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

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  • (PMID = 20207848.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / SEC31A protein, human; 0 / Vesicular Transport Proteins; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2833084
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2. Beltran B, Castillo J, Salas R, Quiñones P, Morales D, Hurtado F, Riva L, Winer E: ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature. J Hematol Oncol; 2009;2:11
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature.
  • BACKGROUND: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma (ALK-DLBCL) is a rare lymphoma with several clinicopathological differences from ALK-positive anaplastic large cell lymphoma (ALCL).
  • The latest WHO classification of lymphomas recognizes ALK-DLBCL as a separate entity.
  • By immunohistochemistry, cases were positive for cytoplasmic ALK, MUM1, CD45, and EMA; they marked negative for CD3, CD30 and CD20.
  • CONCLUSION: ALK-DLBCL is a distinct variant of DLBCL with plasmacytic differentiation, which is characterized by a bimodal age incidence curve, primarily nodal involvement, plasmablastic morphology, lack of expression of CD20, aggressive behavior and poor response to standard therapies, although some cases can have prolonged survival as the cases reported in this study.
  • ALK-DLBCL does not seem associated to immunosuppression or the presence of EBV or HHV8.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 19250532.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 39
  • [Other-IDs] NLM/ PMC2651189
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3. Li S: Anaplastic lymphoma kinase-positive large B-cell lymphoma: a distinct clinicopathological entity. Int J Clin Exp Pathol; 2009;2(6):508-18
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  • [Title] Anaplastic lymphoma kinase-positive large B-cell lymphoma: a distinct clinicopathological entity.
  • Anaplastic lymphoma kinase-positive large B-cell lymphoma (ALK(+) LBCL) represents a distinct subtype of mature B-cell neoplasms in the most recent WHO classification of hematolymphoid neoplasms.
  • With the advent of new ALK inhibitors for possible targeted therapy clinical trials, it is important to recognize this new entity, particularly in the pediatric population because the prognosis is worse than the more common ALK+ anaplastic large cell lymphoma.

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  • (PMID = 19636398.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2713458
  • [Keywords] NOTNLM ; ALK / Anaplastic lymphoma kinase / CLTC/ALK / diffuse large B-cell lymphoma / t(2;17)
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4. Lee HW, Kim K, Kim W, Ko YH: ALK-positive diffuse large B-cell lymphoma: report of three cases. Hematol Oncol; 2008 Jun;26(2):108-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ALK-positive diffuse large B-cell lymphoma: report of three cases.
  • Diffuse large B-cell lymphoma positive for anaplastic lymphoma kinase (ALK(+) DLBCL) is a rare variant of diffuse large B-cell lymphoma, with characteristic morphological, immunohistochemical and cytogenetic features.
  • Only 34 cases of ALK-positive diffuse large B-cell lymphoma have so far been reported in the literature.
  • We examined three new cases, which showed similar characteristics to previously reported cases, but with peculiar nuclear-membrane staining for ALK protein in one patient and a 5'-ALK gene deletion in another.
  • The tumour cells showed immunoblastic/plasmablastic histology and were positive for ALK and Oct2, but negative for CD3, CD20, CD79a, CD30 and PAX5.
  • The staining pattern of ALK protein was cytoplasmic in two patients and associated with the nuclear membrane in one patient.
  • Fluorescence in situ hybridization (FISH) analysis using the ALK break-apart probe revealed ALK gene rearrangements in all three patients, with a 5'-ALK gene deletion in one patient.
  • These three cases suggest that different types of cytogenetic aberrations may involve the ALK gene in ALK-positive diffuse large B-cell lymphoma leading to peculiar immunohistochemical staining patterns.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / therapy. Protein-Tyrosine Kinases / biosynthesis. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Cell Nucleus / metabolism. Chromosome Aberrations. Cytogenetics. Female. Gene Deletion. Humans. Immunohistochemistry. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Receptor Protein-Tyrosine Kinases. Treatment Outcome

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  • (PMID = 18220322.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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5. Cluzeau T, Pécuchet N, Mounier N, Vignot S: [Implications of ALK (anaplastic lymphoma kinase) in oncohematology]. Bull Cancer; 2010 Aug;97(8):991-6
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  • [Title] [Implications of ALK (anaplastic lymphoma kinase) in oncohematology].
  • [Transliterated title] Implications d'ALK (anaplastic lymphoma kinase) en oncohématologie.
  • The anaplastic lymphoma kinase gene (ALK) code for a receptor tyrosine-kinase.
  • The fusion proteins from the ALK gene have been identified in oncohaematology malignancies including ALK positive anaplastic lymphoma large cell and non small cells lung cancer with EML4-ALK fusion gene.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / enzymology. Lung Neoplasms / enzymology. Lymphoma, Large-Cell, Anaplastic / enzymology. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 20483705.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Nucleoplasmins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 27
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6. 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.
  • Expression of the antiapoptotic proteins survivin and BCL-X(L), which were believed to be the targets of STAT 3, was investigated.
  • 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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7. Reichard KK, McKenna RW, Kroft SH: ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature. Mod Pathol; 2007 Mar;20(3):310-9
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature.
  • We report detailed clinical and pathologic features of four cases of anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma (ALK-DLBCL), a rare entity with only 29 currently reported cases.
  • By immunohistochemistry and/or flow cytometry, they expressed cytoplasmic ALK-1, CD138, VS38 (3/3), monoclonal cytoplasmic light chain, CD45, EMA, CD4, and CD57 (2/3), and were negative for CD3, CD30, CD56, and TIA-1.
  • Two showed variable CD79a expression, and one had rare CD20(+) cells.
  • [MeSH-major] Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 17277765.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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8. Bubała H, Małdyk J, Włodarska I, Sońta-Jakimczyk D, Szczepański T: ALK-positive diffuse large B-cell lymphoma. Pediatr Blood Cancer; 2006 May 1;46(5):649-53
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  • [Title] ALK-positive diffuse large B-cell lymphoma.
  • Anaplastic lymphoma kinase (ALK) positive diffuse large B-cell lymphoma (DLBCL) is a rare subtype of non-Hodgkins lymphoma.
  • We present a 9-year-old boy, in whom diagnosis of DLBCL has been established in addition to congenital multiple enchondromatosis.
  • Immunohistopathological evaluation of tumor biopsy established the final diagnosis of ALK + DLBCL.
  • The clathrin gene (CLTC)-ALK fusion underlying aberrant expression of ALK in the present case was demonstrated by interphase fluorescence in situ hybridization (FISH) using break-apart rearrangement probes for ALK and CLTC.
  • Analysis of the disease course in our patient and review of other cases reported previously show that ALK + DLBCL can be an aggressive malignancy that can be cured with conventional chemotherapy protocols only at stage of localized disease.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 15852431.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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9. Zhang D, Denley RC, Filippa DA, Teruya-Feldstein J: ALK-positive diffuse large B-cell lymphoma with the t(2;17)(p23;q23). Appl Immunohistochem Mol Morphol; 2009 Mar;17(2):172-7
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  • [Title] ALK-positive diffuse large B-cell lymphoma with the t(2;17)(p23;q23).
  • Diffuse large B-cell lymphoma (DLBCL) with plasmablastic features associated with t(2;17)(p23;q23) and characteristic granular cytoplasmic anaplastic lymphoma kinase-1 (ALK1) protein expression is a rare lymphoma subtype.
  • Lymph node biopsy showed large atypical cells with prominent plasmablastic differentiation, abundant amphophilic cytoplasm, and prominent central nucleoli.
  • Paraffin immunohistochemistry showed finely granular cytoplasmic ALK1 expression, positive CD138, IgA, p63 (VS38), focal positive epithelial membrane antigen and CD4, and lambda light chain restriction whereas negative CD20 and CD30 staining.
  • While reports show detection of the unique CLTC-ALK fusion by either reverse transcription-polymerase chain reaction or fluorescence in situ hybridization, our case represents the second case in the literature to detect the t(2;17)(p23;q23) translocation by multiplex karyotyping (multiplex fluorescence in situ hybridization) and the usefulness of this technique to detect hidden translocations not seen by G-banding.
  • Differential diagnoses of neoplasms with plasmablastic differentiation and a comprehensive molecular/cytogenetic literature review of ALK+DLBCL is discussed.

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  • (PMID = 19521280.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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10. 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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  • [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.
  • 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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11. 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.
  • 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.
  • Patients were of median age 39 years with a male:female ratio of 7:1.
  • T-cell receptor gene rearrangement was present in all cases, CD30 was positive in 22 (96%), and the vast majority (90%) were ALK-negative.
  • Many (68%) patients died, with a median survival of 9 months.
  • Death was caused by either lymphoma progression (42%) or infection (58%).
  • 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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12. 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.
  • [Title] Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells.
  • METHODS: PD-L1 expression was analyzed in 16 NHL cell lines by flow cytometry (FC) and in 111 lymphoma specimens by immunohistochemistry (IHC) (n=92) or FC (n=19).
  • In functional studies, irradiated anaplastic large cell lymphoma (ALCL) cells were co-cultured with allogeneic T cells in the presence of anti-PD-L1 blocking antibody, and IFNγ secretion and thymidine incorporation was used to assess T cell function and proliferation.
  • To further test tumor-T cell interactions, malignant ascites from a patient with ALK+ ALCL and peripheral blood mononuclear cells from a patient with leukemic mantle cell lymphoma, both containing PD-L1-expressing tumor cells and tumor-associated T cells, were stimulated with phytohemagglutinin (a polyclonal T cell activator) and incubated with anti-PD-L1 antibody.
  • Levels of 16 inflammatory cytokines were measured as an assessment of T cell activity.
  • RESULTS: All 9 B cell lymphoma lines were negative for PD-L1, while all 5 ALCL cell lines were strongly positive.
  • One T-cell ALL line was positive, and one peripheral T cell lymphoma was negative.
  • Strong PD-L1 staining was detected by IHC in all 14 ALCL specimens and in 83% of diffuse large B cell lymphomas (DLBCL) analyzed (n=35).
  • In the autologous setting using cultures of ALCL and mantle cell lymphoma specimens containing host T cells, secretion of inflammatory cytokines by tumor-associated T cells, including GMCSF, IFNγ, IL-1, IL-6, IL-8, TNFα, and MIP1α, were increased by incubation with anti-PD-L1 antibody.
  • 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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13. Siordia-Reyes AG, Ferman-Cano F, Rodríguez-Velasco A: [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case]. Gac Med Mex; 2005 Nov-Dec;141(6):531-4
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  • [Title] [ALK-1 positive anaplastic large cell lymphoma of the lung. Report of a pediatric case].
  • [Transliterated title] Linfoma anaplásico de células grandes ALK-1 positivo, primario de pulmón. Informe de un caso pediátrico.
  • Ki-1 anaplastic large cell non-Hodgkin lymphoma is a well recognized clinical entity.
  • Anaplastic large cell lymphoma is more common among young people, in whom the prognosis is more favorable.
  • Primary anaplastic large cell lymphoma of the lung is a rare clinical entity.
  • Its clinical expression is similar to a high grade malignant lymphoma, and in most cases the diagnosis is made in advanced stages.
  • We present a pediatric case with ALK-1 positive anaplastic large cell lymphoma of the lung.
  • [MeSH-major] Lung Neoplasms / chemistry. Lymphoma, Large B-Cell, Diffuse / chemistry. Membrane Proteins / analysis

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  • (PMID = 16381509.001).
  • [ISSN] 0016-3813
  • [Journal-full-title] Gaceta médica de México
  • [ISO-abbreviation] Gac Med Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
  • [Number-of-references] 16
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14. Li C, Takino H, Eimoto T, Ishida T, Inagaki A, Ueda R, Suzuki R, Yoshino T, Nakagawa A, Nakamura S, Inagaki H: Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma. Mod Pathol; 2007 Jun;20(6):648-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma.
  • In anaplastic large-cell lymphomas positive for anaplastic lymphoma kinase (ALK) protein, the ALK gene is most commonly fused to the NPM gene, and less commonly to TPM3, TFG, ATIC, and other rare genes.
  • Although this lymphoma is generally associated with a favorable clinical outcome, 25% of the patients die of the disease within 5 years.
  • (1) a sensitive reverse transcription-polymerase chain reaction (RT-PCR) assay for various X-ALK fusion genes, (2) a 5' rapid amplification of cDNA ends (RACE) assay to identify unknown fusion partners, and (3) a real-time RT-PCR assay to quantify the amount of the NPM-ALK fusion transcript.
  • In 26 cases of ALK(+) anaplastic large-cell lymphoma, the RT-PCR assay showed that the ALK was fused to NPM in 21 cases, to TPM3 in three, and to TFG in one.
  • The 5' RACE assay detected ATIC-ALK fusion in the remaining case.
  • The real-time quantitative RT-PCR assay showed that the NPM-ALK transcript was over expressed in four of 20 quantifiable cases.
  • Patients with NPM-ALK overexpression showed a significantly unfavorable overall survival compared with those with a low expression of this transcript.
  • The RT-PCR and 5' RACE assays developed here may be useful for identification of known and unknown gene partners fused to the ALK gene.
  • Overexpression of the NPM-ALK fusion transcript may be associated with a poor prognosis of the patients with ALK(+) anaplastic large-cell lymphomas.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Protein-Tyrosine Kinases / biosynthesis

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  • (PMID = 17464320.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Fixatives; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; 1HG84L3525 / Formaldehyde; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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15. Sjostrom C, Seiler C, Crockett DK, Tripp SR, Elenitoba Johnson KS, Lim MS: Global proteome profiling of NPM/ALK-positive anaplastic large cell lymphoma. Exp Hematol; 2007 Aug;35(8):1240-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Global proteome profiling of NPM/ALK-positive anaplastic large cell lymphoma.
  • OBJECTIVE: Constitutive overexpression of nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) is a key oncogenic event in anaplastic large cell lymphomas (ALCL) that carry the t(2;5)(p23;q35) translocation.
  • Global proteomic analysis of NPM/ALK-positive ALCL would improve understanding of the disease pathogenesis and yield new candidate targets for novel treatment and diagnostic strategies.
  • MATERIALS AND METHODS: To comprehensively determine the inventory of proteins from NPM/ALK-positive ALCL SUDHL-1 cells, the membrane, cytoplasm, and nuclear subcellular fractions were resolved by one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS).
  • RESULTS: A total of 623 proteins consisting of 210 membrane, 229 cytoplasm, and 184 nuclear proteins were identified with a <or=5% error rate.
  • CONCLUSION: We present an extensive catalog of proteins expressed by NPM/ALK-positive ALCL.
  • This study illustrates the potential for novel pathogenetic discovery in NPM/ALK-positive ALCL and the utility of combining cellular subfractionation, 1D SDS-PAGE, and LC-MS/MS for the comprehensive protein analysis of lymphoma.
  • [MeSH-major] Gene Expression Profiling. Lymphoma, Large B-Cell, Diffuse / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proteome
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. Humans. Molecular Sequence Data. Neoplasm Proteins / genetics

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  • (PMID = 17560012.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proteome; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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16. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • 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.
  • [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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17. Ishii K, Yamamoto Y, Nomura S: [CD30-negative diffuse large B-cell lymphoma expressing ALK]. Rinsho Ketsueki; 2005 Jul;46(7):501-6
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  • [Title] [CD30-negative diffuse large B-cell lymphoma expressing ALK].
  • An open-abdominal lymph node biopsy was performed from which a diagnosis of anaplastic large cell lymphoma was made.
  • He underwent allogeneic peripheral blood stem cell transplantation (PBSCT) from his HLA-matched sister while in non-CR in November 2002.
  • The tumor cells were ALK-positive, CD30-negative and JH rearrangement was detected, and were therefore classified as diffuse large B-cell lymphoma with expression of ALK according to the WHO classification, though they differed from this subtype in some points.
  • Although this case was refractory for chemotherapy with a complex karyotype, the graft-versus-lymphoma effect might have contributed to the sustained CR following the PBSCT.
  • [MeSH-major] Lymphoma, B-Cell. Lymphoma, Large B-Cell, Diffuse. Protein-Tyrosine Kinases
  • [MeSH-minor] Adult. Antigens, CD30. Combined Modality Therapy. Fatal Outcome. Humans. Male. Peripheral Blood Stem Cell Transplantation. Peripheral Vascular Diseases / etiology. Receptor Protein-Tyrosine Kinases. Transplantation, Homologous

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  • (PMID = 16440742.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [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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18. 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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19. Bohling SD, Jenson SD, Crockett DK, Schumacher JA, Elenitoba-Johnson KS, Lim MS: Analysis of gene expression profile of TPM3-ALK positive anaplastic large cell lymphoma reveals overlapping and unique patterns with that of NPM-ALK positive anaplastic large cell lymphoma. Leuk Res; 2008 Mar;32(3):383-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of gene expression profile of TPM3-ALK positive anaplastic large cell lymphoma reveals overlapping and unique patterns with that of NPM-ALK positive anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) comprises a group of non-Hodgkin lymphomas characterized by the expression of the CD30/Ki-1 antigen.
  • A subset of ALCL is characterized by chromosomal translocations involving the anaplastic lymphoma kinase (ALK) gene on chromosome 2.
  • While the most common translocation is the t(2;5)(p23;q35) involving the nucleophosmin (NPM) gene on chromosome 5, up to 12 other translocations partners of the ALK gene have been identified.
  • One of these is the t(1;2)(q25;p23) which results in the formation of the chimeric protein TPM3-ALK.
  • While several of the signaling pathways induced by NPM-ALK have been elucidated, those involved in ALCLs harboring TPM3-ALK are largely unknown.
  • In order to investigate the expression profiles of ALCLs carrying the NPM-ALK and TPM3-ALK fusions, we carried out cDNA microarray analysis of two ALCL tissue samples, one expressing the NPM-ALK fusion protein and the other the TPM3-ALK fusion protein.
  • Our results show a significant overlap of genes deregulated in the NPM-ALK and TPM-ALK positive lymphomas.
  • These deregulated genes are involved in diverse cellular functions, such as cell cycle regulation, apoptosis, proliferation, and adhesion.
  • Interestingly, a subset of the genes was distinct in their expression pattern in the two types of lymphomas.
  • More importantly, many genes that were not previously associated with ALK positive lymphomas were identified.
  • Our results demonstrate the overlapping and unique transcriptional patterns associated with the NPM-ALK and TPM3-ALK fusions in ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Tropomyosin / genetics
  • [MeSH-minor] Adult. Child. Gene Expression Profiling. Humans. Male. Oligonucleotide Array Sequence Analysis. Receptor Protein-Tyrosine Kinases. Translocation, Genetic

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  • (PMID = 17720243.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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20. 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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21. 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.
  • These results were compared with phosphorylated (activated) STAT3 (pSTAT3) expression.
  • 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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22. Salaverria I, Beà S, Lopez-Guillermo A, Lespinet V, Pinyol M, Burkhardt B, Lamant L, Zettl A, Horsman D, Gascoyne R, Ott G, Siebert R, Delsol G, Campo E: Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas. Br J Haematol; 2008 Mar;140(5):516-26
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  • [Title] Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is a T/null-cell neoplasm characterized by chromosomal translocations involving the anaplastic lymphoma kinase (ALK) gene (ALK).
  • Tumours with similar morphology and phenotype but negative for ALK have been also recognized.
  • We have examined 74 ALCL, 43 ALK-positive and 31 ALK-negative, cases by comparative genomic hybridization (CGH), and locus-specific alterations for TP53 and ATM were examined by fluorescence in situ hybridization and real-time quantitative polymerase chain reaction.
  • Chromosomal imbalances were detected in 25 (58%) ALK-positive and 20 (65%) ALK-negative ALCL.
  • ALK-positive ALCL with NPM-ALK or other ALK variant translocations showed a similar profile of secondary genetic alterations.
  • Gains of 17p and 17q24-qter and losses of 4q13-q21, and 11q14 were associated with ALK-positive cases (P = 0.05), whereas gains of 1q and 6p21 were more frequent in ALK-negative tumours (P = 0.03).
  • ALCL-negative tumours had a significantly worse prognosis than ALK-positive.
  • In conclusion, ALK-positive and negative ALCL have different secondary genomic aberrations, suggesting they correspond to different genetic entities.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromosome Aberrations. Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adult. Aged. Female. Gene Expression Profiling / methods. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Nucleic Acid Hybridization. Prognosis. Receptor Protein-Tyrosine Kinases. Survival Analysis

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  • (PMID = 18275429.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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23. 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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24. Lai R, Rassidakis GZ, Lin Q, Atwell C, Medeiros LJ, Amin HM: Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma. Hum Pathol; 2005 Sep;36(9):939-44
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  • [Title] Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma.
  • Janus kinase 3 (Jak3) is a tyrosine kinase that activates signal transducer and activator of transcription 3 (Stat3) in response to cytokine stimulation.
  • In previous studies of anaplastic large cell lymphoma (ALCL), we showed that inhibition of Jak3 down-regulates activated/phosphorylated Stat3 (pStat3), decreases anaplastic lymphoma kinase (ALK) enzymatic activity, and induces cell-cycle arrest and apoptosis in ALK-positive ALCL.
  • These findings implicate Jak3 as playing a significant role in the pathogenesis of ALK-positive ALCL; most likely via Stat3 and ALK activation.
  • To assess this possibility, we used immunohistochemical staining to evaluate the frequency of expression of Jak3 and its activated/phosphorylated form (pJak3) in 48 systemic ALCL tumors included in a tissue microarray. pJak3 was detected in 17 (81%) of 21 ALK-positive tumors, compared with 3 (11%) of 27 ALK-negative tumors (P < .0001, Fisher exact test).
  • pStat3 was present in 12 (86%) of 14 ALK-positive tumors and in 10 (40%) of 25 ALK-negative tumors assessed (P = .0078).
  • Of 12 ALK-positive/pStat3-positive tumors, 8 (67%) expressed pJak3, but none of 10 ALK-negative/pStat3-positive tumors expressed pJak3.
  • We conclude that Jak3 activation is predominantly restricted to ALK-positive ALCL tumors.
  • Most likely, Jak3 collaborates with ALK in activating Stat3, leading to cell survival, cell-cycle progression, and tumor growth.
  • In contrast, the mechanism of Stat3 activation in ALK-negative ALCL tumors appears to be independent of Jak3.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Child. Enzyme Activation. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Janus Kinase 3. Male. Middle Aged. Phosphorylation. Receptor Protein-Tyrosine Kinases

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  • (PMID = 16153455.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / JAK3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3
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25. Choung HS, Kim HJ, Kim WS, Kim K, Kim SH: [Cytomorphology and molecular characterization of CLTC-ALK rearrangement in 2 cases of ALK-positive diffuse large B-cell lymphoma with extensive bone marrow involvement]. Korean J Lab Med; 2008 Apr;28(2):89-94
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  • [Title] [Cytomorphology and molecular characterization of CLTC-ALK rearrangement in 2 cases of ALK-positive diffuse large B-cell lymphoma with extensive bone marrow involvement].
  • Aanaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma (DLBCL) is an unusual disease entity first reported in 1997 as DLBCL with expression of full-length ALK protein.
  • The World Health Organization classification enlists the disease as a rare variant of DLBCL.
  • Herein we describe two cases of ALK-positive DLBCL with cytomorphologic and molecular characteristics for the first time in Korea.
  • Immunohistochemical studies on the lymph nodes revealed large sized neoplastic cells with plasmablastic differentiation, which were negative for CD30 and positive for ALK with the characteristic granular staining in the cytoplasmic region.
  • Extensive involvement of bone marrow was observed in both cases showing large, extremely atypical cells.
  • Fluorescence in situ hybridization and molecular studies on the bone marrow aspirate specimens led to the detection of a clathrin (CLTC)/ALK rearrangement.
  • This is the first report demonstrating the cytomorphologic findings of ALK-positive DLBCL cells on bone marrow aspirates.
  • [MeSH-major] Bone Marrow / pathology. Clathrin / genetics. Gene Fusion. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / genetics

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  • (PMID = 18458503.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Clathrin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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31. 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.
  • This decrease in viability was associated with apoptosis, as confirmed by the increase in the subG(0/1) fraction, poly(ADP-ribose)polymerase cleavage and expression of active caspase 3.
  • 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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32. 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.
  • CCAAT/enhancer binding protein beta (C/EBPbeta) is one of a 6-member family of C/EBPs.
  • 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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33. 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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34. Dien Bard J, Gelebart P, Anand M, Zak Z, Hegazy SA, Amin HM, Lai R: IL-21 contributes to JAK3/STAT3 activation and promotes cell growth in ALK-positive anaplastic large cell lymphoma. Am J Pathol; 2009 Aug;175(2):825-34
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  • [Title] IL-21 contributes to JAK3/STAT3 activation and promotes cell growth in ALK-positive anaplastic large cell lymphoma.
  • Interleukin (IL)-21 has been reported to both stimulate cell growth and promote survival in benign lymphoid cells and several types of hematopoietic neoplasms.
  • It induces JAK3/STAT3 signaling, a biologically important cellular pathway activated in most cases of anaplastic lymphoma kinase (ALK)-expressing anaplastic large cell lymphoma (ALK(+)ALCL).
  • Therefore, we hypothesize that IL-21 may contribute to JAK3/STAT3 activation and cell growth in ALK(+)ALCL.
  • By reverse transcription-PCR, we found consistent expression of IL-21 receptor (IL-21R) in all ALK(+)ALCL cell lines and frozen tumors examined.
  • IL-21 was also consistently expressed in ALK(+)ALCL tumors, although its mRNA was detectable in only one of three cell lines tested.
  • By immunohistochemistry, we examined 10 paraffin-embedded ALK(+)ALCL tumors; all cases were positive for both IL-21 and IL-21R in these neoplastic cells.
  • IL-21 signaling is biologically significant in ALK(+)ALCL since the addition of recombinant IL-21 enhanced the activation of JAK3/STAT3 and significantly increased cell growth in ALK(+)ALCL cell lines.
  • However, small interfering RNA down-regulation of IL-21R significantly decreased both STAT3 activation and cell growth.
  • IL-21R expression is not linked to nucleophosmin-ALK since forced expression of nucleophosmin-ALK and small interfering RNA down-regulation of nucleophosmin-ALK did not significantly change the expression of either IL-21R or IL-21.
  • Our findings thus support the enhancement of JAK3/STAT3 activation and cell growth in ALK(+)ALCL via IL-21 signaling.
  • [MeSH-major] Interleukins / metabolism. Janus Kinase 3 / biosynthesis. Lymphoma, Large-Cell, Anaplastic / pathology. STAT3 Transcription Factor / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Protein-Tyrosine Kinases / analysis. RNA, Small Interfering / genetics. Receptor Protein-Tyrosine Kinases. Receptors, Interleukin-21 / metabolism

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  • (PMID = 19608866.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukins; 0 / JAK3 protein, human; 0 / RNA, Small Interfering; 0 / Receptors, Interleukin-21; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / interleukin-21; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3
  • [Other-IDs] NLM/ PMC2716977
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35. Tamiolakis D, Papadopoulos N, Venizelos J, Kakagia D, Nikolaidou S, Bolioti S, Kouskoukis C: ALK-positive neutrophil-rich variant of anaplastic large cell lymphoma diagnosed after head trauma. Onkologie; 2005 Jun;28(6-7):356-8
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  • [Title] ALK-positive neutrophil-rich variant of anaplastic large cell lymphoma diagnosed after head trauma.
  • BACKGROUND: Anaplastic lymphoma kinase (ALK) expression has not been described in neutrophil-rich anaplastic large cell lymphoma (NR-ALCL).
  • CASE REPORT: A 12-year old female with a 4-weeks history of a non-resolving bump over the forehead resulting from injury, was diagnosed of stage IE cutaneous T-cell lymphoma, and radiation was employed.
  • A fine-needle aspiration of the hand mass was performed, and a diagnosis of CD30+/ALK+ NR-ALCL, was rendered.
  • METHODS: We studied the morphological characteristics of CD30+/ALK+ NR-ALCL using histological methods.
  • 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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36. 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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  • [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 gradually restored SHP1 expression in Karpas 299 and SU-DHL-1 cells over 5 days.
  • The initially low level of SHP1 expression did not result in significant changes to the expression or tyrosine phosphorylation of JAK3 and STAT3.
  • 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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37. Thornber K, Colomba A, Ceccato L, Delsol G, Payrastre B, Gaits-Iacovoni F: Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas. Oncogene; 2009 Jul 23;28(29):2690-6
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  • [Title] Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas.
  • The chimera nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), the tyrosine kinase activity of which is constitutively upregulated, is the causative agent of 75% of the anaplastic large-cell lymphomas (ALCLs).
  • We have demonstrated that NPM-ALK induces the production of reactive oxygen species (ROS) by a pathway involving the arachidonic acid-metabolizing enzymes of the lipoxygenase (LOX) family.
  • The use of the LOX inhibitor nordihydroguaiaretic acid (NDGA) and of the anti-oxidant N-acetylcysteine (NAC) demonstrated that ROS are important in maintaining the ALK kinase active.
  • Consistent with this, NDGA treatment resulted in the inhibition of key pathways, such as Akt, signal transducer and activator of transcription factor 3 (STAT3) and extracellular signal-regulated kinase (ERK), which are involved in NPM-ALK antiapoptotic and pro-mitogenic functions.
  • Conversely, the stress-activated kinase p38, described in some instances as a mediator of apoptosis, was activated.
  • Interestingly, 5-LOX, an isoform involved in many cancers, was found to be activated in NPM-ALK(+) cells.
  • Together, these data point to the ROS/LOX pathway as a potential new target for therapy in NPM-ALK-positive tumors.
  • [MeSH-major] Arachidonate 5-Lipoxygenase / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Humans. Lipoxygenase Inhibitors / pharmacology. Masoprocol / analysis

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  • (PMID = 19503098.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipoxygenase Inhibitors; 0 / Reactive Oxygen Species; 7BO8G1BYQU / Masoprocol; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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38. Damm-Welk C, Klapper W, Oschlies I, Gesk S, Röttgers S, Bradtke J, Siebert R, Reiter A, Woessmann W: Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation. Br J Haematol; 2009 Aug;146(3):306-9
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  • [Title] Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation.
  • Anaplastic large cell lymphomas (ALCL) in children express anaplastic lymphoma kinase (ALK) fusion genes, most commonly NPM1-ALK.
  • The distribution of X-ALK among 66 childhood ALCLs was analysed.
  • One ALCL was ALK-negative.
  • Reverse transcription polymerase chain reaction detected NPM1-ALK in 58 tumours, all showing nuclear and cytoplasmic ALK staining.
  • The remaining seven ALCL stained for ALK in the cytoplasm only: two expressed TPM3-ALK, one ATIC-ALK, one MYH9-ALK; three no TPM3-, TFG-, ATIC-, CLTC- or MYH9-ALK.
  • Almost 90% of paediatric ALK-positive ALCLs express NPM1-ALK.
  • There was complete concordance between ALK staining pattern and the presence of a typical/variant ALK fusion partner.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19545284.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / MYH9 protein, human; 0 / Molecular Motor Proteins; 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; 0 / oncoprotein CLTCL-ALK; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.6.4.1 / Myosin Heavy Chains
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39. 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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40. Lamant L, Pileri S, Sabattini E, Brugières L, Jaffe ES, Delsol G: Cutaneous presentation of ALK-positive anaplastic large cell lymphoma following insect bites: evidence for an association in five cases. Haematologica; 2010 Mar;95(3):449-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cutaneous presentation of ALK-positive anaplastic large cell lymphoma following insect bites: evidence for an association in five cases.
  • BACKGROUND: Skin involvement is frequent in ALK-positive anaplastic large cell lymphomas.
  • DESIGN AND METHODS: We retrospectively investigated five cases of ALK-positive anaplastic large cell lymphoma who presented with skin lesions occurring after an insect bite.
  • Biopsies were immunostained with antibodies against CD30, ALK, T- and B-cell antigens.
  • In four cases the correct diagnosis was delayed due to misinterpretation of the findings as a reactive infiltrate in the skin (n=2) or lymph nodes (n=2); all cases subsequently showed small numbers of cells with nuclear and cytoplasmic staining for ALK.
  • The final diagnoses were lymphohistiocytic variant (n=3) and composite common/small cell type (n=2) anaplastic large cell lymphoma.
  • CONCLUSIONS: In these cases the sequence of events between the insect bites and the occurrence of both skin lesions and satellite lymphadenopathy suggest a direct relationship between the bite and the presentation with anaplastic large cell lymphoma.
  • The subsequent release of cytokines at the site of the bite could act as a 'second hit', eliciting activation of the latter cells, which would then express the oncogenic NPM-ALK protein and undergo uncontrolled proliferation.

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  • (PMID = 19951975.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2833075
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41. 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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42. Georgakis GV, Li Y, Rassidakis GZ, Medeiros LJ, Younes A: The HSP90 inhibitor 17-AAG synergizes with doxorubicin and U0126 in anaplastic large cell lymphoma irrespective of ALK expression. Exp Hematol; 2006 Dec;34(12):1670-9
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  • [Title] The HSP90 inhibitor 17-AAG synergizes with doxorubicin and U0126 in anaplastic large cell lymphoma irrespective of ALK expression.
  • OBJECTIVE: Heat shock protein 90 (HSP90) chaperones and maintains the molecular integrity of a variety of signal transduction proteins, including the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) oncogenic protein, a genetic abnormality that is frequently observed in anaplastic large cell lymphoma (ALCL) cells.
  • Here we demonstrate that HSP90 is overexpressed in primary and cultured ALK-positive and ALK-negative ALCL cells, and we evaluate the potential role of the small molecule inhibitor of HSP90, 17-allylamino-17-demethoxygeldanamycin (17-AAG) in treating ALCL.
  • Apoptosis and cell-cycle arrest were determined by Annexin-V/propidium iodide and propidium iodide staining, respectively, and fluorescein-activated cell sorting analysis.
  • Expression of HSP90 was evaluated by immunohistochemistry, and molecular changes were determined by Western blot.
  • RESULTS: Treatment of cultured ALCL cells with 17-AAG induced cell-cycle arrest and apoptosis, irrespective of ALK expression.
  • At the molecular level, 17-AAG induced degradation of ALK and Akt proteins, dephosphorylated extracellular signal-regulated kinase, and degraded the cell-cycle regulatory protein cyclin D1 and its cyclin-dependent kinases, CDK4 and CDK6, but had a differential effect on p27 and p53 proteins.
  • Inhibition of extracellular signal-regulated kinase phosphorylation by the mitogen activated protein kinase inhibitor U0126 induced cell death in all ALCL cell lines, and sublethal concentration 17-AAG showed synergistic antiproliferative effects when combined with U0126 or doxorubicin.
  • [MeSH-major] Benzoquinones / pharmacology. Butadienes / pharmacology. Doxorubicin / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / pharmacology. Lymphoma, Large-Cell, Anaplastic / metabolism. Nitriles / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis / drug effects. Caspase 3 / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D. Cyclin-Dependent Kinase 4 / drug effects. Cyclin-Dependent Kinase 4 / metabolism. Cyclin-Dependent Kinase 6 / drug effects. Cyclin-Dependent Kinase 6 / metabolism. Cyclins / drug effects. Cyclins / metabolism. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Drug Synergism. Extracellular Signal-Regulated MAP Kinases / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. G0 Phase / drug effects. G1 Phase / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / drug effects. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / drug effects. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphorylation. Receptor Protein-Tyrosine Kinases. Time Factors

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  • (PMID = 17157164.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Butadienes; 0 / Cyclin D; 0 / Cyclins; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Nitriles; 0 / U 0126; 4GY0AVT3L4 / tanespimycin; 80168379AG / Doxorubicin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.22.- / Caspase 3
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43. Liu A, Sugisaki Y, Hosone M, Namimatsu S, Maeda S, Naito Z, Ghazizadeh M: CD30-positive diffuse large B-cell lymphoma with microvillous features: so-called microvillous lymphoma. J Clin Pathol; 2009 Sep;62(9):840-4
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  • [Title] CD30-positive diffuse large B-cell lymphoma with microvillous features: so-called microvillous lymphoma.
  • A case of CD30-positive microvillous lymphoma (MVL) in an 87-year-old man who was encountered generalised lymphadenopathy is presented.
  • Histopathologically, the tumour showed a morphological mimic of anaplastic large cell lymphoma (ALCL) with sinusoidal growth pattern.
  • Immunohistochemically (IHC), the tumour cells were CD30(+), CD20(+), CD45(+), BCL-2(+), BCL-6(+), MUM1(+), Ki-67(+), CD45RO(-), CD3(-), CD10(-), CD15(-), CD56(-), EMA(-), TIA-1(-) and ALK(-).
  • Electron microscopically, the tumour cells were similar to large transformed lymphocytes and had circumferentially profuse microvillous projections resembling those of epithelial mesothelioma cells.
  • In conclusion, CD30-positive MVLs are indistinguishable from ALCLs that have ultrastructural microvillous projections by morphology alone.
  • However, the lack of EMA, TIA-1 and ALK expression in this MVL case facilitated a definite distinction from ALCLs.
  • The results of a panel of three markers (CD10(-), Bcl-6(+) and MUM1(+)) suggested that the present case of CD30-positive MVLs has an activated non-germinal centre B-cell origin.
  • [MeSH-major] Antigens, CD30 / analysis. Lymphoma, Large B-Cell, Diffuse / ultrastructure
  • [MeSH-minor] Aged, 80 and over. Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Lymphoma, Large-Cell, Anaplastic / diagnosis. Male. Microscopy, Electron. Microvilli / ultrastructure

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  • (PMID = 19126565.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor
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44. 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 patient presented with a 3-month history of progressive right breast swelling and erythema.
  • 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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45. Zhang Q, Wang HY, Bhutani G, Liu X, Paessler M, Tobias JW, Baldwin D, Swaminathan K, Milone MC, Wasik MA: Lack of TNFalpha expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis. Proc Natl Acad Sci U S A; 2009 Sep 15;106(37):15843-8
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  • [Title] Lack of TNFalpha expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis.
  • Here we report that T-cell lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express the TNFalpha and frequently display DNA methylation of the TNFalpha gene promoter.
  • While only a subset of the ALK+ TCL-derived cell lines showed a high degree of the promoter methylation, all 6 showed low to nondetectable expression of the TNFalpha mRNA, and none expressed the TNFalpha protein.
  • All 14 ALK+ TCL tissue samples examined displayed some degree of the TNFalpha promoter methylation, which was the most prominent in the distal portion of the the promoter.
  • Treatment with a DNA methyltransferase inhibitor, 5'-aza-2'-deoxy-cytidine (5-ADC), reversed the promoter methylation and led to the expression of TNFalpha mRNA and protein.
  • Notably, the ALK+ TCL cell lines uniformly expressed the type 1 TNFalpha receptor (TNF-R1) protein known to transduce the TNFalpha-induced pro-apoptotic signals.
  • Moreover, exogenous TNFalpha inhibited growth of the ALK+ TCL cell lines in a dose-dependent manner and induced activation of the members of the cell apoptotic pathway: Caspase 8 and caspase 3.
  • These findings provide additional rationale for the therapeutic inhibition of DNA methyltransferases in ALK+ TCL.
  • They also suggest that treatment with TNFalpha may be highly effective in this type of lymphoma.

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  • (PMID = 19717436.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089194; United States / NCI NIH HHS / CA / R01 CA096856; United States / NCI NIH HHS / CA / R01-CA89194; United States / NCI NIH HHS / CA / R01-CA96856
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2747206
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46. Ait-Tahar K, Damm-Welk C, Burkhardt B, Zimmermann M, Klapper W, Reiter A, Pulford K, Woessmann W: Correlation of the autoantibody response to the ALK oncoantigen in pediatric anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor dissemination and relapse risk. Blood; 2010 Apr 22;115(16):3314-9
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  • [Title] Correlation of the autoantibody response to the ALK oncoantigen in pediatric anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor dissemination and relapse risk.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) constitutes an ideal model disease to study tumor-specific immune responses.
  • All the tumor cells express oncogenic ALK resulting from a chromosomal translocation involved in lymphomagenesis.
  • Although antibodies and T-cell responses to ALK have previously been detected in ALK-positive ALCL patients, their prognostic significance is unknown.
  • We investigated a large cohort of uniformly treated ALK-positive pediatric ALCL patients to ascertain whether the titers of preexisting ALK autoantibodies correlated with clinical and histologic characteristics, tumor dissemination, and patient outcome.
  • ALK autoantibodies were analyzed in pretherapeutic serum samples from 95 patients enrolled into 2 therapy studies between 1996 and 2007.
  • ALK autoantibodies were detected in 87/95 patients.
  • Our results provide the first clinical evidence that a robust preexisting immune response to an oncoantigen resulting from an oncogenic chromosomal translocation inhibits lymphoma dissemination and decreases the risk of relapse.
  • [MeSH-major] Autoantibodies / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasm Recurrence, Local / immunology. Protein-Tyrosine Kinases / immunology

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  • (PMID = 20185586.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Autoantigens; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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47. Gonin J, Kadiri H, Bensaci S, Le Tourneau A, Molina TJ, Diebold J, Abdellouche DJ, Audouin J: Primary mediastinal anaplastic alk-1-positive large-cell lymphoma of T/NK-cell type expressing CD20. Virchows Arch; 2007 Mar;450(3):355-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary mediastinal anaplastic alk-1-positive large-cell lymphoma of T/NK-cell type expressing CD20.
  • We describe an unusual case of ALK-1-positive primary mediastinal lymphoma with the morphology of an anaplastic large-cell lymphoma (ALCL) of T/NK cell type but expressing CD20.
  • This tumour had T/NK morphology and immunophenotype, as demonstrated by its expression of CD30, EMA, ALK-1, CD7 and TiA-1 and the lack of expression of B-cell markers other than CD20.
  • The significance of such a co-expression of a B cell-associated antigen in a case of ALCL of T/NK cell type is discussed.
  • [MeSH-major] Activin Receptors, Type II / metabolism. Antigens, CD20 / metabolism. Killer Cells, Natural / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Mediastinal Neoplasms / pathology. T-Lymphocytes / pathology

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  • (PMID = 17252228.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Biomarkers, Tumor; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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48. Matsubara K, Tanaka T, Taki T, Nakagawa A, Nigami H, Tamura A, Fukaya T: [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature]. Rinsho Ketsueki; 2008 May;49(5):325-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature].
  • We report a 10-year-old girl with ATIC-anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • Pathological findings showed that staining of ALK was restricted to the cytoplasm of ALCL cells.
  • ATIC-ALK chimeric transcripts were detected by reverse transcriptase polymerase chain reaction.
  • To date, 7 genes have been identified as a fusion partner of ALK, with the highest frequency in nucleophosmin (NPM).
  • Little is known about the clinical implications of subtypes of ALCL harboring each of the 7 fusion genes, especially those of variant fusion genes other than NPM-ALK.
  • In this paper, we review 9 patients with ATIC-ALK-positive ALCL in the literature in addition to discussing our patient.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Oncogene Proteins, Fusion / analysis

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  • (PMID = 18572809.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 18
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49. 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).
  • METHODS: A 39-year-old man presented with a rapidly growing exophytic mass on the left upper eyelid, with a protuberant, ulcerated aspect and with discharge.
  • 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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50. Stachurski D, Miron PM, Al-Homsi S, Hutchinson L, Harris NL, Woda B, Wang SA: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma with a complex karyotype and cryptic 3' ALK gene insertion to chromosome 4 q22-24. Hum Pathol; 2007 Jun;38(6):940-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma with a complex karyotype and cryptic 3' ALK gene insertion to chromosome 4 q22-24.
  • Anaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma (DLBCL) is a rare tumor that is frequently associated with t(2;17)(p23;q23), a translocation fusing the ALK gene at 2p23 to the clathrin heavy chain gene (CLTC) at 17q23.
  • Here, we report a unique case of ALK-positive DLBCL with plasmablastic morphology and focal cytoplasmic granular ALK stain in an HIV-negative 33-year-old man.
  • By conventional karyotyping, the lymphoma cells were near-tetraploid and included 4 structurally normal copies each of chromosomes 2 and 17.
  • Fluorescence in situ hybridization revealed an apparently normal, intact ALK gene on each of the 4 chromosome 2 homologs plus a cytogenetically cryptic ALK gene insertion into 2 of the 4 chromosome 4 homologs at band 4q22-24.
  • The lymphoma cells expressed CD138, lambda light chain, focal and weak CD30, and exhibited aberrant T-cell antigens, including perforin.
  • This case indicates that ALK-positive DLBCL is more heterogeneous at the cytogenetic/molecular level than previously recognized.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 4 / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 17509395.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [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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51. 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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52. 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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53. Fernandez-Vidal A, Mazars A, Gautier EF, Prévost G, Payrastre B, Manenti S: Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation. Cell Cycle; 2009 May 1;8(9):1373-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation.
  • Here, we demonstrate that the expression of the dual specificity phosphatase CDC25A, a key regulator of cell cycle progression, is deregulated in Ba/F3 cells expressing the oncogenic protein NPM/ALK and in human cell lines derived from NPM/ALK-positive anaplastic large cell lymphomas (ALCL).
  • Both transcriptional and post-translational mechanisms account for the constitutive expression of the protein, and the PI3K/Akt pathway is essential for this process.
  • Importantly, pharmacological inhibition of CDC25 dramatically inhibits the proliferation of NPM/ALK-expressing cells, while moderately affecting the proliferation of control Ba/F3 cells.
  • RNA interference-mediated downregulation of CDC25A confirmed that NPM/ALK-expressing cells are highly dependent on this protein for their proliferation.
  • Moreover, similar PI3K/AKt-mediated constitutive expression of CDC25A takes place down-stream of other hematological oncogenes, including BCR/ABL in Chronic Myeloid Leukemia and FLT3-ITD in Acute Myeloid Leukemia.
  • Altogether, our data point to the functional link between hematopoietic oncogenic tyrosine kinases and the G(1) cell cycle regulator CDC25A, and we propose that this protein may be a potential therapeutic target in ALCL and other hematological malignancies.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / pathology. Oncogenes. Protein-Tyrosine Kinases / metabolism. Up-Regulation. cdc25 Phosphatases / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. Oncogene Proteins, Fusion / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction

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  • (PMID = 19305144.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.16 / Cdc25a protein, mouse; EC 3.1.3.48 / CDC25A protein, human; EC 3.1.3.48 / cdc25 Phosphatases
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54. Damm-Welk C, Busch K, Burkhardt B, Schieferstein J, Viehmann S, Oschlies I, Klapper W, Zimmermann M, Harbott J, Reiter A, Woessmann W: Prognostic significance of circulating tumor cells in bone marrow or peripheral blood as detected by qualitative and quantitative PCR in pediatric NPM-ALK-positive anaplastic large-cell lymphoma. Blood; 2007 Jul 15;110(2):670-7
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  • [Title] Prognostic significance of circulating tumor cells in bone marrow or peripheral blood as detected by qualitative and quantitative PCR in pediatric NPM-ALK-positive anaplastic large-cell lymphoma.
  • Clinical and histopathological characteristics have limited prognostic value for children with anaplastic large-cell lymphoma (ALCL).
  • We evaluated the presence, extent, and prognostic impact of circulating tumor cells in bone marrow (BM) and peripheral blood (PB) of children and adolescents with NPM-ALK-positive ALCL at diagnosis using qualitative and quantitative polymerase chain reaction (PCR) for NPM-ALK.
  • Numbers of NPM-ALK transcripts were normalized to 10(4) copies ABL (NCNs).
  • BM was positive for NPM-ALK in 47.5% of patients, and positivity was significantly correlated with clinical stage, mediastinal or visceral involvement, microscopic BM involvement, and histologic subtype.
  • BM PCR was associated with the cumulative incidence of relapses (CI-Rs): CI-R was 50% +/- 10% for 38 PCR-positive and 15% +/- 7% for 42 PCR-negative patients (P < .001).
  • Sixteen patients with more than 10 NCNs NPM-ALK in BM had a CI-R of 71% +/- 14% compared with a CI-R of 18% +/- 6% for 59 patients with 10 or fewer NCNs (P < .001).
  • [MeSH-major] Bone Marrow Cells / physiology. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 17392503.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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55. Takahashi E, Kajimoto K, Fukatsu T, Yoshida M, Eimoto T, Nakamura S: Intravascular large T-cell lymphoma: a case report of CD30-positive and ALK-negative anaplastic type with cytotoxic molecule expression. Virchows Arch; 2005 Dec;447(6):1000-6
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  • [Title] Intravascular large T-cell lymphoma: a case report of CD30-positive and ALK-negative anaplastic type with cytotoxic molecule expression.
  • We reported a case of intravascular T-cell lymphoma (T-IVL) with anaplastic large cell morphology, the hemophagocytic syndrome, and an aggressive clinical course.
  • Phenotypic analysis of the tumor cells revealed CD2+, CD3-, CD4+, CD5-, CD8-, CD30+, CD56-, T-cell receptor alpha/beta-, ALK-, TIA1+, granzyme B+, and perforin+.
  • A review revealed that 25 cases of T-IVL have been reported in the available literature, only two of which were of CD30+ anaplastic large cell or cytotoxic T-cell type.
  • The findings in the present case may highlight the unique clinicopathologic aspects of a subset of CD30-positive T-IVLs with an ALK-negative cytotoxic phenotype.
  • [MeSH-major] Alkaline Phosphatase / metabolism. Antigens, CD30 / metabolism. Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, T-Cell / pathology

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  • (PMID = 16189700.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 3.1.3.1 / Alkaline Phosphatase
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56. 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.
  • 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


57. Li HL, Jiang HY, Ji TH, Chu HJ, Liu F, Chen XY, Wang X, Zhang G, Zhao T: [Nuclear microarray combined with fluorescence in situ hybridization for detecting ALK gene translocation in paraffin-embedded anaplastic large cell lymphoma and its significance]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Apr;28(4):572-5
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  • [Title] [Nuclear microarray combined with fluorescence in situ hybridization for detecting ALK gene translocation in paraffin-embedded anaplastic large cell lymphoma and its significance].
  • OBJECTIVE: To compare the efficacy of nuclear microarray combined with fluorescence in situ hybridization (FISH) and immunohistochemistry in detecting ALK gene translocation and ALK fusion protein in anaplastic large cell lymphoma (ALCL).
  • METHODS: ALK gene translocation and ALK fusion protein in 17 paraffin-embedded ALCL specimens were detected using nuclear microarray combined with FISH and immunohistochemical straining, respectively.
  • RESULTS: The expression of ALK fusion protein was detected immunohistochemically with ALK antibody in 8 of the 17 specimens of systemic ALCL, including 4 with both nuclear and cytoplasmic positivity and 4 with only cytoplasmic positivity.
  • Dual-color FISH identified 6 positive specimens, including the 4 specimens with both nuclear and cytoplasmic positivity as identified immunohistochemically, and 2 with immunohistochemical cytoplasmic positivity.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics. Translocation, Genetic

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  • (PMID = 18495593.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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58. 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.
  • 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.
  • 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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59. 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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60. 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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  • [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.


61. 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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  • [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.
  • 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).
  • Multivariate analysis confirmed that the type 1 phenotype with CM expression was an independent prognostic factor.
  • 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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62. Hsu FY, Zhao Y, Anderson WF, Johnston PB: Downregulation of NPM-ALK by siRNA causes anaplastic large cell lymphoma cell growth inhibition and augments the anti cancer effects of chemotherapy in vitro. Cancer Invest; 2007 Jun;25(4):240-8
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  • [Title] Downregulation of NPM-ALK by siRNA causes anaplastic large cell lymphoma cell growth inhibition and augments the anti cancer effects of chemotherapy in vitro.
  • The fusion protein, nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), results from the chromosome translocation t(2;5)(p23;q25) and is present in 50-70 percent of anaplastic large-cell lymphomas (ALCLs).
  • NPM-ALK is a constitutively activated kinase that transforms cells through stimulating several mitogenic signaling pathways.
  • To examine if the NPM-ALK is a potential therapeutic target in ALCL, we used siRNA to specifically downregulate the expression of the NPM-ALK in ALCL cell lines.
  • In this report, we demonstrated viability loss in t(2;5)-positive ALCL cell lines, SUDHL-1 and Karpas 299 cells, but not in lymphoma cell lines without the chromosome translocation, Jurkat and Granta 519 cells.
  • Further study demonstrated that the downregulation of NPM-ALK resulted in decreased cell proliferation and increased cell apoptosis.
  • When used in combination with chemotherapeutic agents, such as doxorubicin, the inhibition of the NPM-ALK augments the chemosensitivity of the tumor cells.
  • These results revealed the importance of continuous expression of NPM-ALK in maintaining the growth of ALCL cells.
  • Our data also suggested that the repression of the fusion gene might be a potential novel therapeutic strategy for NPM-ALK positive ALCLs.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. RNA, Small Interfering / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 5. Down-Regulation. Humans. Signal Transduction. Translocation, Genetic

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  • (PMID = 17612934.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59318
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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63. Staber PB, Vesely P, Haq N, Ott RG, Funato K, Bambach I, Fuchs C, Schauer S, Linkesch W, Hrzenjak A, Dirks WG, Sexl V, Bergler H, Kadin ME, Sternberg DW, Kenner L, Hoefler G: The oncoprotein NPM-ALK of anaplastic large-cell lymphoma induces JUNB transcription via ERK1/2 and JunB translation via mTOR signaling. Blood; 2007 Nov 1;110(9):3374-83
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  • [Title] The oncoprotein NPM-ALK of anaplastic large-cell lymphoma induces JUNB transcription via ERK1/2 and JunB translation via mTOR signaling.
  • Anaplastic large cell lymphomas (ALCLs) are highly proliferating tumors that commonly express the AP-1 transcription factor JunB.
  • ALK fusions occur in approximately 50% of ALCLs, and among these, 80% have the t(2;5) translocation with NPM-ALK expression.
  • We report greater activity of JunB in NPM-ALK-positive than in NPM-ALK-negative ALCLs.
  • Specific knockdown of JUNB mRNA using small interfering RNA and small hairpin RNA in NPM-ALK-expressing cells decreases cellular proliferation as evidenced by a reduced cell count in the G2/M phase of the cell cycle.
  • Expression of NPM-ALK results in ERK1/2 activation and transcriptional up-regulation of JUNB.
  • Both NPM-ALK-positive and -negative ALCL tumors demonstrate active ERK1/2 signaling.
  • In contrast to NPM-ALK-negative ALCL, the mTOR pathway is active in NPM-ALK-positive lymphomas.
  • Pharmacological inhibition of mTOR in NPM-ALK-positive cells down-regulates JunB protein levels by shifting JUNB mRNA translation from large polysomes to monosomes and ribonucleic particles (RNPs), and decreases cellular proliferation.
  • Thus, JunB is a critical target of mTOR and is translationally regulated in NPM-ALK-positive lymphomas.
  • In conjunction with NPM-ALK, JunB enhances cell cycle progression and may therefore represent a therapeutic target.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Protein Kinases / physiology. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins c-jun / genetics. Proto-Oncogene Proteins c-jun / metabolism. Transcriptional Activation
  • [MeSH-minor] Catalytic Domain / physiology. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. Protein Binding. Protein Biosynthesis. RNA, Messenger / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction / physiology. TOR Serine-Threonine Kinases. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism. Transcription Factor AP-1 / physiology. Tumor Cells, Cultured


64. Bakshi NA, Finn WG, Schnitzer B, Valdez R, Ross CW: Fascin expression in diffuse large B-cell lymphoma, anaplastic large cell lymphoma, and classical Hodgkin lymphoma. Arch Pathol Lab Med; 2007 May;131(5):742-7
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  • [Title] Fascin expression in diffuse large B-cell lymphoma, anaplastic large cell lymphoma, and classical Hodgkin lymphoma.
  • Fascin is a sensitive marker for classical Reed-Sternberg cells and has a high negative predictive value for diagnosis of classical Hodgkin lymphoma (CHL).
  • Fascin has been used to distinguish CHL from non-Hodgkin lymphoma.
  • Recently, it was shown that fascin might not help differentiate CHL from anaplastic large cell lymphoma (ALCL).
  • Moreover, fascin has not been extensively studied in the context of other large cell lymphomas.
  • OBJECTIVE: To analyze fascin expression in diffuse large B-cell lymphoma (DLBCL) and also reexamine its usefulness in discriminating CHL from ALCL.
  • DESIGN: Formalin-fixed, paraffin-embedded tissue samples from 41 cases of DLBCL, 30 cases of CHL, and 30 cases of ALCL were analyzed.
  • Fascin expression was compared across each type of lymphoma with additional correlation between fascin positivity and ALK-1 expression in ALCL performed.
  • RESULTS: Only 6 (14.6%) of 41 cases of DLBCL stained positively for fascin, with most neoplastic large cells exhibiting a weak staining pattern.
  • Fifteen (50%) of 30 cases of ALCL showed positivity for fascin, with most large cells staining strongly.
  • All 30 cases of CHL demonstrated intense positive staining.
  • Sixty percent of fascin-positive ALCLs were positive for ALK-1, while 66.7% of fascin-negative ALCLs were positive for ALK-1.
  • CONCLUSIONS: Fascin is highly sensitive for CHL and has a very high negative predictive value (100% in this series) for distinguishing CHL from DLBCL or ALCL.
  • However, the specificity and positive predictive value for fascin are much higher in distinguishing CHL from DLBCL than in distinguishing CHL from ALCL.
  • Expression of fascin appears more useful in the differential diagnosis of CHL versus DLBCL than in the differential diagnosis of CHL versus ALCL.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carrier Proteins / biosynthesis. Hodgkin Disease / metabolism. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Microfilament Proteins / biosynthesis


65. Colomba A, Courilleau D, Ramel D, Billadeau DD, Espinos E, Delsol G, Payrastre B, Gaits-Iacovoni F: Activation of Rac1 and the exchange factor Vav3 are involved in NPM-ALK signaling in anaplastic large cell lymphomas. Oncogene; 2008 Apr 24;27(19):2728-36
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  • [Title] Activation of Rac1 and the exchange factor Vav3 are involved in NPM-ALK signaling in anaplastic large cell lymphomas.
  • The majority of anaplastic large cell lymphomas (ALCLs) express the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion protein, which is oncogenic due to its constitutive tyrosine kinase activity.
  • Transformation by NPM-ALK not only increases proliferation, but also modifies cell shape and motility in both lymphoid and fibroblastic cells.
  • We report that the Rac1 GTPase, a known cytoskeletal regulator, is activated by NPM-ALK in ALCL cell lines (Karpas 299 and Cost) and transfected cells (lymphoid Ba/F3 cells, NIH-3T3 fibroblasts).
  • Stimulation of Vav3 and Rac1 by NPM-ALK is under the control of Src kinases.
  • It involves formation of a signaling complex between NPM-ALK, pp60(c-src), Lyn and Vav3, in which Vav3 associates with tyrosine 343 of NPM-ALK via its SH2 domain.
  • Moreover, Vav3 is phosphorylated in NPM-ALK positive biopsies from patients suffering from ALCL, demonstrating the pathological relevance of this observation.
  • The use of Vav3-specific shRNA and a dominant negative Rac1 mutant demonstrates the central role of GTPases in NPM-ALK elicited motility and invasion.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Lymphoma, Large-Cell, Anaplastic / enzymology. Protein-Tyrosine Kinases / metabolism. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction / physiology. rac1 GTP-Binding Protein / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. NIH 3T3 Cells. Nuclear Proteins / physiology. Phosphatidylinositol 3-Kinases / physiology. Receptor Protein-Tyrosine Kinases. src-Family Kinases / physiology

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  • (PMID = 17998938.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-vav; 0 / VAV3 protein, human; 0 / Vav3 protein, mouse; 117896-08-9 / nucleophosmin; 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 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases; EC 3.6.5.2 / rac1 GTP-Binding Protein
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66. Donella-Deana A, Marin O, Cesaro L, Gunby RH, Ferrarese A, Coluccia AM, Tartari CJ, Mologni L, Scapozza L, Gambacorti-Passerini C, Pinna LA: Unique substrate specificity of anaplastic lymphoma kinase (ALK): development of phosphoacceptor peptides for the assay of ALK activity. Biochemistry; 2005 Jun 14;44(23):8533-42
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  • [Title] Unique substrate specificity of anaplastic lymphoma kinase (ALK): development of phosphoacceptor peptides for the assay of ALK activity.
  • The anaplastic lymphoma kinase (ALK), whose constitutively active fusion proteins are responsible for 5-10% of non-Hodgkin's lymphomas, shares with the other members of the insulin receptor kinase (IRK) subfamily an activation loop (A-loop) with the triple tyrosine motif Y-x-x-x-Y-Y.
  • However, the amino acid sequence of the ALK A-loop differs significantly from the sequences of both the IRK A-loop and the consensus A-loop for this kinase subfamily.
  • A major difference is the presence of a unique "RAS" triplet between the first and second tyrosines of the ALK A-loop, which in IRK is replaced by "ETD".
  • Here we show that a peptide reproducing the A-loop of ALK is readily phosphorylated by ALK, while a homologous IRK A-loop peptide is not unless its "ETD" triplet is substituted by "RAS".
  • Consequently, a peptide in which the first tyrosine had been replaced by phenylalanine (FYY) was almost unaffected by ALK.
  • A number of substitutions in the YFF peptide outlined the importance of Ile and Arg at positions n - 1 and n + 6 in addition to the central triplet, to ensure efficient phosphorylation by ALK.
  • Such a peculiar substrate specificity allows the specific monitoring of ALK activity in crude extracts of NPM-ALK positive cells, using the YFF peptide, which is only marginally phosphorylated by a number of other tyrosine kinases.
  • [MeSH-minor] Amino Acid Sequence. Amino Acid Substitution. Cell Line, Tumor. Enzyme Activation. Humans. Lymphoma, Large-Cell, Anaplastic / enzymology. Molecular Sequence Data. Oligopeptides / chemical synthesis. Phosphorylation. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases / chemistry. Receptor Protein-Tyrosine Kinases / metabolism. Substrate Specificity. Tyrosine / metabolism

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  • (PMID = 15938644.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Peptides; 42HK56048U / Tyrosine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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67. 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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  • [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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68. Ezra N, Van Dyke GS, Binder SW: CD30 positive anaplastic large-cell lymphoma mimicking Langerhans cell histiocytosis. J Cutan Pathol; 2010 Jul;37(7):787-92
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  • [Title] CD30 positive anaplastic large-cell lymphoma mimicking Langerhans cell histiocytosis.
  • The presence of CD 1a+ dendritic cells (DC) has been well described in T-cell lymphoproliferative disorders, and the presence of large numbers of DCs has rarely been reported as a mimicker of Langerhans cell histiocytsis (LCH).
  • We present the case of a 56-year-old female with a solitary nodule on the chin whose case was referred to our institution for confirmation of the diagnosis of LCH.
  • Skin biopsy showed an ulcerated nodule containing a wedge-shaped infiltrate comprised of large atypical cells and cells with prominent grooved nuclei.
  • The constellation of histologic and immunologic features favored a CD30 lymphoproliferative disorder of T-cell lineage even though there were accompanying numerous dendritic histiocytes and CD1a positive Langerhans cells.
  • The sheets of CD30 positive atypical lymphoid cells which express T-cell markers were consistent with CD30 positive lymphoproliferative disease and favor CD30 positive anaplastic large-cell lymphoma (ALCL) over Langerhans histiocytosis.
  • The absence of Anaplastic Lymphoma Kinase (ALK) staining favored a primary cutaneous origin.
  • CD30 positive anaplastic large-cell lymphoma (ALCL) mimicking Langerhans cell histiocytosis (LCH).
  • [MeSH-major] Antigens, CD30 / biosynthesis. Histiocytosis, Langerhans-Cell / pathology. Lymphoma, Large-Cell, Anaplastic / pathology


69. Laurent C, Do C, Gascoyne RD, Lamant L, Ysebaert L, Laurent G, Delsol G, Brousset P: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis. J Clin Oncol; 2009 Sep 1;27(25):4211-6
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  • [Title] Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis.
  • PURPOSE: Anaplastic lymphoma kinase (ALK) -positive diffuse large B-cell lymphoma (DLBCL) is a rare variant of DLBCL that has been described only in small case reports.
  • PATIENTS AND METHODS: We retrospectively analyzed 38 patients with ALK-positive DLBCL treated with cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP) or CHOP-like regimens from different institutions to better define the presenting features, clinical course, and response to treatment.
  • All patients expressed ALK fusion proteins, but virtually all were CD30 and CD20 negative.
  • The median age was 43 years with a 5:1 ratio of males to females.
  • CONCLUSION: ALK-positive DLBCLs display clinicopathologic features that distinguish them from common DLBCL.
  • Conventional therapy, as used for typical DLBCL, is of limited efficacy.
  • Recognition of this new entity and the characteristic lack of CD20 expression are paramount.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD20 / analysis. Antigens, CD30 / analysis. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Oncogene Proteins, Fusion / analysis. Prednisone / administration & dosage. Receptor Protein-Tyrosine Kinases. Retrospective Studies. Risk Assessment. Time Factors. Treatment Outcome. Vincristine / administration & dosage. Young Adult

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  • [ErratumIn] J Clin Oncol. 2010 Jan 1;28(1):182
  • (PMID = 19636007.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / oncoprotein CLTCL-ALK; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
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70. 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.
  • 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.
  • All cases showed unusually strong expression of neuron-specific enolase (NSE).
  • 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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71. Kodama K, Hokama M, Kawaguchi K, Tanaka Y, Hongo K: Primary ALK-1-negative anaplastic large cell lymphoma of the brain: case report and review of the literature. Neuropathology; 2009 Apr;29(2):166-71
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  • [Title] Primary ALK-1-negative anaplastic large cell lymphoma of the brain: case report and review of the literature.
  • Anaplastic large cell lymphoma (ALCL) is a type of non-Hodgkin lymphoma composed of CD30-positive cells.
  • Anaplastic lymphoma kinase (ALK) -1 positive ALCL frequently involves both lymph nodes and extranodal sites.
  • While primary extranodal involvement of ALK-1 negative ALCL is rare, this case is unique in that it is a case of primary ALK-1 negative ALCL of the brain.
  • The tumor was excised and histological diagnosis of primary ALK-1-negative ALCL was made.
  • Primary ALK-1-negative ALCL in this case showed aggressive clinical behavior and fatal outcome.
  • [MeSH-major] Activin Receptors, Type II / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 18564100.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
  • [Number-of-references] 29
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72. 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.
  • [MeSH-major] Adenocarcinoma / diagnosis. Genetic Variation / genetics. Lung Neoplasms / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

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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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73. Kalinova M, Krskova L, Brizova H, Kabickova E, Kepak T, Kodet R: Quantitative PCR detection of NPM/ALK fusion gene and CD30 gene expression in patients with anaplastic large cell lymphoma--residual disease monitoring and a correlation with the disease status. Leuk Res; 2008 Jan;32(1):25-32
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  • [Title] Quantitative PCR detection of NPM/ALK fusion gene and CD30 gene expression in patients with anaplastic large cell lymphoma--residual disease monitoring and a correlation with the disease status.
  • Anaplastic large cell lymphoma (ALCL) represents a heterogeneous group of malignant lymphoproliferative diseases with a consistent expression of the cytokine receptor CD30.
  • ALCL is frequently associated with a NPM/ALK fusion gene which is found in up to 75% of pediatric ALCLs.
  • Real-time quantitative RT-PCR (RQ-RT-PCR) of NPM/ALK and CD30 gene expression was employed to analyze minimal residual disease (MRD) in 10 patients with NPM/ALK positive ALCL in 79 follow-up bone marrow (BM) and/or peripheral blood (PB) samples.
  • In all BM samples from relapses and/or closely before a relapse, BM samples revealed NPM/ALK and CD30 positivity in at least one of the iliac BM trephines.
  • Five out of nine relapses were preceded or were accompanied by minimally half log increased NPM/ALK levels in the BM.
  • We found that RQ-RT-PCR of the CD30 expression is not suitable for MRD detection--only two relapses were accompanied by an increase of the CD30 level above a level which was detected in BM/PB samples from healthy individuals.
  • RQ-RT-PCR of NPM/ALK expression is a promising and rapid approach for monitoring MRD.
  • [MeSH-major] Antigens, CD30 / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. Neoplasm, Residual / genetics. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Gene Expression. Humans. Male. Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17320171.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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74. 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)".
  • 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-.
  • [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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75. Voena C, Conte C, Ambrogio C, Boeri Erba E, Boccalatte F, Mohammed S, Jensen ON, Palestro G, Inghirami G, Chiarle R: The tyrosine phosphatase Shp2 interacts with NPM-ALK and regulates anaplastic lymphoma cell growth and migration. Cancer Res; 2007 May 1;67(9):4278-86
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  • [Title] The tyrosine phosphatase Shp2 interacts with NPM-ALK and regulates anaplastic lymphoma cell growth and migration.
  • Anaplastic large cell lymphomas (ALCL) are mainly characterized by the reciprocal translocation t(2;5)(p23;q35) that involves the anaplastic lymphoma kinase (ALK) gene and generates the fusion protein NPM-ALK with intrinsic tyrosine kinase activity.
  • NPM-ALK triggers several signaling cascades, leading to increased cell growth, resistance to apoptosis, and changes in morphology and migration of transformed cells.
  • To search for new NPM-ALK interacting molecules, we developed a mass spectrometry-based proteomic approach in HEK293 cells expressing an inducible NPM-ALK and identified the tyrosine phosphatase Shp2 as a candidate substrate.
  • We found that NPM-ALK was able to bind Shp2 in coprecipitation experiments and to induce its phosphorylation in the tyrosine residues Y542 and Y580 both in HEK293 cells and ALCL cell lines.
  • In primary lymphomas, antibodies against the phosphorylated tyrosine Y542 of Shp2 mainly stained ALK-positive cells.
  • In ALCL cell lines, Shp2-constitutive phosphorylation was dependent on NPM-ALK, as it significantly decreased after short hairpin RNA (shRNA)-mediated NPM-ALK knock down.
  • In addition, only the constitutively active NPM-ALK, but not the kinase dead NPM-ALK(K210R), formed a complex with Shp2, Gab2, and growth factor receptor binding protein 2 (Grb2), where Grb2 bound to the phosphorylated Shp2 through its SH2 domain.
  • Shp2 knock down by specific shRNA decreased the phosphorylation of extracellular signal-regulated kinase 1/2 and of the tyrosine residue Y416 in the activation loop of Src, resulting in impaired ALCL cell proliferation and growth disadvantage.
  • These findings show a direct involvement of Shp2 in NPM-ALK lymphomagenesis, highlighting its critical role in lymphoma cell proliferation and migration.
  • [MeSH-major] Cell Movement / physiology. Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Amino Acid Sequence. Apoptosis / physiology. Cell Growth Processes / physiology. Down-Regulation. Enzyme Activation. GRB2 Adaptor Protein / metabolism. Humans. K562 Cells. Mass Spectrometry. Molecular Sequence Data. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 11. RNA, Small Interfering / genetics. SH2 Domain-Containing Protein Tyrosine Phosphatases. Transfection

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  • [ErratumIn] Cancer Res. 2016 Mar 15;76(6):1669 [26979794.001]
  • (PMID = 17483340.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA64033
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / GAB2 protein, human; 0 / GRB2 Adaptor Protein; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / SH2 Domain-Containing Protein Tyrosine Phosphatases
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76. 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.
  • 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.
  • [MeSH-major] Biopsy, Fine-Needle. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism. Soft Tissue Neoplasms / 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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77. 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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  • [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.
  • The AKT/mTOR signaling pathway did not have any influence on C/EBPbeta expression or C/EBPbeta phosphorylation.
  • 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


78. Damm-Welk C, Schieferstein J, Schwalm S, Reiter A, Woessmann W: Flow cytometric detection of circulating tumour cells in nucleophosmin/anaplastic lymphoma kinase-positive anaplastic large cell lymphoma: comparison with quantitative polymerase chain reaction. Br J Haematol; 2007 Aug;138(4):459-66
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  • [Title] Flow cytometric detection of circulating tumour cells in nucleophosmin/anaplastic lymphoma kinase-positive anaplastic large cell lymphoma: comparison with quantitative polymerase chain reaction.
  • Quantification of occult circulating tumour cells in blood or bone marrow (BM) enables the identification of patients with a high risk for relapse in nucleophosmin/anaplastic lymphoma kinase (NPM-ALK)-positive anaplastic large cell lymphoma (ALCL).
  • We have developed a flow cytometric (FCM) assay to quantify the rare ALK- and CD30-positive ALCL cells.
  • When ALCL cells were admixed with normal peripheral blood or BM, ALK- and CD30-positive cells could be detected above background level at an added concentration of 10(-5) for all three cell lines tested.
  • Sensitivity and costs of the assay were compared with quantitative real-time polymerase chain reaction (PCR) for NPM-ALK.
  • The results of the FCM assay and quantitative PCR for NPM-ALK correlated.
  • FCM using antibodies against ALK and CD30 can sensitively and specifically detect the circulating ALCL cells in BM or blood.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Neoplastic Cells, Circulating / pathology

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  • (PMID = 17608768.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / Nuclear Proteins; 0 / RNA, Messenger; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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79. Karikari IO, Thomas KK, Lagoo A, Cummings TJ, George TM: Primary cerebral ALK-1-positive anaplastic large cell lymphoma in a child. Case report and literature review. Pediatr Neurosurg; 2007;43(6):516-21
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  • [Title] Primary cerebral ALK-1-positive anaplastic large cell lymphoma in a child. Case report and literature review.
  • An MRI of the brain revealed a pineal region mass with diffuse leptomeningeal enhancement and compression of the basilar cisterns.
  • A biopsy of the brain revealed histologic and immunophenotypic findings characteristic of ALK-1+ anaplastic large cell lymphoma (ALCL).
  • We describe a case of a rapidly deteriorating clinical course in a child with central nervous system ALCL and review the current literature on ALCL occurring in the central nervous system.
  • [MeSH-major] Activin Receptors, Type II / analysis. Biomarkers, Tumor / analysis. Brain Neoplasms / diagnosis. Brain Neoplasms / enzymology. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / enzymology


80. Bonvini P, Zorzi E, Mussolin L, Monaco G, Pigazzi M, Basso G, Rosolen A: The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity. Haematologica; 2009 Jul;94(7):944-55
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  • [Title] The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity.
  • BACKGROUND: The loss of cell cycle regulation due to abnormal function of cyclin-dependent kinases (cdk) occurs in tumors and leads to genetic instability of chemotherapy-resistant cells.
  • In this study, we investigated the effect of the cdk inhibitor flavopiridol in anaplastic large cell lymphomas, in which unrestrained proliferation depends on NPM-ALK tyrosine kinase activity.
  • DESIGN AND METHODS: Effects of flavopiridol were examined in ALK-positive and -negative anaplastic large cell lymphoma cells by means of immunoblotting and immunofluorescence analyses to assess cdk expression and activity, quantitative real time reverse transcriptase polymerase chain reaction to measure drug-induced changes in transcription, and FACS analyses to monitor changes in proliferation and survival.
  • RESULTS: Treatment with flavopiridol resulted in growth inhibition of anaplastic large cell lymphoma cells, along with accumulation of subG(1) cells and disappearance of S phase without cell cycle arrest.
  • This correlated with induction of cell death through rapid mitochondrial damage, inhibition of DNA synthesis, and down-regulation of anti-apoptotic proteins and transcripts.
  • Notably, flavopiridol was less active in ALK-positive cells, as apoptosis was observed at higher concentrations and later time points, and resistance to treatment was observed in cells maintaining NPM-ALK signaling.
  • NPM-ALK inhibition affected proliferation but not survival of anaplastic large cell lym-phoma cells, whereas it resulted in a dramatic increase in apoptosis when combined with flavopiridol.
  • CONCLUSIONS: This work provides the first demonstration that targeting cdk is effective against anaplastic large cell lymphoma cells, and proves the critical role of NPM-ALK in the regulation of responsiveness of tumor cells with cdk dysregulation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Flavonoids / pharmacology. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / drug therapy. Piperidines / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis. Bromodeoxyuridine / pharmacology. Cell Cycle. Cell Separation. Cell Survival. Dose-Response Relationship, Drug. Humans. Reverse Transcriptase Polymerase Chain Reaction. Subcellular Fractions. Time Factors


81. 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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  • [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.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Neoplasms, Second Primary / pathology. Protein-Tyrosine Kinases / metabolism


82. Dargent JL, Lespagnard L, Feoli F, Debusscher L, Greuse M, Bron D: De novo CD5-positive diffuse large B-cell lymphoma of the skin arising in chronic limb lymphedema. Leuk Lymphoma; 2005 May;46(5):775-80
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  • [Title] De novo CD5-positive diffuse large B-cell lymphoma of the skin arising in chronic limb lymphedema.
  • We report the case of a 79-year-old woman with a longstanding lymphedema of the right arm who developed a skin lymphoma involving the right wrist area.
  • Phenotypic investigations showed expression of CD20, CD79a, and bcl-2 protein by neoplastic cells.
  • In addition, these cells were CD5 positive.
  • No expression of anaplastic large cell lymphoma kinase (ALK), CD10, CD23, CD30, CD43, bcl-6, cyclin D1, p53 or p16INK4a could be seen.
  • This study further illustrates that lymphoma of the skin may complicate chronic limb lymphedema.
  • Like most of the previously reported cases, this neoplasm belonged to the category of diffuse large B-cell lymphoma.
  • However, it showed CD5 expression as a singular feature.
  • [MeSH-major] Antigens, CD5 / biosynthesis. Lymphedema / complications. Lymphoma, B-Cell / complications. Lymphoma, Large B-Cell, Diffuse / complications. Skin Neoplasms / complications


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


85. Chen CH, Chen SW, Shen WL, Chen TY, Tsao CJ, Huang WT: Successful allogeneic stem cell transplantation for an adult with refractory anaplastic lymphoma kinase-positive anaplastic large cell lymphoma. Int J Hematol; 2007 Feb;85(2):105-7
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  • [Title] Successful allogeneic stem cell transplantation for an adult with refractory anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK) expression exists in approximately 60% of anaplastic large cell lymphoma (ALCL) cases.
  • Compared with the ALK-negative cases, ALK-positive cases are usually characterized by a good response to chemotherapy and a good prognosis.
  • In the relapsed or refractory ALCL cases, high-dose chemotherapy followed by autologous stem cell transplantation has been widely used as a salvage therapy.
  • However, 40% of patients who received transplants after more than 2 complete remissions eventually experienced disease progression, despite receiving autologous stem cell transplantation.
  • Allogeneic stem cell transplantation has been proposed as a therapeutic option in refractory ALCL cases, but clinical reports of adult patients are rare.
  • Herein, we report the case of an adult with refractory ALK-positive ALCL who was successfully treated with salvage high-dose chemotherapy followed by allogeneic stem cell transplantation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, Large-Cell, Anaplastic / therapy. Stem Cell Transplantation

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  • [Cites] Ann Oncol. 2000 Jan;11(1):53-8 [10690387.001]
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  • (PMID = 17321986.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CEOP protocol 1; CVAD protocol
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86. Fornari A, Piva R, Chiarle R, Novero D, Inghirami G: Anaplastic large cell lymphoma: one or more entities among T-cell lymphoma? Hematol Oncol; 2009 Dec;27(4):161-70
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  • [Title] Anaplastic large cell lymphoma: one or more entities among T-cell lymphoma?
  • Anaplastic large cell lymphoma (ALCL) is a subtype of peripheral T-cell lymphoma (PTCL) first described in 1985 as a lymphoid malignancy characterized by marked cellular pleomorphism, propensity to grow cohesively, tendency to invade lymph node sinuses and diffuse expression of CD30 1.
  • The discovery of the t(2;5), involving the anaplastic lymphoma kinase (ALK) gene on chromosome 2 and the nucleophosmin (NPM) gene on chromosome 5 in the majority of systemic ALCL, has soon pointed out that ALCL is a clinically and biologically heterogeneous disease.
  • While ALK-positive (ALK+) ALCL is usually characterized by onset in children and young adults and better prognosis, epidemiology, poor outcome and possibly genetic defects of ALK-negative (ALK-) ALCL suggest that this neoplasms should be considered an independent pathological entity.
  • The aim of this review is to illustrate clinical features, histology, immunophenotype, genetics and biology of ALCL and discuss possible relationship(s) among different T-non-Hodgkin lymphoma (T-NHL).
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, T-Cell, Peripheral / pathology

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19358142.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 82
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87. Gómez-Román JJ, Cobo ML, Val-Bernal JF: Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma presenting as a bladder neoplasm. Pathol Int; 2008 Apr;58(4):249-52
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  • [Title] Anaplastic lymphoma kinase-positive anaplastic large cell lymphoma presenting as a bladder neoplasm.
  • Malignant lymphoma presenting in the bladder has been classified in primary cases, as the first sign of disseminated disease and as a secondary infiltration.
  • Reported herein is the case of a 45-year-old man with an anaplastic large cell lymphoma (anaplastic lymphoma kinase (ALK) and granzyme B positive) that presented as a bladder neoplasm.
  • The morphological differential diagnosis was complex because the EMA-positive immunophenotype, CD45 and CD3 negativity and the clinical manifestation simulated a transitional cell carcinoma.
  • It is important to be aware of its existence because a poorly differentiated bladder carcinoma cannot be ruled out if CD30 and ALK immunostaining are not performed.
  • T-cell receptor-gamma clonal rearrangement could be also helpful in these cases.
  • Although bladder involvement by recurrent lymphoma is a sign of widely disseminated disease and it is associated with a very poor prognosis, it seems that chemotherapeutic regimens in this kind of ALK-positive lymphoma could be effective, given that the present patient had an impressive response to chemotherapy treatment.
  • [MeSH-major] Carcinoma, Transitional Cell / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis. Protein-Tyrosine Kinases / metabolism. Urinary Bladder Neoplasms / diagnosis

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  • (PMID = 18324919.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Mucin-1; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; Q20Q21Q62J / Cisplatin; X4W7ZR7023 / Methylprednisolone
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88. Jokoji R, Yamasaki T, Minami S, Komuta K, Sakamaki Y, Takeuchi K, Tsujimoto M: Combination of morphological feature analysis and immunohistochemistry is useful for screening of EML4-ALK-positive lung adenocarcinoma. J Clin Pathol; 2010 Dec;63(12):1066-70
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  • [Title] Combination of morphological feature analysis and immunohistochemistry is useful for screening of EML4-ALK-positive lung adenocarcinoma.
  • BACKGROUND: A subset of lung cancers harbours the fusion gene echinoderm microtubule-associated protein-like-4-anaplastic lymphoma kinase (EML4-ALK).
  • Recently, immunohistochemistry for ALK has shown sensitivity for the detection of EML4-ALK-positive lung adenocarcinoma almost equal to that of the fluorescence in situ hybridisation (FISH) assay.
  • AIMS: To study the clinicopathological features of EML4-ALK-positive lung adenocarcinoma in a large number of surgically resected samples using immunohistochemistry, in order to establish a useful screening method for EML4-ALK-positive lung adenocarcinoma.
  • METHODS: Immunohistochemistry for ALK was used to screen for EML4-ALK-positive lung adenocarcinomas in 254 cases of surgically resected samples.
  • RESULTS: EML4-ALK-positive cases were detected in 3.1% of lung adenocarcinomas (8/254).
  • EML4-ALK-positive lung adenocarcinomas showed significant associations with intra- and/or extra-cytoplasmic mucin (p=0.0001), and cribriform pattern with excessive extracytoplasmic mucin (p<0.0001).
  • Signet-ring cell appearance alone lacked significance (p=0.149).
  • CONCLUSION: EML4-ALK-positive lung adenocarcinoma has a tendency to express a characteristic morphological pattern.
  • The combined use of morphological feature analysis and immunohistochemistry may be a useful and cost effective screening method for EML4-ALK lung adenocarcinoma.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Cytoplasm / enzymology. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Proteins / metabolism

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  • (PMID = 20935334.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion
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89. Tan BT, Seo K, Warnke RA, Arber DA: The frequency of immunoglobulin heavy chain gene and T-cell receptor gamma-chain gene rearrangements and Epstein-Barr virus in ALK+ and ALK- anaplastic large cell lymphoma and other peripheral T-cell lymphomas. J Mol Diagn; 2008 Nov;10(6):502-12
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  • [Title] The frequency of immunoglobulin heavy chain gene and T-cell receptor gamma-chain gene rearrangements and Epstein-Barr virus in ALK+ and ALK- anaplastic large cell lymphoma and other peripheral T-cell lymphomas.
  • We previously identified a relatively high frequency of B-cell proliferations along with simultaneous T-cell receptor gamma-chain gene (TRG) and immunoglobulin heavy chain gene (IGH) rearrangements in a series of angioimmunoblastic T-cell lymphoma and peripheral T-cell lymphoma, unspecified.
  • Here, we report on a series of 74 peripheral T-cell lymphoma (PTCL) cases composed entirely of specific PTCL subtypes, including 28 cases of ALK+ anaplastic large-cell lymphoma (ALCL), 35 cases of ALK- ALCL, and 11 cases that represent other specific PTCL subtypes.
  • We performed IGH and TRG gene rearrangement studies and in situ hybridization for Epstein-Barr virus (EBV) to determine the frequency of IGH clonality and to investigate the relationship between EBV, clonality, and associated B-cell proliferations.
  • Using BIOMED-2 PCR assays, we detected TRG clones in 64 of 74 (86%) cases and IGH clones in 6 of 74 (8%) cases, with all IGH-positive cases exhibiting a concurrent TRG clone.
  • Despite the detection of occasional IGH clones, there was no correlation between IGH clonality and EBV, and B-cell proliferations were not identified in any of the cases.
  • These findings suggest that other factors contribute to IGH clonality and demonstrate that, in the absence of an associated B-cell proliferation, IGH clonality occurs infrequently (8%) in specific PTCL subtypes.
  • [MeSH-major] Gene Rearrangement. Genes, T-Cell Receptor gamma. Herpesvirus 4, Human / immunology. Immunoglobulin Heavy Chains / genetics. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, T-Cell, Peripheral / genetics. Protein-Tyrosine Kinases / metabolism. Receptors, Antigen, T-Cell, gamma-delta / genetics

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  • (PMID = 18832464.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2570633
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90. 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 AKT activation contributes to mTOR phosphorylation, at least in part, as forced expression of constitutively active AKT by myristoylated AKT adenovirus results in increased phosphorylation of mTOR and its downstream effectors.
  • Conversely, inhibition of AKT expression or activity results in decreased mTOR phosphorylation.
  • 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).
  • Apoptosis following inhibition of mTOR expression or function was associated with down-regulation of antiapoptotic proteins, including c-FLIP, MCL-1, and BCL-2.
  • 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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91. Honorat JF, Ragab A, Lamant L, Delsol G, Ragab-Thomas J: SHP1 tyrosine phosphatase negatively regulates NPM-ALK tyrosine kinase signaling. Blood; 2006 May 15;107(10):4130-8
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  • [Title] SHP1 tyrosine phosphatase negatively regulates NPM-ALK tyrosine kinase signaling.
  • Anaplastic large-cell lymphoma (ALCL) is frequently associated with the 2;5 translocation and expresses the NPM-ALK fusion protein, which possesses a constitutive tyrosine kinase activity.
  • We analyzed SHP1 tyrosine phosphatase expression and activity in 3 ALK-positive ALCL cell lines (Karpas 299, Cost, and SU-DHL1) and in lymph node biopsies (n = 40).
  • We found an inverse correlation between the level of NPM-ALK phosphorylation and SHP1 phosphatase activity.
  • Pull-down and coimmunoprecipitation experiments demonstrated a SHP1/NPM-ALK association.
  • Furthermore, confocal microscopy performed on ALCL cell lines and biopsy specimens showed the colocalization of the 2 proteins in cytoplasmic bodies containing Y664-phosphorylated NPM-ALK.
  • Dephosphorylation of NPM-ALK by SHP1 demonstrated that NPM-ALK was a SHP1 substrate.
  • Downregulation of SHP1 expression by RNAi in Karpas cells led to hyperphosphorylation of NPM-ALK, STAT3 activation, and increase in cell proliferation.
  • Furthermore, SHP1 overexpression in 3T3 fibroblasts stably expressing NPM-ALK led to the decrease of NPM-ALK phosphorylation, lower cell proliferation, and tumor progression in nude mice.
  • These findings show that SHP1 is a negative regulator of NPM-ALK signaling.
  • The use of tissue microarrays revealed that 50% of ALK-positive ALCLs were positive for SHP1.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / enzymology. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / physiology
  • [MeSH-minor] Base Sequence. Cell Line. Cytoplasm / physiology. DNA Primers. Humans. Microscopy, Confocal. Phosphoric Monoester Hydrolases / metabolism. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 6. RNA, Small Interfering / genetics. Recombinant Fusion Proteins / metabolism. Signal Transduction / physiology

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  • (PMID = 16469875.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.1.3.- / Phosphoric Monoester Hydrolases; 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
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92. Lim MS, Carlson ML, Crockett DK, Fillmore GC, Abbott DR, Elenitoba-Johnson OF, Tripp SR, Rassidakis GZ, Medeiros LJ, Szankasi P, Elenitoba-Johnson KS: The proteomic signature of NPM/ALK reveals deregulation of multiple cellular pathways. Blood; 2009 Aug 20;114(8):1585-95
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  • [Title] The proteomic signature of NPM/ALK reveals deregulation of multiple cellular pathways.
  • Constitutive expression of the chimeric NPM/ALK fusion protein encoded by the t(2;5)(p32;q35) is a key oncogenic event in the pathogenesis of most anaplastic large cell lymphomas (ALCLs).
  • Using a mass spectrometry (MS)-driven approach to identify changes in protein expression caused by the NPM/ALK fusion, we identified diverse NPM/ALK-induced changes affecting cell proliferation, ribosome synthesis, survival, apoptosis evasion, angiogenesis, and cytoarchitectural organization.
  • MS-based findings were confirmed using Western blotting and/or immunostaining of NPM/ALK-transfected cells and ALK-deregulated lymphomas.
  • A subset of the proteins distinguished NPM/ALK-positive ALCLs from NPM/ALK-negative ALCLs and Hodgkin lymphoma.
  • The multiple NPM/ALK-deregulated pathways identified by MS analysis also predicted novel biologic effects of NPM/ALK expression.
  • In this regard, we showed loss of cell adhesion as a consequence of NPM/ALK expression in a kinase-dependent manner, and sensitivity of NPM/ALK-positive ALCLs to inhibition of the RAS, p42/44ERK, and FRAP/mTOR signaling pathways.
  • These findings reveal that the NPM/ALK alteration affects diverse cellular pathways, and provide novel insights into NPM/ALK-positive ALCL pathobiology.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Metabolic Networks and Pathways. Protein-Tyrosine Kinases / metabolism. Proteome / analysis
  • [MeSH-minor] Amino Acid Sequence. Gene Expression Regulation, Neoplastic. Humans. Jurkat Cells. Models, Biological. Molecular Sequence Data. Proteomics. Ribosomal Protein S6 Kinases / chemistry. Ribosomal Protein S6 Kinases / metabolism. Tissue Array Analysis. Transfection. Tumor Cells, Cultured

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  • (PMID = 19531656.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proteome; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases
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93. Shiran MS, Tan GC, Sabariah AR, Chye PC, Pathmanathan R: Small cell variant of anaplastic large cell lymphoma with positive immunoreactivity for CD99. Med J Malaysia; 2008 Jun;63(2):150-1
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  • [Title] Small cell variant of anaplastic large cell lymphoma with positive immunoreactivity for CD99.
  • A 13 year old boy presented with a huge mass on his right arm of 6 months duration.
  • Histopathological examination revealed sheets of malignant small round blue cells with immunopositivity for LCA, CD43, CD45Ro, CD30, EMA, ALK-1 and CD99, and negativity for CD20, TdT, myogenin, myoD1, NSE, bcl-6, bcl-2 and CD10.
  • Pathologists need to be aware of the diagnosis of a small cell variant of ALCL, as well as of the fact that CD99 expression commonly occurs in cases of ALK-positive ALCL, in order to distinguish this entity from Ewing's sarcoma/PNET.
  • [MeSH-major] Antigens, CD / immunology. Cell Adhesion Molecules / immunology. Lymphoma, Large B-Cell, Diffuse / immunology. Soft Tissue Neoplasms / immunology


94. Piccaluga PP, Gazzola A, Mannu C, Agostinelli C, Bacci F, Sabattini E, Sagramoso C, Piva R, Roncolato F, Inghirami G, Pileri SA: Pathobiology of anaplastic large cell lymphoma. Adv Hematol; 2010;:345053
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  • [Title] Pathobiology of anaplastic large cell lymphoma.
  • The authors revise the concept of anaplastic large cell lymphoma (ALCL) in the light of the recently updated WHO classification of Tumors of Hematopoietic and Lymphoid Tissues both on biological and clinical grounds.
  • The phenotype is reported in detail: the expression of the ALK protein as well as the chromosomal abnormalities is discussed with their potential pathogenetic implications.
  • The clinical features of ALCL are presented by underlining the difference in terms of response to therapy and survival between the ALK-positive and ALK-negative forms.

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  • (PMID = 21331150.001).
  • [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/ PMC3038421
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95. Teruya-Feldstein J: Diffuse large B-cell lymphomas with plasmablastic differentiation. Curr Oncol Rep; 2005 Sep;7(5):357-63
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  • [Title] Diffuse large B-cell lymphomas with plasmablastic differentiation.
  • Recent evidence suggests that diffuse large B-cell lymphoma (DLBCL) with plasmablastic differentiation represents a clinically heterogeneous spectrum with different clinicopathologic characteristics representing distinct entities.
  • Subtypes of DLBCL with plasmablastic features and terminal B-cell differentiation include plasmablastic lymphoma (PBL) of oral mucosa type; PBL with plasmacytic differentiation; primary effusion lymphoma (PEL); KSHV-positive solid lymphoma/extracavitary PEL/HHV-8 associated DLBCL; and DLBCL expressing ALK.
  • In contrast, PBL associated with multicentric Castleman disease, DLBCL with secretory differentiation, pyothorax-associated lymphoma, and atypical Burkitt lymphoma with plasmacytoid differentiation have morphologic appearances of plasma cell differentiation but maintain a mature B-cell (CD20 positive) phenotype.
  • In this review, we discuss recently described clinicopathologic insights, case observations, and recently reported molecules involved in terminal B-cell or plasma cell differentiation and their possible roles in disease pathogenesis.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adult. Antigens, CD20 / metabolism. B-Lymphocytes / cytology. Cell Differentiation. Cell Proliferation. Empyema, Pleural / metabolism. Giant Lymph Node Hyperplasia / metabolism. Giant Lymph Node Hyperplasia / therapy. Humans. Lymphoma / metabolism. Male. Middle Aged. Mouth Mucosa / pathology. Multiple Myeloma / metabolism. Neoplasms / metabolism. Phenotype. Plasmacytoma / metabolism

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  • (PMID = 16091196.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20
  • [Number-of-references] 50
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96. Asano H, Imai Y, Ota S, Yamamoto G, Takahashi T, Fukayama M, Kurokawa M: CD30-positive anaplastic variant diffuse large B cell lymphoma: a rare case presented with cutaneous involvement. Int J Hematol; 2010 Oct;92(3):550-2
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  • [Title] CD30-positive anaplastic variant diffuse large B cell lymphoma: a rare case presented with cutaneous involvement.
  • Biopsy of the cervical lymph node showed pleomorphic large cells containing large atypical nuclei.
  • Immunohistochemical stains of these cells were positive for CD30, but negative for CD3 and CD20.
  • Large pleomorphic cells with constricted nuclei and Reed-Sternberg-like cells existed in the dermis and epidermis.
  • Immunohistochemical stains of the former cells were positive for CD30, CD45 and PAX5, but negative for CD3, CD10, CD20, CD15, Bcl-2, EBER ISH, EMA and ALK.
  • He was diagnosed with diffuse large B cell lymphoma, anaplastic variant.
  • CD30-positive DLBCL, anaplastic variant is a rare B cell lymphoma.
  • Most of the patients presented with primary nodal disease, and skin involvement of lymphoma is very rare.
  • This is the report of a rare case of CD30-positive DLBCL, anaplastic variant, with both nodal and skin lesions.
  • [MeSH-major] Antigens, CD30 / immunology. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large-Cell, Anaplastic / immunology. Lymphoma, Large-Cell, Anaplastic / pathology. Skin / pathology


97. Plaza JA, Ortega P, Lynott J, Mullane M, Kroft S, Olteanu H: CD8-positive primary cutaneous anaplastic large T-cell lymphoma (PCALCL): case report and review of this unusual variant of PCALCL. Am J Dermatopathol; 2010 Jul;32(5):489-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD8-positive primary cutaneous anaplastic large T-cell lymphoma (PCALCL): case report and review of this unusual variant of PCALCL.
  • Primary cutaneous anaplastic large T-cell lymphoma (PCALCL) is a well-defined CD30-positive lymphoproliferative disorder with relatively good prognosis and response to treatment.
  • Histopathologic sections showed an ulcerated epidermis with a diffuse lymphocytic infiltrate in the superficial dermis with focal epidermotropism.
  • The large cohesive atypical cells were admixed with a reactive infiltrate composed of neutrophils, eosinophils, and small lymphocytes.
  • Immunohistochemical studies showed the tumor cells to be strongly positive for CD8, CD30, and TIA-1, focally positive for CD3, and negative for CD4, CD20, CD56, Anaplastic Lymphoma Kinase (ALK-1), and HSV.
  • The diagnosis of a CD8+ PCALCL was confirmed.
  • There is limited precedent literature regarding CD8-positive PCALCL and this case falls within the clinical and histopathologic spectrum of CD30+ lymphoproliferative disorders.
  • [MeSH-major] CD8-Positive T-Lymphocytes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Skin Neoplasms / pathology


98. Giuriato S, Faumont N, Bousquet E, Foisseau M, Bibonne A, Moreau M, Al Saati T, Felsher DW, Delsol G, Meggetto F: Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy. Cancer Biol Ther; 2007 Aug;6(8):1318-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of a conditional bioluminescent transplant model for TPM3-ALK-induced tumorigenesis as a tool to validate ALK-dependent cancer targeted therapy.
  • Overexpression and activation of TPM3-ALK tyrosine kinase fusion protein is a causal oncogenic event in the development of Anaplastic Large Cell Lymphoma and Inflammatory Myofibroblastic ALK-positive tumors.
  • Thus, the development of ALK specific tyrosine kinase inhibitors is a current therapeutic challenge.
  • Animal models are essential to assess, in vivo, the efficiency of ALK-oncogene inhibitors and to identify new and/or additional therapeutic targets in the ALK tumorigenesis pathway.
  • Using the tetracycline system to allow conditional and concomitant TPM3-ALK and luciferase expression, we have developed a unique transplant model for bioluminescent TPM3-ALK-induced fibroblastic tumors in athymic nude mice.
  • The reversible TPM3-ALK expression allowed us to demonstrate that this oncogene is essential for the tumor growth and its maintenance.
  • In addition, we showed that this model could be used to precisely assess tumor growth inhibition upon ALK chemical inactivation.
  • As proof of principle, we used the general tyrosine kinase inhibitor herbimycin A to inhibit ALK oncoprotein activity.
  • We conclude that this transplant model for TPM3-ALK-induced tumors represents a valuable tool not only to accurately and rapidly evaluate in vivo ALK-targeted therapies but also to gain insight into the mechanism of ALK-positive tumor development.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Disease Models, Animal. Lymphoma, Large-Cell, Anaplastic / drug therapy. Mice. Oncogene Proteins, Fusion / antagonists & inhibitors. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Tropomyosin / antagonists & inhibitors
  • [MeSH-minor] Animals. Benzoquinones / pharmacology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Drug Screening Assays, Antitumor / methods. Genes, Reporter. Lactams, Macrocyclic / pharmacology. Luciferases / analysis. Luciferases / genetics. Luminescent Agents / analysis. Mice, Nude. Neoplasm Transplantation. Receptor Protein-Tyrosine Kinases. Rifabutin / analogs & derivatives

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  • (PMID = 17660712.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Benzoquinones; 0 / Lactams, Macrocyclic; 0 / Luminescent Agents; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; 0 / Tpm3 protein, mouse; 0 / Tropomyosin; 1W306TDA6S / Rifabutin; 70563-58-5 / herbimycin; EC 1.13.12.- / Luciferases; 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. Belousova IE, Kazakov DV, Sosna B, Sulc M, Michal M: [Small-cell variant of CD30+ -anaplastic large-cell lymphoma of the skin]. Arkh Patol; 2008 Mar-Apr;70(2):40-3
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  • [Title] [Small-cell variant of CD30+ -anaplastic large-cell lymphoma of the skin].
  • Three cases of the so-called variant of primary cutaneous CD30+ anaplastic large cell lymphoma (ALCL) are presented.
  • Microscopically, the tumors were composed of small cells with irregular nuclei that were immunohistochemically positive for CD3, CD5, CD7, and CD30 and negative for B-cell markers; there was focal ALK-1 positivity in 1 case.
  • Fhedium to large CD30+ cells were rarely found scattered in the infiltrate.
  • Two patients were alive and well 4 and 6 years after surgery, without evidence of cutaneous and extractaneous involvement (including the ALK+ patient).
  • [MeSH-major] Antigens, CD30. Lymphoma, Large B-Cell, Diffuse / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD / immunology. Cell Size. Gene Rearrangement, B-Lymphocyte / immunology. Gene Rearrangement, T-Lymphocyte / immunology. Humans. Immunoglobulin Heavy Chains / immunology. Male. Middle Aged. Receptors, Antigen, T-Cell / immunology


100. Wang WY, Ma ZG, Li GD, Liu WP, Zhong L, Wang Y, Li JM, Li L, Jiang W, Tang Y, Liao DY: [Diffuse large B-cell lymphoma with expression of anaplastic lymphoma kinase protein: clinicopathologic and immunohistochemical study of 5 cases]. Zhonghua Bing Li Xue Za Zhi; 2006 Sep;35(9):529-34
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  • [Title] [Diffuse large B-cell lymphoma with expression of anaplastic lymphoma kinase protein: clinicopathologic and immunohistochemical study of 5 cases].
  • OBJECTIVE: To study the clinicopathologic features of diffuse large B-cell lymphoma (DLBCL) with expression of anaplastic lymphoma kinase (ALK) protein.
  • METHODS: Nine hundred and forty-five (945) cases of DLBCL (including 177 consultation cases) diagnosed according to the 2001 World Health Organization classification of tumors of hematopoietic and lymphoid tissues were enrolled into the study.
  • Immunohistochemical study for anti-ALK-11 was performed using LSAB technique.
  • The ALK-positive cases were further confirmed by immunohistochemical study using EnVision technique.
  • Only ALK-positive cases by EnVision technique were further analyzed by immunostaining for antigens including CD20, CD3, CD30, EMA, granzyme-B, TIA-1 and PC.
  • RESULTS: There were altogether 5 (4 males and 1 female) cases of DLBCL showing expression of ALK protein.
  • All were primary nodal DLBCL.
  • Morphologic subtypes included centroblastic 2, anaplastic 1, immunoblastic with plasmacytoid differentiation 1 and plasmablastic 1.
  • Immunohistochemically, 4 cases were CD20 positive (including 2 centroblastic, 1 anaplastic and 1 immunoblastic cases).
  • As for ALK protein staining, a mixed membranous and cytoplasmic (1 immunoblastic case), granular cytoplasmic (2 centroblastic and 1 anaplastic cases) and mixed nuclear and cytoplasmic (1 plasmablastic case) patterns were observed.
  • CONCLUSIONS: Expression of ALK protein is a rare phenomenon in DLBCL and can be seen in centroblastic, anaplastic, immunoblastic and plasmablastic subtypes.
  • A new pattern of ALK protein expression, mixed membranous and cytoplasmic, is reported.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 17134546.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Immunoglobulin kappa-Chains; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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