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.
  • Highly effective short hairpin RNA sequences and/or pharmacological inhibitors were used to abrogate the expression or activity of C/EBPbeta, signal transducer and activator of transcription 3 (STAT3), AKT, extracellular signal-related kinase 1/2 (ERK1/2) and mammalian target of rapamycin (mTOR).
  • 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


95. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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96. Zhang W, McQueen T, Schober W, Rassidakis G, Andreeff M, Konopleva M: Leukotriene B4 receptor inhibitor LY293111 induces cell cycle arrest and apoptosis in human anaplastic large-cell lymphoma cells via JNK phosphorylation. Leukemia; 2005 Nov;19(11):1977-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukotriene B4 receptor inhibitor LY293111 induces cell cycle arrest and apoptosis in human anaplastic large-cell lymphoma cells via JNK phosphorylation.
  • Anaplastic large-cell lymphoma (ALCL) is a heterogeneous lymphoma category in which a subset of cases carry the t(2;5)(p23;q35) or variant translocations resulting in overexpression of anaplastic lymphoma kinase (ALK).
  • In this study, we investigated the potential therapeutic effects and mechanisms of action of LY293111 in ALCL cell lines.
  • LY293111 inhibited proliferation of both ALK(+) and ALK(-) ALCL cell in a dose-dependent fashion and induced complete G(1)-S cell cycle arrest, which was accompanied by upregulation of p27 and downregulation of cyclin E.
  • Pretreatment with LY293111 for 4 h resulted in profound inhibition of serum-induced phosphorylation of extracellular-regulated kinases-1 and 2 and Akt and a concomitant increase in the phosphorylation of the stress-activated kinase c-jun N-terminal kinases (JNK).
  • The phospho-JNK inhibitor SP600125 partially protected Sup-M2 cells from LY293111-induced apoptosis, PARP cleavage and ROS generation, suggesting a role for JNK in LY293111-induced cell death.
  • These results warrant further studies of LY293111 in ALCL.
  • [MeSH-major] Apoptosis / drug effects. Benzoates / pharmacology. Cell Cycle / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Cell Cycle Proteins / biosynthesis. Cyclin E / biosynthesis. Cyclin-Dependent Kinase Inhibitor p27. Dose-Response Relationship, Drug. Down-Regulation. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. MAP Kinase Kinase 4. Membrane Potentials. Mitochondria / physiology. Mitogen-Activated Protein Kinase Kinases / metabolism. Phosphorylation. Reactive Oxygen Species. Receptors, Leukotriene B4. Tumor Cells, Cultured. Tumor Suppressor Proteins / biosynthesis. Up-Regulation

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  • (PMID = 16151469.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA55164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzoates; 0 / Cell Cycle Proteins; 0 / Cyclin E; 0 / LY 293111; 0 / Reactive Oxygen Species; 0 / Receptors, Leukotriene B4; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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97. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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98. Kapur S, Tiemann M, Menke MA, Schubert C, Parwaresch R: The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases. Indian J Med Res; 2005 Jan;121(1):46-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases.
  • BACKGROUND AND OBJECTIVES: Molecular events that precede transformations from lymphomatoid palulosis (LyP) to mycosis fungoides (MF) or to cutaneous anaplastic large cell lymphoma (ALCL) in the CD 30(+) cutaneous lymphoproliferative diseases (LPDs) are not known.
  • Expression of the anaplastic lymphoma kinase (ALK) gene product has also been described as an important prognostic indicator in ALCL.
  • 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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99. 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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100. 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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