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41. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma 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.
  • Histologically, the tumor cells exhibited plasmablastic morphology with expression of Bob-1, CD4, CD10, CD45, CD56, CD138, EMA, MUM1, Oct-2, and kappa immunoglobulin light chain, but negative for CD20, CD30, CD79a, PAX-5, and lambda.
  • 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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42. 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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43. Drakos E, Rassidakis GZ, Tsioli P, Lai R, Jones D, Medeiros LJ: Differential expression of WT1 gene product in non-Hodgkin lymphomas. Appl Immunohistochem Mol Morphol; 2005 Jun;13(2):132-7
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  • The authors assessed for WT1 expression in six lymphoma/leukemia cell lines using Western blot methods after subcellular fractionation.
  • The B-cell NHLs analyzed were 18 diffuse large B-cell lymphomas, 13 marginal zone B-cell lymphomas, 9 small lymphocytic lymphomas, (DLBCLs), 8 follicular lymphomas, 6 mantle cell lymphomas, 5 Burkitt lymphomas, 3 lymphoplasmacytic lymphomas, and 2 B-cell lymphoblastic lymphomas.
  • The T-cell NHLs analyzed were 43 anaplastic large cell lymphomas (ALCLs), 26 peripheral T-cell lymphomas unspecified, 13 angioimmunoblastic T-cell lymphomas, 6 cutaneous ALCLs, 6 cases of mycosis fungoides, 5 extranodal NK/T-cell lymphomas of nasal type, and 4 T-cell lymphoblastic lymphomas.
  • WT1 levels were higher in cytoplasmic extracts than in nuclear extracts of the Karpas 299 and SU-DHL-1 lymphoma cell lines but were higher in nuclear extracts than in the cytoplasmic extracts of the Jurkat, HH, U-937, and K562 leukemia cell lines.
  • In NHLs, WT1 was positive in 4 of 5 (80%) Burkitt lymphomas, 9 of 12 (75%) ALK-positive ALCLs, 3 of 6 (50%) lymphoblastic lymphomas (2 of 4 T-cell, 1 of 2 B-cell), 14 of 31 (45%) ALK-negative ALCLs, 6 of 18 (33%) DLBCLs, and 1 of 6 (17%) cutaneous ALCLs.
  • WT1 was negative in all other NHLs tested.
  • WT1 immunoreactivity was primarily cytoplasmic in all positive NHLs except T-cell lymphoblastic lymphoma.

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  • (PMID = 15894924.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / WT1 Proteins
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4
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4. Honorat JF, Ragab A, Lamant L, Delsol G, Ragab-Thomas J: SHP1 tyrosine phosphatase negatively regulates NPM-ALK tyrosine kinase signaling. Blood; 2006 May 15;107(10):4130-8
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  • [Title] SHP1 tyrosine phosphatase negatively regulates NPM-ALK tyrosine kinase signaling.
  • Anaplastic large-cell lymphoma (ALCL) is frequently associated with the 2;5 translocation and expresses the NPM-ALK fusion protein, which possesses a constitutive tyrosine kinase activity.
  • We analyzed SHP1 tyrosine phosphatase expression and activity in 3 ALK-positive ALCL cell lines (Karpas 299, Cost, and SU-DHL1) and in lymph node biopsies (n = 40).
  • We found an inverse correlation between the level of NPM-ALK phosphorylation and SHP1 phosphatase activity.
  • Pull-down and coimmunoprecipitation experiments demonstrated a SHP1/NPM-ALK association.
  • Furthermore, confocal microscopy performed on ALCL cell lines and biopsy specimens showed the colocalization of the 2 proteins in cytoplasmic bodies containing Y664-phosphorylated NPM-ALK.
  • Dephosphorylation of NPM-ALK by SHP1 demonstrated that NPM-ALK was a SHP1 substrate.
  • Downregulation of SHP1 expression by RNAi in Karpas cells led to hyperphosphorylation of NPM-ALK, STAT3 activation, and increase in cell proliferation.
  • Furthermore, SHP1 overexpression in 3T3 fibroblasts stably expressing NPM-ALK led to the decrease of NPM-ALK phosphorylation, lower cell proliferation, and tumor progression in nude mice.
  • These findings show that SHP1 is a negative regulator of NPM-ALK signaling.
  • The use of tissue microarrays revealed that 50% of ALK-positive ALCLs were positive for SHP1.
  • Our results suggest that SHP1 could be a critical enzyme in ALCL biology and a potential therapeutic target.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / enzymology. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / physiology
  • [MeSH-minor] Base Sequence. Cell Line. Cytoplasm / physiology. DNA Primers. Humans. Microscopy, Confocal. Phosphoric Monoester Hydrolases / metabolism. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 6. RNA, Small Interfering / genetics. Recombinant Fusion Proteins / metabolism. Signal Transduction / physiology

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  • (PMID = 16469875.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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45. 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


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

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  • (PMID = 18755494.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Clathrin; 0 / Oncogene Proteins, Fusion; 0 / STAT3 Transcription Factor; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
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48. Streubel B, Vinatzer U, Willheim M, Raderer M, Chott A: Novel t(5;9)(q33;q22) fuses ITK to SYK in unspecified peripheral T-cell lymphoma. Leukemia; 2006 Feb;20(2):313-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel t(5;9)(q33;q22) fuses ITK to SYK in unspecified peripheral T-cell lymphoma.
  • Among peripheral T-cell lymphomas (PTCL), the heterogeneous category of unspecified PTCL represents the most common subtype.
  • Nevertheless, recurrent chromosomal translocations are unknown in this aggressive type of lymphoma.
  • Molecular analyses delineated the breakpoints to ITK and SYK resulting in a previously undescribed expression of the Syk tyrosine kinase by Itk.
  • ITK-SYK transcripts were detected in five of 30 (17%) unspecified PTCL, but not in cases of angioimmunoblastic T-cell lymphoma (n=9) and anaplastic lymphoma kinase-negative anaplastic large-cell lymphoma (n=7).
  • In all five translocation-positive cases, the breakpoints were identical fusing the N-terminal pleckstrin homology domain and proline-rich region of ITK to the tyrosine kinase domain of SYK.
  • [MeSH-major] Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 9 / genetics. Intracellular Signaling Peptides and Proteins / genetics. Lymphoma, Non-Hodgkin / genetics. Lymphoma, T-Cell, Peripheral / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

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  • [CommentIn] Leukemia. 2006 Feb;20(2):208-9 [16307012.001]
  • (PMID = 16341044.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; EC 2.7.10.2 / emt protein-tyrosine kinase
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49. Mussolin L, Pillon M, d'Amore ES, Santoro N, Lombardi A, Fagioli F, Zanesco L, Rosolen A: Prevalence and clinical implications of bone marrow involvement in pediatric anaplastic large cell lymphoma. Leukemia; 2005 Sep;19(9):1643-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and clinical implications of bone marrow involvement in pediatric anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) harbors the reciprocal chromosomal translocation t(2;5)(p23;q35) in approximately 80% of the cases.
  • The genes involved are nucleophosmin (NPM) and anaplastic lymphoma kinase (ALK) and the resulting chimeric NPM-ALK protein is thought to play a key role in the pathogenesis of t(2;5) positive ALCL.
  • Few data on bone marrow (BM) involvement in ALCL have been published and they mostly rely on morphological examination of BM smears.
  • We studied 52 ALCL for NPM-ALK expression by RT-PCR: 47/52 biopsies were positive.
  • In 41 of the 47 cases we obtained the BM at diagnosis and investigated the prevalence of minimal BM infiltration by RT-PCR and real-time PCR.
  • Survival analysis demonstrated a 5-year progression-free survival of 41 +/- 11% for patients with molecularly positive BM vs 100% for patients with negative BM (P = 0.001).
  • These results suggest that minimal BM involvement at diagnosis is a common event in pediatric ALCL and that minimal BM disease monitoring could identify patients at risk of relapse.
  • [MeSH-major] Bone Marrow / metabolism. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / genetics

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  • (PMID = 16049513.001).
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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50. Recavarren RA, Yang J: Cytomorphologic features of primary anaplastic large cell lymphoma of the psoas muscle: a case report and literature review. Diagn Cytopathol; 2010 Mar;38(3):208-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytomorphologic features of primary anaplastic large cell lymphoma of the psoas muscle: a case report and literature review.
  • Ki-1 (CD30) positive anaplastic large cell lymphoma (ALCL) is an uncommon malignancy, which may present with nodal as well as extra-nodal disease.
  • Primary skeletal muscle Ki-1 (CD30) positive ALCL is an even rarer event with few cases reported in the literature and only some with published cytomorphologic features.
  • Smears demonstrated a predominantly discohesive population of large pleomorphic cells.
  • Morphologic and immunohistochemical features later revealed a primary psoas muscle Ki-1 (CD30) positive ALCL with negative staining for anaplastic large cell lymphoma kinase (ALK).
  • Cytologic features of ALCL mimic epithelial neoplasms, sarcomas, melanoma and other lymphomas.
  • Although rare, ALCL should be a diagnostic consideration when discohesive pleomorphic malignant cells are encountered on FNA of a muscle neoplasm.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Muscle Neoplasms / pathology. Psoas Muscles / pathology
  • [MeSH-minor] Aged, 80 and over. Antigens, CD30 / metabolism. Biomarkers, Tumor / metabolism. Biopsy, Fine-Needle. Carcinoma / diagnosis. Cell Nucleus / metabolism. Cell Nucleus / pathology. Diagnosis, Differential. Female. Humans. Melanoma / diagnosis. Melanoma / secondary. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Skin Neoplasms / diagnosis

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  • (PMID = 19760764.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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51. Perez-Pinera P, Chang Y, Astudillo A, Mortimer J, Deuel TF: Anaplastic lymphoma kinase is expressed in different subtypes of human breast cancer. Biochem Biophys Res Commun; 2007 Jun 29;358(2):399-403
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic lymphoma kinase is expressed in different subtypes of human breast cancer.
  • Since inappropriate expression of Ptn stimulates progression of breast cancer in transgenic mice and a dominant negative PTN reverses the transformed phenotype of human breast cancer cells that inappropriately express Ptn, it is suggested that constitutive PTN signaling in breast cancer cells that inappropriately express Ptn activates pathways that promote a more aggressive breast cancer phenotype.
  • Pleiotrophin signals by inactivating its receptor, the receptor protein tyrosine phosphatase (RPTP)beta/zeta, and, recently, PTN was found to activate anaplastic lymphoma kinase (ALK) through the PTN/RPTPbeta/zeta signaling pathway in PTN-stimulated cells, not through a direct interaction of PTN with ALK and thus not through the PTN-enforced dimerization of ALK.
  • Since full-length ALK is activated in different malignant cancers and activated ALK is a potent oncogenic protein, we examined human breast cancers to test the possibility that ALK may be expressed in breast cancers and potentially activated through the PTN/RPTPbeta/zeta signaling pathway; we now demonstrate that ALK is strongly expressed in different histological subtypes of human breast cancer; furthermore, ALK is expressed in both nuclei and cytoplasm and, in the ;;dotted" pattern characteristic of ALK fusion proteins in anaplastic large cell lymphoma.
  • This study thus supports the possibility that activated ALK may be important in human breast cancers and potentially activated either through the PTN/RPTPbeta/zeta signaling pathway, or, alternatively, as an activated fusion protein to stimulate progression of breast cancer in humans.

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  • (PMID = 17490616.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA084400-06; United States / NIDDK NIH HHS / DK / 2 T32 DK007022-26; United States / NCI NIH HHS / CA / R01 CA084400-06; United States / NCI NIH HHS / CA / CA88440; United States / NIDDK NIH HHS / DK / T32 DK007022
  • [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 / Carrier Proteins; 0 / Cytokines; 134034-50-7 / pleiotrophin; 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 3.1.3.48 / PTPRZ1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 5
  • [Other-IDs] NLM/ NIHMS24272; NLM/ PMC1945107
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52. Damm-Welk C, Klapper W, Oschlies I, Gesk S, Röttgers S, Bradtke J, Siebert R, Reiter A, Woessmann W: Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation. Br J Haematol; 2009 Aug;146(3):306-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation.
  • Anaplastic large cell lymphomas (ALCL) in children express anaplastic lymphoma kinase (ALK) fusion genes, most commonly NPM1-ALK.
  • The distribution of X-ALK among 66 childhood ALCLs was analysed.
  • One ALCL was ALK-negative.
  • 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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53. 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


54. 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


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

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16114011.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes, B-Lymphocyte; 0 / Epitopes, T-Lymphocyte; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Peptide Fragments; 82115-62-6 / Interferon-gamma; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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56. 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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57. Rassidakis GZ, Feretzaki M, Atwell C, Grammatikakis I, Lin Q, Lai R, Claret FX, Medeiros LJ, Amin HM: Inhibition of Akt increases p27Kip1 levels and induces cell cycle arrest in anaplastic large cell lymphoma. Blood; 2005 Jan 15;105(2):827-9
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  • [Title] Inhibition of Akt increases p27Kip1 levels and induces cell cycle arrest in anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is a highly proliferative neoplasm that frequently carries the t(2;5)(p23;q35) and aberrantly expresses nucleophosmin-anaplastic lymphoma kinase (NPM-ALK).
  • Previously, NPM-ALK had been shown to activate the phosphatidylinositol 3 kinase (PI3K)/Akt pathway.
  • As the cyclin-dependent kinase (CDK) inhibitor p27(Kip1) (p27) is usually not expressed in ALCL, we hypothesized that activated Akt (pAkt) phosphorylates p27 resulting in increased p27 proteolysis and cell cycle progression.
  • Here we demonstrate that inhibition of pAkt activity in ALCL decreases p27 phosphorylation and degradation, resulting in increased p27 levels and cell cycle arrest.
  • Using immunohistochemistry, pAkt was detected in 24 (57%) of 42 ALCL tumors, including 8 (44%) of 18 ALK-positive tumors and 16 (67%) of 24 ALK-negative tumors, and was inversely correlated with p27 levels.
  • The mean percentage of p27-positive tumor cells was 5% in the pAkt-positive group compared with 26% in the pAkt-negative group (P = .0076).
  • These findings implicate that Akt activation promotes cell cycle progression through inactivation of p27 in ALCL.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins / antagonists & inhibitors. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Cell Division / physiology. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p27. Cytoplasm / metabolism. Down-Regulation. Humans. Proto-Oncogene Proteins c-akt


58. Ait-Tahar K, Barnardo MC, Pulford K: CD4 T-helper responses to the anaplastic lymphoma kinase (ALK) protein in patients with ALK-positive anaplastic large-cell lymphoma. Cancer Res; 2007 Mar 1;67(5):1898-901
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  • [Title] CD4 T-helper responses to the anaplastic lymphoma kinase (ALK) protein in patients with ALK-positive anaplastic large-cell lymphoma.
  • We have previously shown both humoral and CTL responses to anaplastic lymphoma kinase (ALK) in patients with ALK-positive anaplastic large-cell lymphoma (ALCL).
  • However, because CD4(+) T-helper (Th) cells also play a vital role in developing and maintaining tumor immunity, we investigated the presence of a CD4(+) Th response in ALK-positive ALCL.
  • Using an IFN-gamma ELISPOT assay, we identified two ALK-derived DRB1-restricted 24-mer promiscuous peptides, ALK1(278-301) and ALK2(233-256), as being immunogenic in six ALK-positive ALCL patients but not in two ALK-negative ALCL patients or five normal subjects.
  • A significant interleukin-4 response to the ALK peptides was detected in only one ALK-positive patient.
  • CD4(+) Th cell lines lysed ALK-positive ALCL cell lines in a MHC class II-restricted manner.
  • This first report of a CD4(+) Th response to ALK provides valuable information for developing future immunotherapeutic options for ALK-positive ALCL patients who fail to respond well to conventional therapies.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / immunology. Protein-Tyrosine Kinases / immunology. T-Lymphocytes, Helper-Inducer / immunology

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  • (PMID = 17332315.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes, T-Lymphocyte; 0 / Peptide Fragments; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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59. Tartari CJ, Gunby RH, Coluccia AM, Sottocornola R, Cimbro B, Scapozza L, Donella-Deana A, Pinna LA, Gambacorti-Passerini C: Characterization of some molecular mechanisms governing autoactivation of the catalytic domain of the anaplastic lymphoma kinase. J Biol Chem; 2008 Feb 15;283(7):3743-50
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  • [Title] Characterization of some molecular mechanisms governing autoactivation of the catalytic domain of the anaplastic lymphoma kinase.
  • NPM/ALK is an oncogenic fusion protein expressed in approximately 50% of anaplastic large cell lymphoma cases.
  • It derives from the t(2;5)(p23;q35) chromosomal translocation that fuses the catalytic domain of the tyrosine kinase, anaplastic lymphoma kinase (ALK), with the dimerization domain of the ubiquitously expressed nucleophosmin (NPM) protein.
  • Dimerization of the ALK kinase domain leads to its autophosphorylation and constitutive activation.
  • Activated NPM/ALK stimulates downstream survival and proliferation signaling pathways leading to malignant transformation.
  • Herein, we investigated the molecular mechanisms of autoactivation of the catalytic domain of ALK.
  • Because kinases are typically regulated by autophosphorylation of their activation loops, we systematically mutated (Tyr --> Phe) three potential autophosphorylation sites contained in the "YXXXYY" motif of the ALK activation loop, and determined the effect of these mutations on the catalytic activity and biological function of NPM/ALK.
  • We observed that mutation of both the second and third tyrosine residues (YFF mutant) did not affect the kinase activity or transforming ability of NPM/ALK.
  • In contrast, mutation of the first and second (FFY), first and third (FYF), or all three (FFF) tyrosine residues impaired both kinase activity and transforming ability of NPM/ALK.
  • Furthermore, a DFF mutant, in which the aspartic residue introduces a negative charge similar to a phosphorylated tyrosine, possessed catalytic activity similar to the YFF mutant.
  • Together, our findings indicate that phosphorylation of the first tyrosine of the YXXXYY motif is necessary for the autoactivation of the ALK kinase domain and the transforming activity of NPM/ALK.

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  • (PMID = 18070884.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [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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60. Balachandran I, Walker JW Jr, Broman J: Fine needle aspiration cytology of ALK1(-), CD30+ anaplastic large cell lymphoma post renal transplantation: a case report and literature review. Diagn Cytopathol; 2010 Mar;38(3):213-6
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  • [Title] Fine needle aspiration cytology of ALK1(-), CD30+ anaplastic large cell lymphoma post renal transplantation: a case report and literature review.
  • Epstein-Barr virus (EBV) related non-Hodgkin's lymphomas of B-cell type is more common than those of T-cell origin.
  • CD30 positive Anaplastic Large Cell Lymphoma (ALCL) is a Non-Hodgkin's lymphoma (B or T cell type) that accounts for a small percentage of PTLD's.
  • ALCL of T-cell type are a spectrum of disease ranging from primary cutaneous to systemic nodal ALCL.
  • The systemic nodal ALCL is further subdivided into anaplastic lymphoma kinase-1 (ALK-1) positive or negative.
  • ALK-1 protein is a gene fusion product of translocation (2;5) and carries prognostic implications.
  • We present an unusual manifestation of ALK-1 negative CD30 positive ALCL in a post renal transplant patient in FNA cytology with all supportive adjuvant studies and differential diagnoses and review the cytology literature on this topic.
  • [MeSH-major] Antigens, CD30 / analysis. Kidney Transplantation / adverse effects. Lymphoma, Large-Cell, Anaplastic / pathology. Mediastinal Neoplasms / pathology. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Carcinoma / diagnosis. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Humans. Immunocompromised Host. Immunohistochemistry. Male. Melanoma / diagnosis. Postoperative Complications. Prednisone / therapeutic use. Receptor Protein-Tyrosine Kinases. Remission Induction. Seminoma / diagnosis. Seminoma / secondary. Testicular Neoplasms / diagnosis. Vincristine / therapeutic use

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  • (PMID = 19774614.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
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61. 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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62. Sung CO, Ko YH, Park S, Kim K, Kim W: Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma. J Korean Med Sci; 2005 Dec;20(6):952-6
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  • [Title] Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma.
  • To verify the spectrum of CD99-expressing lymphoid malignancy, an immunohistochemical study for CD99 was carried out in 182 cases of non-Hodgkin's lymphoma, including 21 lymphoblastic lymphomas, 11 small lymphocytic lymphomas, 9 mantle cell lymphomas, 12 follicular lymphomas, 37 diffuse large B cell lymphomas, 18 Burkitt's lymphomas, 28 NK/T-cell lymphomas, 8 angioimmunoblastic T-cell lymphomas, 23 peripheral T-cell lymphomas, unspecified, and 15 systemic anaplastic large cell lymphomas.
  • Majority of T and NK cell lymphomas were negative for CD99, except anaplastic large cell lymphomas (ALCLs).
  • Seven of 10 (70%) ALK positive ALCLs expressed CD99, whereas only 1 of 5 (20%) ALK negative ALCLs were positive.
  • Of the mature B-cell lymphomas, 5.4% (2/37) of diffuse large B cell lymphomas and 11.1% (2/18) of Burkitt's lymphomas expressed CD99.
  • In conclusion, CD99 is infrequently expressed in mature B and T cell lymphomas, except ALK-positive ALCL.
  • High expression of CD99 in ALK-positive ALCL is unexpected finding and its biologic and clinical significances have yet to be clarified.
  • [MeSH-major] Antigens, CD / metabolism. Cell Adhesion Molecules / metabolism. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Non-Hodgkin / immunology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16361803.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2779325
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63. Cannizzo E, Sohani AR, Ferry JA, Hochberg EP, Kluk MJ, Dorn ME, Sadowski C, Bucci JJ, Ackerman AM, Longtine JA, Carulli G, Preffer FI: Carcinoma and multiple lymphomas in one patient: establishing the diagnoses and analyzing risk factors. J Hematop; 2009;2(3):163-70
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  • We report the case of a patient who showed the sequential occurrence of four different lymphoid neoplasms together with a squamous cell carcinoma of the lung.
  • A 62-year-old man with adenopathy was admitted to the hospital, and lymph node biopsy was positive for low-grade follicular lymphoma.
  • Two years later, a PET-CT scan showed a left hilar mass in the lung; biopsy showed a squamous cell carcinoma.
  • Simultaneously, he was diagnosed with diffuse large B cell lymphoma in a neck lymph node; after chemo- and radiotherapy, he achieved a complete response.
  • A restaging PET-CT scan 2 years later revealed a retroperitoneal nodule, and biopsy again showed a low-grade follicular lymphoma, while a biopsy of a cutaneous scalp lesion showed a CD30-positive peripheral T cell lymphoma.
  • After some months, a liver biopsy and a right cervical lymph node biopsy showed a CD30-positive peripheral T cell lymphoma consistent with anaplastic lymphoma kinase-negative anaplastic large cell lymphoma.
  • Flow cytometry and cytogenetic and molecular genetic analysis performed at diagnosis and during the patient's follow-up confirmed the presence of two clonally distinct B cell lymphomas, while the two T cell neoplasms were confirmed to be clonally related.

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  • (PMID = 20309424.001).
  • [ISSN] 1865-5785
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2766444
  • [Keywords] NOTNLM ; Anaplastic large cell lymphoma / Cytogenetics / Diffuse large B cell lymphoma / Follicular lymphoma / Multiple malignancies / Risk factors
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64. 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


65. Nasr MR, Laver JH, Chang M, Hutchison RE: Expression of anaplastic lymphoma kinase, tyrosine-phosphorylated STAT3, and associated factors in pediatric anaplastic large cell lymphoma: A report from the children's oncology group. Am J Clin Pathol; 2007 May;127(5):770-8
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  • [Title] Expression of anaplastic lymphoma kinase, tyrosine-phosphorylated STAT3, and associated factors in pediatric anaplastic large cell lymphoma: A report from the children's oncology group.
  • In anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK) activates (phosphorylates) signal transducer and activator of transcription 3 (STAT3) with subsequent cytoplasmic expression, in some cases, of survivin and tissue inhibitor of metalloprotease 1 (TIMP1).
  • These are inhibitors of apoptosis and negative prognostic factors.
  • CD56 is also a negative prognostic marker in ALCL.
  • We assayed 40 cases of predominantly ALK+ pediatric ALCL for pSTAT3, survivin, TIMP1, and CD56 using immunohistochemical analysis.
  • The patients were derived from a Pediatric Oncology Group treatment protocol that showed 72% event-free survival at 4 years for ALCL.
  • The results show that in advanced-stage pediatric ALCL, although most tumors express ALK and a majority show activated STAT3, cytoplasmic localization of survivin and TIMP1 is not frequent, nor is expression of CD56.
  • This may help, in part, explain the relatively good prognosis of pediatric ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / chemistry. Protein-Tyrosine Kinases / analysis. STAT3 Transcription Factor / analysis

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  • (PMID = 17439836.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 30969; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / STAT3 Transcription Factor; 0 / Tissue Inhibitor of Metalloproteinase-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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66. 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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67. Cağlar K, Akyüz C, Uner A, Kutluk T, Yalçin B, Varan A, Büyükpamukçu M: Anaplastic large cell lymphoma in a child presenting with cutaneous nodules and blisters. Turk J Pediatr; 2005 Apr-Jun;47(2):188-90
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  • [Title] Anaplastic large cell lymphoma in a child presenting with cutaneous nodules and blisters.
  • In another hospital, histopathological diagnosis of a skin biopsy was reported to be consistent with tuberculosis and she was treated with antimycobacterial drugs.
  • At our center, histopathological diagnosis was anaplastic lymphoma kinase (ALK)-negative anaplastic large cell lymphoma (ALCL).
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / diagnosis

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  • (PMID = 16052864.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
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68. 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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69. 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


70. 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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  • 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.
  • 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.
  • [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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71. Bakshi NA, Finn WG, Schnitzer B, Valdez R, Ross CW: Fascin expression in diffuse large B-cell lymphoma, anaplastic large cell lymphoma, and classical Hodgkin lymphoma. Arch Pathol Lab Med; 2007 May;131(5):742-7
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  • [Title] Fascin expression in diffuse large B-cell lymphoma, anaplastic large cell lymphoma, and classical Hodgkin lymphoma.
  • Fascin is a sensitive marker for classical Reed-Sternberg cells and has a high negative predictive value for diagnosis of classical Hodgkin lymphoma (CHL).
  • Fascin has been used to distinguish CHL from non-Hodgkin lymphoma.
  • Recently, it was shown that fascin might not help differentiate CHL from anaplastic large cell lymphoma (ALCL).
  • Moreover, fascin has not been extensively studied in the context of other large cell lymphomas.
  • OBJECTIVE: To analyze fascin expression in diffuse large B-cell lymphoma (DLBCL) and also reexamine its usefulness in discriminating CHL from ALCL.
  • DESIGN: Formalin-fixed, paraffin-embedded tissue samples from 41 cases of DLBCL, 30 cases of CHL, and 30 cases of ALCL were analyzed.
  • Fascin expression was compared across each type of lymphoma with additional correlation between fascin positivity and ALK-1 expression in ALCL performed.
  • RESULTS: Only 6 (14.6%) of 41 cases of DLBCL stained positively for fascin, with most neoplastic large cells exhibiting a weak staining pattern.
  • Fifteen (50%) of 30 cases of ALCL showed positivity for fascin, with most large cells staining strongly.
  • Sixty percent of fascin-positive ALCLs were positive for ALK-1, while 66.7% of fascin-negative ALCLs were positive for ALK-1.
  • CONCLUSIONS: Fascin is highly sensitive for CHL and has a very high negative predictive value (100% in this series) for distinguishing CHL from DLBCL or ALCL.
  • However, the specificity and positive predictive value for fascin are much higher in distinguishing CHL from DLBCL than in distinguishing CHL from ALCL.
  • Expression of fascin appears more useful in the differential diagnosis of CHL versus DLBCL than in the differential diagnosis of CHL versus ALCL.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carrier Proteins / biosynthesis. Hodgkin Disease / metabolism. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Microfilament Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Middle Aged. Predictive Value of Tests. Sensitivity and Specificity


72. Majhail NS, Burns LJ: Hematopoietic stem cell transplantation in the treatment of peripheral T-cell lymphomas. Curr Hematol Rep; 2005 Jul;4(4):252-9
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  • [Title] Hematopoietic stem cell transplantation in the treatment of peripheral T-cell lymphomas.
  • Peripheral T-cell lymphomas (PTCL) are a rare group of heterogeneous lymphoproliferative disorders with their origin in the post-thymic T cells.
  • Anaplastic large cell lymphoma (ALCL) has a better prognosis compared with other subtypes of PTCL.
  • As with aggressive B-cell non-Hodgkin's lymphoma, high-dose chemotherapy followed by autologous stem cell transplantation should be offered to patients with PTCL in their first relapse.
  • Patients with poor-risk features (alk-negative ALCL, histologic subtypes other than ALCL, and high International Prognostic Index score at presentation) may be candidates for autologous stem cell transplantation as first-line therapy.
  • Initial results of allogeneic stem cell transplantation, both with standard and nonmyeloablative conditioning, look promising.
  • Randomized, multi-institutional clinical trials are needed to optimally define the role of stem cell transplantation in PTCL.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, T-Cell, Peripheral / surgery
  • [MeSH-minor] Humans. Immunophenotyping. Prognosis. Stem Cell Transplantation. Transplantation, Autologous

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  • (PMID = 16009039.001).
  • [ISSN] 1541-0714
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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73. Brooks JK, Nikitakis NG, Frankel BF, Papadimitriou JC, Sauk JJ: Oral inflammatory myofibroblastic tumor demonstrating ALK, p53, MDM2, CDK4, pRb, and Ki-67 immunoreactivity in an elderly patient. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2005 Jun;99(6):716-26
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  • [Title] Oral inflammatory myofibroblastic tumor demonstrating ALK, p53, MDM2, CDK4, pRb, and Ki-67 immunoreactivity in an elderly patient.
  • Numerous large ganglion cell-like cells were seen, some exhibiting emperipolesis of neutrophils.
  • Tumor cells were immunoreactive for vimentin, smooth muscle actin, and KP1 (CD68), and negative for desmin, S-100, and EBV-LMP.
  • The recorded positivity for ALK, p53, MDM2, CDK4, pRb, and Ki-67, despite the absence of bcl-2 reactivity, strongly favors the neoplastic origin of the studied tumor.
  • [MeSH-major] Granuloma, Plasma Cell / pathology. Mandibular Diseases / pathology
  • [MeSH-minor] Actins / analysis. Aged. Aged, 80 and over. Cyclin-Dependent Kinase 4 / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Mandibular Neoplasms / diagnosis. Mouth Mucosa / chemistry. Neoplasms, Muscle Tissue / diagnosis. Protein-Tyrosine Kinases / analysis. Proto-Oncogene Proteins c-mdm2 / analysis. Receptor Protein-Tyrosine Kinases. Retinoblastoma Protein / analysis. Tumor Suppressor Protein p53 / analysis. Vimentin / analysis

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  • (PMID = 15897859.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Ki-67 Antigen; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 0 / Vimentin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Number-of-references] 91
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74. Perkins SL, Pickering D, Lowe EJ, Zwick D, Abromowitch M, Davenport G, Cairo MS, Sanger WG: Childhood anaplastic large cell lymphoma has a high incidence of ALK gene rearrangement as determined by immunohistochemical staining and fluorescent in situ hybridisation: a genetic and pathological correlation. Br J Haematol; 2005 Dec;131(5):624-7
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  • [Title] Childhood anaplastic large cell lymphoma has a high incidence of ALK gene rearrangement as determined by immunohistochemical staining and fluorescent in situ hybridisation: a genetic and pathological correlation.
  • Anaplastic large cell lymphoma (ALCL) comprises 10-15% of childhood non-Hodgkin lymphomas (NHL).
  • Systemic ALCL is highly associated with anaplastic lymphoma kinase (ALK) gene translocations with over-expression of ALK protein.
  • We studied ALK rearrangements using fluorescence in situ hybridisation (FISH) and ALK immunohistochemical staining in 43 paediatric systemic ALCLs.
  • Immunohistochemistry identified ALK over-expression in 42/43 cases (97%) with the single ALK-negative case demonstrating an ALK rearrangement by FISH, indicating 100% incidence of ALK translocations.
  • [MeSH-major] Gene Rearrangement. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 16351638.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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75. Tamaru J, Tokuhira M, Nittsu N, Nakamura S, Ichinohasama R, Suzuki R, Mori H, Takagi T, Suzuki T, Itami J, Itoyama S, Mikata A: Hodgkin-like anaplastic large cell lymphoma (previously designated in the REAL classification) has same immunophenotypic features to classical Hodgkin lymphoma. Leuk Lymphoma; 2007 Jun;48(6):1127-38
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  • [Title] Hodgkin-like anaplastic large cell lymphoma (previously designated in the REAL classification) has same immunophenotypic features to classical Hodgkin lymphoma.
  • In the WHO classification, the majority of Hodgkin-like ALCL cases as defined by the REAL classification are considered to be CHL.
  • However, establishing a histological diagnosis for the gray zone between CHL and ALCL is often confusing.
  • Expression of PAX-5/BSAP was observed in 88% (76/87) of CHL specimens and none (0/11) of ALK-positive ALCL specimens.
  • Among specimens of Hodgkin-like ALCL and ALK-negative ALCL, expression of PAX-5/BSAP was observed in 77% (20/26) and 18% (3/17), respectively.
  • Most of the PAX-5/BSAP-positive specimens were negative for Oct.2 and/or BOB.1/OBF.1 except for four CHL specimens.
  • Our results may support the WHO classification in which most cases of Hodgkin-like ALCL are classified as CHL.
  • However, the patients with Hodgkin-like ALCL with CHL-immunophenotype (PAX-5/BSAP-positive and negative for Oct.2 and/or BOB.1) did not have a favorable outcome, with a 5-year OS rate of 58%.
  • [MeSH-major] Hodgkin Disease / diagnosis. Hodgkin Disease / pathology. Immunophenotyping. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. B-Cell-Specific Activator Protein / genetics. Biomarkers, Tumor / genetics. Diagnosis, Differential. Female. Gene Expression Regulation, Leukemic. Humans. Male. Middle Aged. Neoplasm Staging. Octamer Transcription Factor-2 / genetics. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Retrospective Studies. Survival Analysis. Trans-Activators / genetics

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  • (PMID = 17577776.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / Octamer Transcription Factor-2; 0 / PAX5 protein, human; 0 / POU2AF1 protein, human; 0 / Trans-Activators; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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76. Choung HS, Kim HJ, Kim WS, Kim K, Kim SH: [Cytomorphology and molecular characterization of CLTC-ALK rearrangement in 2 cases of ALK-positive diffuse large B-cell lymphoma with extensive bone marrow involvement]. Korean J Lab Med; 2008 Apr;28(2):89-94
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  • [Title] [Cytomorphology and molecular characterization of CLTC-ALK rearrangement in 2 cases of ALK-positive diffuse large B-cell lymphoma with extensive bone marrow involvement].
  • Aanaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma (DLBCL) is an unusual disease entity first reported in 1997 as DLBCL with expression of full-length ALK protein.
  • 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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77. Savopoulos CG, Tsesmeli NE, Kaiafa GD, Zantidis AT, Bobos MT, Hatzitolios AI, Papavramidis ST, Kostopoulos IS: Primary pancreatic anaplastic large cell lymphoma, ALK negative: a case report. World J Gastroenterol; 2005 Oct 21;11(39):6221-4
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  • [Title] Primary pancreatic anaplastic large cell lymphoma, ALK negative: a case report.
  • We present the fourth case of a primary pancreatic anaplastic large cell lymphoma (ALCL), ALK-.
  • Duodenal and surgical biopsies identified an ALCL of T-cell lineage, ALK-.
  • Our case is the first one indicating that primary pancreatic lymphoma should be suspected in a patient with pancreatic mass and elevated serum LDH and beta(2) microglobulin.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Pancreatic Neoplasms / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16273656.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 12
  • [Other-IDs] NLM/ PMC4436646
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78. Wong WS, Liu BW, Lam FS, Wong KF: ALK-negative anaplastic large cell lymphoma in leukemic phase with near-pentaploidy. Leuk Lymphoma; 2010 Oct;51(10):1927-30
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  • [Title] ALK-negative anaplastic large cell lymphoma in leukemic phase with near-pentaploidy.
  • [MeSH-major] Chromosome Aberrations. Leukemia / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 20846102.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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79. Koizumi K, Minauchi K, Odani T, Kondo M, Takada A, Mukai M: [ALK-negative primary gastric anaplastic large cell lymphoma]. Rinsho Ketsueki; 2007 May;48(5):397-401
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  • [Title] [ALK-negative primary gastric anaplastic large cell lymphoma].
  • Gastroendoscopy revealed a Borrmann III type tumor which was diagnosed from the biopsied specimen as an anaplastic large cell lymphoma (ALCL).
  • CT scan revealed para-aortic and left-supra clavicular lymph node swelling, so her clinical stage was defined as IIIE according to the Ann Arbor classification.
  • The patient first of all received CHOP therapy, however her lymphoma lesions increased in size.
  • Therefore she underwent salvage chemotherapy regimens and autologous peripheral blood stem cell transplantation (APBSCT).
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / therapy. Protein-Tyrosine Kinases / analysis. Stomach Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Combined Modality Therapy. Epirubicin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Ifosfamide / administration & dosage. Middle Aged. Peripheral Blood Stem Cell Transplantation. Receptor Protein-Tyrosine Kinases. Remission Induction. Salvage Therapy. Transplantation, Autologous


80. Kodama K, Hokama M, Kawaguchi K, Tanaka Y, Hongo K: Primary ALK-1-negative anaplastic large cell lymphoma of the brain: case report and review of the literature. Neuropathology; 2009 Apr;29(2):166-71
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  • [Title] Primary ALK-1-negative anaplastic large cell lymphoma of the brain: case report and review of the literature.
  • Anaplastic large cell lymphoma (ALCL) is a type of non-Hodgkin lymphoma composed of CD30-positive cells.
  • Anaplastic lymphoma kinase (ALK) -1 positive ALCL frequently involves both lymph nodes and extranodal sites.
  • While primary extranodal involvement of ALK-1 negative ALCL is rare, this case is unique in that it is a case of primary ALK-1 negative ALCL of the brain.
  • The tumor was excised and histological diagnosis of primary ALK-1-negative ALCL was made.
  • Primary ALK-1-negative ALCL in this case showed aggressive clinical behavior and fatal outcome.
  • It is of great importance to avoid any delay in reaching an accurate diagnosis, as even primary ALCL of the brain is too seldom suspected clinically.
  • [MeSH-major] Activin Receptors, Type II / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adolescent. Aged. Blotting, Southern. Brain / metabolism. Brain / pathology. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Young Adult


81. Farkash EA, Ferry JA, Harris NL, Hochberg EP, Takvorian RW, Zuckerman DS, Sohani AR: Rare lymphoid malignancies of the breast: a report of two cases illustrating potential diagnostic pitfalls. J Hematop; 2009;2(4):237-44
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  • Breast involvement by lymphoma is uncommon and poses challenges in diagnosis.
  • The first case, ALK-negative anaplastic large-cell lymphoma involving a seroma associated with a breast implant, is an emerging clinicopathologic entity.
  • Anaplastic large-cell lymphoma has been identified in association with breast implants and seroma formation relatively recently.
  • The second case, hairy cell leukemia involving the breast and ipsilateral axillary sentinel lymph node, is, to our knowledge, the first reported case of hairy cell leukemia involving the breast at the time of diagnosis.
  • While a localized bone lesion was present at time of diagnosis, bone marrow involvement was relatively mild in comparison to that seen in the breast and lymph node.
  • In the first case, lymphoma occurred in a clinical setting where malignancy was unsuspected, highlighting the importance of careful morphologic evaluation of paucicellular samples, as well as awareness of rare clinicopathologic entities, in avoiding a misdiagnosis of a benign inflammatory infiltrate.
  • Knowledge of the patient's concurrent diagnosis of hairy cell leukemia involving the bone marrow and bone helped avoid a misdiagnosis of carcinoma rather than lymphoma.

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  • (PMID = 20309431.001).
  • [ISSN] 1865-5785
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2798933
  • [Keywords] NOTNLM ; Anaplastic large cell lymphoma / Anaplastic lymphoma kinase / Breast / Breast implant / Hairy cell leukemia / Primary breast lymphoma / Seroma / T-cell neoplasm
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82. Kesler MV, Paranjape GS, Asplund SL, McKenna RW, Jamal S, Kroft SH: Anaplastic large cell lymphoma: a flow cytometric analysis of 29 cases. Am J Clin Pathol; 2007 Aug;128(2):314-22
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  • [Title] Anaplastic large cell lymphoma: a flow cytometric analysis of 29 cases.
  • We report our experience with flow cytometric (FC) analysis of 29 cases of anaplastic large cell lymphoma (ALCL).
  • Of 21 cases, 13 were anaplastic lymphoma kinase (ALK)+, all of which were CD4+, vs 5 of 8 ALK - cases (P = .042).
  • However, light scatter gating on typical lymphoid regions may yield false-negative results in a substantial number of cases.
  • [MeSH-major] Antigens, CD / analysis. Flow Cytometry / methods. Lymphoma, Large B-Cell, Diffuse / immunology

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  • (PMID = 17638668.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / 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; EC 3.1.3.48 / Antigens, CD45; EC 3.1.3.48 / PTPRC protein, human
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83. Ziarkiewicz-Wróblewska B, Górnicka B, Gierej B, Suleiman W, Nowacka-Cieciura E, Durlik M, Bogdańska M, Wasiutyński A, Pileri SA: Hodgkin-like lymphoma, simulating anaplastic large cell lymphoma in the patient after renal transplantation--unusual case report and literature review. Pol J Pathol; 2008;59(1):63-9
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  • [Title] Hodgkin-like lymphoma, simulating anaplastic large cell lymphoma in the patient after renal transplantation--unusual case report and literature review.
  • We report the atypical case of posttransplant lymphoproliferative disorder (PTLD) diagnosed in 55-year men 9 years after renal transplantation.
  • It was evaluated only by bone marrow biopsy, which showed its total involvement with malignant lymphoma.
  • It was composed of two populations of lymphoid cells: large RS-like cells and small to medium ones, with slightly angular nuclei without visible nucleoli.
  • Both cellpopulations did not show positive reaction for typical B cell markers (CD20, CD79a).
  • Large RS-like cells were positive with CD30 and EBV-LMP.
  • However, negative reaction with CD15 and positive reactions with UCHL1 and EMA were not consistent with classical type of Hodgkin lymphoma.
  • Morphological picture and immunophenotype had suggested anaplastic T cell lymphoma.
  • Because of negative reaction with ALK1, initial diagnosis was ALCL ALK-negative.
  • Taking it into account the diagnosis was changed; finally Hodgkin-like B lymphoma was diagnosed.
  • 2. Negative reactions with typical immunohistochemical markers for lymphocytes of B cell line do not exclude the possibility of B-cell proliferation.
  • [MeSH-major] Hodgkin Disease / diagnosis. Kidney Transplantation / adverse effects. Lymphoma, Large-Cell, Anaplastic / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antiviral Agents / therapeutic use. Biomarkers, Tumor / metabolism. Bone Marrow / metabolism. Bone Marrow / pathology. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Epstein-Barr Virus Infections / complications. Epstein-Barr Virus Infections / pathology. Ganciclovir / therapeutic use. Humans. Immunosuppression. Male. Middle Aged. Postoperative Complications. Prednisone / therapeutic use. Treatment Outcome. Vincristine / therapeutic use


84. Rudolph C, Bittner C, Feller AC, Merz H, Schlegelberger B: Cytogenetic characteristics of a murine in vitro model for the human anaplastic large cell lymphoma (ALCL). Cytogenet Genome Res; 2006;114(3-4):292-5
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  • [Title] Cytogenetic characteristics of a murine in vitro model for the human anaplastic large cell lymphoma (ALCL).
  • Anaplastic large cell lymphoma (ALCL) is an entity of non-Hodgkin lymphomas (NHL) that often occurs in young children and adolescents.
  • In the majority of cases, ALCL are of T-cell origin and contain the t(2;5)(p23;q35) leading to an NPM-ALK fusion or variant ALK translocations.
  • In addition, there is an ALK-negative subtype of ALCL.
  • The anaplastic lymphoid cell line TS1G6 established by interleukin (IL)-9 transfection of T-helper cells represents a murine model of this subtype.
  • Here, we describe the cytogenetic features of this cell line using spectral karyotyping (SKY) and single-color fluorescence in situ hybridization (FISH).
  • [MeSH-major] Chromosome Aberrations. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16954669.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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85. Cotta CV, Leventaki V, Atsaves V, Vidaki A, Schlette E, Jones D, Medeiros LJ, Rassidakis GZ: The helix-loop-helix protein Id2 is expressed differentially and induced by myc in T-cell lymphomas. Cancer; 2008 Feb 1;112(3):552-61
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  • [Title] The helix-loop-helix protein Id2 is expressed differentially and induced by myc in T-cell lymphomas.
  • Recent studies have shown that Id2 is overexpressed in some types of B-cell lymphoma, including classical Hodgkin lymphoma.
  • The authors of the current study hypothesized that Id2 also is overexpressed in T-cell lymphomas.
  • METHODS: By using reverse-transcriptase polymerase chain reaction (RT-PCR) and Western blot analyses, high Id2 messenger RNA (mRNA) and protein levels, respectively, were detected in all 4 T-cell anaplastic large cell lymphoma (ALCL) cell lines that were tested.
  • RESULTS: Immunohistochemistry results indicated that Id2 was expressed strongly in 21 of 27 (78%) ALCL tumors (79% anaplastic lymphoma kinase [ALK]-negative and 75% ALK-positive), in 5 of 10 (50%) extranodal natural killer/T (NK/T)-cell lymphomas of the nasal type, in 2 of 8 (25%) cutaneous ALCLs, in 2 of 9 (22%) enteropathy type T-cell lymphomas, in 1 of 5 (20%) peripheral T-cell lymphomas not otherwise specified, and in 1 of 8 (13%) T-cell prolymphocytic leukemias.
  • Other types of T-cell lymphoma were negative for Id2.
  • Because it is known that myc is expressed in ALCL, myc was inhibited selectively in 2 ALCL cell lines, resulting in a concentration-dependent decrease in Id2 mRNA and protein levels.
  • CONCLUSIONS: Taken together, the current data suggest that Id2 commonly is overexpressed in highly proliferative T-cell lymphomas, and its expression may result from transcriptional activation of myc in these tumors.
  • [MeSH-major] Inhibitor of Differentiation Protein 2 / metabolism. Lymphoma, T-Cell / metabolism. Proto-Oncogene Proteins c-myc / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Gene Expression Regulation, Neoplastic / physiology. Hodgkin Disease / metabolism. Hodgkin Disease / pathology. Humans. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, Non-Hodgkin / metabolism. Lymphoma, Non-Hodgkin / pathology. Lymphomatoid Papulosis / metabolism. Lymphomatoid Papulosis / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Skin Neoplasms / metabolism. Skin Neoplasms / pathology. Up-Regulation / physiology

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  • (PMID = 18085637.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger
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86. Zhang D, Denley RC, Filippa DA, Teruya-Feldstein J: ALK-positive diffuse large B-cell lymphoma with the t(2;17)(p23;q23). Appl Immunohistochem Mol Morphol; 2009 Mar;17(2):172-7
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  • [Title] ALK-positive diffuse large B-cell lymphoma with the t(2;17)(p23;q23).
  • Diffuse large B-cell lymphoma (DLBCL) with plasmablastic features associated with t(2;17)(p23;q23) and characteristic granular cytoplasmic anaplastic lymphoma kinase-1 (ALK1) protein expression is a rare lymphoma subtype.
  • Lymph node biopsy showed large atypical cells with prominent plasmablastic differentiation, abundant amphophilic cytoplasm, and prominent central nucleoli.
  • Paraffin immunohistochemistry showed finely granular cytoplasmic ALK1 expression, positive CD138, IgA, p63 (VS38), focal positive epithelial membrane antigen and CD4, and lambda light chain restriction whereas negative CD20 and CD30 staining.
  • While reports show detection of the unique CLTC-ALK fusion by either reverse transcription-polymerase chain reaction or fluorescence in situ hybridization, our case represents the second case in the literature to detect the t(2;17)(p23;q23) translocation by multiplex karyotyping (multiplex fluorescence in situ hybridization) and the usefulness of this technique to detect hidden translocations not seen by G-banding.
  • Differential diagnoses of neoplasms with plasmablastic differentiation and a comprehensive molecular/cytogenetic literature review of ALK+DLBCL is discussed.

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  • (PMID = 19521280.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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87. Bishara MR, Ross C, Sur M: Primary anaplastic large cell lymphoma of the breast arising in reconstruction mammoplasty capsule of saline filled breast implant after radical mastectomy for breast cancer: an unusual case presentation. Diagn Pathol; 2009;4:11
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  • [Title] Primary anaplastic large cell lymphoma of the breast arising in reconstruction mammoplasty capsule of saline filled breast implant after radical mastectomy for breast cancer: an unusual case presentation.
  • BACKGROUND: Primary non-Hodgkin lymphoma (NHL) of the breast represents 0.04-0.5% of malignant lesions of the breast and accounts for 1.7-2.2% of extra-nodal NHL.
  • Most primary cases are of B-cell phenotype and only rare cases are of T-cell phenotype.
  • Anaplastic large cell lymphoma (ALCL) is a rare T-cell lymphoma typically seen in children and young adults with the breast being one of the least common locations.
  • There are a total of eleven cases of primary ALCL of the breast described in the literature.
  • However in contrast to acute myeloid leukemia (AML), the association between lymphoma and administration of chemotherapy has never been clearly demonstrated.
  • CASE PRESENTATION: In this report we present a case of primary ALCL of the breast arising in reconstruction mammoplasty capsule of saline filled breast implant after radical mastectomy for infiltrating ductal carcinoma followed by postoperative chemotherapy twelve years ago.
  • CONCLUSION: Primary ALK negative ALCL arising at the site of saline filled breast implant is rare.
  • However, it is important to be aware of these complications and need for careful pathologic examination of tissue removed for implant related complications to make the correct diagnosis for further patient management and treatment.
  • It is important to be aware of this entity at this site as it can be easily misdiagnosed on histologic grounds and to exclude sarcomatoid carcinoma, malignant melanoma and pleomorphic sarcoma by an appropriate panel of immunostains to arrive at the correct diagnosis of ALCL.

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  • (PMID = 19341480.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2678081
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88. Drakos E, Leventaki V, Schlette EJ, Jones D, Lin P, Medeiros LJ, Rassidakis GZ: c-Jun expression and activation are restricted to CD30+ lymphoproliferative disorders. Am J Surg Pathol; 2007 Mar;31(3):447-53
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  • Cellular Jun (c-Jun), a member of the JUN family, is an activator protein-1 transcription factor involved in cell differentiation, proliferation, and apoptosis that can be activated by phosphorylation at serine-73 and -63 residues.
  • Using tissue microarrays and immunohistochemistry, we investigated c-Jun expression and serine-73 phosphorylation in 112 CD30 lymphomas and 232 CD30 lymphomas of B- or T-cell lineage, and 24 cases of lymphomatoid papulosis. c-Jun was expressed exclusively by CD30 lymphoproliferative disorders including 41/41 (100%) classical Hodgkin lymphoma (cHL), 20/23 (87%) anaplastic lymphoma kinase (ALK)+ anaplastic large cell lymphoma (ALCL), 18/26 (69%) ALK- ALCL, 5/9 (56%) primary cutaneous ALCL, 4/11 (36%) CD30 diffuse large B-cell lymphoma (DLBCL), and 11/24 (46%) cases of lymphomatoid papulosis.
  • The percentage of c-Jun-positive tumor cells was highest in cHL and ALCL (P=0.002).
  • In contrast, all CD30 lymphomas, including nodular lymphocyte predominant HL and CD30 non-Hodgkin lymphomas of B- or T-cell lineage were negative for c-Jun.
  • Serine-73 phosphorylated c-Jun (p-c-Jun), the activated form of c-Jun, was expressed more frequently and at a higher level in cHL and ALK+ ALCL than other CD30 tumors.
  • [MeSH-major] Antigens, CD30 / metabolism. Hodgkin Disease / pathology. Lymphoma, Non-Hodgkin / pathology. Lymphomatoid Papulosis / pathology. Proto-Oncogene Proteins c-jun / metabolism. Transcriptional Activation
  • [MeSH-minor] Biomarkers, Tumor / biosynthesis. Cell Count. Cell Line, Tumor. Cell Nucleus / metabolism. Cell Nucleus / pathology. Humans. Phosphorylation. Serine / metabolism. Tissue Array Analysis


89. 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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90. Gjerdrum LM, Woetmann A, Odum N, Hother C, Henrik-Nielsen R, Gniadecki R, Ralfkiaer E: FOXP3 positive regulatory T-cells in cutaneous and systemic CD30 positive T-cell lymphoproliferations. Eur J Haematol; 2008 Jun;80(6):483-9
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  • [Title] FOXP3 positive regulatory T-cells in cutaneous and systemic CD30 positive T-cell lymphoproliferations.
  • In this study, skin biopsies from lymphomatoid papulosis (LyP) (n = 14), primary cutaneous anaplastic large cells lymphoma (C-ALCL) (n = 13) and systemic anaplastic large cells lymphoma (S-ALCL) with (n = 9) or without (n = 6) ALK expression were examined by immunohistology for FOXP3 expression in tumour cells and tumour infiltrating Tregs.
  • Labelling of a majority of the neoplastic cells was seen in one case of C-ALCL.
  • Another three cases (one LyP and two C-ALCL) displayed weak labelling of very occasional atypical T-cells.
  • In the remaining 38 cases the atypical lymphoid infiltrate was FOXP3 negative.
  • Significant higher numbers were recorded in ALK negative S-ALCL and LyP than in C-ALCL and S-ALCL positive for ALK.
  • These cells may have influence upon the clinical behaviour, possibly depending upon the net degree of Treg mediated immune suppression of tumour cells relative to tumour infiltrating, cytotoxic effector cells, thereby implicating the more favourable outcome of LyP compared to C-ALCL.
  • [MeSH-major] Antigens, CD30 / immunology. Cell Proliferation. Forkhead Transcription Factors / metabolism. Lymphoproliferative Disorders / metabolism. Skin / immunology. T-Lymphocytes / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Blotting, Western. Cell Line. Humans. Immunohistochemistry

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  • (PMID = 18331599.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
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91. 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


92. Merlin E, Chabrier S, Verkarre V, Cramer E, Delabesse E, Stéphan JL: Primary leptomeningeal ALK+ lymphoma in a 13-year-old child. J Pediatr Hematol Oncol; 2008 Dec;30(12):963-7
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  • [Title] Primary leptomeningeal ALK+ lymphoma in a 13-year-old child.
  • A distinct pathologic entity characterized by expression of the anaplastic lymphoma kinase (ALK) protein (hence described as ALK lymphoma) has emerged within the heterogeneous group of CD30 anaplastic large-cell lymphomas.
  • Central nervous system (CNS) involvement is extremely rare in anaplastic large-cell lymphoma.
  • Cerebrospinal fluid was infiltrated with atypical large granular lymphocytes.
  • A frontal lobe biopsy showed a pleomorphic neoplasm diffusely infiltrating the meninges composed of large cells with bizarre nuclei similar to those evidenced in cerebrospinal fluid.
  • Immunohistochemical stains showed diffuse strong positivity for CD8, CD30, anaplastic lymphoma kinase protein: p80 and negative monocyte-macrophage and B cell markers.
  • This finding was confirmed by reverse transcription-polymerase chain reaction analysis of the NPM/ALK fusion protein.
  • This case is the first reported occurrence of a primary meningeal ALK lymphoma in a child.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Meningeal Neoplasms / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. DNA, Neoplasm / analysis. Fatal Outcome. Gene Rearrangement. Genes, T-Cell Receptor gamma / genetics. Humans. Immunophenotyping. Male. Multiple Organ Failure. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19131793.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 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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93. Wang WY, Ma ZG, Li GD, Liu WP, Zhong L, Wang Y, Li JM, Li L, Jiang W, Tang Y, Liao DY: [Diffuse large B-cell lymphoma with expression of anaplastic lymphoma kinase protein: clinicopathologic and immunohistochemical study of 5 cases]. Zhonghua Bing Li Xue Za Zhi; 2006 Sep;35(9):529-34
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  • [Title] [Diffuse large B-cell lymphoma with expression of anaplastic lymphoma kinase protein: clinicopathologic and immunohistochemical study of 5 cases].
  • OBJECTIVE: To study the clinicopathologic features of diffuse large B-cell lymphoma (DLBCL) with expression of anaplastic lymphoma kinase (ALK) protein.
  • Immunohistochemical study for anti-ALK-11 was performed using LSAB technique.
  • The ALK-positive cases were further confirmed by immunohistochemical study using EnVision technique.
  • Only ALK-positive cases by EnVision technique were further analyzed by immunostaining for antigens including CD20, CD3, CD30, EMA, granzyme-B, TIA-1 and PC.
  • RESULTS: There were altogether 5 (4 males and 1 female) cases of DLBCL showing expression of ALK protein.
  • Morphologic subtypes included centroblastic 2, anaplastic 1, immunoblastic with plasmacytoid differentiation 1 and plasmablastic 1.
  • Immunohistochemically, 4 cases were CD20 positive (including 2 centroblastic, 1 anaplastic and 1 immunoblastic cases).
  • The plasmablastic case expressed kappa light chain and was negative for CD20.
  • As for ALK protein staining, a mixed membranous and cytoplasmic (1 immunoblastic case), granular cytoplasmic (2 centroblastic and 1 anaplastic cases) and mixed nuclear and cytoplasmic (1 plasmablastic case) patterns were observed.
  • CONCLUSIONS: Expression of ALK protein is a rare phenomenon in DLBCL and can be seen in centroblastic, anaplastic, immunoblastic and plasmablastic subtypes.
  • A new pattern of ALK protein expression, mixed membranous and cytoplasmic, is reported.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 17134546.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Immunoglobulin kappa-Chains; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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94. Takahashi E, Kajimoto K, Fukatsu T, Yoshida M, Eimoto T, Nakamura S: Intravascular large T-cell lymphoma: a case report of CD30-positive and ALK-negative anaplastic type with cytotoxic molecule expression. Virchows Arch; 2005 Dec;447(6):1000-6
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  • [Title] Intravascular large T-cell lymphoma: a case report of CD30-positive and ALK-negative anaplastic type with cytotoxic molecule expression.
  • We reported a case of intravascular T-cell lymphoma (T-IVL) with anaplastic large cell morphology, the hemophagocytic syndrome, and an aggressive clinical course.
  • Phenotypic analysis of the tumor cells revealed CD2+, CD3-, CD4+, CD5-, CD8-, CD30+, CD56-, T-cell receptor alpha/beta-, ALK-, TIA1+, granzyme B+, and perforin+.
  • A review revealed that 25 cases of T-IVL have been reported in the available literature, only two of which were of CD30+ anaplastic large cell or cytotoxic T-cell type.
  • The findings in the present case may highlight the unique clinicopathologic aspects of a subset of CD30-positive T-IVLs with an ALK-negative cytotoxic phenotype.
  • [MeSH-major] Alkaline Phosphatase / metabolism. Antigens, CD30 / metabolism. Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, T-Cell / pathology

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  • (PMID = 16189700.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 3.1.3.1 / Alkaline Phosphatase
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95. 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].
  • He had multiple para-aorta lymphadenopathy and splenomegaly in December 2001.
  • 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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96. 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(-).
  • In situ hybridisation for Epstein-Barr virus RNA was negative.
  • Electron microscopically, the tumour cells were similar to large transformed lymphocytes and had circumferentially profuse microvillous projections resembling those of epithelial mesothelioma cells.
  • 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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97. 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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98. 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.
  • 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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99. Drakos E, Atsaves V, Schlette E, Li J, Papanastasi I, Rassidakis GZ, Medeiros LJ: The therapeutic potential of p53 reactivation by nutlin-3a in ALK+ anaplastic large cell lymphoma with wild-type or mutated p53. Leukemia; 2009 Dec;23(12):2290-9
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  • [Title] The therapeutic potential of p53 reactivation by nutlin-3a in ALK+ anaplastic large cell lymphoma with wild-type or mutated p53.
  • p53 is expressed frequently, but is rarely mutated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) tumours.
  • Nutlin-3a is a recently developed small molecule that targets Mdm2, a critical negative regulator of p53, and disrupts the p53-Mdm2 interaction resulting in p53 stabilization and activation.
  • We show that nutlin-3a activates p53 in ALK+ ALCL cells carrying a wild type (wt) or mutated but partially functional p53 gene resulting in p53-dependent cell-cycle arrest and apoptosis.
  • Cell-cycle arrest was associated with upregulation of the cyclin-dependent kinase inhibitor p21.
  • Nutlin-3a-induced apoptotic cell death was accompanied by Bax and Puma upregulation, downregulation of Bcl-xl, survivin, and caspase-3 cleavage, and this was reduced when p53-dependent transactivation activity was inhibited by pifithrin-alpha, or when pifithrin-mu was used to inhibit direct p53 targeting of mitochondria.
  • Nutlin-3a sensitized the activation of the extrinsic apoptotic pathway in wt-p53 ALK+ ALCL cells, in part, through upregulation of DR-5 and downregulation of c-Flip(S/L), and was synergistic with TRAIL in cell death induction.
  • In addition, nutlin-3a treatment enhanced doxorubicin cytotoxicity against ALK+ ALCL cells harbouring mt p53, and this was associated with p73 upregulation.
  • These data suggest that disruption of the p53-mdm2 interaction by nutlin-3a offers a novel therapeutic approach for ALK+ ALCL patients.
  • [MeSH-major] Imidazoles / pharmacology. Lymphoma, Large-Cell, Anaplastic / drug therapy. Mutation. Piperazines / pharmacology. Tumor Suppressor Protein p53 / drug effects
  • [MeSH-minor] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. Cell Cycle. Cell Line, Tumor. Doxorubicin / pharmacology. Drug Synergism. Humans. TNF-Related Apoptosis-Inducing Ligand / pharmacology


100. Lee CC, Jia Y, Li N, Sun X, Ng K, Ambing E, Gao MY, Hua S, Chen C, Kim S, Michellys PY, Lesley SA, Harris JL, Spraggon G: Crystal structure of the ALK (anaplastic lymphoma kinase) catalytic domain. Biochem J; 2010 Sep 15;430(3):425-37
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  • [Title] Crystal structure of the ALK (anaplastic lymphoma kinase) catalytic domain.
  • ALK (anaplastic lymphoma kinase) is an RTK (receptor tyrosine kinase) of the IRK (insulin receptor kinase) superfamily, which share an YXXXYY autophosphorylation motif within their A-loops (activation loops).
  • A common activation and regulatory mechanism is believed to exist for members of this superfamily typified by IRK and IGF1RK (insulin-like growth factor receptor kinase-1).
  • Chromosomal translocations involving ALK were first identified in anaplastic large-cell lymphoma, a subtype of non-Hodgkin's lymphoma, where aberrant fusion of the ALK kinase domain with the NPM (nucleophosmin) dimerization domain results in autophosphosphorylation and ligand-independent activation.
  • Activating mutations within the full-length ALK kinase domain, most commonly R1275Q and F1174L, which play a major role in neuroblastoma, were recently identified.
  • To provide a structural framework for understanding these mutations and to guide structure-assisted drug discovery efforts, the X-ray crystal structure of the unphosphorylated ALK catalytic domain was determined in the apo, ADP- and staurosporine-bound forms.
  • The structures reveal a partially inactive protein kinase conformation distinct from, and lacking, many of the negative regulatory features observed in inactive IGF1RK/IRK structures in their unphosphorylated forms.
  • The structure helps explain the reported unique peptide substrate specificity and the importance of phosphorylation of the first A-loop Tyr1278 for kinase activity and NPM-ALK transforming potential.
  • A single amino acid difference in the ALK substrate peptide binding P-1 site (where the P-site is the phosphoacceptor site) was identified that, in conjunction with A-loop sequence variation including the RAS (Arg-Ala-Ser)-motif, rationalizes the difference in the A-loop tyrosine autophosphorylation preference between ALK and IGF1RK/IRK.
  • Enzymatic analysis of recombinant R1275Q and F1174L ALK mutant catalytic domains confirms the enhanced activity and transforming potential of these mutants.
  • The transforming ability of the full-length ALK mutants in soft agar colony growth assays corroborates these findings.
  • The availability of a three-dimensional structure for ALK will facilitate future structure-function and rational drug design efforts targeting this receptor tyrosine kinase.
  • [MeSH-minor] Adenosine Diphosphate / chemistry. Adenosine Diphosphate / metabolism. Amino Acid Motifs / genetics. Amino Acid Sequence. Animals. Cell Line. Crystallization. Crystallography, X-Ray. Humans. Kinetics. Models, Molecular. Molecular Sequence Data. Mutagenesis. Neuroblastoma / enzymology. Neuroblastoma / genetics. Phosphorylation. Protein Binding. Receptor Protein-Tyrosine Kinases. Sequence Homology, Amino Acid. Spodoptera. Staurosporine / chemistry. Staurosporine / metabolism. Substrate Specificity

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  • (PMID = 20632993.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mutant Proteins; 61D2G4IYVH / Adenosine Diphosphate; 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; H88EPA0A3N / Staurosporine
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