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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


2. Takahashi D, Nagatoshi Y, Nagayama J, Inagaki J, Itonoaga N, Takeshita M, Okamura J: Anaplastic large cell lymphoma in leukemic presentation: a case report and a review of the literature. J Pediatr Hematol Oncol; 2008 Sep;30(9):696-700
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  • [Title] Anaplastic large cell lymphoma in leukemic presentation: a case report and a review of the literature.
  • It is extremely rare that a patient with anaplastic large cell lymphoma (ALCL) demonstrates circulating lymphoma cells.
  • The white cell count was 26.2x10(9)/L with 95% of abnormal lymphoid cells, which were small to medium-sized with a high nucleus/cytoplasm ratio, basophilic cytoplasm, condensed nuclear chromatins, and 1 or 2 distinct nucleoli, hemoglobin 6.4 g/dL, and platelet 0.9x10(9)/L.
  • A flow cytometric analysis of abnormal cells in both the peripheral blood and bone marrow samples was strongly positive for CD30 on their cell membranes.
  • Reverse transcriptase-polymerase chain reaction of peripheral blood cell-derived mRNA also indicated the fusion gene product of anaplastic lymphoma kinase and nucleophosmin.
  • Subsequently, the patient was diagnosed to have ALCL with a rare clinical feature of a peripheral leukemic presentation, and his disease revealed to be refractory to chemotherapy.
  • On the basis of the 11 childhood cases of ALCL with leukemic presentation so far published and reviewed herein, the prognosis is very poor.
  • [MeSH-major] Leukemia / diagnosis. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 18776764.001).
  • [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 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 25
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3. 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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  • [Title] Hyperactivated STAT3 in ALK-positive diffuse large B-cell lymphoma with clathrin-ALK fusion.
  • Anaplastic lymphoma kinase (ALK)-positive large B-cell lymphoma is a rare subtype of diffuse large B-cell lymphoma (DLBCL).
  • Although a few cases of ALK-positive large B-cell lymphoma harbor nucleophosmin-ALK chromosomal translocation similar to ALK-positive anaplastic large cell lymphoma, most reported cases are characterized by t(2;17)(p23;q23) involving the clathrin gene.
  • Here, we report 2 cases of ALK-positive DLBCL.
  • The 2 cases presented similar morphologic features and immunohistochemical characteristics, that is, positivity for ALK, IgA, CD138, and MUM1; weak positivity for CD30 and CD79a; and negativity for CD20.
  • The clathrin-ALK transcript was identified by reverse transcription-polymerase chain reaction, and the sequence was determined by direct sequencing.
  • Recently, the essential role of STAT3 activation as well as STAT 5 activation in nucleophosmin-ALK fusion protein-mediated lymphomagenesis was reported.
  • However, differential effects of ALK-fusion variant proteins on proliferation, transformation, and invasion properties were reported.
  • Thus, we evaluated the phosphorylation status of STAT 3 and STAT 5, and found highly hyperphosphorylated STAT 3 on tyrosine 705 but not STAT 5 in our 2 cases of ALK-positive DLBCL with clathrin-ALK fusion.
  • Furthermore, STAT 5A expression was not detected in either of the ALK-positive DLBCL cases, although 11 of the 36 ALK-negative DLBCL cases revealed STAT 5A expression.
  • However, there were no significant associations between expression of survivin or BCL-X(L) and ALK positivity among the diffuse large B-cell lymphomas.
  • In summary, similar signaling transduction mechanism involving STAT proteins seems to underlie DLBCL harboring the clathrin-ALK or nucleophosmin-ALK fusion gene.
  • [MeSH-major] Clathrin / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Adult. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Cytarabine / administration & dosage. Doxorubicin / therapeutic use. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Prednisone / therapeutic use. Receptor Protein-Tyrosine Kinases. Recurrence. Remission Induction. Stem Cell Transplantation. Time Factors. Treatment Outcome. Vincristine / therapeutic use

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  • (PMID = 18755494.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Clathrin; 0 / Oncogene Proteins, Fusion; 0 / STAT3 Transcription Factor; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
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4. Daneshbod Y, Oryan A, Khojasteh HN, Rasekhi A, Ahmadi N, Mohammadianpanah M: Primary ALK-positive anaplastic large cell lymphoma of the breast: a case report and review of the literature. J Pediatr Hematol Oncol; 2010 Mar;32(2):e75-8
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  • [Title] Primary ALK-positive anaplastic large cell lymphoma of the breast: a case report and review of the literature.
  • BACKGROUND: Non-Hodgkin lymphomas of the breast are uncommon, which represent less than 1% of all breast malignancies and predominantly are of B-cell origin.
  • OBSERVATION: In this report, a rare case of anaplastic lymphoma kinase (ALK)-positive anaplastic large T-cell lymphoma in the breast of a 16-year-old female without breast implant is described.
  • The immunohistochemical profile showed positivity for CD30 and ALK and confirmed the diagnosis of ALK-positive anaplastic large T-cell lymphoma of the breast.
  • CONCLUSION: Anaplastic large T-cell lymphoma of the breast is rare, and can clinically mimic inflammatory breast carcinoma in adolescence.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / analysis


5. Li K, Tipps AM, Wang HY: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma presenting as an isolated nasopharyngeal mass: a case report and review of literature. Int J Clin Exp Pathol; 2011;4(2):190-6
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  • [Title] Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma presenting as an isolated nasopharyngeal mass: a case report and review of literature.
  • Anaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma is a rare and distinct variant of diffuse large B-cell lymphoma with characteristic morphologic, immunophenotypic, and cytogenetic features.
  • We report a case of ALK-positive diffuse large B-cell lymphoma in a 44-year-old male with progressively worsening unilateral nasal congestion and obstruction secondary to a nasopharyngeal mass.
  • More importantly, the neoplastic cells showed positive immunoreactivity for ALK with exclusive cytoplasmic granular staining pattern.
  • This case represented the second reported ALK-positive diffuse large B-cell lymphoma in the nasopharyngeal region.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / diagnosis. Nasopharyngeal Neoplasms / diagnosis. Receptor Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Cytoplasm / enzymology. Cytoplasm / pathology. Diagnosis, Differential. Humans. Male. Tomography, X-Ray Computed

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  • (PMID = 21326807.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC3037206
  • [Keywords] NOTNLM ; Anaplastic lymphoma kinase (ALK) / CD10 / CD4 / diffuse large B-cell lymphoma / nasopharyngeal mass
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6. Coluccia AM, Gunby RH, Tartari CJ, Scapozza L, Gambacorti-Passerini C, Passoni L: Anaplastic lymphoma kinase and its signalling molecules as novel targets in lymphoma therapy. Expert Opin Ther Targets; 2005 Jun;9(3):515-32
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  • [Title] Anaplastic lymphoma kinase and its signalling molecules as novel targets in lymphoma therapy.
  • Anaplastic lymphoma kinase (ALK) is a transmembrane receptor tyrosine kinase, normally expressed at low levels in the nervous system.
  • As a consequence of chromosomal translocations involving the alk gene (2p23), ALK is also aberrantly expressed and constitutively activated in approximately 60% of CD30+ anaplastic large cell lymphomas (ALCLs).
  • Due to the selective overexpression of ALK in tumour cells, its direct involvement in the process of malignant transformation and its frequent expression in ALCL patients, the authors recognise ALK as a suitable candidate for the development of molecularly targeted strategies for the therapeutic treatment of ALK-positive lymphomas.
  • Strategies targeting ALK directly or indirectly via the inhibition of the protein networks responsible for ALK oncogenic signalling are discussed.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Lymphoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Signal Transduction / drug effects

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  • (PMID = 15948671.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 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] 189
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7. Sano F, Tasaka T, Nishimura H, Akiyama T, Kubo Y, Matsuhashi Y, Wada H, Sugihara T, Sadahira Y: Small cell variant of anaplastic large cell lymphoma diagnosed by a novel chromosomal abnormality t(2;5;3)(p23;q35;p21) of bone marrow cells. Pathol Int; 2008 Aug;58(8):494-7
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  • [Title] Small cell variant of anaplastic large cell lymphoma diagnosed by a novel chromosomal abnormality t(2;5;3)(p23;q35;p21) of bone marrow cells.
  • Because of the rarity and the morphological variations, small cell variant of anaplastic large cell lymphoma (ALCL) represents a diagnostic challenge.
  • Herein is reported a case of leukemic type of small cell variant of ALCL, in which the diagnosis was established by a cytogenetic analysis.
  • The initial differential diagnosis on bone marrow trephine biopsy sections included viral infection and peripheral T-cell lymphoma unspecified.
  • But a cytogenetic study on bone marrow cells indicated a novel complex translocation, t(2;5;3)(p23;q35;p21), which led to confirmation of anaplastic lymphoma kinase (ALK)-positive pleomorphic small to medium-sized cells scattered in bone marrow cells, on immunohistochemistry.
  • ALK was distributed in both nuclear and cytoplasmic regions of neoplastic cells.
  • The patient achieved complete remission after four courses of combination chemotherapy, and received autologous peripheral stem cell transplantation (auto-PBSCT) after two additional courses of combination chemotherapy, but relapsed 2 months after auto-PBSCT in the bilateral lung.
  • Allogeneic stem cell transplantation led to a second remission.
  • This case demonstrates the diagnostic importance of cytogenetic study for malignant lymphoma involving bone marrow.
  • [MeSH-major] Bone Marrow Cells / pathology. Chromosomes, Human, 1-3 / genetics. Chromosomes, Human, Pair 5 / genetics. Lymphoma, Large-Cell, Anaplastic / diagnosis. Translocation, Genetic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Chromosome Banding. Diagnosis, Differential. Female. Humans. Lymphoma, T-Cell, Peripheral / diagnosis. Protein-Tyrosine Kinases / immunology. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Remission Induction. Spectral Karyotyping. Virus Diseases / diagnosis

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  • (PMID = 18705769.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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8. Piva R, Pellegrino E, Inghirami G: Identification and validation of the anaplastic large cell lymphoma signature. Adv Exp Med Biol; 2007;604:129-36
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  • [Title] Identification and validation of the anaplastic large cell lymphoma signature.
  • Anaplastic large cell lymphomas (ALCL) represent a subset of lymphomas in which the anaplastic lymphoma kinase (ALK) gene is fused to several partners, most frequently to the NPM gene.
  • We have previously demonstrated that the constitutive expression and phosphorylation of ALK chimeric proteins is sufficient for cellular transformation, and its activity is strictly required for the survival of ALCL cells.
  • To unravel signaling pathways required for NPM-ALK-mediated transformation and tumor maintenance, we analyzed the transcriptomes of ALK positive ALCL cell lines through experimentally controlled approaches in which ALK signaling was abrogated by an inducible ALKshRNA or by ALK inhibitors.
  • Transcripts derived from the gene expression profiling analyses uncovered a reproducible signature, which includes a novel group of ALK-regulated genes.
  • A functional RNAi screening identified new ALK transcriptional targets instrumental to cell transformation and/or to sustain the growth and survival of ALK positive ALCL cells.
  • [MeSH-major] Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / genetics

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  • (PMID = 17695725.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [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 / RNA, Messenger
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9. 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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10. Li C, Takino H, Eimoto T, Ishida T, Inagaki A, Ueda R, Suzuki R, Yoshino T, Nakagawa A, Nakamura S, Inagaki H: Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma. Mod Pathol; 2007 Jun;20(6):648-55
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  • [Title] Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma.
  • In anaplastic large-cell lymphomas positive for anaplastic lymphoma kinase (ALK) protein, the ALK gene is most commonly fused to the NPM gene, and less commonly to TPM3, TFG, ATIC, and other rare genes.
  • Although this lymphoma is generally associated with a favorable clinical outcome, 25% of the patients die of the disease within 5 years.
  • (1) a sensitive reverse transcription-polymerase chain reaction (RT-PCR) assay for various X-ALK fusion genes, (2) a 5' rapid amplification of cDNA ends (RACE) assay to identify unknown fusion partners, and (3) a real-time RT-PCR assay to quantify the amount of the NPM-ALK fusion transcript.
  • In 26 cases of ALK(+) anaplastic large-cell lymphoma, the RT-PCR assay showed that the ALK was fused to NPM in 21 cases, to TPM3 in three, and to TFG in one.
  • The 5' RACE assay detected ATIC-ALK fusion in the remaining case.
  • The real-time quantitative RT-PCR assay showed that the NPM-ALK transcript was over expressed in four of 20 quantifiable cases.
  • Patients with NPM-ALK overexpression showed a significantly unfavorable overall survival compared with those with a low expression of this transcript.
  • The RT-PCR and 5' RACE assays developed here may be useful for identification of known and unknown gene partners fused to the ALK gene.
  • Overexpression of the NPM-ALK fusion transcript may be associated with a poor prognosis of the patients with ALK(+) anaplastic large-cell lymphomas.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Protein-Tyrosine Kinases / biosynthesis

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  • (PMID = 17464320.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Fixatives; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; 1HG84L3525 / Formaldehyde; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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11. Matsumoto N, Ohki H, Mukae S, Amano Y, Harada D, Nishimura S, Komiyama K: Anaplastic large cell lymphoma in gingiva: case report and literature review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2008 Oct;106(4):e29-34
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  • [Title] Anaplastic large cell lymphoma in gingiva: case report and literature review.
  • We report an unusual case of gingival anaplastic large-cell lymphoma (ALCL) that occurred in a 76-year-old Japanese woman who showed marked gingival swelling in both the maxilla and mandible.
  • The specimens showed proliferation of large atypical and amphophilic epithelioid cells beneath the covering epithelium.
  • Immunohistochemical analysis of the proliferating cells revealed positivity for CD30 and T-cell markers, such as CD45RB, as well as CD45RO antibodies, and they were weakly positive for the granzyme B antibody.
  • In contrast, the tumor cells were negative for all B-cell markers as well as for CD3, CD56, S-100 protein, epithelial membrane antigen, and p80(NPM/ALK) antibodies.
  • Based on the clinical and histopathologic features, the lesion was diagnosed as an ALCL in both the upper and the lower gingiva.
  • This is an extremely rare case, in which a specific subtype of T-cell lymphoma appeared in the oral cavity.
  • [MeSH-major] Gingival Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 18656392.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 3.1.3.48 / Antigens, CD45
  • [Number-of-references] 30
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12. 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.
  • At the diagnosis the patient manifested with the stage IIIB.
  • The patient died of massive bleeding from his decomposing tumor 3 months after the diagnosis.
  • The tumor showed immunoblastic/anaplastic morphology, with some Reed-Sternberg-like cells positive for ALK.
  • ALK immunostaining was cytoplasmic, weak in a routine immunostain, enhanced with double (proteinase + pressure cooker) antigen retrieval.
  • FISH was consistent with the t(2;5)/nucleophosmin(NPM)-ALK rearrangement.
  • ALK-positive DLBCL affects mostly middle-aged men, shows generally poor but stage-dependent prognosis (at least 60% mortality rate), presents typically as a lymph node-based disseminated disease, and very rarely involves the bone marrow.
  • Genetic studies showed that the majority of ALK+DLBCL cases are characterized by the clathrin (CLTC)-ALK fusion and in a few cases the NPM-ALK rearrangement has been found.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 15921012.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
  • [Number-of-references] 17
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13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • Despite aggressive chemotherapy, the patients died 15 and 17 months after the diagnosis, indicating poor prognosis of the disease entity.
  • 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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14. Tokura Y, Sugita K, Yagi H, Shimauchi T, Kabashima K, Takigawa M: Primary cutaneous anaplastic large cell lymphoma with fatal leukemic outcome in association with CLA and CCR4-negative conversion. J Am Acad Dermatol; 2007 Nov;57(5 Suppl):S92-6
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  • [Title] Primary cutaneous anaplastic large cell lymphoma with fatal leukemic outcome in association with CLA and CCR4-negative conversion.
  • A 70-year-old Japanese male presented with a 1-year history of skin tumors, which were diagnosed as primary cutaneous anaplastic large cell lymphoma (ALCL) because of the CD3(low+), CD4(+), CD25(+), CD30(+), CD45RO(+), CD71(+), HLA-DR(+), CD8(-), CD56(-), and NPM/ALK(-) phenotype and monoclonal T-cell receptor-rearranged property of tumor cells as well as the absence of systemic involvement.
  • At this time, the tumor cell was positive for cutaneous lymphocyte-associated antigen (CLA) and TH(2) chemokine receptor CCR4.
  • The eruption had repeatedly appeared and spontaneously regressed or regressed by virtue of several therapeutic modalities, including radiotherapy, interferon-alpha and chemotherapy, until the tumor cell invaded the gastric mucosa and spread to the peripheral blood 5 years later.
  • Flow cytometric monitoring of the phenotype of peripheral blood and skin-infiltrating lymphocytes disclosed that the expression of CLA and CCR4 on the tumor cells was converted from positive to negative in association with the leukemic change.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Leukemia / etiology. Lymphoma, Large B-Cell, Diffuse / complications. Lymphoma, Large B-Cell, Diffuse / metabolism. Membrane Glycoproteins / metabolism. Receptors, Chemokine / metabolism

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  • (PMID = 17938033.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / CCR4 protein, human; 0 / CTAGE1 protein, human; 0 / Membrane Glycoproteins; 0 / Receptors, CCR4; 0 / Receptors, Chemokine
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15. Prochazka V, Faber E, Raida L, Vondrakova J, Kucerova L, Jarosova M, Indrak K, Papajik T: Prolonged survival of patients with peripheral T-cell lymphoma after first-line intensive sequential chemotherapy with autologous stem cell transplantation. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub; 2009 Mar;153(1):63-6
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  • [Title] Prolonged survival of patients with peripheral T-cell lymphoma after first-line intensive sequential chemotherapy with autologous stem cell transplantation.
  • BACKGROUND: Nodal peripheral T-cell lymphomas (PTCLs) are infrequent subtypes of non-Hodgkin's lymphomas.
  • The WHO classification recognizes three subgroups of nodal PTCL: peripheral T-cell lymphoma not otherwise specified (PTCL, NOS), anaplastic large cell lymphoma (ALCL) and angioimmunoblastic lymphoma (AIL).
  • Optimal first-line chemotherapy is not established and the role of high-dose therapy with autologous stem cell support is still controversial.
  • Consolidation was provided with myeloablative conditioning (BEAM 200) and autologous stem cell support.
  • Eighty-four patients with aggressive high-risk lymphoma were treated with the sequential protocol from 2000 to 2007 in our institution.
  • Here we report our experience with 18 patients with nodal PTCL (10 PTCL, NOS; 3 ALCL, ALKnegative; 2 ALCL, ALK-positive; 2 ALCL, unknown ALK status; 1 AIL).
  • After a median follow-up of 25.7 months, nine patients relapsed or progressed (6 PTCL, NOS; 2 ALCL ALK-positive; 1 ALCL ALK-negative; median 14.1 months) and four patients died (lymphoma progression).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Lymphoma, T-Cell, Peripheral / mortality. Lymphoma, T-Cell, Peripheral / therapy

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  • (PMID = 19365529.001).
  • [ISSN] 1213-8118
  • [Journal-full-title] Biomedical papers of the Medical Faculty of the University Palacký, Olomouc, Czechoslovakia
  • [ISO-abbreviation] Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
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16. Niitsu N, Kohri M, Hayama M, Tamaru J, Miura I: ALK-positive anaplastic large cell lymphoma with dic(2;4)(p23;q33). Leuk Res; 2009 Jun;33(6):e23-5
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  • [Title] ALK-positive anaplastic large cell lymphoma with dic(2;4)(p23;q33).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 4. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / metabolism. Translocation, Genetic

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  • (PMID = 19036440.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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17. Christensen JG, Zou HY, Arango ME, Li Q, Lee JH, McDonnell SR, Yamazaki S, Alton GR, Mroczkowski B, Los G: Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma. Mol Cancer Ther; 2007 Dec;6(12 Pt 1):3314-22
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  • [Title] Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma.
  • A t(2;5) chromosomal translocation resulting in expression of an oncogenic kinase fusion protein known as nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) has been implicated in the pathogenesis of anaplastic large-cell lymphoma (ALCL).
  • PF-2341066 was recently identified as a p.o. bioavailable, small-molecule inhibitor of the catalytic activity of c-Met kinase and the NPM-ALK fusion protein.
  • PF-2341066 also potently inhibited NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells (mean IC(50) value, 24 nmol/L).
  • In biochemical and cellular screens, PF-2341066 was shown to be selective for c-Met and ALK at pharmacologically relevant concentrations across a panel of >120 diverse kinases.
  • PF-2341066 potently inhibited cell proliferation, which was associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells (IC(50) values, approximately 30 nmol/L) but not ALK-negative lymphoma cells.
  • The induction of apoptosis was confirmed using terminal deoxyribonucleotide transferase-mediated nick-end labeling and Annexin V staining (IC(50) values, 25-50 nmol/L). P.o. administration of PF-2341066 to severe combined immunodeficient-Beige mice bearing Karpas299 ALCL tumor xenografts resulted in dose-dependent antitumor efficacy with complete regression of all tumors at the 100 mg/kg/d dose within 15 days of initial compound administration.
  • A strong correlation was observed between antitumor response and inhibition of NPM-ALK phosphorylation and induction of apoptosis in tumor tissue.
  • In addition, inhibition of key NPM-ALK signaling mediators, including phospholipase C-gamma, signal transducers and activators of transcription 3, extracellular signal-regulated kinases, and Akt by PF-2341066 were observed at concentrations or dose levels, which correlated with inhibition of NPM-ALK phosphorylation and function.
  • Collectively, these data illustrate the potential clinical utility of inhibitors of NPM-ALK in treatment of patients with ALK-positive ALCL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Lymphoma, Large-Cell, Anaplastic / pathology. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-met / antagonists & inhibitors. Pyridines / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Drug Screening Assays, Antitumor. Enzyme-Linked Immunosorbent Assay. Female. Humans. Mice. Mice, SCID. Phosphorylation. Receptor Protein-Tyrosine Kinases


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

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20451371.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GSK 1838705A; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase
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19. 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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  • (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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20. Hwang YY, Liang RH: An update in management of noncutaneous T-cell lymphomas. Adv Hematol; 2010;2010:424786
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  • [Title] An update in management of noncutaneous T-cell lymphomas.
  • T-cell lymphoma is a heterogeneous group of diseases.
  • Except for ALK positive anaplastic large cell lymphoma, T-cell lymphoma responds to conventional chemotherapy unfavourably, and most patients carry poor prognosis.
  • In recent years, efforts have been made to improve the outcome of T-cell lymphoma patients.
  • Novel agents, high-dose therapy, and allogeneic stem cell transplantation are studied, and various results are reported in literature.
  • This paper looks into the prognostication and treatment approach of different entities of noncutaneous T-cell lymphoma and would focus on the latest updates in its management.

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  • (PMID = 21188274.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3003949
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21. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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22. Ma L, Katz Y, Sharan KP, Schwarting R, Kim AS: Epstein-Barr virus positive anaplastic large cell lymphoma: myth or reality? Int J Clin Exp Pathol; 2010;4(1):100-10
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  • [Title] Epstein-Barr virus positive anaplastic large cell lymphoma: myth or reality?
  • The World Health Organization (WHO) Classification of Tumours of Haematopoietic and Lymphoid Tissue, 2008 edition, states that anaplastic large cell lymphoma (ALCL) is "consistently negative for Epstein-Barr virus (EBV)".
  • The statement made by the WHO has led to the widespread belief that EBV can have no pathogenic role in ALCL.
  • Herein we report a case of an immunocompetent 35-year-old male who presented with hemophagocytic syndrome secondary to lymphoma for which diagnostic material consisted solely of a bone marrow biopsy.
  • The biopsy demonstrated large anaplastic cells which were uniformly positive for surface CD3, CD30 (strong membranous and Golgi expression), CD45, TIA-1 and Granzyme B but negative for ALK-1.
  • In-situ hybridization was strongly positive for EBER in the large neoplastic cells.
  • The uniformity of CD30 expression and positivity for cytotoxic markers on the anaplastic tumor cells raised the diagnostic possibility of an EBV-associated ALCL, ALK-.
  • Discussion of this case as well as a retrospective review of 64 cases of reported of EBV+ ALCL are presented.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Herpesvirus 4, Human / isolation & purification. Lymphoma, Large-Cell, Anaplastic / virology. Tumor Virus Infections / complications

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  • (PMID = 21228932.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC3016108
  • [Keywords] NOTNLM ; ALK / Epstein-Barr virus / anaplastic large cell lymphoma
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23. Rannan-Eliya YF, Pulford K, Johnson R, Peart I, Kokai G, Baillie C, Ait-Tahar K, Pizer B: Isolated cutaneous anaplastic large cell lymphoma progressing to severe systemic disease with myocardial involvement and central nervous system infiltration. Pediatr Blood Cancer; 2008 Apr;50(4):879-81
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  • [Title] Isolated cutaneous anaplastic large cell lymphoma progressing to severe systemic disease with myocardial involvement and central nervous system infiltration.
  • Anaplastic large cell lymphoma (ALCL) is a rare tumor comprising around 10-15% of childhood lymphomas.
  • However, she subsequently relapsed with widespread systemic ALK-positive ALCL that included lymphoma deposits in the myocardium, a very rare manifestation.
  • We also present data on an immune response to ALK, demonstrating a fluctuation in the levels of circulating antibodies to ALK corresponding to the different phases of her illness.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Heart Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Skin Neoplasms / pathology

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 17914741.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 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
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24. Hughes M, Morrison A, Jackson R: Primary bladder lymphoma: management and outcome of 12 patients with a review of the literature. Leuk Lymphoma; 2005 Jun;46(6):873-7
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  • [Title] Primary bladder lymphoma: management and outcome of 12 patients with a review of the literature.
  • Primary bladder non-Hodgkin's lymphoma (NHL) is rare.
  • Using the Scotland and Newcastle lymphoma group database, 12 patients with primary bladder lymphoma were identified between 1980 and 2001, the largest single group of patients available to date.
  • Six cases were low-grade extranodal marginal zone lymphoma, 4 diffuse large B-cell lymphoma, one an ALK 1 positive anaplastic large cell lymphoma (ALKoma) and one a low-grade lymphoma unspecified.
  • A review of 88 additional cases in the literature support the findings that primary bladder lymphoma is associated with a good prognosis.
  • Patients with low-grade extranodal marginal zone lymphoma may respond well to simple therapies.
  • Patients with diffuse large B-cell lymphoma respond well to first-line chemotherapy regimens.
  • [MeSH-major] Lymphoma, B-Cell / diagnosis. Lymphoma, B-Cell / therapy. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / therapy. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / therapy. Urinary Bladder Neoplasms / diagnosis. Urinary Bladder Neoplasms / therapy

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  • (PMID = 16019532.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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25. 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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26. Lim ZY, Grace R, Salisbury JR, Creamer D, Jayaprakasam A, Ho AY, Devereux S, Mufti GJ, Pagliuca A: Cardiac presentation of ALK positive anaplastic large cell lymphoma. Eur J Haematol; 2005 Dec;75(6):511-4
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  • [Title] Cardiac presentation of ALK positive anaplastic large cell lymphoma.
  • Cardiac involvement as an initial presentation of malignant lymphoma is a rare occurrence.
  • Transcutaneous cardiac biopsy was non-diagnostic, therefore an open cardiac biopsy was performed from which a provisional diagnosis of a cardiac inflammatory pseudotumour was made.
  • Histological and immunophenotypic review of the initial cardiac biopsy revealed features consistent with a diagnosis of CD30, ALK1 positive anaplastic large cell lymphoma (ALCL).
  • Despite intensive treatment with combination chemotherapy, there was significant progression of disease, and he died 11 months after diagnosis.
  • The overall prognosis of cardiac lymphoma remains poor, which may be due to the often late presentation of the tumour.
  • To our knowledge, this is the first reported case of a cardiac ALK positive ALCL.
  • Although rare, cardiac presentation of ALCL should be added to the list of differential diagnoses of cardiac lymphomas.
  • [MeSH-major] Activin Receptors, Type I. Heart Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 16313264.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type I; EC 2.7.11.30 / Activin Receptors, Type II
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27. 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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28. 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.
  • A biopsy of the brain revealed histologic and immunophenotypic findings characteristic of ALK-1+ anaplastic large cell lymphoma (ALCL).
  • ALCL rarely occurs in the central nervous system and poses a significant diagnostic challenge often leading to a delay in the initiation of appropriate treatment.
  • 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


29. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • [MeSH-major] Antigens, CD5 / biosynthesis. Lymphedema / complications. Lymphoma, B-Cell / complications. Lymphoma, Large B-Cell, Diffuse / complications. Skin Neoplasms / complications


30. Wong AK, Lopategui J, Clancy S, Kulber D, Bose S: Anaplastic large cell lymphoma associated with a breast implant capsule: a case report and review of the literature. Am J Surg Pathol; 2008 Aug;32(8):1265-8
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  • [Title] Anaplastic large cell lymphoma associated with a breast implant capsule: a case report and review of the literature.
  • Primary lymphomas of the breast are rare and predominately of B-cell phenotype.
  • Anaplastic large cell lymphoma is a T-cell lymphoma that accounts for only 3% of all non-Hodgkin lymphomas.
  • We present a rare case of primary anaplastic large cell lymphoma of the breast in association with a silicone breast implant capsule in a healthy 40-year-old woman.
  • Histology, immunohistochemistry, and T-cell gene rearrangement studies were supportive of a CD 30-positive ALK-1 negative anaplastic large cell lymphoma.
  • This case represents the 14th reported case of primary breast lymphoma in association with breast prosthesis.
  • Of interest is that 11 of these cases were T-cell lymphomas with 8 specifically of the CD30-positive anaplastic large cell lymphoma type.
  • [MeSH-major] Breast Implantation. Breast Implants / adverse effects. Breast Neoplasms / etiology. Lymphoma, Large-Cell, Anaplastic / etiology. Silicone Gels


31. Gudgin E, Rashbass J, Pulford KJ, Erber WN: Primary and isolated anaplastic large cell lymphoma of the bone marrow. Leuk Lymphoma; 2005 Mar;46(3):461-3
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  • [Title] Primary and isolated anaplastic large cell lymphoma of the bone marrow.
  • Anaplastic large cell lymphoma (ALCL) is a T-cell lymphoma in which the majority of patients present with advanced stage III or IV disease.
  • Here we report a case of ALCL where bone marrow was the only site of disease, in a 60-year-old man with pyrexia and pancytopenia.
  • The diagnosis of ALCL was made on detection of CD30-positive anaplastic cells in the bone marrow, together with prominent hemophagocytosis.
  • Genetics confirmed the clonal nature of the disease and showed it to be anaplastic lymphoma kinase (ALK) negative.
  • Primary isolated bone marrow ALCL should be considered in the diagnosis of pancytopenia associated with hemophagocytosis.
  • [MeSH-major] Bone Marrow / pathology. Lymphoma, Large-Cell, Anaplastic / pathology


32. Wang C, Zhang WM, Zhang ZH, Li BZ: [ALK-positive anaplastic large cell lymphoma with obvious nodular growth pattern: report of a case]. Zhonghua Bing Li Xue Za Zhi; 2010 Nov;39(11):779-80
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  • [Title] [ALK-positive anaplastic large cell lymphoma with obvious nodular growth pattern: report of a case].
  • [MeSH-major] Lymph Nodes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Receptor Protein-Tyrosine Kinases / metabolism

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  • (PMID = 21215175.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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33. Paolo C, Lucia F, Anna D: Hematopoietic stem cell transplantation in peripheral T-cell lymphomas. Leuk Lymphoma; 2007 Aug;48(8):1496-501
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  • [Title] Hematopoietic stem cell transplantation in peripheral T-cell lymphomas.
  • Peripheral T-cell lymphomas (PTCL) are a rare entity with a dismal outcome.
  • After conventional chemotherapy they showed a worse prognosis compared with B-cell non-Hodgkin's lymphoma (NHL), except for anaplastic lymphoma-kinase (ALK)-positive anaplastic large cell lymphomas (ALCL).
  • High-dose chemotherapy followed by autologous stem cell transplantation (SCT) has been evaluated in relapsed patients as well as in the upfront setting.
  • Available data showed an advantage for patients who received transplant as first line treatment whereas results of autografting at relapse have been satisfactory only for ALK-positive ALCLs compared to other PTCL subtypes.
  • Whether or not the postulated graft-versus-lymphoma effect may overcome the poor prognosis of T-cell NHL patients has to be established.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, T-Cell, Peripheral / therapy

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  • (PMID = 17701579.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 38
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34. Rassidakis GZ, Thomaides A, Wang S, Jiang Y, Fourtouna A, Lai R, Medeiros LJ: p53 gene mutations are uncommon but p53 is commonly expressed in anaplastic large-cell lymphoma. Leukemia; 2005 Sep;19(9):1663-9
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  • [Title] p53 gene mutations are uncommon but p53 is commonly expressed in anaplastic large-cell lymphoma.
  • Anaplastic large-cell lymphoma (ALCL), as defined in the World Health Organization, is a heterogeneous category in which a subset of cases is associated with the t(2;5)(p23;q35) or variant translocations resulting in overexpression of anaplastic lymphoma kinase (ALK).
  • p53 has not been assessed in currently defined subsets of ALCL tumors.
  • In this study, we assessed ALK+ and ALK- ALCL tumors for p53 gene alterations using PCR, single-strand conformation polymorphism and direct sequencing methods.
  • We also immunohistochemically assessed ALCL tumors for p53 expression.
  • Three of 36 (8%) ALCL tumors (1/14 ALK+, 2/22 ALK-) with adequate DNA showed p53 gene mutations.
  • By contrast, p53 was overexpressed in 36 of 55 (65%) ALCL tumors (16 ALK+, 20 ALK-).
  • p21, a target of p53, was expressed in 15 of 31 (48%) ALCL tumors including seven of 15 (47%) p53-positive tumors. p21 expression in a subset of ALCL suggests the presence of functional p53 protein.
  • Apoptotic rate was significantly higher in p53-positive than p53-negative tumors (mean 2.78 vs 0.91%, P = 0.0003).
  • We conclude that the p53 gene is rarely mutated in ALK+ and ALK- ALCL tumors.
  • Nevertheless, wild-type p53 gene product is commonly overexpressed in ALCL and may be functional in a subset of these tumors.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, p53 / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Apoptosis / physiology. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Cell Proliferation. Cloning, Molecular. Cyclin-Dependent Kinase Inhibitor p21. Humans. Middle Aged. Mutation. Nuclear Proteins / biosynthesis. Nuclear Proteins / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-mdm2. Receptor Protein-Tyrosine Kinases. Sequence Analysis, DNA / methods

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  • (PMID = 15990866.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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35. 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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36. Boccalatte FE, Voena C, Riganti C, Bosia A, D'Amico L, Riera L, Cheng M, Ruggeri B, Jensen ON, Goss VL, Lee K, Nardone J, Rush J, Polakiewicz RD, Comb MJ, Chiarle R, Inghirami G: The enzymatic activity of 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase is enhanced by NPM-ALK: new insights in ALK-mediated pathogenesis and the treatment of ALCL. Blood; 2009 Mar 19;113(12):2776-90
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  • [Title] The enzymatic activity of 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase is enhanced by NPM-ALK: new insights in ALK-mediated pathogenesis and the treatment of ALCL.
  • Anaplastic large cell lymphoma represents a subset of neoplasms caused by translocations that juxtapose the anaplastic lymphoma kinase (ALK) to dimerization partners.
  • The constitutive activation of ALK fusion proteins leads to cellular transformation through a complex signaling network.
  • To elucidate the ALK pathways sustaining lymphomagenesis and tumor maintenance, we analyzed the tyrosine-kinase protein profiles of ALK-positive cell lines using 2 complementary proteomic-based approaches, taking advantage of a specific ALK RNA interference (RNAi) or cell-permeable inhibitors.
  • A well-defined set of ALK-associated tyrosine phosphopeptides, including metabolic enzymes, kinases, ribosomal and cytoskeletal proteins, was identified.
  • Validation studies confirmed that vasodilator-stimulated phosphoprotein and 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/inosine monophosphate cyclohydrolase (ATIC) associated with nucleophosmin (NPM)-ALK, and their phosphorylation required ALK activity.
  • ATIC phosphorylation was documented in cell lines and primary tumors carrying ALK proteins and other tyrosine kinases, including TPR-Met and wild type c-Met.
  • Functional analyses revealed that ALK-mediated ATIC phosphorylation enhanced its enzymatic activity, dampening the methotrexate-mediated transformylase activity inhibition.
  • These findings demonstrate that proteomic approaches in well-controlled experimental settings allow the definition of informative proteomic profiles and the discovery of novel ALK downstream players that contribute to the maintenance of the neoplastic phenotype.

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  • (PMID = 18845790.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090773; United States / NCI NIH HHS / CA / R01-CA90773
  • [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 / Antimetabolites, Antineoplastic; 0 / CEP 11988; 0 / CEP 14083; 0 / Carbazoles; 0 / Cell Adhesion Molecules; 0 / Indazoles; 0 / Microfilament Proteins; 0 / Multienzyme Complexes; 0 / Neoplasm Proteins; 0 / Phenylurea Compounds; 0 / Phosphoproteins; 0 / Protein Kinase Inhibitors; 0 / inosine monophosphate synthase; 0 / vasodilator-stimulated phosphoprotein; 21820-51-9 / Phosphotyrosine; EC 2.1.2.- / Hydroxymethyl and Formyl Transferases; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.5.4.- / Nucleotide Deaminases; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC2661863
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37. 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
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38. Dunleavy K, Piekarz RL, Zain J, Janik JE, Wilson WH, O'Connor OA, Bates SE: New strategies in peripheral T-cell lymphoma: understanding tumor biology and developing novel therapies. Clin Cancer Res; 2010 Dec 1;16(23):5608-17
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  • [Title] New strategies in peripheral T-cell lymphoma: understanding tumor biology and developing novel therapies.
  • Peripheral T-cell lymphomas (PTCL) constitute a group of heterogeneous diseases that are uncommon, representing, in Western countries, only approximately 10% of all non-Hodgkin lymphomas.
  • They are typically associated with a poor prognosis compared with their B-cell counterparts and are much less well understood with respect to tumor biology, owing to their rarity and biologic heterogeneity, and to the fact that characteristic cytogenetic abnormalities are few compared with B-cell lymphomas.
  • Although the outcome for patients with anaplastic large cell lymphoma (ALCL), particularly anaplastic lymphoma kinase (ALK)-positive ALCL, is good, other types of PTCLs are associated with a poor prognosis, even with aggressive anthracycline-based chemotherapy.
  • [MeSH-major] Lymphoma, T-Cell, Peripheral / diagnosis. Lymphoma, T-Cell, Peripheral / etiology. Lymphoma, T-Cell, Peripheral / therapy. Therapies, Investigational / trends
  • [MeSH-minor] Animals. Antineoplastic Agents / chemical synthesis. Antineoplastic Agents / therapeutic use. Cell Biology. Comprehension. Drug Discovery / methods. Drug Discovery / trends. Gene Expression Profiling. Humans. Molecular Targeted Therapy / methods

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  • (PMID = 21138864.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ NIHMS236831; NLM/ PMC3058794
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39. Delsol G: [Molecular abnormalities in lymphomas]. Bull Cancer; 2010 Nov;97(11):1347-64
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  • In the present review, molecular abnormalities observed in the most frequent B, T or NK cell lymphomas are discussed.
  • In the broad spectrum of diffuse large B-cell lymphomas microarray analysis shows mostly two subgroups of tumors, one with gene expression signature corresponding to germinal center B-cell-like (GCB: CD10+, BCL6 [B-Cell Lymphoma 6]+, centerine+, MUM1-) and a subgroup expressing an activated B-cell-like signature (ABC: CD10-, BCL6-, centerine-, MUM1+).
  • Among other B-cell lymphomas with well characterized molecular abnormalies are follicular lymphoma (BCL2 deregulation), MALT lymphoma (Mucosa Associated Lymphoid Tissue) [API2-MALT1 (mucosa-associated-lymphoid-tissue-lymphoma-translocation-gene1) fusion protein or deregulation BCL10, MALT1, FOXP1.
  • MALT1 transcription factors], mantle cell lymphoma (cycline D1 [CCND1] overexpression) and Burkitt lymphoma (c-Myc expression).
  • Except for ALK (anaplastic lymphoma kinase)-positive anaplastic large cell lymphoma, well characterized molecular anomalies are rare in lymphomas developed from T or NK cells.
  • Peripheral T cell lymphomas not otherwise specified are a heterogeneous group of tumors with frequent but not recurrent molecular abnormalities.
  • In angio-immunoblastic T-cell lymphomas molecular abnormalities are found in follicular helper T-cell (TFH) that express some distinctive markers such as CD10, PD-1, CXCR5 and the CXCL13 chemokine.
  • ALK-positive anaplastic large cell lymphoma is a paradigme of T-cell lymphoma since it is associated with an X-ALK oncogenic fusion protein due to a translocation involving ALK gene at 2p23.
  • ALK tyrosine kinase activates downstream pathways (Stat3/5b, Src kinases, PLCγ, PI3 kinase) implicated in lymphomagenesis, proliferation and protection against apoptosis.
  • Specific ALK inhibitors are currently in clinical evaluation.
  • Helicobacter pylori in MALT lymphoma) in lymphomagenesis.
  • [MeSH-major] Gene Amplification / genetics. Genes, Tumor Suppressor. Lymphoma / genetics. Mutation / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Gene Deletion. Gene Expression Regulation, Neoplastic / genetics. Genetic Techniques. Humans. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / metabolism. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell / metabolism. Neoplasm Proteins / metabolism


40. 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.


41. Khor TS, Alessandri AJ, Jevon GP: Infant anaplastic large cell lymphoma with hemophagocytic syndrome. Pediatr Dev Pathol; 2010 Jan-Feb;13(1):72-6
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  • [Title] Infant anaplastic large cell lymphoma with hemophagocytic syndrome.
  • Anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK)-positive, is uncommon in infancy.
  • We present an unusual occurrence of infant ALCL, ALK-positive, associated with hemophagocytic syndrome.
  • To the best of our knowledge, there have been no cases of infant ALCL, ALK-positive, described that have been associated with hemophagocytic syndrome.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 19863446.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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42. Gualco G, Klumb CE, Barber GN, Weiss LM, Bacchi CE: Pediatric lymphomas in Brazil. Clinics (Sao Paulo); 2010;65(12):1267-77
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  • METHODS: A retrospective analyses of diagnosed pediatric lymphoma cases in a 10-year period was performed.
  • RESULTS: Non-Hodgkin lymphomas represented 68% of the cases, including those of precursor (36%) and mature (64%) cell origin.
  • Mature cell lymphomas comprised 81% of the B-cell phenotype and 19% of the T-cell phenotype.
  • Among mature B-cell lymphomas, most of the cases were Burkitt lymphomas (65%), followed by diffuse large B-cell lymphomas (24%).
  • In the mature T-cell group, anaplastic large cell lymphoma, ALK-positive was the most prevalent (57%), followed by peripheral T-cell lymphoma, then not otherwise specified (25%).
  • [MeSH-major] Lymphoma / epidemiology

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  • (PMID = 21340214.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / P30 AI073961
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC3020336
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43. Li JF, Li GD, Liu WP, Wang Y, Cheng JR, Chen Y, Yang H, Tang HL, Bai YQ, Lin DG, DU LH, Peng FX, Yang YH, Zhao C: [Expression of anaplastic lymphoma kinase and survivin proteins in anaplastic large cell lymphoma and its significance]. Zhonghua Bing Li Xue Za Zhi; 2006 Apr;35(4):213-7
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  • [Title] [Expression of anaplastic lymphoma kinase and survivin proteins in anaplastic large cell lymphoma and its significance].
  • OBJECTIVE: To study the expression of anaplastic lymphoma kinase (ALK) and survivin proteins in anaplastic large cell lymphoma (ALCL) and there clinical significance.
  • Immunohistochemical staining for ALK and survivin proteins was performed using LSAB method.
  • RESULTS: ALK protein was positive in 51 cases (63%) and negative in 30 cases (37%) of the 81 cases of ALCL studied.
  • The prognosis of patients with ALK protein expression was better than those without ALK expression (P < 0.05).
  • As for survivin protein, there were various degrees of expression in all the 77 ALCL cases studied.
  • The expression of survivin protein did not correlate with that of ALK protein (P > 0.05).
  • In cases with ALK protein expression, the prognosis was less favorable if there was also high co-expression of survivin protein (P < 0.05).
  • In ALK protein negative cases, prognosis did not significantly correlate with the expression of survivin protein (P > 0.05).
  • In addition, multivariate analysis confirmed the prognosis value of ALK protein expression, survivin protein expression and constitutional symptoms.
  • CONCLUSION: Survivin protein expression can serve as an independent prognostic predictor of unfavorable clinical outcome in patients with ALCL, especially when ALK protein is positive.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16776978.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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44. Schumacher JA, Crockett DK, Elenitoba-Johnson KS, Lim MS: Proteome-wide changes induced by the Hsp90 inhibitor, geldanamycin in anaplastic large cell lymphoma cells. Proteomics; 2007 Aug;7(15):2603-16
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  • [Title] Proteome-wide changes induced by the Hsp90 inhibitor, geldanamycin in anaplastic large cell lymphoma cells.
  • The molecular chaperone heat shock protein 90 (Hsp90) affects the function of many oncogenic signaling proteins including nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expressed in anaplastic large cell lymphoma (ALCL).
  • While ALK-positive ALCL cells are sensitive to the Hsp90 inhibitor and the geldanamycin (GA) analog, 17-allylamino-17-demethoxygeldanamycin (17-AAG), the proteomic effects of these drugs on ALK-positive ALCL cells are unpublished.
  • In this study, we investigated the cellular, biologic, and proteomic changes occurring in ALK-positive ALCL cells in response to GA treatment.
  • GA induced G2/M cell cycle arrest and caspase-3-mediated apoptosis.
  • Our studies reveal some of the molecular and proteomic consequences of Hsp90 inhibition in ALK-positive ALCL cells and provide novel insights into the mechanisms of its diverse cellular effects.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Benzoquinones / pharmacology. Enzyme Inhibitors / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / pharmacology. Lymphoma, Large B-Cell, Diffuse / metabolism. Proteome / analysis
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Caspase 3 / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA, Neoplasm / analysis. Humans. Models, Biological. Reproducibility of Results

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  • (PMID = 17610208.001).
  • [ISSN] 1615-9853
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Benzoquinones; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Proteome; EC 3.4.22.- / Caspase 3; Z3K3VJ16KU / geldanamycin
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45. Chuang SS, Hsieh YC, Ye H, Hwang WS: Lymphohistiocytic anaplastic large cell lymphoma involving skin: a diagnostic challenge. Pathol Res Pract; 2009;205(4):283-7
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  • [Title] Lymphohistiocytic anaplastic large cell lymphoma involving skin: a diagnostic challenge.
  • Systemic anaplastic large cell lymphoma (ALCL) involving the skin should be differentiated from primary cutaneous CD30-positive T-cell lymphoproliferative disorders.
  • The lymphohistiocytic variant of ALCL (LH-ALCL) is rich in reactive histiocytes with relatively few neoplastic cells, which pose a diagnostic challenge.
  • We present a case of LH-ALCL involving skin mimicking granulomatous inflammation.
  • Biopsy of the cervical lymph node showed LH-ALCL with null cell phenotype.
  • Microscopically, the cutaneous lesion was located predominately around the hair follicle, with numerous reactive histiocytes and scanty medium-sized lymphoma cells expressing CD30 and anaplastic lymphoma kinase (ALK) protein.
  • Furthermore, an ALK gene rearrangement was demonstrated by locus-specific interphase fluorescent in situ hybridization, confirming cutaneous involvement with LH-ALCL.
  • LH-ALCL involving the skin is a rare event, and the numerous reactive histiocytes may mask scanty tumor cells.
  • In addition to B-and T-cell markers, (dermato) pathologists must be aware of this entity in cutaneous lymphohistiocytic proliferations and perform immunostaining for CD30 and ALK to reach a correct diagnosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Skin Neoplasms / pathology

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  • (PMID = 19091487.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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46. Cussac D, Pichereaux C, Colomba A, Capilla F, Pont F, Gaits-Iacovoni F, Lamant L, Espinos E, Burlet-Schiltz O, Monsarrat B, Delsol G, Payrastre B: Proteomic analysis of anaplastic lymphoma cell lines: identification of potential tumour markers. Proteomics; 2006 May;6(10):3210-22
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  • [Title] Proteomic analysis of anaplastic lymphoma cell lines: identification of potential tumour markers.
  • Anaplastic large-cell lymphomas (ALCL) are high grade lymphomas of T or null phenotype often associated with the t(2;5) translocation leading to the expression of a chimeric protein consisting of the N-terminal portion of nucleophosmin (NPM) and the intracellular domain of the anaplastic lymphoma kinase (ALK).
  • Although ALCL are recognized as distinct clinical, biological and cytogenetic entities, heterogeneities persist in this group of tumours, which exhibit a broad spectrum of morphological features.
  • Particularly, the common type tumour consisting in large cells contrast with the small cell variant that is sometimes associated with a leukemic phase.
  • The ALK-negative ALCL is often associated with a poor prognosis.
  • Here, we investigated the proteome of these subtypes of tumours using patient-derived cell lines.
  • We compared the proteome of the cytosolic fraction of NPM-ALK-positive versus NPM-ALK-negative cells on one hand, and the proteome of common cell type versus small cell variant on the other hand.
  • The identification of a set of proteins differentially expressed in the subtypes of ALCL points to new diagnosis/prognosis markers.
  • This study also provides interesting information on the molecular mechanisms responsible for the different subtypes of ALCL.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Lymphoma, Large B-Cell, Diffuse / metabolism. Proteome / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Cytosol / metabolism. Electrophoresis, Gel, Two-Dimensional. Humans. Immunohistochemistry. Nuclear Proteins / biosynthesis. Phenotype. Prognosis. Protein-Tyrosine Kinases / biosynthesis. Receptor Protein-Tyrosine Kinases. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization


47. Gofrit ON, Pode D, Shapiro A, Zorn KC, Pizov G: Significance of inflammatory pseudotumors in patients with a history of bladder cancer. Urology; 2007 Jun;69(6):1064-7
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  • The original histologic blocks were reviewed and immunostained for vimentin, anaplastic large cell lymphoma (ALK), and pancytokeratin.
  • Immunostaining for vimentin was positive in all patients, ALK was negative in all patients, and pancytokeratin positive in only 2 patients.
  • [MeSH-major] Granuloma, Plasma Cell / pathology. Urinary Bladder Neoplasms / complications

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  • (PMID = 17572187.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. 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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  • [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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49. Mergan F, Jaubert F, Sauvat F, Hartmann O, Lortat-Jacob S, Révillon Y, Nihoul-Fékété C, Sarnacki S: Inflammatory myofibroblastic tumor in children: clinical review with anaplastic lymphoma kinase, Epstein-Barr virus, and human herpesvirus 8 detection analysis. J Pediatr Surg; 2005 Oct;40(10):1581-6
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  • [Title] Inflammatory myofibroblastic tumor in children: clinical review with anaplastic lymphoma kinase, Epstein-Barr virus, and human herpesvirus 8 detection analysis.
  • Differential diagnosis with other tumor processes is sometimes difficult.
  • Similar anaplastic lymphoma kinase (ALK) gene abnormalities as in anaplastic large cell lymphoma have been reported.
  • This article aims to evaluate ALK, EBV, and HHV-8 expression in children with IMT and to correlate our findings with clinical features.
  • Formalin-fixed, paraffin-embedded archival tissues were stained for HHV-8 and ALK with immunohistochemistry.
  • ALK was positive in 3 (18.8%) cases and EBV in 1 pulmonary and 1 bladder tumor, all of them without recurrence or metastasis.
  • None of the cases were positive for HHV-8.
  • Larger multicentric studies would be necessary to understand the prognostic significance of ALK, EBV, and HHV-8 and their relationships with the origins of the tumor.
  • [MeSH-major] Granuloma, Plasma Cell / enzymology. Granuloma, Plasma Cell / virology. Herpesvirus 4, Human / isolation & purification. Herpesvirus 8, Human / isolation & purification. Protein-Tyrosine Kinases / analysis. Receptor Protein-Tyrosine Kinases / analysis

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  • (PMID = 16226988.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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50. 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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51. Reimer P, Hentrich M: [Peripheral T-cell lymphoma: diagnosis and treatment]. Dtsch Med Wochenschr; 2006 Mar 31;131(13):685-90
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  • [Title] [Peripheral T-cell lymphoma: diagnosis and treatment].
  • Peripheral T/NK-cell lymphomas (PTCL) comprise a heterogeneous group of rare diseases accounting for approximately 10-15% of all non-Hodgkin"s lymphomas.
  • Compared to B-cell lymphomas, PTCL more frequently involve extranodal sites and have a worse prognosis.
  • Because of their usually indolent course, primary cutaneous T/NK-cell lymphomas should be distinguished from the other PTCL.
  • The International Prognostic Index, established for aggressive B-cell lymphomas, has also proved relevant for PTCL.
  • Apart from (ALK-positive) anaplastic large cell lymphoma it thus gives poorer results than those obtained in patients with aggressive B-cell lymphomas.
  • Data for high-dosage therapy with autologous stem cell transplantation (autoSCT) for relapsing and refractory PTCL are similar to those reported for aggressive B-cell lymphomas.
  • Allogeneic stem cell transplantation following reduced conditioning regimens has also given promising results in patients with relapse.
  • [MeSH-major] Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / therapy
  • [MeSH-minor] Humans. Stem Cell Transplantation. Survival Analysis. Transplantation, Homologous

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  • [CommentIn] Dtsch Med Wochenschr. 2006 Aug 25;131(34-35):1884; author reply 1884 [16915558.001]
  • (PMID = 16555177.001).
  • [ISSN] 0012-0472
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 56
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52. 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


53. Thornber K, Colomba A, Ceccato L, Delsol G, Payrastre B, Gaits-Iacovoni F: Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas. Oncogene; 2009 Jul 23;28(29):2690-6
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  • [Title] Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas.
  • The chimera nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), the tyrosine kinase activity of which is constitutively upregulated, is the causative agent of 75% of the anaplastic large-cell lymphomas (ALCLs).
  • We have demonstrated that NPM-ALK induces the production of reactive oxygen species (ROS) by a pathway involving the arachidonic acid-metabolizing enzymes of the lipoxygenase (LOX) family.
  • The use of the LOX inhibitor nordihydroguaiaretic acid (NDGA) and of the anti-oxidant N-acetylcysteine (NAC) demonstrated that ROS are important in maintaining the ALK kinase active.
  • Consistent with this, NDGA treatment resulted in the inhibition of key pathways, such as Akt, signal transducer and activator of transcription factor 3 (STAT3) and extracellular signal-regulated kinase (ERK), which are involved in NPM-ALK antiapoptotic and pro-mitogenic functions.
  • Interestingly, 5-LOX, an isoform involved in many cancers, was found to be activated in NPM-ALK(+) cells.
  • Together, these data point to the ROS/LOX pathway as a potential new target for therapy in NPM-ALK-positive tumors.
  • [MeSH-major] Arachidonate 5-Lipoxygenase / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Humans. Lipoxygenase Inhibitors / pharmacology. Masoprocol / analysis

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  • (PMID = 19503098.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipoxygenase Inhibitors; 0 / Reactive Oxygen Species; 7BO8G1BYQU / Masoprocol; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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54. Eckerle S, Brune V, Döring C, Tiacci E, Bohle V, Sundström C, Kodet R, Paulli M, Falini B, Klapper W, Chaubert AB, Willenbrock K, Metzler D, Bräuninger A, Küppers R, Hansmann ML: Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma. Leukemia; 2009 Nov;23(11):2129-38
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  • [Title] Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is a main type of T-cell lymphomas and comprises three distinct entities: systemic anaplastic lymphoma kinase (ALK) positive, systemic ALK(-) and cutaneous ALK(-) ALCL (cALCL).
  • Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK(-) ALCL and classical Hodgkin lymphoma (cHL).
  • We conducted gene expression profiling of microdissected lymphoma cells of five ALK(+) and four ALK(-) systemic ALCL, seven cALCL and sixteen cHL, and of eight subsets of normal T and NK cells.
  • The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4(+), CD8(+) or CD30(+) T-cell origin.
  • Indeed, ALCL display a down-modulation of many T-cell characteristic molecules.
  • All ALCL types show significant expression of NFkappaB target genes and upregulation of genes involved in oncogenesis (e.g. EZH2).
  • Surprisingly, few genes are differentially expressed between systemic and cALCL despite their different clinical behaviour, and between ALK(-) ALCL and cHL despite their different cellular origin.
  • ALK(+) ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK.
  • This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Hodgkin Disease / genetics. Lymphoma, Large-Cell, Anaplastic / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line. Female. Humans. Immunohistochemistry. Killer Cells, Natural / cytology. Killer Cells, Natural / physiology. Male. Microdissection. Middle Aged. NF-kappa B / metabolism. Phenotype. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / cytology. T-Lymphocytes / physiology. Young Adult


55. Kaliyadan F, Ray S, Mathew MK, Pai S, Sasikala L, Pai R: A rapidly progressing, fatal case of primary systemic anaplastic large cell lymphoma presenting as erythroderma--association with carbamazepine. Dermatol Online J; 2008;14(12):5
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  • [Title] A rapidly progressing, fatal case of primary systemic anaplastic large cell lymphoma presenting as erythroderma--association with carbamazepine.
  • A 73-year-old male patient admitted with erythroderma was diagnosed to have primary systemic Analpastic Lymphoma Kinase (ALK) positive, CD 30 positive, anaplastic large cell lymphoma.
  • The patient's condition deteriorated rapidly during the period after the diagnosis was confirmed, with subsequent death before chemotherapy could be started.
  • Here we highlight the possibility of carbamazepine inducing anaplastic large cell lymphomas and the need for a high level of suspicion to make an early diagnosis allowing rapid appropriate treatment in such cases.
  • [MeSH-major] Carbamazepine / adverse effects. Dermatitis, Exfoliative / complications. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / etiology

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  • (PMID = 19265618.001).
  • [ISSN] 1087-2108
  • [Journal-full-title] Dermatology online journal
  • [ISO-abbreviation] Dermatol. Online J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 33CM23913M / Carbamazepine
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56. 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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57. Lai R, Rassidakis GZ, Lin Q, Atwell C, Medeiros LJ, Amin HM: Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma. Hum Pathol; 2005 Sep;36(9):939-44
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  • [Title] Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma.
  • In previous studies of anaplastic large cell lymphoma (ALCL), we showed that inhibition of Jak3 down-regulates activated/phosphorylated Stat3 (pStat3), decreases anaplastic lymphoma kinase (ALK) enzymatic activity, and induces cell-cycle arrest and apoptosis in ALK-positive ALCL.
  • These findings implicate Jak3 as playing a significant role in the pathogenesis of ALK-positive ALCL; most likely via Stat3 and ALK activation.
  • To assess this possibility, we used immunohistochemical staining to evaluate the frequency of expression of Jak3 and its activated/phosphorylated form (pJak3) in 48 systemic ALCL tumors included in a tissue microarray. pJak3 was detected in 17 (81%) of 21 ALK-positive tumors, compared with 3 (11%) of 27 ALK-negative tumors (P < .0001, Fisher exact test).
  • pStat3 was present in 12 (86%) of 14 ALK-positive tumors and in 10 (40%) of 25 ALK-negative tumors assessed (P = .0078).
  • Of 12 ALK-positive/pStat3-positive tumors, 8 (67%) expressed pJak3, but none of 10 ALK-negative/pStat3-positive tumors expressed pJak3.
  • We conclude that Jak3 activation is predominantly restricted to ALK-positive ALCL tumors.
  • Most likely, Jak3 collaborates with ALK in activating Stat3, leading to cell survival, cell-cycle progression, and tumor growth.
  • In contrast, the mechanism of Stat3 activation in ALK-negative ALCL tumors appears to be independent of Jak3.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16153455.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / JAK3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3
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58. Salaverria I, Beà S, Lopez-Guillermo A, Lespinet V, Pinyol M, Burkhardt B, Lamant L, Zettl A, Horsman D, Gascoyne R, Ott G, Siebert R, Delsol G, Campo E: Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas. Br J Haematol; 2008 Mar;140(5):516-26
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  • [Title] Genomic profiling reveals different genetic aberrations in systemic ALK-positive and ALK-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is a T/null-cell neoplasm characterized by chromosomal translocations involving the anaplastic lymphoma kinase (ALK) gene (ALK).
  • Tumours with similar morphology and phenotype but negative for ALK have been also recognized.
  • We have examined 74 ALCL, 43 ALK-positive and 31 ALK-negative, cases by comparative genomic hybridization (CGH), and locus-specific alterations for TP53 and ATM were examined by fluorescence in situ hybridization and real-time quantitative polymerase chain reaction.
  • Chromosomal imbalances were detected in 25 (58%) ALK-positive and 20 (65%) ALK-negative ALCL.
  • ALK-positive ALCL with NPM-ALK or other ALK variant translocations showed a similar profile of secondary genetic alterations.
  • Gains of 17p and 17q24-qter and losses of 4q13-q21, and 11q14 were associated with ALK-positive cases (P = 0.05), whereas gains of 1q and 6p21 were more frequent in ALK-negative tumours (P = 0.03).
  • ALCL-negative tumours had a significantly worse prognosis than ALK-positive.
  • In conclusion, ALK-positive and negative ALCL have different secondary genomic aberrations, suggesting they correspond to different genetic entities.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromosome Aberrations. Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 18275429.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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59. Watanabe M, Sasaki M, Itoh K, Higashihara M, Umezawa K, Kadin ME, Abraham LJ, Watanabe T, Horie R: JunB induced by constitutive CD30-extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase signaling activates the CD30 promoter in anaplastic large cell lymphoma and reed-sternberg cells of Hodgkin lymphoma. Cancer Res; 2005 Sep 1;65(17):7628-34
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  • [Title] JunB induced by constitutive CD30-extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase signaling activates the CD30 promoter in anaplastic large cell lymphoma and reed-sternberg cells of Hodgkin lymphoma.
  • High expression of CD30 and JunB is characteristic of tumor cells in anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL).
  • We found that the CD30 promoter in tumor cells of both nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK)-positive and NPM-ALK-negative ALCL and HL is regulated by a constitutively active CD30-extracellular signal-regulated kinase (ERK) 1/2 mitogen-activated protein kinase (MAPK).
  • Phosphorylation of ERK1/2 MAPK was confirmed in nuclei of tumor cells in both ALCL and HL.
  • JunB induction seems to be largely independent of nuclear factor kappaB in ALCL and HL.
  • These results show a common mechanism of CD30 overexpression in ALCL and HL, although the outcome of CD30 signaling differs between NPM-ALK-positive ALCL and NPM-ALK-negative ALCL, cutaneous ALCL, and HL as we recently reported.
  • [MeSH-major] Antigens, CD30 / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. MAP Kinase Signaling System / physiology. Proto-Oncogene Proteins c-jun / biosynthesis. Reed-Sternberg Cells / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. K562 Cells. NF-kappa B / metabolism. Promoter Regions, Genetic. Protein Binding. Transcription Factor AP-1 / metabolism


60. Bakshi NA, Ross CW, Finn WG, Valdez R, Ruiz R, Koujok K, Schnitzer B: ALK-positive anaplastic large cell lymphoma with primary bone involvement in children. Am J Clin Pathol; 2006 Jan;125(1):57-63
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  • [Title] ALK-positive anaplastic large cell lymphoma with primary bone involvement in children.
  • We describe the clinical, radiologic, and pathologic features of primary bone anaplastic large cell lymphoma (ALCL) in 3 boys.
  • Differential diagnoses included osteomyelitis and small round cell tumors of childhood, particularly Ewing sarcoma.
  • Preoperatively, ALCL was not a diagnostic consideration in any case.
  • Two cases showed classic large pleomorphic cells; 1 showed a composite pattern with a distinct small cell component and the more typical large cell type.
  • Neoplastic cells in all cases showed strong CD30 and anaplastic lymphoma kinase expression with relatively weak epithelial membrane antigen positivity.
  • Two patients were disease-free at last follow-up (15 months and 11 years); 1 patient died of disseminated disease within a year of diagnosis.
  • ALCL should be considered a diagnostic possibility when evaluating neoplastic bone lesions in children.
  • Although expression of NSE in ALCL has not been emphasized in the literature, it is worth noting because it may pose a diagnostic pitfall.
  • [MeSH-major] Bone Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / analysis

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  • (PMID = 16482992.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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61. Kapur S, Tiemann M, Menke MA, Schubert C, Parwaresch R: The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases. Indian J Med Res; 2005 Jan;121(1):46-54
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  • [Title] The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases.
  • BACKGROUND AND OBJECTIVES: Molecular events that precede transformations from lymphomatoid palulosis (LyP) to mycosis fungoides (MF) or to cutaneous anaplastic large cell lymphoma (ALCL) in the CD 30(+) cutaneous lymphoproliferative diseases (LPDs) are not known.
  • Expression of the anaplastic lymphoma kinase (ALK) gene product has also been described as an important prognostic indicator in ALCL.
  • ALK positive systemic nodal ALCL are associated with a good prognosis.
  • However, primary cutaneous ALCL that are ALK negative have a better overall survival.
  • The current study was done to see if mutated p(53) gene or ALK reactivity were poor prognostic indicators in those patients with CD 30(+) cutaneous LPD who showed progression of the disease.
  • METHODS: Mutations of the p(53) gene and expression of the ALK gene product were analysed in 36 patients (23 of LyP and 13 of CD30(+) cutaneous ALCL).
  • Transformation occurred in 5 patients (4 from LyP to ALCL and 1 from MF to ALCL) and clinical progression in 4 patients with ALCL.
  • ALK gene products were not detected in any of the biopsy specimens of LyP and primary cutaneous ALCL.
  • INTERPRETATION AND CONCLUSION: Although 9 of 36 patients with cutaneous CD30(+) LPDs had progression of their disease, neither mutations of the p(53) gene nor ALK immunoreactivity were found in any of these biopsies.

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  • (PMID = 15713979.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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62. 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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  • [Title] Analysis of gene expression profile of TPM3-ALK positive anaplastic large cell lymphoma reveals overlapping and unique patterns with that of NPM-ALK positive anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) comprises a group of non-Hodgkin lymphomas characterized by the expression of the CD30/Ki-1 antigen.
  • A subset of ALCL is characterized by chromosomal translocations involving the anaplastic lymphoma kinase (ALK) gene on chromosome 2.
  • While the most common translocation is the t(2;5)(p23;q35) involving the nucleophosmin (NPM) gene on chromosome 5, up to 12 other translocations partners of the ALK gene have been identified.
  • One of these is the t(1;2)(q25;p23) which results in the formation of the chimeric protein TPM3-ALK.
  • While several of the signaling pathways induced by NPM-ALK have been elucidated, those involved in ALCLs harboring TPM3-ALK are largely unknown.
  • In order to investigate the expression profiles of ALCLs carrying the NPM-ALK and TPM3-ALK fusions, we carried out cDNA microarray analysis of two ALCL tissue samples, one expressing the NPM-ALK fusion protein and the other the TPM3-ALK fusion protein.
  • Our results show a significant overlap of genes deregulated in the NPM-ALK and TPM-ALK positive lymphomas.
  • These deregulated genes are involved in diverse cellular functions, such as cell cycle regulation, apoptosis, proliferation, and adhesion.
  • More importantly, many genes that were not previously associated with ALK positive lymphomas were identified.
  • Our results demonstrate the overlapping and unique transcriptional patterns associated with the NPM-ALK and TPM3-ALK fusions in ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Tropomyosin / genetics

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  • (PMID = 17720243.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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63. Lü Z, Shi YK, He XH, Qin Y, Zhou SY, Zhang CG, Liu P, Yang JL: [Primary cutaneous anaplastic large cell lymphoma: clinical presentation, therapy and prognosis study of 10 cases]. Zhonghua Yi Xue Za Zhi; 2010 May 11;90(18):1247-50
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  • [Title] [Primary cutaneous anaplastic large cell lymphoma: clinical presentation, therapy and prognosis study of 10 cases].
  • OBJECTIVE: To explore the clinical presentation, therapy and prognosis study of primary cutaneous anaplastic large cell lymphoma (PCALCL).
  • Two patients had lymphadenopathy and one had bone involvement with anaplastic lymphoma kinase (ALK) positive and high cell proliferation ratio index (ki-67 > 80%).
  • [MeSH-major] Lymphoma, Primary Cutaneous Anaplastic Large Cell / diagnosis. Lymphoma, Primary Cutaneous Anaplastic Large Cell / therapy. Skin Neoplasms / diagnosis. Skin Neoplasms / therapy


64. Costello R, Sanchez C, Le Treut T, Rihet P, Imbert J, Sébahoun G: Peripheral T-cell lymphoma gene expression profiling and potential therapeutic exploitations. Br J Haematol; 2010 Jul;150(1):21-7
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  • [Title] Peripheral T-cell lymphoma gene expression profiling and potential therapeutic exploitations.
  • Peripheral T-cell lymphomas constitute a heterogeneous group with regard to diagnosis, treatment and prognosis.
  • Molecular profiling has contributed to novel insights in the biology of T-cell lymphoma.
  • Regarding anaplastic large cell lymphoma, low expression T-cell receptor signalling and high STAT3 target signatures have been associated with the ALK-positive subgroup.
  • Gene expression profiling differentiates angioblastic T-cell lymphoma from other T-cell malignancies, suggests that the normal counterpart of lymphoma cells are follicular helper T cells, and supports the involvement of vascular endothelial growth factor deregulation in its physiopathology.
  • In peripheral T-cell lymphoma unspecified, gene profiling suggests the normal counterpart of tumour cells are activated CD4(+) or CD8(+) T-lymphocytes, delineates prognostic groups depending on the proliferative signature, and suggests therapeutic options aimed at regulating nuclear factor-kappaB and platelet-derived growth factor receptor-alpha phosphorylation.
  • Gene expression profiling of primary cutaneous T cell lymphomas highlighted the importance of abnormal methylation patterns, suggested a pivotal role for JUNB/AP-1, and defined a predictive model for response to interferon-alpha.
  • In conclusion, gene expression profiling is beginning to change the pathological classification, the prognosis profiles and the therapeutic approach in T-cell lymphomas.
  • [MeSH-major] Lymphoma, T-Cell, Peripheral / genetics
  • [MeSH-minor] Gene Expression Profiling. Humans. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / therapy. Oligonucleotide Array Sequence Analysis


65. 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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66. Benner MF, Jansen PM, Meijer CJ, Willemze R: Diagnostic and prognostic evaluation of phenotypic markers TRAF1, MUM1, BCL2 and CD15 in cutaneous CD30-positive lymphoproliferative disorders. Br J Dermatol; 2009 Jul;161(1):121-7
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  • [Title] Diagnostic and prognostic evaluation of phenotypic markers TRAF1, MUM1, BCL2 and CD15 in cutaneous CD30-positive lymphoproliferative disorders.
  • BACKGROUND: CD30 is expressed in various types of cutaneous lymphomas, including lymphomatoid papulosis (LyP), primary cutaneous anaplastic large cell lymphoma (C-ALCL), some cases of mycosis fungoides showing large cell transformation (MF-TR) and skin localizations of systemic anaplastic lymphoma kinase (ALK)-positive or ALK-negative ALCL.
  • OBJECTIVE: To evaluate the diagnostic and prognostic significance of these markers in a large group of cutaneous CD30-positive lymphoproliferations.
  • METHODS: An immunohistochemical study on the expression of TRAF1, MUM1, BCL2 and CD15 was performed on skin biopsies from 28 patients with C-ALCL, 39 patients with LyP, 11 patients with CD30-positive MF-TR, two with ALK-positive ALCL and six with ALK-negative ALCL.
  • RESULTS: TRAF1 was expressed in roughly 70-80% and MUM1 was expressed in 70-100% of all the groups of cutaneous CD30-positive lymphoproliferations.
  • Highest levels of BCL2 were expressed in MF-TR (73%), in contrast to 21% in C-ALCL and 36% in LyP.
  • Highest levels of CD15 were expressed in C-ALCL (43%), compared with 18% in LyP and 9% in MF-TR.
  • CONCLUSIONS: The results of the present study suggest that TRAF1, MUM1, BCL2 and CD15 cannot be considered as useful diagnostic or prognostic marker in cutaneous CD30-positive lymphoproliferations.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoproliferative Disorders / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD15 / analysis. Antigens, CD30 / analysis. Biopsy. Child. Female. Humans. Immunohistochemistry / methods. Interferon Regulatory Factors / analysis. Lymphoma, Primary Cutaneous Anaplastic Large Cell / chemistry. Lymphoma, Primary Cutaneous Anaplastic Large Cell / diagnosis. Lymphoma, Primary Cutaneous Anaplastic Large Cell / immunology. Lymphomatoid Papulosis / diagnosis. Lymphomatoid Papulosis / immunology. Lymphomatoid Papulosis / metabolism. Male. Middle Aged. Mycosis Fungoides / chemistry. Mycosis Fungoides / immunology. Mycosis Fungoides / pathology. Proto-Oncogene Proteins c-bcl-2 / analysis. TNF Receptor-Associated Factor 1 / analysis. Young Adult

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  • (PMID = 19416236.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD15; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TNF Receptor-Associated Factor 1; 0 / interferon regulatory factor-4
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67. Pant V, Jambhekar NA, Madur B, Shet TM, Agarwal M, Puri A, Gujral S, Banavali M, Arora B: Anaplastic large cell lymphoma (ALCL) presenting as primary bone and soft tissue sarcoma--a study of 12 cases. Indian J Pathol Microbiol; 2007 Apr;50(2):303-7
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  • [Title] Anaplastic large cell lymphoma (ALCL) presenting as primary bone and soft tissue sarcoma--a study of 12 cases.
  • This study highlights the rare presentation of anaplastic large cell lymphoma as primary bone and soft tissue tumour.
  • Clinical impression was non Hodgkin's lymphoma in 4 cases, sarcoma in 6 (osteosarcoma-2, Ewing's/primitive neuroectodermal tumour-1, and sarcoma NOS-3), and tuberculosis of thoracic spine in 1 and the last case involving the rib had a differential diagnosis of tuberculosis and NHL.
  • Immunohistochemically all tumours were CD30 positive and 8 of 9 cases (88.9%) showed ALK-1 positivity.
  • This alone will lead to an accurate recognition of ALCL and the appropriate chemotherapy.
  • [MeSH-major] Bone Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Sarcoma / pathology. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Activin Receptors, Type II / metabolism. Adolescent. Adult. Antigens, CD30 / metabolism. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male


68. 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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  • [Title] [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature].
  • We report a 10-year-old girl with ATIC-anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • Pathological findings showed that staining of ALK was restricted to the cytoplasm of ALCL cells.
  • ATIC-ALK chimeric transcripts were detected by reverse transcriptase polymerase chain reaction.
  • The patient was assigned to the standard risk group proposed by the international multicenter study for pediatric ALCL, ALCL99.
  • To date, 7 genes have been identified as a fusion partner of ALK, with the highest frequency in nucleophosmin (NPM).
  • Little is known about the clinical implications of subtypes of ALCL harboring each of the 7 fusion genes, especially those of variant fusion genes other than NPM-ALK.
  • In this paper, we review 9 patients with ATIC-ALK-positive ALCL in the literature in addition to discussing our patient.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Oncogene Proteins, Fusion / analysis

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  • (PMID = 18572809.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 18
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69. 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


70. 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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71. 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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72. Rust R, Blokzijl T, Harms G, Lim M, Visser L, Kamps WA, Poppema S, van den Berg A: TIMP-1 expression in anaplastic large cell lymphoma is usually restricted to macrophages and only seldom observed in tumour cells. J Pathol; 2005 Aug;206(4):445-50
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  • [Title] TIMP-1 expression in anaplastic large cell lymphoma is usually restricted to macrophages and only seldom observed in tumour cells.
  • Anaplastic large cell lymphomas (ALCLs) can be subdivided into two subgroups on the basis of their expression of the ALK protein.
  • ALK protein expression leads to activation of signal transducer and activator of transcription (STAT) 3, which is more commonly expressed in ALK-positive than in ALK-negative tumours.
  • In this study, we analysed TIMP-1 expression in five ALCL cell lines and 11 tumours by quantitative RT-PCR and immunohistochemistry.
  • We identified high-level TIMP-1 expression by RT-PCR in three ALK-positive ALCL-derived cell lines and in all ALK-positive ALCLs, whereas ALK-negative ALCLs generally demonstrated a lower level of TIMP-1 expression.
  • Concordant with these results, we observed TIMP-1 immunostaining in all ALK-positive ALCLs and in only two of six ALK-negative ALCLs.
  • No relationship was observed between the levels of ALK and TIMP-1 expression in the ALK-positive tumours.
  • STAT3 expression levels were similar in all ALCL samples.
  • Double staining with either CD30 or CD68 demonstrated that TIMP-1 expression was restricted to macrophages in the majority of TIMP-1-positive tumours.
  • Expression of the TIMP-1 substrate MMP-2 was more prominent in ALK-negative tumours, while MMP-9 levels were low in all cases.
  • Expression levels of IL-6 and TGF-beta1, which are cytokines known to induce TIMP-1, were higher in ALK-negative ALCLs and moderate in ALK-positive tumours.
  • No clear relationship was observed between IL-10 expression and ALK positivity.
  • Lack of TIMP-1 expression in the tumour cells of ALK-positive ALCLs argues against a direct role for ALK-induced activation of STAT3 in the regulation of TIMP-1 expression in ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / chemistry. Macrophages / chemistry. Tissue Inhibitor of Metalloproteinase-1 / analysis
  • [MeSH-minor] Antigens, CD / analysis. Cell Line, Tumor. Cytokines / analysis. DNA-Binding Proteins / analysis. Gene Expression Regulation, Neoplastic / genetics. Humans. Immunohistochemistry / methods. Matrix Metalloproteinases / analysis. Neoplasm Proteins / analysis. Protein-Tyrosine Kinases / analysis. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction / methods. STAT3 Transcription Factor. Trans-Activators / analysis

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  • [Copyright] Copyright 2005 Pathological Society of Great Britain and Ireland
  • (PMID = 15920698.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-1; 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; EC 3.4.24.- / Matrix Metalloproteinases
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73. Piva R, Pellegrino E, Mattioli M, Agnelli L, Lombardi L, Boccalatte F, Costa G, Ruggeri BA, Cheng M, Chiarle R, Palestro G, Neri A, Inghirami G: Functional validation of the anaplastic lymphoma kinase signature identifies CEBPB and BCL2A1 as critical target genes. J Clin Invest; 2006 Dec;116(12):3171-82
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  • [Title] Functional validation of the anaplastic lymphoma kinase signature identifies CEBPB and BCL2A1 as critical target genes.
  • Anaplastic large cell lymphomas (ALCLs) represent a subset of lymphomas in which the anaplastic lymphoma kinase (ALK) gene is frequently fused to the nucleophosmin (NPM) gene.
  • We previously demonstrated that the constitutive phosphorylation of ALK chimeric proteins is sufficient to induce cellular transformation in vitro and in vivo and that ALK activity is strictly required for the survival of ALK-positive ALCL cells.
  • To elucidate the signaling pathways required for ALK-mediated transformation and tumor maintenance, we analyzed the transcriptomes of multiple ALK-positive ALCL cell lines, abrogating their ALK-mediated signaling by inducible ALK RNA interference (RNAi) or with potent and cell-permeable ALK inhibitors.
  • Transcripts derived from the gene expression profiling (GEP) analysis uncovered a reproducible signature, which included a novel group of ALK-regulated genes.
  • Functional RNAi screening on a set of these ALK transcriptional targets revealed that the transcription factor C/EBPbeta and the antiapoptotic protein BCL2A1 are absolutely necessary to induce cell transformation and/or to sustain the growth and survival of ALK-positive ALCL cells.

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  • (PMID = 17111047.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [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 / BCL2-related protein A1; 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / STAT3 Transcription Factor; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC1636692
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74. Kisacik B, Akdogan A, Maras Y, Kalyoncu U, Karadag O, Kilickap S, Calguneri M: Anaplastic large cell lymphoma presenting with symmetric polyarthritis in pregnancy. Rheumatol Int; 2008 Jul;28(9):909-11
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  • [Title] Anaplastic large cell lymphoma presenting with symmetric polyarthritis in pregnancy.
  • Anaplastic large-cell lymphoma (ALCL) is a rare T-cell lymphoma and typically is seen in children and young adults.
  • Primary bone infiltration of ALCL is exceedingly rare.
  • Herein we report ALCL of bone in a pregnant admitted with symmetric polyarthritis.
  • Excisional biopsy from the destructive mass showed anaplastic large cell lymphoma (CD 30 was positive and ALK negative).
  • [MeSH-major] Arthritis / etiology. Bone Neoplasms / complications. Lymphoma, Large-Cell, Anaplastic / complications. Pregnancy Complications, Neoplastic


75. 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.
  • We present the histopathologic, molecular, and cytogenetic findings of this patient's initial presentation with systemic ALCL as well as his secondary presentation with CML 4 years later.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Neoplasms, Second Primary / pathology. Protein-Tyrosine Kinases / metabolism


76. Wu L, Wang Y, Fu SL, Huang L, Tongji FC, Qi JY: Anaplastic large cell lymphoma with primary involvement of skeletal muscle: a rare case report and review of the literature. Pediatr Hematol Oncol; 2009 Apr-May;26(3):142-9
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  • [Title] Anaplastic large cell lymphoma with primary involvement of skeletal muscle: a rare case report and review of the literature.
  • Primary skeletal muscle ALCL is very rare.
  • Here the authors report a case of skeletal muscle ALCL that was proven pathologically.
  • Histopathological examination revealed a diffuse infiltration of large and atypical cells with pleomorphic nuclei and abundant cytoplasm.
  • Immunohistological staining showed these atypical cells were positive for CD30 (Ki-l), anaplastic lymphoma kinase (ALK), epithelial membrane antigen (EMA), CD3, CD45RO, and CD68.
  • The morphology and immunophenotype were consistent with CD30-positive, ALK-positive, and ALCL of T-cell lineage.
  • The patient's condition was diagnosed as CD30-positive primary skeletal muscle ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / diagnosis. Muscle Neoplasms / diagnosis


77. Weinberg OK, Seo K, Arber DA: Prevalence of bone marrow involvement in systemic anaplastic large cell lymphoma: are immunohistochemical studies necessary? Hum Pathol; 2008 Sep;39(9):1331-40
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  • [Title] Prevalence of bone marrow involvement in systemic anaplastic large cell lymphoma: are immunohistochemical studies necessary?
  • The frequency of bone marrow involvement in anaplastic large cell lymphoma has been reported with great variation.
  • A prior study found that anaplastic large cell lymphoma involvement of bone marrow was often not evident on routine stains and advocated using immunohistochemical studies.
  • We evaluated 70 bone marrow biopsies from 41 patients with anaplastic large cell lymphoma and found 10 morphologically involved cases (14% of all biopsies, 22% of all patients).
  • In most cases (9/10 biopsies), the involvement of the bone marrow by anaplastic large cell lymphoma was massive and, thus, was evident on the hematoxylin and eosin section.
  • To determine if the hematoxylin and eosin evaluation missed bone marrow involvement, we used a panel of antibodies including CD30, ALK-1, epithelial membrane antigen, and granzyme.
  • Only the 10 morphologically involved cases showed anaplastic large cell lymphoma cells with distinct CD30 expression.
  • Other stains highlighted only a subset of the CD30-positive cases.
  • Overall, marrow involvement in anaplastic large cell lymphoma was relatively uncommon, and when present, it was identified on hematoxylin and eosin sections.
  • [MeSH-major] Bone Marrow / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 18602674.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [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; TDQ283MPCW / Eosine Yellowish-(YS); YKM8PY2Z55 / Hematoxylin
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78. Osoegawa A, Nosaki K, Miyamoto H, Kometani T, Hirai F, Ondo K, Seto T, Sugio K, Choi YL, Soda M, Mano H, Ichinose Y: Incidentally proven pulmonary "ALKoma". Intern Med; 2010;49(6):603-6
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  • [Title] Incidentally proven pulmonary "ALKoma".
  • Genetic alterations of echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) inversion were recently found in lung cancer.
  • Biopsy from her supraclavicular lymph nodes was performed to differentiate the diagnosis between lymphoma and lung cancer.
  • On the other hand, the commercially available chromosomal fluorescent in situ hybridization (FISH) analysis showed split signals of ALK, which was confirmed to be the EML4-ALK inversion.
  • The commercial-based ALK FISH is useful for screening pulmonary ALKoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / genetics. Cell Cycle Proteins / genetics. Chromosome Inversion / genetics. Lung Neoplasms / diagnosis. Lung Neoplasms / genetics. Microtubule-Associated Proteins / genetics. Protein-Tyrosine Kinases / genetics. Serine Endopeptidases / genetics
  • [MeSH-minor] Adult. Biopsy. Diagnosis, Differential. Female. Humans. In Situ Hybridization, Fluorescence. Lymph Nodes / pathology. Lymphoma / diagnosis. Lymphoma / pathology. Receptor Protein-Tyrosine Kinases

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  • (PMID = 20228600.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Microtubule-Associated Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases
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79. Yamamoto H, Kohashi K, Oda Y, Tamiya S, Takahashi Y, Kinoshita Y, Ishizawa S, Kubota M, Tsuneyoshi M: Absence of human herpesvirus-8 and Epstein-Barr virus in inflammatory myofibroblastic tumor with anaplastic large cell lymphoma kinase fusion gene. Pathol Int; 2006 Oct;56(10):584-90
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  • [Title] Absence of human herpesvirus-8 and Epstein-Barr virus in inflammatory myofibroblastic tumor with anaplastic large cell lymphoma kinase fusion gene.
  • Some populations of IMT have anaplastic large cell lymphoma kinase (ALK) gene rearrangements.
  • Infection with Epstein-Barr virus (EBV) and human herpesvirus-8 (HHV-8) in tumor cells of IMT has been reported; these reports, however, have been limited to ALK-negative IMT.
  • Immunohistochemically, 15 cases were ALK positive and six were negative.
  • Of eight cases analyzed using reverse transcription-polymerase chain reaction, tropomyosin 3 (TPM3)-ALK, TPM4-ALK and clathrin heavy chain-ALK fusion genes were detected in one, two and two cases, respectively.
  • All 21 IMT, irrespective of ALK expression, were negative for EBV by in situ hybridization for EBV-encoded RNA and immunohistochemical stain for latent membrane antigen-1.
  • These results suggest that IMT may be a heterogeneous group in terms of pathogenesis, and EBV and HHV-8 do not play a major role in the pathogenesis of ALK-positive tumor.

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  • (PMID = 16984614.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / TPM4 protein, human; 0 / Tropomyosin; 0 / latency-associated nuclear antigen; 114899-12-6 / Clathrin Heavy 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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80. Proca DM, De Renne L, Marsh WL Jr, Keyhani-Rofagha S: Anaplastic large cell lymphoma in a human immunodeficiency virus-positive patient with cytologic findings in bladder wash: a case report. Acta Cytol; 2008 Jan-Feb;52(1):83-6
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  • [Title] Anaplastic large cell lymphoma in a human immunodeficiency virus-positive patient with cytologic findings in bladder wash: a case report.
  • BACKGROUND: Anaplastic large cell lymphoma (ALCL) (Ki-1/CD-30 positive) is an uncommon lymphoproliferative disorder that may be of T cell or null cell type.
  • ALCL has been reported in fine needle aspirations of lymph nodes and pleural or peritoneal fluid cytology.
  • In human immunodeficiency virus (HIV)-positive patients, ALCL appears to be more common and run a more aggressive course.
  • Bladder wash cytology and subsequent biopsy of the mass were diagnostic of ALCL.
  • The ALCL was CD30+ and null cell type, with negative CD2, CD3, CD4, CD5, CD7, CD8, CD20, CD45, CD79a, ALK-1, granzyme B, cytokeratin (AE1/AE3), placental alkaline phosphatase (PLAP) and S-100.
  • The patient expired 9 months after the diagnosis, despite aggressive therapy.
  • CONCLUSION: This is a rare occurrence of ALCL (CD 30 positive, null cell type) in the urinary bladder in an HIV+ patient.
  • Presumptive diagnosis was made by bladder wash cytology and subsequently confirmed by biopsy.
  • In HIV+/immunosuppressed patients with urinary symptoms and an obstructive mass, ALCL should be considered in the differential diagnosis.
  • [MeSH-major] HIV Infections / complications. Lymphoma, Large-Cell, Anaplastic / diagnosis. Urinary Bladder / pathology


81. Droc C, Cualing HD, Kadin ME: Need for an improved molecular/genetic classification for CD30+ lymphomas involving the skin. Cancer Control; 2007 Apr;14(2):124-32
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  • BACKGROUND: The spectrum of diseases that constitute the CD30+ lymphomas, with lymphomatoid papulosis (LyP) at one end, and anaplastic large-cell lymphoma (ALCL) at the other end, shows variable morphology, immunophenotype, and clinical behavior.
  • METHODS: We reviewed the clinical and research literature and guided by our experiences attempted to discern molecular and phenotypic criteria to improve the classification and identify molecular targets for therapy of CD30-positive cutaneous lymphomas.
  • RESULTS: Functional studies of ALCL cell lines clonally derived from LyP have revealed loss of growth inhibition by transforming growth factor beta (TGF-beta), due to TGF-beta receptor mutations.
  • Studies of genetic variants of the CD30 promoter showed distinct microsatellite alleles associated with development of LyP and lymphoma progression.
  • Studies of LyP and cutaneous ALCL tissues and cell lines suggest a dual role for CD30/CD30 ligand interactions in regression of LyP and progression to lymphoma.
  • CD30 signaling activates NF-kappaB in cell lines derived from cutaneous ALCL but not anaplastic lymphoma kinase (ALK)-positive systemic ALCL in which growth arrest occurs through cell cycle inhibitor p21WAF1/Cip1.
  • Other likely biomarkers of disease progression include differential expression of Bcl-2, fascin, cutaneous lymphocyte antigen, and T-cell receptor clonality.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Skin Neoplasms / pathology

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  • (PMID = 17387297.001).
  • [ISSN] 1073-2748
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Grant] United States / PHS HHS / / P50 96343
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 85
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82. Schmitz N, Trümper L, Ziepert M, Nickelsen M, Ho AD, Metzner B, Peter N, Loeffler M, Rosenwald A, Pfreundschuh M: Treatment and prognosis of mature T-cell and NK-cell lymphoma: an analysis of patients with T-cell lymphoma treated in studies of the German High-Grade Non-Hodgkin Lymphoma Study Group. Blood; 2010 Nov 4;116(18):3418-25
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  • [Title] Treatment and prognosis of mature T-cell and NK-cell lymphoma: an analysis of patients with T-cell lymphoma treated in studies of the German High-Grade Non-Hodgkin Lymphoma Study Group.
  • To evaluate outcome and prognosis of patients with T-cell lymphoma we analyzed 343 patients treated within trials of the German High-Grade Non-Hodgkin Lymphoma Study Group (DSHNHL).
  • Two hundred eighty-nine patients belonged to 1 of the 4 major T-cell lymphoma subtypes: anaplastic large cell lymphoma (ALCL), anaplastic large cell lymphoma kinase (ALK)-positive (n = 78); ALCL, ALK-negative (n = 113); peripheral T-cell lymphoma, unspecified (PTCLU; n = 70); and angioimmunoblastic T-cell lymphoma (AITL; n = 28).
  • Three-year event-free survival (EFS) and overall survival were 75.8% and 89.8% (ALK-positive ALCL), 50.0% and 67.5% (AITL), 45.7% and 62.1% (ALK-negative ALCL), and 41.1% and 53.9% (PTCLU), respectively.
  • Patients with ALK-negative ALCL, PTCLU, or AITL presenting with IPI > 1 have a poor prognosis and should be considered candidates for novel treatment strategies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Cohort Studies. Cyclophosphamide / administration & dosage. Cyclophosphamide / therapeutic use. Doxorubicin / administration & dosage. Doxorubicin / therapeutic use. Female. Humans. Killer Cells, Natural / pathology. Lymphoma, Extranodal NK-T-Cell / diagnosis. Lymphoma, Extranodal NK-T-Cell / drug therapy. Lymphoma, Extranodal NK-T-Cell / pathology. Male. Middle Aged. Prednisone / administration & dosage. Prednisone / therapeutic use. Prognosis. Treatment Outcome. Vincristine / administration & dosage. Vincristine / therapeutic use. Young Adult


83. 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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84. 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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85. 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


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

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  • (PMID = 17071493.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.5.4.4 / Adenosine Deaminase
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87. Allory Y, Merabet Z, Copie-Bergman C, Lange F, Yiou R, Gaulard P: Sarcomatoid variant of anaplastic large cell lymphoma mimics ALK-1-positive inflammatory myofibroblastic tumor in bladder. Am J Surg Pathol; 2005 Jun;29(6):838-9; author reply 839
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  • [Title] Sarcomatoid variant of anaplastic large cell lymphoma mimics ALK-1-positive inflammatory myofibroblastic tumor in bladder.
  • [MeSH-major] Activin Receptors, Type I / immunology. Biomarkers, Tumor / immunology. Lung Neoplasms / immunology. Lymphoma, Large B-Cell, Diffuse / immunology. Urinary Bladder Neoplasms / immunology


88. Hosoi M, Ichikawa M, Imai Y, Kurokawa M: A case of anaplastic large cell lymphoma, ALK positive, primary presented in the skin and relapsed with systemic involvement and leukocytosis after years of follow-up period. Int J Hematol; 2010 Nov;92(4):667-8
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  • [Title] A case of anaplastic large cell lymphoma, ALK positive, primary presented in the skin and relapsed with systemic involvement and leukocytosis after years of follow-up period.
  • [MeSH-major] Leukocytosis. Lymphoma, Large-Cell, Anaplastic. Lymphoma, Primary Cutaneous Anaplastic Large Cell. Neoplasm Recurrence, Local. Protein-Tyrosine Kinases / metabolism. Skin Neoplasms

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  • (PMID = 20976631.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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89. Fernandez-Vidal A, Mazars A, Gautier EF, Prévost G, Payrastre B, Manenti S: Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation. Cell Cycle; 2009 May 1;8(9):1373-9
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  • [Title] Upregulation of the CDC25A phosphatase down-stream of the NPM/ALK oncogene participates to anaplastic large cell lymphoma enhanced proliferation.
  • Here, we demonstrate that the expression of the dual specificity phosphatase CDC25A, a key regulator of cell cycle progression, is deregulated in Ba/F3 cells expressing the oncogenic protein NPM/ALK and in human cell lines derived from NPM/ALK-positive anaplastic large cell lymphomas (ALCL).
  • Importantly, pharmacological inhibition of CDC25 dramatically inhibits the proliferation of NPM/ALK-expressing cells, while moderately affecting the proliferation of control Ba/F3 cells.
  • RNA interference-mediated downregulation of CDC25A confirmed that NPM/ALK-expressing cells are highly dependent on this protein for their proliferation.
  • Altogether, our data point to the functional link between hematopoietic oncogenic tyrosine kinases and the G(1) cell cycle regulator CDC25A, and we propose that this protein may be a potential therapeutic target in ALCL and other hematological malignancies.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / pathology. Oncogenes. Protein-Tyrosine Kinases / metabolism. Up-Regulation. cdc25 Phosphatases / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. Oncogene Proteins, Fusion / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction

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  • (PMID = 19305144.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.16 / Cdc25a protein, mouse; EC 3.1.3.48 / CDC25A protein, human; EC 3.1.3.48 / cdc25 Phosphatases
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90. Krishnan C, Moline S, Anders K, Warnke RA: Intravascular ALK-positive anaplastic large-cell lymphoma mimicking inflammatory breast carcinoma. J Clin Oncol; 2009 May 20;27(15):2563-5
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  • [Title] Intravascular ALK-positive anaplastic large-cell lymphoma mimicking inflammatory breast carcinoma.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adult. Antigens, CD30 / biosynthesis. Biomarkers, Tumor / metabolism. Cellulitis / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Inflammation / pathology. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19364961.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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91. Das P, Iyer VK, Mathur SR, Ray R: Anaplastic large cell lymphoma: a critical evaluation of cytomorphological features in seven cases. Cytopathology; 2010 Aug;21(4):251-8
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  • [Title] Anaplastic large cell lymphoma: a critical evaluation of cytomorphological features in seven cases.
  • OBJECTIVE: Anaplastic large cell lymphoma (ALCL) is a rare subtype of non-Hodgkin's lymphoma that is difficult to diagnose on fine needle aspiration cytology (FNAC).
  • Detailed descriptions about the cytomorphological features of ALCL are few and do not illustrate the various categories of cells, which we have done in this study.
  • METHODS: Eight FNAC specimens from seven patients with biopsy-proven ALCL over a period of 6 years were reviewed.
  • Cytomorphological details were analysed and the various cell types identified were enumerated on Papanicolaou and May-Grünwald-Giemsa (MGG)-stained smears.
  • RESULTS: Of the seven cases, five were of conventional type, one of the lymphohistiocytic variant and one of the small cell variant.
  • Aspiration from the lymphohistiocytic and small cell variants showed a small number of similar characteristic giant cells.
  • All cases were confirmed as ALK-1 positive.
  • CONCLUSIONS: The morphological spectrum of ALCL is wide and it may be misdiagnosed as a metastatic poorly differentiated malignant tumour on FNAC.
  • Identification of unusual giant cells on FNAC helps in establishing a diagnosis on an early lymph node biopsy.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 19744187.001).
  • [ISSN] 1365-2303
  • [Journal-full-title] Cytopathology : official journal of the British Society for Clinical Cytology
  • [ISO-abbreviation] Cytopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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92. Wang FH, Li YH, Zeng J, Rao HL, Xia ZJ, Sun XF, Huang HQ, Lin TY, Jiang WQ, Guan ZZ: Clinical analysis of primary systemic anaplastic large cell lymphoma: a report of 57 cases. Ai Zheng; 2009 Jan;28(1):49-53
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  • [Title] Clinical analysis of primary systemic anaplastic large cell lymphoma: a report of 57 cases.
  • BACKGROUND AND OBJECTIVE: The clinical characteristics and prognosis of primary systemic anaplastic large cell lymphoma (ALCL) are various according to different reports.
  • Anaplastic lymphoma kinase (ALK), a specific marker of primary systemic ALCL, is related with its clinical characteristics and prognosis.
  • This study was to investigate the clinical characteristics and prognosis of primary systemic ALCL, and to explore the expression and clinical significance of ALK.
  • METHODS: Clinical data of 57 primary systemic ALCL patients, treated in Cancer Center of Sun Yat-sen University from January 1997 to January 2006, were reviewed.
  • The expression of ALK in 46 tumor specimens was detected by SP immunohisochemistry.
  • Of the 57 patients, 33 (57.9%) had B symptoms, 23 (40.4%) had Ann Arbor stage III-IV tumors, and 23 (40.4%) had extranodal disease at diagnosis.
  • The positive rate of ALK was 63.0% in the 46 cases detected.
  • Compared with ALK-negative patients, ALK-positive patients were younger (p = 0.001) and had higher expected 5-year survival rate (p < 0.01).
  • Multivariate analysis confirmed the independent prognostic values of ALK expression, primary disease site and lactate dehydrogenase (LDH) level.
  • CONCLUSIONS: Primary systemic ALCL usually occurs in young patients, with good response to chemotherapy and good prognosis.
  • No ALK expression, high-intermediate/high IPI, extranodal disease and elevated LDH level are correlated to unfavorable prognosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / drug therapy. Protein-Tyrosine Kinases / analysis

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  • (PMID = 19448428.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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93. Shi Y, Chen G, Zhou XG, Gong LP, Yu R, Zheng YY, Xie JL, Jin Y: [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study]. Zhonghua Bing Li Xue Za Zhi; 2010 Apr;39(4):235-9
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  • [Title] [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study].
  • OBJECTIVE: To study the clinicopathologic features of 66 cases of primary systemic anaplastic large cell lymphoma (ALCL), with emphasis on the differences between ALK-positive and ALK-negative cases.
  • METHODS: The clinical data of 66 cases of ALCL was analyzed.
  • Immunohistochemical study for CD30, ALK protein, epithelial membrane antigen, CD2, CD3, granzyme B and TIA-1 was carried out.
  • The differences between ALK-positive and ALK-negative cases were statistically analyzed.
  • RESULTS: There were 48 cases of ALK-positive ALCL and 18 cases of ALK-negative ALCL.
  • The patients with ALK-positive ALCL were younger than those with ALK-negative ALCL (P < 0.05), with the median age being 18 years and 36 years, respectively.
  • Fever, especially hyperpyrexia, was more commonly observed in ALK-positive ALCL patients than in ALK-negative ALCL patients (33 cases versus 4 cases, P < 0.05).
  • The overall survival rate and median duration of survival in patients with ALK-positive ALCL were higher and longer than those in patients with ALK-negative ALCL (80% versus 71%; 21 months versus 12.5 months, P > 0.05).
  • There were however no significant differences in histology between ALK-positive ALCL and ALK-negative ALCL.
  • "Hallmark" cells were seen in most of the ALCL cases.
  • Most ALK-positive cases belonged to the common variant (35 cases).
  • Small cell variant and sarcomatoid subtype were found only in few cases (3 cases and 2 cases, respectively).On the other hand, common variant (17 cases) constituted the majority of ALK-negative ALCL.
  • Immunohistochemical study showed that ALK-positive ALCL always expressed CD30 and epithelial membrane antigen.
  • ALK-positive ALCL more often expressed epithelial membrane antigen (100% versus 72%; P < 0.05) but less so for T-cell markers (including CD2, CD3, CD43 and CD45RO).
  • Cytotoxic molecules were more commonly expressed in ALK-positive ALCL (P > 0.05).
  • FISH showed that in ALK-positive ALCL, 1 case had normal ALK gene, 1 had deletion and multicopy and 2 had deletion.
  • On the other hand, 1 case of ALK-negative ALCL had normal ALK gene.
  • CONCLUSIONS: While there are no significant morphologic differences between ALK-positive ALCL and ALK-negative ALCL, the clinical features, immunophenotypes and genetic features of both groups vary.
  • These differences are helpful in guiding the differential diagnosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antigens, CD30 / metabolism. Child. Child, Preschool. Diagnosis, Differential. Female. Follow-Up Studies. Gene Deletion. Humans. Male. Malignant Hyperthermia / etiology. Middle Aged. Mucin-1 / metabolism. Neoplasm Recurrence, Local. Receptor Protein-Tyrosine Kinases. Survival Rate. Young Adult

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  • (PMID = 20654121.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Mucin-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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94. Quintanilla-Martinez L, Pittaluga S, Miething C, Klier M, Rudelius M, Davies-Hill T, Anastasov N, Martinez A, Vivero A, Duyster J, Jaffe ES, Fend F, Raffeld M: NPM-ALK-dependent expression of the transcription factor CCAAT/enhancer binding protein beta in ALK-positive anaplastic large cell lymphoma. Blood; 2006 Sep 15;108(6):2029-36
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  • [Title] NPM-ALK-dependent expression of the transcription factor CCAAT/enhancer binding protein beta in ALK-positive anaplastic large cell lymphoma.
  • Although C/EBPbeta has important functions in B- and T-cell differentiation, its expression has not been well studied in lymphoid tissues.
  • We, therefore, analyzed its expression by immunohistochemistry and Western blot in normal lymphoid tissues and in 248 well-characterized lymphomas and lymphoma cell lines.
  • Nonneoplastic lymphoid tissues and most B-cell, T-cell, and Hodgkin lymphomas lacked detectable levels of C/EBPbeta.
  • In contrast, most (40 of 45; 88%) cases of ALK-positive anaplastic large cell lymphoma (ALCL) strongly expressed C/EBPbeta.
  • Western blot analysis confirmed C/EBPbeta expression in the ALK-positive ALCLs and demonstrated elevated levels of the LIP isoform, which has been associated with increased proliferation and aggressiveness in carcinomas.
  • Transfection of Ba/F3 and 32D cells with NPM-ALK and a kinase-inhibitable modified NPM-ALK resulted in the induction of C/EBPbeta and demonstrated dependence on NPM-ALK kinase activity.
  • In conclusion, we report the constitutive expression of C/EBPbeta in ALK-positive ALCL and show its relationship to NPM-ALK.
  • We suggest that C/EBPbeta is likely to play an important role in the pathogenesis and unique phenotype of this lymphoma.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / genetics. CCAAT-Enhancer-Binding Protein-beta / metabolism. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Cell Line, Tumor. Gene Expression. Humans. Immunohistochemistry. Lymphoid Tissue / metabolism. Receptor Protein-Tyrosine Kinases. Transfection

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  • (PMID = 16709933.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-beta; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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95. Asano N, Suzuki R, Matsuo K, Kagami Y, Ishida F, Tamaru JI, Jin GS, Sato Y, Shimoyama Y, Yoshino T, Morishima Y, Nakamura S: Cytotoxic molecule expression is predictive of prognosis in Hodgkin's-like anaplastic large cell lymphoma. Histopathology; 2007 May;50(6):705-15
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  • [Title] Cytotoxic molecule expression is predictive of prognosis in Hodgkin's-like anaplastic large cell lymphoma.
  • AIMS: The Revised European American Lymphoma classification uses the term Hodgkin's-like anaplastic large cell lymphoma (HD-like ALCL) for borderline cases with features of both anaplastic large cell lymphoma (ALCL) and classical Hodgkin's lymphoma (HL).
  • The aim of this study was to clarify the association between cytotoxic molecule (CM) expression and clinical outcome in HD-like ALCL.
  • METHODS AND RESULTS: Subjects were 59 patients with HD-like ALCL, defined by nodal presentation without mediastinal bulky lesions, T- or null-cell phenotype, CD30+ anaplastic lymphoma kinase (ALK)- phenotype and by confluent sheets or nodules of large cells mimicking classic Hodgkin and Reed-Sternberg cells.
  • We evaluated the presenting features and prognosis of subjects on categorization into two defined groups, namely CM (TIA1 and/or granzyme B)-positive (n = 21) and CM-negative (n = 38).
  • Multivariate analysis confirmed that CM expression was an independent prognostic factor, in contrast to phenotypic categorization (T-cell vs. null-cell group), which had no prognostic impact on disease-specific survival.
  • CONCLUSION: CM expression is predictive of prognosis in HD-like ALCL.
  • [MeSH-major] Granzymes / metabolism. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / metabolism. Poly(A)-Binding Proteins / metabolism

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  • [ErratumIn] Histopathology. 2007 Jun;50(7):962
  • (PMID = 17493234.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Poly(A)-Binding Proteins; 0 / TIA1 protein, human; EC 3.4.21.- / Granzymes
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96. Savage KJ: Aggressive peripheral T-cell lymphomas (specified and unspecified types). Hematology Am Soc Hematol Educ Program; 2005;:267-77
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  • [Title] Aggressive peripheral T-cell lymphomas (specified and unspecified types).
  • Peripheral T-cell lymphomas (PTCLs) are a biologically diverse and uncommon group of diseases.
  • Compared to their B-cell counterparts, PTCLs remain largely unexplored and the optimal treatment ill-defined due to disease rarity and biological heterogeneity.
  • For the majority of PTCL subtypes, prognosis is poor with a 5-year overall survival of approximately 30% in most series.The notable exception is ALK-positive anaplastic large-cell lymphoma (ALK-pos ALCL), which has a superior outcome.

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  • [ErratumIn] Hematology Am Soc Hematol Educ Program. 2006;()
  • (PMID = 16304391.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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97. 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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98. Iqbal J, Weisenburger DD, Greiner TC, Vose JM, McKeithan T, Kucuk C, Geng H, Deffenbacher K, Smith L, Dybkaer K, Nakamura S, Seto M, Delabie J, Berger F, Loong F, Au WY, Ko YH, Sng I, Armitage JO, Chan WC, International Peripheral T-Cell Lymphoma Project: Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma. Blood; 2010 Feb 4;115(5):1026-36
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  • [Title] Molecular signatures to improve diagnosis in peripheral T-cell lymphoma and prognostication in angioimmunoblastic T-cell lymphoma.
  • Peripheral T-cell lymphoma (PTCL) is often challenging to diagnose and classify.
  • Gene expression profiling was performed on 144 cases of PTCL and natural killer cell lymphoma and robust molecular classifiers were constructed for angioimmunoblastic T-cell lymphoma (AITL), anaplastic lymphoma kinase-positive (ALK(+)) anaplastic large-cell lymphoma (ALCL), and adult T-cell leukemia/lymphoma.
  • Many of the pathologic features and substantial components of the molecular signature of AITL are contributed by the follicular dendritic cells, B-cell, and other stromal components.
  • The expression of Th17-associated molecules in ALK(+) ALCL was noted and may represent aberrant activation of Th17-cell differentiation by abnormal cytokine secretion.
  • Adult T-cell leukemia/lymphoma has a homogeneous molecular signature demonstrating high expression of human T-lymphotropic virus type 1-induced genes.