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1. 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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2. Han Y, Amin HM, Franko B, Frantz C, Shi X, Lai R: Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma. Blood; 2006 Oct 15;108(8):2796-803
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  • [Title] Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma.
  • Previous studies showed that most cases of ALK(+) anaplastic large-cell lymphoma (ALK(+)ALCL) do not express SHP1, a tyrosine phosphatase and an important negative regulator for cellular signaling pathways such as that of JAK/STAT.
  • To fully assess the biologic significance of loss of SHP1 in ALK(+)ALCL, we transfected SHP1 plasmids into 2 SHP1(-), ALK(+)ALCL cell lines, Karpas 299 and SU-DHL-1.
  • Expression of SHP1 in these 2 cell lines also resulted in marked decreases in the protein levels of JAK3 and NPM-ALK, and these effects were reversible by proteosome inhibitor MG132.
  • Conversely, when SHP1 expression in SUP-M2 (a SHP1(+) ALK(+)ALCL cell line) was inhibited using siRNA, pSTAT3, pJAK3, JAK3, and NPM-ALK were all up-regulated.
  • Coimmunoprecipitation studies showed that SHP1 was physically associated with JAK3 and NPM-ALK.
  • SHP1 expression in Karpas 299 and SU-DHL-1 led to significant G(1) cell cycle arrest but not apoptosis.
  • To conclude, loss of SHP1 contributes to the pathogenesis of ALK(+)ALCL by 2 mechanisms:.
  • (1) it leaves the tyrosine phosphorylation and activation of JAK3/STAT3 unchecked and (2) it decreases proteosome degradation of JAK3 and NPM-ALK.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / metabolism. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Apoptosis. Base Sequence. Cell Cycle. Cell Line, Tumor. Gene Expression. Humans. Janus Kinase 3. Proteasome Endopeptidase Complex / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 6. RNA, Neoplasm / genetics. RNA, Small Interfering / genetics. Signal Transduction. Transfection

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  • (PMID = 16825495.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / JAK3 protein, human; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 3; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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3. Rust R, Harms G, Blokzijl T, Boot M, Diepstra A, Kluiver J, Visser L, Peh SC, Lim M, Kamps WA, Poppema S, van den Berg A: High expression of Mcl-1 in ALK positive and negative anaplastic large cell lymphoma. J Clin Pathol; 2005 May;58(5):520-4
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  • [Title] High expression of Mcl-1 in ALK positive and negative anaplastic large cell lymphoma.
  • AIM: To gain more insight into the genes involved in the aetiology and pathogenesis of anaplastic large cell lymphoma (ALCL).
  • METHODS: Serial analysis of gene expression (SAGE) was undertaken on the CD4+ALK+ (anaplastic lymphoma kinase positive) ALCL derived cell line Karpas299 and as comparison on CD4+ T cells.
  • Quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry were performed on five ALCL derived cell lines and 32 tissue samples to confirm the SAGE data.
  • RESULTS: High expression of Mcl-1 was seen in the Karpas299 cell line, whereas the two other antiapoptotic Bcl-2 family members, Bcl-2 and Bcl-X(L), were not detected in the SAGE library.
  • Quantitative RT-PCR confirmed the high expression of Mcl-1 mRNA and low expression of Bcl-2 and Bcl-X(L) in Karpas299 and in four other ALCL cell lines.
  • All 23 ALK+ and nine ALK- ALCL cases were positive for Mcl-1.
  • Bcl-2 and Bcl-X(L) were expressed infrequently in ALK+ ALCL cases, but were present in a higher proportion of ALK- ALCL cases.
  • CONCLUSION: The consistent high expression of Mcl-1 in ALK+ and ALK- ALCL suggests that Mcl-1 is the main antiapoptotic protein in this disease.
  • The high frequency of Mcl-1, Bcl-2, and Bcl-X(L) positive ALCL cases in the ALK- group compared with the ALK+ group indicates that ALK induced STAT3 activation is not the main regulatory pathway in ALCL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Neoplasm Proteins / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Apoptosis / genetics. CD4-Positive T-Lymphocytes / physiology. Cell Line, Tumor. Genes, bcl-2 / genetics. Humans. Immunohistochemistry / methods. Myeloid Cell Leukemia Sequence 1 Protein. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction / methods. bcl-X Protein

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  • [Cites] Trends Biochem Sci. 2001 Jan;26(1):61-6 [11165519.001]
  • [Cites] Am J Pathol. 1999 Jun;154(6):1685-91 [10362793.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3902-9 [11389033.001]
  • [Cites] Am J Pathol. 2001 Aug;159(2):527-35 [11485911.001]
  • [Cites] Oncogene. 2001 Sep 13;20(41):5799-809 [11593385.001]
  • [Cites] Oncogene. 2002 Feb 7;21(7):1038-47 [11850821.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):945-54 [11948098.001]
  • [Cites] Leukemia. 2002 Apr;16(4):444-54 [11960321.001]
  • [Cites] J Hematother Stem Cell Res. 2002 Apr;11(2):423-8 [11983114.001]
  • [Cites] Am J Pathol. 2002 Jun;160(6):2309-10 [12057933.001]
  • [Cites] Br J Haematol. 2002 Sep;118(3):791-8 [12181047.001]
  • [Cites] Pathol Int. 2002 Sep;52(9):578-85 [12406187.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3527-38 [12429644.001]
  • [Cites] Mol Cancer Ther. 2002 Feb;1(4):253-66 [12467221.001]
  • [Cites] J Pathol. 2003 Jan;199(1):84-9 [12474230.001]
  • [Cites] Mol Cancer Ther. 2003 Jan;2(1):73-81 [12533675.001]
  • [Cites] Arch Pathol Lab Med. 2003 Apr;127(4):424-31 [12683869.001]
  • [Cites] J Pathol. 2003 Jun;200(2):240-8 [12754745.001]
  • [Cites] J Pathol. 2003 Jun;200(2):249-54 [12754746.001]
  • [Cites] Oncogene. 2003 May 15;22(19):2950-9 [12771946.001]
  • [Cites] Blood. 2003 Jul 1;102(1):344-52 [12637318.001]
  • [Cites] Oncogene. 2003 Aug 21;22(35):5399-407 [12934099.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3692-9 [14506160.001]
  • [Cites] FEBS Lett. 2000 Jan 21;466(1):6-10 [10648802.001]
  • [Cites] Hematol Oncol. 1999 Dec;17(4):137-48 [10725869.001]
  • [Cites] Blood. 2000 Jul 15;96(2):393-7 [10887097.001]
  • [Cites] Blood. 2000 Jul 15;96(2):398-404 [10887098.001]
  • [Cites] J Biol Chem. 2000 Jul 21;275(29):22136-46 [10766760.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3681-95 [11090048.001]
  • [Cites] Pediatr Dev Pathol. 2001 Mar-Apr;4(2):129-37 [11178628.001]
  • [Cites] J Clin Invest. 2001 Feb;107(3):351-62 [11160159.001]
  • [Cites] Mod Pathol. 2004 Jan;17(1):109-16 [14657946.001]
  • [Cites] Oncogene. 2004 Jul 15;23(32):5426-34 [15184887.001]
  • [Cites] Histopathology. 1987 Jul;11(7):733-40 [3040565.001]
  • [Cites] Br J Haematol. 1989 Jan;71(1):31-6 [2917127.001]
  • [Cites] Pathol Res Pract. 1990 Oct;186(5):582-8 [2287585.001]
  • [Cites] Science. 1995 Oct 20;270(5235):484-7 [7570003.001]
  • [Cites] Am J Pathol. 1996 Jul;149(1):177-85 [8686741.001]
  • [Cites] Blood. 1997 Jan 15;89(2):630-43 [9002967.001]
  • [Cites] Am J Pathol. 1997 Aug;151(2):343-51 [9250148.001]
  • [Cites] Am J Surg Pathol. 1997 Dec;21(12):1420-32 [9414185.001]
  • [Cites] Am J Pathol. 2001 May;158(5):1889-90 [11337388.001]
  • (PMID = 15858125.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / bcl-X Protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC1770666
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4. Asano N, Suzuki R, Ohshima K, Kagami Y, Ishida F, Yoshino T, Ogawa H, Morishima Y, Nakamura S: Linkage of expression of chemokine receptors (CXCR3 and CCR4) and cytotoxic molecules in peripheral T cell lymphoma, not otherwise specified and ALK-negative anaplastic large cell lymphoma. Int J Hematol; 2010 Apr;91(3):426-35
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  • [Title] Linkage of expression of chemokine receptors (CXCR3 and CCR4) and cytotoxic molecules in peripheral T cell lymphoma, not otherwise specified and ALK-negative anaplastic large cell lymphoma.
  • Peripheral T cell lymphoma not otherwise specified (PTCL-N) and ALK-negative anaplastic large cell lymphoma (ALCL) are heterogeneous categories with poor diagnostic reproducibility.
  • To clarify the biologic features of these categories, we investigated the expression of two chemokine receptors, type 1 (Th1/Tc1)-associated CXCR3 and type 2 (Th2/Tc2)-associated CCR4 in 110 PTCL-N and 35 ALK-negative ALCL cases, as well as the expression of cytotoxic molecules (CM).
  • CXCR3 and CCR4 were expressed in 69 (63%) and 37 (34%) of PTCL-N, and in 12 (34%) and 6 (17%) of ALK-negative ALCL, respectively.
  • In PTCL-N, type 1 pattern (CXCR3(+)CCR4(-)) was dominant (52%), whereas in ALK-negative ALCL, 54% were negative for both (P < 0.0001).
  • CM was expressed in 38% of PTCL-N and 51% of ALK-negative ALCL.
  • In contrast, type 2 pattern (CXCR3(-)CCR4(+)) was recognized in the CM-negative group only.
  • Among type 1 disease, CM-positive cases had a higher female ratio and more aggressive clinical features than CM-negative cases and a poorer prognosis (P = 0.006).
  • In both PTCL-N and ALK-negative ALCL, CM-positive type 1 disease had an extremely poor prognosis.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, T-Cell / metabolism. Receptors, CCR4 / metabolism. Receptors, CXCR3 / metabolism

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  • (PMID = 20217288.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CCR4 protein, human; 0 / CXCR3 protein, human; 0 / Receptors, CCR4; 0 / Receptors, CXCR3
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5. Wu F, Wang P, Zhang J, Young LC, Lai R, Li L: Studies of phosphoproteomic changes induced by nucleophosmin-anaplastic lymphoma kinase (ALK) highlight deregulation of tumor necrosis factor (TNF)/Fas/TNF-related apoptosis-induced ligand signaling pathway in ALK-positive anaplastic large cell lymphoma. Mol Cell Proteomics; 2010 Jul;9(7):1616-32
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  • [Title] Studies of phosphoproteomic changes induced by nucleophosmin-anaplastic lymphoma kinase (ALK) highlight deregulation of tumor necrosis factor (TNF)/Fas/TNF-related apoptosis-induced ligand signaling pathway in ALK-positive anaplastic large cell lymphoma.
  • The oncogenic fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), found exclusively in a subset of ALK-positive anaplastic large cell lymphoma, promotes tumorigenesis by exerting its constitutively active tyrosine kinase activity.
  • Thus, characterization of the NPM-ALK-induced changes in the phosphoproteome will likely provide insights into the biology of this oncoprotein.
  • GP293 cells transfected with either NPM-ALK or an NPM-ALK mutant with decreased tyrosine kinase activity (negative control) were used.
  • We identified 506 phosphoproteins detectable in NPM-ALK-expressing cells but not in the negative control.
  • Bioinformatics analysis revealed that these phosphoproteins carry a wide diversity of biological functions, some of which have not been described in association with NPM-ALK, such as the tumor necrosis factor (TNF)/Fas/tumor necrosis factor-related apoptosis-induced ligand (TRAIL) signaling pathway and the ubiquitin proteasome degradation pathway.
  • In particular, modulations of the TNF/Fas/TRAIL pathway by NPM-ALK were supported by our antibody microarray data.
  • Further validation of the TNF/Fas/TRAIL pathway was performed in ALK(+) anaplastic large cell lymphoma (ALCL) cell lines with knockdown of NPM-ALK using short interference RNA, resulting in the loss of the tyrosine phosphorylation of tumor necrosis factor receptor-associated protein 1 (TRAP1) and receptor-interacting protein 1, two crucial TNF signaling molecules.
  • Functional analyses revealed that knockdown of TRAP1 facilitated cell death induced by TRAIL or doxorubicin in ALK(+) ALCL cells.
  • This suggests that down-regulation of TRAP1 in combination with TRAIL or doxorubicin might be a potential novel therapeutic strategy for ALK(+) ALCL.
  • These findings demonstrated that our strategy allowed the identification of novel proteins downstream of NPM-ALK that contribute to the maintenance of neoplastic phenotype and holds great potential for future studies of cellular tyrosine kinases in normal states and diseases.


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

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  • (PMID = 20644462.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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7. Monaco S, Tsao L, Murty VV, Nandula SV, Donovan V, Oesterheld J, Bhagat G, Alobeid B: Pediatric ALK+ anaplastic large cell lymphoma with t(3;8)(q26.2;q24) translocation and c-myc rearrangement terminating in a leukemic phase. Am J Hematol; 2007 Jan;82(1):59-64
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  • [Title] Pediatric ALK+ anaplastic large cell lymphoma with t(3;8)(q26.2;q24) translocation and c-myc rearrangement terminating in a leukemic phase.
  • Pediatric ALK-positive anaplastic large cell lymphoma (ALK+ ALCL) is usually associated with a favorable prognosis.
  • ALK+ ALCL associated with a leukemic phase is uncommon, but has been associated with an aggressive clinical course and unfavorable prognosis.
  • Overexpression of c-myc has been shown to be a consistent finding in ALK+, but not ALK-negative ALCL (ALK- ALCL), and the c-myc gene is considered a downstream target of deregulated ALK signaling.
  • We describe a pediatric ALK+ ALCL with a leukemic phase at relapse.
  • Lymphoma cells showed aberrant ALK expression and c-myc overexpression.
  • The findings in this case demonstrate the association of peripheral blood leukemic involvement and aggressive clinical course, and suggest that other factors, such as c-myc rearrangement, may be responsible for the aggressive clinical behavior in ALK+ ALCL.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Gene Rearrangement. Leukemia / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins c-myc / genetics. Translocation, Genetic

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  • (PMID = 16955462.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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8. Zhou X, Sun C, Wang J, Mao J, Guo H: Rapid fatal pulmonary complications in a Chinese patient after bortezomib treatment for ALK-negative anaplastic large-cell lymphoma. Clin Lymphoma Myeloma Leuk; 2010 Apr;10(2):152-4
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  • [Title] Rapid fatal pulmonary complications in a Chinese patient after bortezomib treatment for ALK-negative anaplastic large-cell lymphoma.
  • Herein, we present a case of rapid fatal pulmonary complications in a patient with ALK-negative anaplastic large-cell lymphoma after receiving a treatment with bortezomib.
  • [MeSH-minor] Aged. Asian Continental Ancestry Group. Bortezomib. Enzyme Inhibitors / therapeutic use. Fatal Outcome. Hematologic Neoplasms / chemically induced. Hematologic Neoplasms / enzymology. Humans. Lung / enzymology. Lung / metabolism. Lymphoma, Large B-Cell, Diffuse / chemically induced. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large-Cell, Anaplastic / chemically induced. Lymphoma, Large-Cell, Anaplastic / enzymology. Male

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  • (PMID = 20371451.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
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9. Lu Y, Zhao X, Wang E, Chen W, Huang Q: ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as "leukemic phase". Leuk Res; 2010 Apr;34(4):475-82
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  • [Title] ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as "leukemic phase".
  • CD30-positive anaplastic large cell lymphoma (ALCL) is a distinctive malignant large cell lymphoma of T-cell lineage, often presenting in lymph node or extranodal sites.
  • ALCL cases with extensive bone marrow and peripheral blood involvement manifested as "leukemic phase" are extremely rare and the most of those cases reported are anaplastic large cell lymphoma kinase (ALK) positive ALCL in childhood population.
  • Here we report four adult cases of ALK-negative ALCL with extensive bone marrow and peripheral blood involvement manifested as "leukemic phase".
  • Circulating large lymphoma cells varied from 20 to 80% in peripheral blood and bone marrow biopsy showed various nodular or interstitial infiltrates.
  • By reviewing the clinicopathologic data of previously reported ALCL cases with extensive bone marrow and peripheral blood involvement, there appears to be of large variations in regard to the patient's age, morphologic variants, immunophenotypic or genotypic characteristics of the disease.
  • While most cases of ALCL with peripheral blood and bone marrow involvement were ALK-positive or carrying t(2;5) translocation, rare ALK-negative cases were also present.
  • Leukemic ALCL patients usually have unfavourable prognosis, regardless of ALK expression.
  • [MeSH-major] Bone Marrow Neoplasms / secondary. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / genetics

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19695703.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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10. Kameoka J, Ichinohasama R, Inoue H, Yamamoto J, Yokoyama H, Tomiya Y, Yamada M, Ishizawa K, Harigae H, Sawai T, Sasaki T: CD26, together with cell surface adenosine deaminase, is selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma. Leuk Lymphoma; 2006 Oct;47(10):2181-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD26, together with cell surface adenosine deaminase, is selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma.
  • CD26/dipeptidyl peptidase IV is a cell surface antigen with multiple biological functions.
  • Although its involvement in tumor biology has been suggested, the significance of its expression in malignant lymphoma has not been clarified in detail.
  • This study examined the expression of CD26 and cell surface adenosine deaminase (ADA) in 42 cases of Hodgkin's lymphoma (HL) and T-cell lymphoma by immunohistochemistry on frozen sections.
  • CD26 was expressed in three of 14 cases of HL, in four of eight cases of anaplastic large cell lymphoma (ALCL), in two of nine cases of peripheral T-cell lymphoma, in one of six cases of lymphoblastic lymphoma and in none of three cases of adult T-cell lymphoma/leukemia.
  • Expression of cell surface ADA was fully correlated with the expression of CD26 and expression of CD26/ADA in ALCL and HL was also completely correlated with the expression of p80 and epithelial membrane antigen.
  • Of 10 CD26-positive patients, seven had fever and elevated CRP at initial diagnosis and over a median follow-up of 61 months (range, 7 - 152 months) only three survived.
  • This study suggested that CD26 is selectively expressed on ALK-positive, but not on ALK-negative, ALCL and HL.
  • This is also the first report to demonstrate that ADA is coexpressed with CD26 on the cell surface of malignant neoplasms in vivo.
  • [MeSH-major] Adenosine Deaminase / biosynthesis. Cell Membrane / enzymology. Dipeptidyl Peptidase 4 / biosynthesis. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / biosynthesis

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  • (PMID = 17071493.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.5.4.4 / Adenosine Deaminase
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11. Mencía-Gutiérrez E, Gutiérrez-Díaz E, Salamanca J, Martínez-González MA: Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL). Int J Dermatol; 2006 Jun;45(6):766-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cutaneous presentation on the eyelid of primary, systemic, CD30+, anaplastic lymphoma kinase (ALK)-negative, anaplastic large-cell lymphoma (ALCL).
  • AIM: To report an unusual case of cutaneous presentation on the eyelid of systemic (or nodal), CD30+, anaplastic large-cell lymphoma (ALCL).
  • RESULTS: The histopathologic and immunohistochemical diagnosis was ALCL, T-cell phenotype, strongly positive for CD43 and CD30, and negative for CD3, anaplastic lymphoma kinase (ALK), and B-cell antigens.
  • CONCLUSIONS: Primary, systemic, CD30+, ALK-negative, ALCL presentations generally have a poor prognosis and tend to occur in older individuals, although the clinical outcome is highly variable and difficult to predict in individual cases.
  • Only three cases of ALCL have been described in the ocular adnexae and none was ALK-negative.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Eyelid Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / analysis

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  • (PMID = 16796648.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD30; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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12. Shi X, Franko B, Frantz C, Amin HM, Lai R: JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells. Br J Haematol; 2006 Oct;135(1):26-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells.
  • As STAT3 activation is pathogenetically important in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ ALCL), we investigated whether JSI-124 can mediate significant inhibitory effects in this cell type.
  • In two ALK+ ALCL cell lines (Karpas 299 and SU-DHL-1), JSI-124 significantly reduced the number of viable cells to 50% of that of negative controls at a dose of 5-10 micromol/l at 24 h and 1-1.25 micromol/l at 48 h.
  • JSI-124 decreased the phosphorylated-STAT3 and -Janus kinase-3 (JAK3) levels in a dose-dependent fashion, and these changes were coupled with significant decreases in several STAT3 downstream targets, including mcl-1, bcl-2, bcl-xL and cyclin D3.
  • Interestingly, JSI-124 also dramatically decreased the protein levels of JAK3 and nucleophosmin (NPM)-ALK, and these effects were reversible by MG132.
  • Our data support that JSI-124 is a potentially useful therapeutic agent for ALK+ ALCL.
  • In addition to its role as a tyrosine kinase inhibitor, JSI-124 appears to be involved in regulating proteosome degradation for proteins such as JAK3 and NPM-ALK.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Triterpenes / pharmacology
  • [MeSH-minor] Blotting, Western. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Janus Kinase 3. Signal Transduction / drug effects. Tumor Cells, Cultured

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  • (PMID = 16939498.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / JAK3 protein, human; 0 / Triterpenes; 2222-07-3 / cucurbitacin I; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 3
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13. 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


14. Castillo J, Milani C, Pantanowitz L: HIV-associated anaplastic large cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19563

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

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  • (PMID = 27961064.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Andorsky DJ, Yamada R, Steward K, De Vos S, Said J, Timmerman J: Expression of programmed death ligand 1 (PD-L1) by non-Hodgkin's lymphomas (NHL) and effect on tumor-associated T cells. J Clin Oncol; 2009 May 20;27(15_suppl):8526

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

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  • (PMID = 27960901.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Vera L, Reategui R, Beltran B, Morales D, Capellino A, Desposorio C, Castillo J: The clinicopathological spectrum of HIV-associated lymphoma: Eleven-year-experience in a general hospital in Peru. J Clin Oncol; 2009 May 20;27(15_suppl):e19561

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

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  • (PMID = 27961062.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Oki M, Isozaki M, Nakamura N, Kikuchi A, Tsuchiya T, Arbogast P, Ogawa Y, Ando K: A multivariate analysis for the survival of nodal peripheral T-cell lymphoma (PTCL). J Clin Oncol; 2009 May 20;27(15_suppl):e19521

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

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  • (PMID = 27960935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Thompson MA, Stumph J, Henrickson SE, Rosenwald A, Wang Q, Olson S, Brandt SJ, Roberts J, Zhang X, Shyr Y, Kinney MC: Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas. Hum Pathol; 2005 May;36(5):494-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression in anaplastic lymphoma kinase-positive and anaplastic lymphoma kinase-negative anaplastic large cell lymphomas.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive large T- or null-cell lymphoma.
  • Most ALCLs arising in children and young adults express a constitutively active receptor tyrosine kinase, anaplastic lymphoma kinase (ALK).
  • Anaplastic large cell lymphomas lacking ALK are clinically heterogeneous and their pathogenesis is unknown.
  • This study is the first complementary DNA (cDNA) microarray analysis using RNA extracted from tumor tissue (7 ALK+ ALCLs and 7 ALK- ALCLs) to identify genes differentially expressed or shared between the ALK+ and ALK- tumors.
  • Unsupervised hierarchical clustering using the top 11 most statistically significant discriminator cDNAs correctly grouped all ALK+ and ALK- tumors.
  • Hierarchical clustering analysis using the 44 cDNAs with the greatest differential expression between ALK+ and ALK- RNAs grouped 6 of 7 ALK+ ALCLs together and 1 ALK+ ALCL with the ALK- group.
  • In general, ALK+ tumors overexpress genes encoding signal transduction molecules (SYK , LYN , CDC37) and underexpress transcription factor genes (including HOXC6 and HOX A3 ) compared with the ALK- group.
  • Cyclin D3 was overexpressed in the ALK+ group and the cell cycle inhibitor p19INK4D was decreased in the ALK- group, suggesting different mechanisms of promoting G 1 /S transition.
  • Genes highly expressed in both ALK- and ALK+ ALCLs included kinases (LCK, protein kinase C, vav2, and NKIAMRE) and antiapoptotic molecules, suggesting possible common pathogenetic mechanisms as well.
  • [MeSH-major] Gene Expression. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Child. Cyclin D3. Cyclin-Dependent Kinase Inhibitor p19. Cyclins / genetics. Cyclins / metabolism. Female. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Receptor Protein-Tyrosine Kinases. Reverse Transcriptase Polymerase Chain Reaction


19. Fornari A, Piva R, Chiarle R, Novero D, Inghirami G: Anaplastic large cell lymphoma: one or more entities among T-cell lymphoma? Hematol Oncol; 2009 Dec;27(4):161-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic large cell lymphoma: one or more entities among T-cell lymphoma?
  • Anaplastic large cell lymphoma (ALCL) is a subtype of peripheral T-cell lymphoma (PTCL) first described in 1985 as a lymphoid malignancy characterized by marked cellular pleomorphism, propensity to grow cohesively, tendency to invade lymph node sinuses and diffuse expression of CD30 1.
  • The discovery of the t(2;5), involving the anaplastic lymphoma kinase (ALK) gene on chromosome 2 and the nucleophosmin (NPM) gene on chromosome 5 in the majority of systemic ALCL, has soon pointed out that ALCL is a clinically and biologically heterogeneous disease.
  • While ALK-positive (ALK+) ALCL is usually characterized by onset in children and young adults and better prognosis, epidemiology, poor outcome and possibly genetic defects of ALK-negative (ALK-) ALCL suggest that this neoplasms should be considered an independent pathological entity.
  • The aim of this review is to illustrate clinical features, histology, immunophenotype, genetics and biology of ALCL and discuss possible relationship(s) among different T-non-Hodgkin lymphoma (T-NHL).
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, T-Cell, Peripheral / pathology

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19358142.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 82
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20. 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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21. Rassidakis GZ, Thomaides A, Wang S, Jiang Y, Fourtouna A, Lai R, Medeiros LJ: p53 gene mutations are uncommon but p53 is commonly expressed in anaplastic large-cell lymphoma. Leukemia; 2005 Sep;19(9):1663-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p53 gene mutations are uncommon but p53 is commonly expressed in anaplastic large-cell lymphoma.
  • Anaplastic large-cell lymphoma (ALCL), as defined in the World Health Organization, is a heterogeneous category in which a subset of cases is associated with the t(2;5)(p23;q35) or variant translocations resulting in overexpression of anaplastic lymphoma kinase (ALK).
  • p53 has not been assessed in currently defined subsets of ALCL tumors.
  • In this study, we assessed ALK+ and ALK- ALCL tumors for p53 gene alterations using PCR, single-strand conformation polymorphism and direct sequencing methods.
  • We also immunohistochemically assessed ALCL tumors for p53 expression.
  • Three of 36 (8%) ALCL tumors (1/14 ALK+, 2/22 ALK-) with adequate DNA showed p53 gene mutations.
  • By contrast, p53 was overexpressed in 36 of 55 (65%) ALCL tumors (16 ALK+, 20 ALK-).
  • p21, a target of p53, was expressed in 15 of 31 (48%) ALCL tumors including seven of 15 (47%) p53-positive tumors. p21 expression in a subset of ALCL suggests the presence of functional p53 protein.
  • Apoptotic rate was significantly higher in p53-positive than p53-negative tumors (mean 2.78 vs 0.91%, P = 0.0003).
  • We conclude that the p53 gene is rarely mutated in ALK+ and ALK- ALCL tumors.
  • Nevertheless, wild-type p53 gene product is commonly overexpressed in ALCL and may be functional in a subset of these tumors.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, p53 / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Apoptosis / physiology. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Cell Proliferation. Cloning, Molecular. Cyclin-Dependent Kinase Inhibitor p21. Humans. Middle Aged. Mutation. Nuclear Proteins / biosynthesis. Nuclear Proteins / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-mdm2. Receptor Protein-Tyrosine Kinases. Sequence Analysis, DNA / methods

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  • (PMID = 15990866.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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22. Nelson M, Horsman DE, Weisenburger DD, Gascoyne RD, Dave BJ, Loberiza FR, Ludkovski O, Savage KJ, Armitage JO, Sanger WG: Cytogenetic abnormalities and clinical correlations in peripheral T-cell lymphoma. Br J Haematol; 2008 May;141(4):461-9
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  • [Title] Cytogenetic abnormalities and clinical correlations in peripheral T-cell lymphoma.
  • Cytogenetic correlations among most types of peripheral T-cell lymphoma (PTCL) have not been very informative to date.
  • This study aimed to identify recurrent chromosomal abnormalities in angioimmunoblastic T-cell lymphoma (AITL), ALK-negative anaplastic large cell lymphoma (ALK-ALCL) and peripheral T-cell lymphoma, unspecified (PTCL-US), and to evaluate their prognostic value.
  • In ALK(-) ALCL, gains of 1q (50%) and 3p (30%), and losses of 16pter (50%), 6q13q21 (30%), 15 (30%), 16qter (30%) and 17p13 (30%) were frequent findings.
  • However, cases with complex karyotypes, most frequently observed in ALK(-) ALCL and PTCL-US, had a significantly shorter OS.
  • [MeSH-major] Chromosome Aberrations. Lymphoma, T-Cell, Peripheral / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Follow-Up Studies. Humans. Immunoblastic Lymphadenopathy / genetics. Karyotyping. Lymphoma, Large-Cell, Anaplastic / genetics. Male. Middle Aged. Prognosis. Survival Analysis

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  • (PMID = 18341637.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
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23. Ma L, Katz Y, Sharan KP, Schwarting R, Kim AS: Epstein-Barr virus positive anaplastic large cell lymphoma: myth or reality? Int J Clin Exp Pathol; 2010;4(1):100-10
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  • [Title] Epstein-Barr virus positive anaplastic large cell lymphoma: myth or reality?
  • The World Health Organization (WHO) Classification of Tumours of Haematopoietic and Lymphoid Tissue, 2008 edition, states that anaplastic large cell lymphoma (ALCL) is "consistently negative for Epstein-Barr virus (EBV)".
  • The statement made by the WHO has led to the widespread belief that EBV can have no pathogenic role in ALCL.
  • Herein we report a case of an immunocompetent 35-year-old male who presented with hemophagocytic syndrome secondary to lymphoma for which diagnostic material consisted solely of a bone marrow biopsy.
  • The biopsy demonstrated large anaplastic cells which were uniformly positive for surface CD3, CD30 (strong membranous and Golgi expression), CD45, TIA-1 and Granzyme B but negative for ALK-1.
  • In-situ hybridization was strongly positive for EBER in the large neoplastic cells.
  • The uniformity of CD30 expression and positivity for cytotoxic markers on the anaplastic tumor cells raised the diagnostic possibility of an EBV-associated ALCL, ALK-.
  • Discussion of this case as well as a retrospective review of 64 cases of reported of EBV+ ALCL are presented.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Herpesvirus 4, Human / isolation & purification. Lymphoma, Large-Cell, Anaplastic / virology. Tumor Virus Infections / complications

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  • [Cites] Blood. 1985 Oct;66(4):848-58 [3876124.001]
  • [Cites] Blood. 2010 Nov 25;116(22):4546-59 [20699441.001]
  • [Cites] J Pathol. 2000 Aug;191(4):400-6 [10918215.001]
  • [Cites] Blood. 2000 Nov 1;96(9):2993-3000 [11049976.001]
  • [Cites] Laryngoscope. 2000 Dec;110(12):2081-4 [11129025.001]
  • [Cites] Br J Cancer. 2001 Apr 6;84(7):920-5 [11286472.001]
  • [Cites] J Virol. 2002 Apr;76(8):4080-6 [11907247.001]
  • [Cites] Hum Pathol. 2002 Feb;33(2):146-52 [11957137.001]
  • [Cites] Mod Pathol. 2002 Nov;15(11):1221-6 [12429802.001]
  • [Cites] Am J Clin Pathol. 2003 Feb;119(2):205-12 [12579990.001]
  • [Cites] Histopathology. 2003 Nov;43(5):462-9 [14636272.001]
  • [Cites] N Engl J Med. 2004 Mar 25;350(13):1328-37 [15044644.001]
  • [Cites] Hum Pathol. 2004 Apr;35(4):455-9 [15116326.001]
  • [Cites] J Clin Pathol. 1987 Sep;40(9):995-1015 [3312308.001]
  • [Cites] Int J Cancer. 1992 Jun 19;51(4):562-7 [1318268.001]
  • [Cites] Am J Pathol. 1992 Jun;140(6):1315-25 [1318639.001]
  • [Cites] Am J Pathol. 1992 Aug;141(2):457-65 [1323222.001]
  • [Cites] Blood. 1991 Nov 15;78(10):2666-73 [1668608.001]
  • [Cites] J Pathol. 1992 Nov;168(3):307-15 [1335046.001]
  • [Cites] Blood. 1994 Mar 15;83(6):1612-8 [8123852.001]
  • [Cites] Am J Surg Pathol. 1995 Jan;19(1):42-9 [7802137.001]
  • [Cites] Br J Dermatol. 1995 Oct;133(4):542-6 [7577580.001]
  • [Cites] Blood. 1996 Feb 1;87(3):1045-55 [8562929.001]
  • [Cites] Leuk Lymphoma. 1996 Jul;22(3-4):319-27 [8819081.001]
  • [Cites] Mod Pathol. 1997 Mar;10(3):210-5 [9071728.001]
  • [Cites] Am J Surg Pathol. 1997 Dec;21(12):1420-32 [9414185.001]
  • [Cites] Hum Pathol. 1997 Dec;28(12):1415-9 [9416699.001]
  • [Cites] Blood. 1998 Mar 15;91(6):2076-84 [9490693.001]
  • [Cites] Am J Hematol. 1999 Mar;60(3):205-14 [10072112.001]
  • [Cites] Am J Surg Pathol. 1999 Oct;23(10):1184-200 [10524519.001]
  • [Cites] Pathol Res Pract. 2004;200(10):669-79 [15648604.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2005 Dec;13(4):323-32 [16280661.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2472-9 [16636342.001]
  • [Cites] Int J Dermatol. 2006 Nov;45(11):1312-6 [17076712.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4163-9 [16902151.001]
  • [Cites] Arch Pathol Lab Med. 2006 Dec;130(12):1859-64 [17149964.001]
  • [Cites] Am J Clin Pathol. 2007 Jun;127(6):887-95 [17509986.001]
  • [Cites] Am J Clin Pathol. 2007 May;127(5):707-22 [17511113.001]
  • [Cites] Am J Clin Pathol. 2007 Aug;128(2):314-22 [17638668.001]
  • [Cites] Br J Haematol. 2008 Mar;140(5):516-26 [18275429.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5496-504 [18385450.001]
  • [Cites] Am J Clin Pathol. 2008 Sep;130(3):343-51 [18701406.001]
  • [Cites] J Mol Diagn. 2008 Nov;10(6):502-12 [18832464.001]
  • [Cites] J Clin Pathol. 2008 Nov;61(11):1160-7 [18755717.001]
  • [Cites] Am J Dermatopathol. 2008 Dec;30(6):567-71 [19033930.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2008;:272-9 [19074096.001]
  • [Cites] Oncogene. 2009 Nov 12;28(45):3997-4008 [19718051.001]
  • [Cites] Blood. 2010 Nov 11;116(19):3695-704 [20671118.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(3):547-61 [10653870.001]
  • (PMID = 21228932.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC3016108
  • [Keywords] NOTNLM ; ALK / Epstein-Barr virus / anaplastic large cell lymphoma
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24. Gustafson S, Medeiros LJ, Kalhor N, Bueso-Ramos CE: Anaplastic large cell lymphoma: another entity in the differential diagnosis of small round blue cell tumors. Ann Diagn Pathol; 2009 Dec;13(6):413-27
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  • [Title] Anaplastic large cell lymphoma: another entity in the differential diagnosis of small round blue cell tumors.
  • We saw in consultation a biopsy specimen from a 6-year old girl with anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • Immunohistochemical workup with a large panel of antibodies at another institution showed immunoreactivity for NB84 and neuron specific enolase (dim).
  • Antibodies specific for CD3, CD20, and CD45/LCA were negative; CD30 or ALK were not assessed.
  • At the time of our review, we considered the possibility of ALCL.
  • Immunohistochemical analysis for CD30 showed bright, uniform expression and ALK was positive in a nuclear and cytoplasmic pattern, confirming the diagnosis of ALK+ ALCL.
  • The purpose of this review is to discuss ALK+ ALCL and many of the other entities included under the rubric of small round blue cell tumor, with a focus on tumors that occur in children.
  • [MeSH-major] Lymphoma / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasms, Complex and Mixed / pathology. Neuroblastoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Rhabdomyosarcoma / pathology. Sarcoma, Ewing / pathology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Child. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Immunohistochemistry. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases


25. Nguyen JT, Condron MR, Nguyen ND, De J, Medeiros LJ, Padula A: Anaplastic large cell lymphoma in leukemic phase: extraordinarily high white blood cell count. Pathol Int; 2009 May;59(5):345-53
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  • [Title] Anaplastic large cell lymphoma in leukemic phase: extraordinarily high white blood cell count.
  • Anaplastic large cell lymphoma (ALCL) is a distinct type of T/null-cell non-Hodgkin lymphoma that commonly involves nodal and extranodal sites.
  • The World Health Organization of lymphoid neoplasms recognizes two types: anaplastic lymphoma kinase (ALK) positive or ALK negative, the former as a result of abnormalities involving the ALK gene at chromosome 2p23.
  • Patients with ALCL rarely develop a leukemic phase of disease, either at the time of initial presentation or during the clinical course.
  • Described herein is a patient with ALK+ ALCL, small cell variant, associated with the t(2;5)(p23;q35), who initially presented with leukemic involvement and an extraordinarily high leukocyte count of 529 x 10(9)/L, which subsequently peaked at 587 x 10(9)/L.
  • Despite chemotherapy the patient died 2(1/2) months after diagnosis.
  • In the literature review 20 well-documented cases are identified of ALCL in leukemic phase reported previously, with a WBC ranging from 15 to 151 x 10(9)/L.
  • Leukemic phase of ALCL occurs almost exclusively in patients with ALK+ ALCL, most often associated with the small cell variant and the t(2;5)(p23;q35), similar to the present case.
  • Patients with leukemic phase ALK+ ALCL appear to have a poorer prognosis than most patients with ALK+ ALCL.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / blood. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 19432678.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 19
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26. Vinogradova IuE, Lutsenko IN, Kaplanskaia IB, Vorob'ev IA, Samoĭlova RS, Gorgidze LA, Ryzhikova NA, Valiev TT, Giliazitdinova EA, Dzhulakian UL, Egorova EK, Zvonkov EE, Krasil'nikova BB, Magomedova AU, Margolin OV, Mar'in DS, Kremenetskaia AM, Kravchenko SK, Vorob'ev AI: [Efficacy of therapy of different variants of anaplastic large T-cell lymphomas]. Ter Arkh; 2008;80(7):33-7
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  • [Title] [Efficacy of therapy of different variants of anaplastic large T-cell lymphomas].
  • AIM: To compare efficacy of NHL-BFM-90 and CHOP-like courses in the treatment of anaplastic large cell lymphoma (ALCL).
  • MATERIAL AND METHODS: Twenty-two patients with ALCL participated in the study.
  • The diagnosis was made basing on the findings of clinical, device, morphological, immunohistochemical and molecular-genetic examinations with application of a panel of monoclonal antibodies to CD30, ALK, CD3, CD4, CDS, CD7, CD34, CD15, CD68, CD20, CD45RO, CD45RA, Ki-67.
  • 14 cases of 22 were negative by kinase of anaplastic lymphocytes (ALK-) and 8 were positive (ALK+).
  • Mean age of ALK-ALCL patients was 39.6 +/- 4.1 years, of ALK+ALCL patients - 23.4 +/- 2.6 years.
  • All 14 patients treated according to NHL-BFM-90 had ALCL stages III-IV with B-symptoms.
  • Of 8 ALCL patients treated initially according to other schemes, a complete remission was achieved in 4 patients (2 had stage II).
  • CONCLUSION: ALCL occurs more frequently in young and middle-aged patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • (PMID = 18763592.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 3.5.1.1 / Asparaginase; Q573I9DVLP / Leucovorin; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; BEACOPP protocol; CHOP protocol; MACOP-B protocol; PVDA protocol
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27. Miranda RN, Lin L, Talwalkar SS, Manning JT, Medeiros LJ: Anaplastic large cell lymphoma involving the breast: a clinicopathologic study of 6 cases and review of the literature. Arch Pathol Lab Med; 2009 Sep;133(9):1383-90
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  • [Title] Anaplastic large cell lymphoma involving the breast: a clinicopathologic study of 6 cases and review of the literature.
  • CONTEXT: Lymphomas involving the breast are rare, and most cases are of B-cell lineage; T-cell neoplasms represent less than 10% of all breast lymphomas.
  • OBJECTIVE: To define the clinicopathologic spectrum of anaplastic large cell lymphomas (ALCLs) involving the breast.
  • DESIGN: Six cases of ALCL involving the breast were identified at a single institution during 21 years.
  • There were 4 anaplastic lymphoma kinase- negative (ALK(-)) ALCL cases; 3 of these neoplasms developed around breast implants.
  • Two patients with ALK(-) ALCL had a history of cutaneous ALCL.
  • There were 2 ALK(+) ALCLs; both patients had stage IV disease.
  • Histologically, all neoplasms were composed of large anaplastic cells that were uniformly CD30(+) and expressed markers of T-cell lineage.
  • Four patients with adequate follow-up are alive, with a mean of 4.1 years (range, 1.5-9 years) after diagnosis of the breast tumor.
  • Included in this group are 2 patients with ALK(-) ALCL associated with breast implants who were alive 4 years and 9 years after diagnosis.
  • CONCLUSIONS: Including the 6 cases we describe, a total of 21 cases of ALCL involving the breast are reported.
  • Fifteen cases, all ALK(-), were associated with breast implants, suggesting a possible pathogenetic relationship, and associated with an excellent prognosis.
  • Patients with cutaneous ALCL can subsequently develop ALK(-) ALCL involving the breast, and these tumors can be associated with breast implants.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adult. Aged. Antigens, CD30 / metabolism. Biomarkers, Tumor / metabolism. Breast Implantation. Combined Modality Therapy. DNA, Neoplasm / analysis. Fatal Outcome. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Humans. Middle Aged. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Young Adult

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  • (PMID = 19722744.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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28. 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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29. 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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30. Lai R, Rassidakis GZ, Lin Q, Atwell C, Medeiros LJ, Amin HM: Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma. Hum Pathol; 2005 Sep;36(9):939-44
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  • [Title] Jak3 activation is significantly associated with ALK expression in anaplastic large cell lymphoma.
  • Janus kinase 3 (Jak3) is a tyrosine kinase that activates signal transducer and activator of transcription 3 (Stat3) in response to cytokine stimulation.
  • In previous studies of anaplastic large cell lymphoma (ALCL), we showed that inhibition of Jak3 down-regulates activated/phosphorylated Stat3 (pStat3), decreases anaplastic lymphoma kinase (ALK) enzymatic activity, and induces cell-cycle arrest and apoptosis in ALK-positive ALCL.
  • These findings implicate Jak3 as playing a significant role in the pathogenesis of ALK-positive ALCL; most likely via Stat3 and ALK activation.
  • To assess this possibility, we used immunohistochemical staining to evaluate the frequency of expression of Jak3 and its activated/phosphorylated form (pJak3) in 48 systemic ALCL tumors included in a tissue microarray. pJak3 was detected in 17 (81%) of 21 ALK-positive tumors, compared with 3 (11%) of 27 ALK-negative tumors (P < .0001, Fisher exact test).
  • pStat3 was present in 12 (86%) of 14 ALK-positive tumors and in 10 (40%) of 25 ALK-negative tumors assessed (P = .0078).
  • Of 12 ALK-positive/pStat3-positive tumors, 8 (67%) expressed pJak3, but none of 10 ALK-negative/pStat3-positive tumors expressed pJak3.
  • We conclude that Jak3 activation is predominantly restricted to ALK-positive ALCL tumors.
  • Most likely, Jak3 collaborates with ALK in activating Stat3, leading to cell survival, cell-cycle progression, and tumor growth.
  • In contrast, the mechanism of Stat3 activation in ALK-negative ALCL tumors appears to be independent of Jak3.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Child. Enzyme Activation. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Janus Kinase 3. Male. Middle Aged. Phosphorylation. Receptor Protein-Tyrosine Kinases

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  • (PMID = 16153455.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / JAK3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3
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31. Savage KJ, Harris NL, Vose JM, Ullrich F, Jaffe ES, Connors JM, Rimsza L, Pileri SA, Chhanabhai M, Gascoyne RD, Armitage JO, Weisenburger DD, International Peripheral T-Cell Lymphoma Project: ALK- anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project. Blood; 2008 Jun 15;111(12):5496-504
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  • [Title] ALK- anaplastic large-cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T-cell lymphoma, not otherwise specified: report from the International Peripheral T-Cell Lymphoma Project.
  • The International Peripheral T-Cell Lymphoma Project is a collaborative effort designed to gain better understanding of peripheral T-cell and natural killer (NK)/T-cell lymphomas (PTCLs).
  • Of the 1314 eligible patients, 181 had anaplastic large-cell lymphoma (ALCL; 13.8%) on consensus review: One hundred fifty-nine had systemic ALCL (12.1%) and 22 had primary cutaneous ALCL (1.7%).
  • Patients with anaplastic lymphoma kinase-positive (ALK(+)) ALCL had a superior outcome compared with those with ALK(-) ALCL (5-year failure-free survival [FFS], 60% vs 36%; P = .015; 5-year overall survival [OS], 70% vs 49%; P = .016).
  • However, contrary to prior reports, the 5-year FFS (36% vs 20%; P = .012) and OS (49% vs 32%; P = .032) were superior for ALK(-) ALCL compared with PTCL, not otherwise specified (PTCL-NOS).
  • Patients with primary cutaneous ALCL had a very favorable 5-year OS (90%), but with a propensity to relapse (5-year FFS, 55%).
  • In summary, ALK(-) ALCL should continue to be separated from both ALK(+) ALCL and PTCL-NOS.
  • Although the prognosis of ALK(-) ALCL appears to be better than that for PTCL-NOS, it is still unsatisfactory and better therapies are needed.
  • Primary cutaneous ALCL is associated with an indolent course.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / mortality. Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, T-Cell, Peripheral / mortality. Lymphoma, T-Cell, Peripheral / pathology. Protein-Tyrosine Kinases / immunology
  • [MeSH-minor] Adult. Asia. Diagnosis, Differential. Europe. Female. Follow-Up Studies. Humans. Immunophenotyping. International Cooperation. Male. Middle Aged. North America. Prognosis. Receptor Protein-Tyrosine Kinases. Recurrence. Retrospective Studies. Skin Neoplasms / immunology. Skin Neoplasms / mortality. Skin Neoplasms / pathology. Skin Neoplasms / therapy. Survival Analysis. Treatment Outcome

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  • (PMID = 18385450.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Investigator] Savage K; Connors J; Gascoyne R; Chhanabhai M; Wilson W; Jaffe E; Armitage J; Vose J; Weisenburger D; Anderson J; Ullrich F; Bast M; Hochberg E; Harris N; Levine A; Nathwani B; Miller T; Rimsza L; Montserrat E; Lopez-Guillermo A; Campo E; Cuadros M; Alvarez Ferreira J; Martinez Delgado B; Holte H; Delabie J; Rüdiger T; Müller-Hermelink K; Reimer P; Adam P; Wilhelm M; Schmitz N; Nerl C; Lister A; Norton A; MacLennan KA; Zinzani PL; Pileri S; Federico M; Bellei M; Coiffier B; Berger F; Tanin I; Wannakrairot P; Au W; Liang R; Loong F; Rajan S; Sng I; Tobinai K; Matsuno Y; Morishima Y; Nakamura S; Seto M; Tanimoto M; Yoshino T; Suzumiya J; Ohshima K; Kim WS; Ko YH
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32. Huang W, Li X, Yao X, Lu Y, Li B, Sheng W, Lu H, Jin A, Zhou X: Expression of ALK protein, mRNA and fusion transcripts in anaplastic large cell lymphoma. Exp Mol Pathol; 2009 Apr;86(2):121-6
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  • [Title] Expression of ALK protein, mRNA and fusion transcripts in anaplastic large cell lymphoma.
  • Systemic anaplastic large cell lymphoma (ALCL) can be divided into two subgroups, anaplastic lymphoma kinase (ALK)-positive and ALK-negative, based on the expression of ALK protein.
  • Expression of this protein is due to genetic alterations of ALK at 2p23.
  • Overall, observations on ALK protein, ALK mRNA, ALK-associated genetic alterations and their relationships, to one another are not often reported in the literature.
  • In this study, we investigated the expression of ALK protein, mRNA and fusion transcripts involving ALK and their relationships in ALCL and analyzed formalin-fixed, paraffin-embedded tissues.
  • Forty-five human cases were analyzed with immunohistochemistry for the ALK protein and RT-PCR for ALK mRNA and seven kinds of ALK involved fusion transcripts.
  • Our results showed that the expression of ALK protein, ALK mRNA and ALK fusion transcripts were significantly related to one another (P<0.01).
  • Consistent with the expression of ALK protein, patients presenting with ALK mRNA or ALK involved fusion transcripts were significantly younger than those lacking ALK gene alteration (P<0.01).
  • This study demonstrates expression of both ALK protein and ALK mRNA are positively correlated with expression of ALK-associated fusion transcripts.
  • Combined detection of ALK protein, ALK mRNA and ALK fusion transcripts can complement each other to aid in the diagnosis of ALCL.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19135051.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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33. 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

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  • (PMID = 17571585.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 3Z8479ZZ5X / Epirubicin; 6PLQ3CP4P3 / Etoposide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; Q20Q21Q62J / Cisplatin; UM20QQM95Y / Ifosfamide; VIP-E protocol
  • [Number-of-references] 15
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34. Vranovsky A, Ladicka M, Lakota J: Autologous stem cell transplantation in first-line treatment of high-risk aggressive non-Hodgkin's lymphoma. Neoplasma; 2008;55(2):107-12
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  • [Title] Autologous stem cell transplantation in first-line treatment of high-risk aggressive non-Hodgkin's lymphoma.
  • A single center, retrospective analysis evaluating the outcome of patients with poor-risk aggressive non-Hodgkin's lymphoma (NHL) treated with high-dose chemotherapy and autologous stem cell transplantation (ASCT) as a part of firstline therapy.
  • Forty-seven patients younger than 65 years with diffuse large B-cell lymphoma (DLBCL), mantle cell lymphoma (MCL), peripheral T-cell lymphoma (PTCL) or alk-negative anaplastic large cell lymphoma (ALCL) underwent ASCT between July 1997 and November 2005.
  • Patients with DLBCL and alk-negative ALCL had 2 or 3 age-adjusted International Prognostic Index risk factors.
  • Our results confirm the efficacy of high-dose therapy with ASCT during first-line treatment of patients with poor-prognosis aggressive lymphoma, with substantial number of patients cured by using this treatment approach.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, Non-Hodgkin / therapy

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  • (PMID = 18652043.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 11056-06-7 / Bleomycin; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; Q20Q21Q62J / Cisplatin; YL5FZ2Y5U1 / Methotrexate; DHAP protocol; MACOP-B regimen
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35. Kapur S, Tiemann M, Menke MA, Schubert C, Parwaresch R: The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases. Indian J Med Res; 2005 Jan;121(1):46-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of p53 and anaplastic lymphoma kinase genes in the progression of cutaneous CD30(+) lymphoproliferative diseases.
  • BACKGROUND AND OBJECTIVES: Molecular events that precede transformations from lymphomatoid palulosis (LyP) to mycosis fungoides (MF) or to cutaneous anaplastic large cell lymphoma (ALCL) in the CD 30(+) cutaneous lymphoproliferative diseases (LPDs) are not known.
  • Expression of the anaplastic lymphoma kinase (ALK) gene product has also been described as an important prognostic indicator in ALCL.
  • ALK positive systemic nodal ALCL are associated with a good prognosis.
  • However, primary cutaneous ALCL that are ALK negative have a better overall survival.
  • The current study was done to see if mutated p(53) gene or ALK reactivity were poor prognostic indicators in those patients with CD 30(+) cutaneous LPD who showed progression of the disease.
  • METHODS: Mutations of the p(53) gene and expression of the ALK gene product were analysed in 36 patients (23 of LyP and 13 of CD30(+) cutaneous ALCL).
  • Transformation occurred in 5 patients (4 from LyP to ALCL and 1 from MF to ALCL) and clinical progression in 4 patients with ALCL.
  • ALK gene products were not detected in any of the biopsy specimens of LyP and primary cutaneous ALCL.
  • INTERPRETATION AND CONCLUSION: Although 9 of 36 patients with cutaneous CD30(+) LPDs had progression of their disease, neither mutations of the p(53) gene nor ALK immunoreactivity were found in any of these biopsies.

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  • (PMID = 15713979.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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36. 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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37. Sung CO, Ko YH, Park S, Kim K, Kim W: Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma. J Korean Med Sci; 2005 Dec;20(6):952-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma.
  • To verify the spectrum of CD99-expressing lymphoid malignancy, an immunohistochemical study for CD99 was carried out in 182 cases of non-Hodgkin's lymphoma, including 21 lymphoblastic lymphomas, 11 small lymphocytic lymphomas, 9 mantle cell lymphomas, 12 follicular lymphomas, 37 diffuse large B cell lymphomas, 18 Burkitt's lymphomas, 28 NK/T-cell lymphomas, 8 angioimmunoblastic T-cell lymphomas, 23 peripheral T-cell lymphomas, unspecified, and 15 systemic anaplastic large cell lymphomas.
  • 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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  • [Cites] Ann Oncol. 1991 Feb;2 Suppl 2:33-8 [1646624.001]
  • [Cites] Am J Pathol. 1990 Nov;137(5):1047-57 [2173409.001]
  • [Cites] Histopathology. 1993 Dec;23(6):557-61 [8314240.001]
  • [Cites] Hum Pathol. 1994 Apr;25(4):396-9 [8163272.001]
  • [Cites] Am J Surg Pathol. 1994 May;18(5):486-94 [7513503.001]
  • [Cites] Blood. 1996 May 15;87(10):4340-7 [8639794.001]
  • [Cites] Hum Pathol. 1996 Dec;27(12):1273-6 [8958297.001]
  • [Cites] Mod Pathol. 1997 Apr;10(4):277-82 [9110287.001]
  • [Cites] J Immunol. 1997 Sep 1;159(5):2250-8 [9278313.001]
  • [Cites] Mod Pathol. 1998 Aug;11(8):769-73 [9720506.001]
  • [Cites] J Immunol. 1998 Nov 1;161(9):4671-8 [9794396.001]
  • [Cites] Br J Haematol. 1999 Jun;105(3):690-5 [10354133.001]
  • [Cites] J Korean Med Sci. 2005 Feb;20(1):50-5 [15716602.001]
  • [Cites] Mod Pathol. 2000 Apr;13(4):452-8 [10786814.001]
  • [Cites] Virchows Arch. 2000 Sep;437(3):270-4 [11037347.001]
  • [Cites] Am J Pathol. 2001 Aug;159(2):527-35 [11485911.001]
  • [Cites] Leuk Lymphoma. 2001 Aug;42(4):587-94 [11697486.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4540-6 [12036886.001]
  • [Cites] J Korean Med Sci. 2002 Aug;17(4):483-9 [12172043.001]
  • [Cites] FEBS Lett. 2003 Nov 20;554(3):478-84 [14623115.001]
  • [Cites] Cancer Cell. 2004 Apr;5(4):353-64 [15093542.001]
  • [Cites] Oncogene. 2004 Jul 22;23(33):5664-74 [15184883.001]
  • [Cites] Cancer Res. 1988 Nov 1;48(21):6127-31 [2844401.001]
  • [Cites] Blood. 1994 Jan 15;83(2):415-25 [7506950.001]
  • (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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38. 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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39. Georgakis GV, Li Y, Rassidakis GZ, Medeiros LJ, Younes A: The HSP90 inhibitor 17-AAG synergizes with doxorubicin and U0126 in anaplastic large cell lymphoma irrespective of ALK expression. Exp Hematol; 2006 Dec;34(12):1670-9
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  • [Title] The HSP90 inhibitor 17-AAG synergizes with doxorubicin and U0126 in anaplastic large cell lymphoma irrespective of ALK expression.
  • OBJECTIVE: Heat shock protein 90 (HSP90) chaperones and maintains the molecular integrity of a variety of signal transduction proteins, including the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) oncogenic protein, a genetic abnormality that is frequently observed in anaplastic large cell lymphoma (ALCL) cells.
  • Here we demonstrate that HSP90 is overexpressed in primary and cultured ALK-positive and ALK-negative ALCL cells, and we evaluate the potential role of the small molecule inhibitor of HSP90, 17-allylamino-17-demethoxygeldanamycin (17-AAG) in treating ALCL.
  • Apoptosis and cell-cycle arrest were determined by Annexin-V/propidium iodide and propidium iodide staining, respectively, and fluorescein-activated cell sorting analysis.
  • RESULTS: Treatment of cultured ALCL cells with 17-AAG induced cell-cycle arrest and apoptosis, irrespective of ALK expression.
  • At the molecular level, 17-AAG induced degradation of ALK and Akt proteins, dephosphorylated extracellular signal-regulated kinase, and degraded the cell-cycle regulatory protein cyclin D1 and its cyclin-dependent kinases, CDK4 and CDK6, but had a differential effect on p27 and p53 proteins.
  • Inhibition of extracellular signal-regulated kinase phosphorylation by the mitogen activated protein kinase inhibitor U0126 induced cell death in all ALCL cell lines, and sublethal concentration 17-AAG showed synergistic antiproliferative effects when combined with U0126 or doxorubicin.
  • CONCLUSION: Our data demonstrate that targeting HSP90 function by 17-AAG may offer a novel therapeutic strategy for ALCL, either as single-agent activity or by combining 17-AAG with conventional or targeted therapeutic schemes.
  • [MeSH-major] Benzoquinones / pharmacology. Butadienes / pharmacology. Doxorubicin / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / pharmacology. Lymphoma, Large-Cell, Anaplastic / metabolism. Nitriles / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis / drug effects. Caspase 3 / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D. Cyclin-Dependent Kinase 4 / drug effects. Cyclin-Dependent Kinase 4 / metabolism. Cyclin-Dependent Kinase 6 / drug effects. Cyclin-Dependent Kinase 6 / metabolism. Cyclins / drug effects. Cyclins / metabolism. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Drug Synergism. Extracellular Signal-Regulated MAP Kinases / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. G0 Phase / drug effects. G1 Phase / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / drug effects. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / drug effects. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphorylation. Receptor Protein-Tyrosine Kinases. Time Factors

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  • (PMID = 17157164.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Butadienes; 0 / Cyclin D; 0 / Cyclins; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Nitriles; 0 / U 0126; 4GY0AVT3L4 / tanespimycin; 80168379AG / Doxorubicin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.22.- / Caspase 3
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40. Momose S, Tamaru J, Kishi H, Mikata I, Mori M, Toyozumi Y, Itoyama S: Hyperactivated STAT3 in ALK-positive diffuse large B-cell lymphoma with clathrin-ALK fusion. Hum Pathol; 2009 Jan;40(1):75-82
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  • [Title] Hyperactivated STAT3 in ALK-positive diffuse large B-cell lymphoma with clathrin-ALK fusion.
  • Anaplastic lymphoma kinase (ALK)-positive large B-cell lymphoma is a rare subtype of diffuse large B-cell lymphoma (DLBCL).
  • Although a few cases of ALK-positive large B-cell lymphoma harbor nucleophosmin-ALK chromosomal translocation similar to ALK-positive anaplastic large cell lymphoma, most reported cases are characterized by t(2;17)(p23;q23) involving the clathrin gene.
  • Here, we report 2 cases of ALK-positive DLBCL.
  • The 2 cases presented similar morphologic features and immunohistochemical characteristics, that is, positivity for ALK, IgA, CD138, and MUM1; weak positivity for CD30 and CD79a; and negativity for CD20.
  • The clathrin-ALK transcript was identified by reverse transcription-polymerase chain reaction, and the sequence was determined by direct sequencing.
  • Recently, the essential role of STAT3 activation as well as STAT 5 activation in nucleophosmin-ALK fusion protein-mediated lymphomagenesis was reported.
  • However, differential effects of ALK-fusion variant proteins on proliferation, transformation, and invasion properties were reported.
  • Thus, we evaluated the phosphorylation status of STAT 3 and STAT 5, and found highly hyperphosphorylated STAT 3 on tyrosine 705 but not STAT 5 in our 2 cases of ALK-positive DLBCL with clathrin-ALK fusion.
  • Furthermore, STAT 5A expression was not detected in either of the ALK-positive DLBCL cases, although 11 of the 36 ALK-negative DLBCL cases revealed STAT 5A expression.
  • However, there were no significant associations between expression of survivin or BCL-X(L) and ALK positivity among the diffuse large B-cell lymphomas.
  • In summary, similar signaling transduction mechanism involving STAT proteins seems to underlie DLBCL harboring the clathrin-ALK or nucleophosmin-ALK fusion gene.
  • [MeSH-major] Clathrin / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Adult. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Cytarabine / administration & dosage. Doxorubicin / therapeutic use. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Prednisone / therapeutic use. Receptor Protein-Tyrosine Kinases. Recurrence. Remission Induction. Stem Cell Transplantation. Time Factors. Treatment Outcome. Vincristine / therapeutic use

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  • (PMID = 18755494.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Clathrin; 0 / Oncogene Proteins, Fusion; 0 / STAT3 Transcription Factor; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
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41. Damm-Welk C, Klapper W, Oschlies I, Gesk S, Röttgers S, Bradtke J, Siebert R, Reiter A, Woessmann W: Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation. Br J Haematol; 2009 Aug;146(3):306-9
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  • [Title] Distribution of NPM1-ALK and X-ALK fusion transcripts in paediatric anaplastic large cell lymphoma: a molecular-histological correlation.
  • Anaplastic large cell lymphomas (ALCL) in children express anaplastic lymphoma kinase (ALK) fusion genes, most commonly NPM1-ALK.
  • The distribution of X-ALK among 66 childhood ALCLs was analysed.
  • One ALCL was ALK-negative.
  • Reverse transcription polymerase chain reaction detected NPM1-ALK in 58 tumours, all showing nuclear and cytoplasmic ALK staining.
  • The remaining seven ALCL stained for ALK in the cytoplasm only: two expressed TPM3-ALK, one ATIC-ALK, one MYH9-ALK; three no TPM3-, TFG-, ATIC-, CLTC- or MYH9-ALK.
  • Almost 90% of paediatric ALK-positive ALCLs express NPM1-ALK.
  • There was complete concordance between ALK staining pattern and the presence of a typical/variant ALK fusion partner.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19545284.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / MYH9 protein, human; 0 / Molecular Motor Proteins; 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / Tropomyosin; 0 / oncoprotein CLTCL-ALK; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.6.4.1 / Myosin Heavy Chains
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42. Vassallo J, Lamant L, Brugieres L, Gaillard F, Campo E, Brousset P, Delsol G: ALK-positive anaplastic large cell lymphoma mimicking nodular sclerosis Hodgkin's lymphoma: report of 10 cases. Am J Surg Pathol; 2006 Feb;30(2):223-9
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  • [Title] ALK-positive anaplastic large cell lymphoma mimicking nodular sclerosis Hodgkin's lymphoma: report of 10 cases.
  • Anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL) are recognized as biologically distinct entities.
  • In the last 10 years, we have collected 380 cases of ALK-positive ALCL of which 10 cases were originally diagnosed as nodular sclerosis classic HL (NSHL) on conventional histopathological examination.
  • After immunostaining, these cases proved to be ALK-positive ALCL mimicking HL (so-called Hodgkin-like ALCL).
  • These cases account for 2.6% of our cases of ALK-positive ALCL (10 of 380 cases).
  • Neoplastic cells were positive for CD30 (10 of 10 cases), ALK protein (10 of 10 cases), epithelial membrane antigen (EMA) (9 of 9 cases), CD43 (6 of 9 cases), and perforin (8 of 8 cases), but negative for CD15 (10 of 10 cases), CD20 (10 of 10 cases), Pax5/BSAP (6 of 6 cases), and EBV (8 of 8 cases).
  • Although rare, Hodgkin-like ALCL may mimic NSHL, and it is advisable to include EMA in the first line panel and to ask for ALK staining in EMA-positive, CD15-negative lesions with morphologic features suggestive of NSHL.
  • [MeSH-major] Biomarkers, Tumor / analysis. Hodgkin Disease / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged, 80 and over. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Receptor Protein-Tyrosine Kinases. Sclerosis / pathology

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  • (PMID = 16434897.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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43. 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

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  • (PMID = 18564100.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
  • [Number-of-references] 29
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44. Ahmed B, Estey E, Manning J, David C, Keating MJ, Kantarjian H, Tsimberidou AM: Anaplastic large cell lymphoma with involvement of the pancreas presenting as panniculitis in a patient with a history of acute myeloid leukemia--case report and review of the literature. Haematologica; 2006 Dec;91(12 Suppl):ECR55
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  • [Title] Anaplastic large cell lymphoma with involvement of the pancreas presenting as panniculitis in a patient with a history of acute myeloid leukemia--case report and review of the literature.
  • An autopsy of the pancreas revealed clusters of large, atypical cells, which morphologically and immunophenotypically were consistent with CD30 positive, ALK-negative anaplastic large cell lymphoma (ALCL) of T-cell lineage and multifocal fat necrosis (panniculitis) in the peripancreatic adipose tissue.
  • This is the first case of ALCL of the pancreas and panniculitis in a patient with history of AML.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Lymphoma, Large-Cell, Anaplastic / diagnosis. Neoplasms, Second Primary / diagnosis. Pancreas / pathology. Panniculitis / etiology


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

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  • (PMID = 18495593.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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46. 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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47. 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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  • [Cites] Histopathology. 1994 Sep;25(3):283-6 [7821899.001]
  • [Cites] Mod Pathol. 1996 Jun;9(6):671-6 [8782206.001]
  • [Cites] Br J Haematol. 2000 Dec;111(3):826-34 [11122144.001]
  • [Cites] Chin Med J (Engl). 1998 Aug;111(8):762-4 [11245038.001]
  • [Cites] Hum Pathol. 2003 Sep;34(9):950-4 [14562294.001]
  • [Cites] J Neurosurg. 1991 May;74(5):757-62 [2013777.001]
  • [Cites] Am J Hematol. 2005 Mar;78(3):207-11 [15726592.001]
  • [Cites] Cancer. 1990 Oct 15;66(8):1781-8 [1698530.001]
  • [Cites] Br J Haematol. 2004 Oct;127(2):173-83 [15461623.001]
  • [Cites] Hum Pathol. 1990 Oct;21(10):1051-8 [2210728.001]
  • [Cites] Histopathology. 1997 Dec;31(6):563-7 [9447389.001]
  • [Cites] J Am Acad Dermatol. 1992 Jan;26(1):101-4 [1732314.001]
  • [Cites] Leuk Lymphoma. 2000 Jun;38(1-2):121-30 [10811454.001]
  • [Cites] J Dermatol. 1992 May;19(5):263-9 [1644950.001]
  • [Cites] Ann Hematol. 2000 Oct;79(10):581-4 [11100751.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2573-9 [7989931.001]
  • [Cites] Cancer. 1993 May 15;71(10):3156-64 [8490846.001]
  • [Cites] N Engl J Med. 1986 Apr 10;314(15):943-8 [3485768.001]
  • [Cites] J Cutan Pathol. 1992 Jun;19(3):226-31 [1401347.001]
  • [Cites] J Korean Med Sci. 1997 Oct;12(5):457-60 [9364306.001]
  • [Cites] Pathol Int. 2000 Sep;50(9):696-702 [11012982.001]
  • [Cites] Hum Pathol. 1991 Feb;22(2):200-2 [2001883.001]
  • [Cites] Histopathology. 1997 Dec;31(6):555-62 [9447388.001]
  • [Cites] Arch Pathol Lab Med. 1999 Apr;123(4):335-7 [10320147.001]
  • [Cites] Am J Surg Pathol. 2005 Oct;29(10):1284-93 [16160469.001]
  • [Cites] Am J Surg Pathol. 2001 Jul;25(7):865-74 [11420457.001]
  • [Cites] Cancer. 1991 Apr 15;67(8):2131-6 [2004333.001]
  • [Cites] Hautarzt. 1959 Aug;10:359-63 [14432547.001]
  • (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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48. Lee HW, Kim K, Kim W, Ko YH: ALK-positive diffuse large B-cell lymphoma: report of three cases. Hematol Oncol; 2008 Jun;26(2):108-13
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of three cases.
  • Diffuse large B-cell lymphoma positive for anaplastic lymphoma kinase (ALK(+) DLBCL) is a rare variant of diffuse large B-cell lymphoma, with characteristic morphological, immunohistochemical and cytogenetic features.
  • Only 34 cases of ALK-positive diffuse large B-cell lymphoma have so far been reported in the literature.
  • We examined three new cases, which showed similar characteristics to previously reported cases, but with peculiar nuclear-membrane staining for ALK protein in one patient and a 5'-ALK gene deletion in another.
  • The tumour cells showed immunoblastic/plasmablastic histology and were positive for ALK and Oct2, but negative for CD3, CD20, CD79a, CD30 and PAX5.
  • The staining pattern of ALK protein was cytoplasmic in two patients and associated with the nuclear membrane in one patient.
  • Fluorescence in situ hybridization (FISH) analysis using the ALK break-apart probe revealed ALK gene rearrangements in all three patients, with a 5'-ALK gene deletion in one patient.
  • These three cases suggest that different types of cytogenetic aberrations may involve the ALK gene in ALK-positive diffuse large B-cell lymphoma leading to peculiar immunohistochemical staining patterns.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / therapy. Protein-Tyrosine Kinases / biosynthesis. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Cell Nucleus / metabolism. Chromosome Aberrations. Cytogenetics. Female. Gene Deletion. Humans. Immunohistochemistry. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Receptor Protein-Tyrosine Kinases. Treatment Outcome

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  • (PMID = 18220322.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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49. Colomba A, Courilleau D, Ramel D, Billadeau DD, Espinos E, Delsol G, Payrastre B, Gaits-Iacovoni F: Activation of Rac1 and the exchange factor Vav3 are involved in NPM-ALK signaling in anaplastic large cell lymphomas. Oncogene; 2008 Apr 24;27(19):2728-36
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  • [Title] Activation of Rac1 and the exchange factor Vav3 are involved in NPM-ALK signaling in anaplastic large cell lymphomas.
  • The majority of anaplastic large cell lymphomas (ALCLs) express the nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) fusion protein, which is oncogenic due to its constitutive tyrosine kinase activity.
  • Transformation by NPM-ALK not only increases proliferation, but also modifies cell shape and motility in both lymphoid and fibroblastic cells.
  • We report that the Rac1 GTPase, a known cytoskeletal regulator, is activated by NPM-ALK in ALCL cell lines (Karpas 299 and Cost) and transfected cells (lymphoid Ba/F3 cells, NIH-3T3 fibroblasts).
  • Stimulation of Vav3 and Rac1 by NPM-ALK is under the control of Src kinases.
  • It involves formation of a signaling complex between NPM-ALK, pp60(c-src), Lyn and Vav3, in which Vav3 associates with tyrosine 343 of NPM-ALK via its SH2 domain.
  • Moreover, Vav3 is phosphorylated in NPM-ALK positive biopsies from patients suffering from ALCL, demonstrating the pathological relevance of this observation.
  • The use of Vav3-specific shRNA and a dominant negative Rac1 mutant demonstrates the central role of GTPases in NPM-ALK elicited motility and invasion.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Lymphoma, Large-Cell, Anaplastic / enzymology. Protein-Tyrosine Kinases / metabolism. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction / physiology. rac1 GTP-Binding Protein / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. NIH 3T3 Cells. Nuclear Proteins / physiology. Phosphatidylinositol 3-Kinases / physiology. Receptor Protein-Tyrosine Kinases. src-Family Kinases / physiology

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  • (PMID = 17998938.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Guanine Nucleotide Exchange Factors; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-vav; 0 / VAV3 protein, human; 0 / Vav3 protein, mouse; 117896-08-9 / nucleophosmin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases; EC 3.6.5.2 / rac1 GTP-Binding Protein
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50. Staber PB, Vesely P, Haq N, Ott RG, Funato K, Bambach I, Fuchs C, Schauer S, Linkesch W, Hrzenjak A, Dirks WG, Sexl V, Bergler H, Kadin ME, Sternberg DW, Kenner L, Hoefler G: The oncoprotein NPM-ALK of anaplastic large-cell lymphoma induces JUNB transcription via ERK1/2 and JunB translation via mTOR signaling. Blood; 2007 Nov 1;110(9):3374-83
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  • [Title] The oncoprotein NPM-ALK of anaplastic large-cell lymphoma induces JUNB transcription via ERK1/2 and JunB translation via mTOR signaling.
  • Anaplastic large cell lymphomas (ALCLs) are highly proliferating tumors that commonly express the AP-1 transcription factor JunB.
  • ALK fusions occur in approximately 50% of ALCLs, and among these, 80% have the t(2;5) translocation with NPM-ALK expression.
  • We report greater activity of JunB in NPM-ALK-positive than in NPM-ALK-negative ALCLs.
  • Specific knockdown of JUNB mRNA using small interfering RNA and small hairpin RNA in NPM-ALK-expressing cells decreases cellular proliferation as evidenced by a reduced cell count in the G2/M phase of the cell cycle.
  • Expression of NPM-ALK results in ERK1/2 activation and transcriptional up-regulation of JUNB.
  • Both NPM-ALK-positive and -negative ALCL tumors demonstrate active ERK1/2 signaling.
  • In contrast to NPM-ALK-negative ALCL, the mTOR pathway is active in NPM-ALK-positive lymphomas.
  • Pharmacological inhibition of mTOR in NPM-ALK-positive cells down-regulates JunB protein levels by shifting JUNB mRNA translation from large polysomes to monosomes and ribonucleic particles (RNPs), and decreases cellular proliferation.
  • Thus, JunB is a critical target of mTOR and is translationally regulated in NPM-ALK-positive lymphomas.
  • In conjunction with NPM-ALK, JunB enhances cell cycle progression and may therefore represent a therapeutic target.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Protein Kinases / physiology. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins c-jun / genetics. Proto-Oncogene Proteins c-jun / metabolism. Transcriptional Activation


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

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  • [Cites] Am J Surg Pathol. 1993 Sep;17(9):859-68 [8394652.001]
  • [Cites] Blood. 1996 Jan 1;87(1):284-91 [8547653.001]
  • [Cites] Blood. 1997 Feb 1;89(3):980-9 [9028330.001]
  • [Cites] Am J Pathol. 1997 Apr;150(4):1207-11 [9094977.001]
  • [Cites] Ann Oncol. 1997 Jun;8(6):583-92 [9261528.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2901-10 [9376569.001]
  • [Cites] Cancer Surv. 1997;30:77-86 [9547987.001]
  • [Cites] Drugs. 2007;67(3):333-50 [17335294.001]
  • [Cites] Haematologica. 2007 Apr;92(4):519-32 [17488663.001]
  • [Cites] Hum Pathol. 2007 Jun;38(6):940-5 [17509395.001]
  • [Cites] Blood Rev. 2007 Jul;21(4):201-16 [17512649.001]
  • [Cites] Cancer Res. 2007 Nov 15;67(22):10703-10 [18006812.001]
  • [Cites] Br J Haematol. 2008 Mar;140(5):516-26 [18275429.001]
  • [Cites] Oncogene. 2002 Apr 11;21(16):2493-503 [11971184.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Aug;34(4):354-62 [12112524.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1919-27 [12424201.001]
  • [Cites] Br J Haematol. 2003 Feb;120(4):671-8 [12588355.001]
  • [Cites] J Clin Oncol. 2004 May 1;22(9):1682-8 [15117990.001]
  • [Cites] Am J Pathol. 2004 Jun;164(6):2259-67 [15161658.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5496-504 [18385450.001]
  • [Cites] J Clin Oncol. 2008 Sep 1;26(25):4124-30 [18626005.001]
  • [Cites] Hematol Oncol. 2009 Dec;27(4):161-70 [19358142.001]
  • [Cites] Blood. 1999 Apr 15;93(8):2697-706 [10194450.001]
  • [Cites] Cancer Res. 1999 Jun 15;59(12):2776-80 [10383129.001]
  • [Cites] Am J Pathol. 1999 Oct;155(4):1353-9 [10514417.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):377-84 [10934142.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1605-7 [10942417.001]
  • [Cites] Haematologica. 2000 Sep;85(9):978-81 [10980638.001]
  • [Cites] Mod Pathol. 2001 Mar;14(3):219-28 [11266530.001]
  • [Cites] Clin Cancer Res. 2001 Jul;7(7):2031-40 [11448921.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):741-60 [11564061.001]
  • [Cites] Blood. 2002 Jan 15;99(2):409-26 [11781220.001]
  • [Cites] Oncogene. 2004 Jul 15;23(32):5426-34 [15184887.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3358-60 [15297316.001]
  • [Cites] Hum Pathol. 2005 May;36(5):494-504 [15948116.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1643-7 [16049513.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1255-64 [16210342.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1617-23 [16254137.001]
  • [Cites] Am J Surg Pathol. 2006 Feb;30(2):223-9 [16434897.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2407-15 [16763206.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2156-64 [17077326.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):270-5 [17185414.001]
  • [Cites] J Biol Chem. 2007 Apr 6;282(14):10252-62 [17261581.001]
  • [Cites] J Clin Invest. 2007 Mar;117(3):823-34 [17304354.001]
  • [Cites] Leuk Res. 2008 Jan;32(1):25-32 [17320171.001]
  • [Cites] Biochem J. 2009 Jun 15;420(3):345-61 [19459784.001]
  • [Cites] Leukemia. 2009 Nov;23(11):2129-38 [19657361.001]
  • [Cites] Blood. 2010 Feb 11;115(6):1226-37 [19965620.001]
  • [Cites] J Clin Oncol. 2010 Mar 20;28(9):1583-90 [20159827.001]
  • [Cites] Curr Hematol Malig Rep. 2009 Oct;4(4):236-44 [20425413.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2010 Dec;18(6):561-72 [20697266.001]
  • [Cites] Blood. 1985 Oct;66(4):848-58 [3876124.001]
  • [Cites] Am J Clin Pathol. 1995 Jan;103(1):82-9 [7817951.001]
  • [Cites] Blood. 1994 Dec 1;84(11):3648-52 [7949120.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] Histopathology. 1993 Aug;23(2):189-91 [8406393.001]
  • [Cites] Blood. 1996 Nov 15;88(10):4005-11 [8916967.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1394-404 [9028963.001]
  • [Cites] Blood. 1998 Mar 15;91(6):2076-84 [9490693.001]
  • [Cites] Am J Pathol. 1998 Sep;153(3):875-86 [9736036.001]
  • [Cites] Am J Surg Pathol. 1999 Jan;23(1):49-58 [9888703.001]
  • [Cites] Leuk Lymphoma. 1998 Apr;29(3-4):249-56 [9684923.001]
  • [Cites] Am J Surg Pathol. 2000 Nov;24(11):1537-43 [11075856.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3681-95 [11090048.001]
  • [Cites] J Clin Pathol. 2002 Nov;55(11):868-71 [12401829.001]
  • [Cites] Oncogene. 2003 Aug 21;22(35):5399-407 [12934099.001]
  • [Cites] Br J Haematol. 1992 Jun;81(2):203-11 [1322690.001]
  • [Cites] Lancet. 1992 May 16;339(8803):1195-6 [1349939.001]
  • [Cites] Histopathology. 2003 Nov;43(5):462-9 [14636272.001]
  • [Cites] Am J Surg Pathol. 2003 Dec;27(12):1513-22 [14657710.001]
  • [Cites] Br J Haematol. 1990 Feb;74(2):161-8 [2156548.001]
  • [Cites] Am J Surg Pathol. 1990 Apr;14(4):305-16 [2157342.001]
  • [Cites] Am J Surg Pathol. 1990 Oct;14(10):983-8 [2206085.001]
  • [Cites] Eur J Immunol. 1989 Jan;19(1):157-62 [2537734.001]
  • [Cites] Leukemia. 1989 Dec;3(12):866-70 [2555633.001]
  • [Cites] Am J Pathol. 1988 Jan;130(1):59-70 [2827494.001]
  • [Cites] Lancet. 1988 Feb 6;1(8580):292-3 [2893097.001]
  • [Cites] Br J Haematol. 1989 Jan;71(1):31-6 [2917127.001]
  • [Cites] Blood. 1995 Sep 1;86(5):1954-60 [7655022.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2139-46 [7718885.001]
  • [Cites] Blood. 1995 Jan 1;85(1):1-14 [7803786.001]
  • [Cites] Blood. 1994 Oct 15;84(8):2467-71 [7919366.001]
  • (PMID = 21331150.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3038421
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52. Macák J, Falková I, Smardová J, Kren L: [Lymphoma of the small intestine]. Cesk Patol; 2010 Jan;46(1):20-4
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  • [Title] [Lymphoma of the small intestine].
  • A series of eight small intestine lymphomas comprised two cases of follicular lymphoma (FL), one anaplastic large cell lymphoma (ALCL) ALK negative, and five cases of diffuse large B-cell lymphoma.
  • Immunohistochemistry revealed that the diffuse large B-cell lymphomas were of the non-germinal center type (non GC-DLBCL).
  • In one case of follicular lymphoma, microscopic foci of tumor were found in the intestinal mucosa which spread far from the primary nodule and probably beyond the resection border.
  • It is difficult to ascertain whether this phenomenon represents colonization of pre-existing non-neoplastic follicles by lymphoma or spreading of the tumor within the same tissue.
  • In this case, surgical removal of the lymphoma is problematic.
  • [MeSH-major] Intestinal Neoplasms / pathology. Intestine, Small. Lymphoma, Follicular / pathology. Lymphoma, Large B-Cell, Diffuse / pathology

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  • (PMID = 21280278.001).
  • [ISSN] 1210-7875
  • [Journal-full-title] Československá patologie
  • [ISO-abbreviation] Cesk Patol
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
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53. 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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54. 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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55. 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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56. 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


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

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  • (PMID = 17392503.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases
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58. Daar G, Küpeli S, Yalçin B, Kesik V, Orhan D, Büyükpamukçu M: Primary cutaneous anaplastic large cell lymphoma. Pediatr Hematol Oncol; 2010 Oct;27(7):558-63
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  • [Title] Primary cutaneous anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is characterized by proliferation of anaplastic large CD 30+ T-cell lymphoid cells with abundant cytoplasm.
  • Primary cutaneous ALCL is a rare form of ALCL, usually seen in elderly patients.
  • In this report, the authors present an unusual case of 15-year-old boy with a solitary left ear lobe mass, previously reported as keratoacanthoma which was later histopathologically and immunohistochemically diagnosed as T-cell phenotype, anaplastic lymphoma kinase (ALK)-negative primary cutaneous anaplastic large cell lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • (PMID = 20624005.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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59. Bonvini P, Zorzi E, Mussolin L, Monaco G, Pigazzi M, Basso G, Rosolen A: The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity. Haematologica; 2009 Jul;94(7):944-55
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  • [Title] The effect of the cyclin-dependent kinase inhibitor flavopiridol on anaplastic large cell lymphoma cells and relationship with NPM-ALK kinase expression and activity.
  • BACKGROUND: The loss of cell cycle regulation due to abnormal function of cyclin-dependent kinases (cdk) occurs in tumors and leads to genetic instability of chemotherapy-resistant cells.
  • In this study, we investigated the effect of the cdk inhibitor flavopiridol in anaplastic large cell lymphomas, in which unrestrained proliferation depends on NPM-ALK tyrosine kinase activity.
  • DESIGN AND METHODS: Effects of flavopiridol were examined in ALK-positive and -negative anaplastic large cell lymphoma cells by means of immunoblotting and immunofluorescence analyses to assess cdk expression and activity, quantitative real time reverse transcriptase polymerase chain reaction to measure drug-induced changes in transcription, and FACS analyses to monitor changes in proliferation and survival.
  • RESULTS: Treatment with flavopiridol resulted in growth inhibition of anaplastic large cell lymphoma cells, along with accumulation of subG(1) cells and disappearance of S phase without cell cycle arrest.
  • This correlated with induction of cell death through rapid mitochondrial damage, inhibition of DNA synthesis, and down-regulation of anti-apoptotic proteins and transcripts.
  • Notably, flavopiridol was less active in ALK-positive cells, as apoptosis was observed at higher concentrations and later time points, and resistance to treatment was observed in cells maintaining NPM-ALK signaling.
  • NPM-ALK inhibition affected proliferation but not survival of anaplastic large cell lym-phoma cells, whereas it resulted in a dramatic increase in apoptosis when combined with flavopiridol.
  • CONCLUSIONS: This work provides the first demonstration that targeting cdk is effective against anaplastic large cell lymphoma cells, and proves the critical role of NPM-ALK in the regulation of responsiveness of tumor cells with cdk dysregulation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Flavonoids / pharmacology. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / drug therapy. Piperidines / pharmacology. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Apoptosis. Bromodeoxyuridine / pharmacology. Cell Cycle. Cell Separation. Cell Survival. Dose-Response Relationship, Drug. Humans. Reverse Transcriptase Polymerase Chain Reaction. Subcellular Fractions. Time Factors


60. Reichard KK, McKenna RW, Kroft SH: ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature. Mod Pathol; 2007 Mar;20(3):310-9
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature.
  • We report detailed clinical and pathologic features of four cases of anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma (ALK-DLBCL), a rare entity with only 29 currently reported cases.
  • By immunohistochemistry and/or flow cytometry, they expressed cytoplasmic ALK-1, CD138, VS38 (3/3), monoclonal cytoplasmic light chain, CD45, EMA, CD4, and CD57 (2/3), and were negative for CD3, CD30, CD56, and TIA-1.
  • [MeSH-major] Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 17277765.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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61. Belousova IE, Kazakov DV, Sosna B, Sulc M, Michal M: [Small-cell variant of CD30+ -anaplastic large-cell lymphoma of the skin]. Arkh Patol; 2008 Mar-Apr;70(2):40-3
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  • [Title] [Small-cell variant of CD30+ -anaplastic large-cell lymphoma of the skin].
  • Three cases of the so-called variant of primary cutaneous CD30+ anaplastic large cell lymphoma (ALCL) are presented.
  • Microscopically, the tumors were composed of small cells with irregular nuclei that were immunohistochemically positive for CD3, CD5, CD7, and CD30 and negative for B-cell markers; there was focal ALK-1 positivity in 1 case.
  • Fhedium to large CD30+ cells were rarely found scattered in the infiltrate.
  • Two patients were alive and well 4 and 6 years after surgery, without evidence of cutaneous and extractaneous involvement (including the ALK+ patient).
  • Chemotherapy was performed and finally the patient underwent allogenic bone marrow transplantation; he died 3 years after the original diagnosis due to acute graft-versus-host disease and sepsis.
  • [MeSH-major] Antigens, CD30. Lymphoma, Large B-Cell, Diffuse / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD / immunology. Cell Size. Gene Rearrangement, B-Lymphocyte / immunology. Gene Rearrangement, T-Lymphocyte / immunology. Humans. Immunoglobulin Heavy Chains / immunology. Male. Middle Aged. Receptors, Antigen, T-Cell / immunology


62. 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


63. Stachurski D, Miron PM, Al-Homsi S, Hutchinson L, Harris NL, Woda B, Wang SA: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma with a complex karyotype and cryptic 3' ALK gene insertion to chromosome 4 q22-24. Hum Pathol; 2007 Jun;38(6):940-5
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  • [Title] Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma with a complex karyotype and cryptic 3' ALK gene insertion to chromosome 4 q22-24.
  • Anaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma (DLBCL) is a rare tumor that is frequently associated with t(2;17)(p23;q23), a translocation fusing the ALK gene at 2p23 to the clathrin heavy chain gene (CLTC) at 17q23.
  • Here, we report a unique case of ALK-positive DLBCL with plasmablastic morphology and focal cytoplasmic granular ALK stain in an HIV-negative 33-year-old man.
  • By conventional karyotyping, the lymphoma cells were near-tetraploid and included 4 structurally normal copies each of chromosomes 2 and 17.
  • Fluorescence in situ hybridization revealed an apparently normal, intact ALK gene on each of the 4 chromosome 2 homologs plus a cytogenetically cryptic ALK gene insertion into 2 of the 4 chromosome 4 homologs at band 4q22-24.
  • The lymphoma cells expressed CD138, lambda light chain, focal and weak CD30, and exhibited aberrant T-cell antigens, including perforin.
  • This case indicates that ALK-positive DLBCL is more heterogeneous at the cytogenetic/molecular level than previously recognized.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 4 / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 17509395.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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64. Chen CH, Chen SW, Shen WL, Chen TY, Tsao CJ, Huang WT: Successful allogeneic stem cell transplantation for an adult with refractory anaplastic lymphoma kinase-positive anaplastic large cell lymphoma. Int J Hematol; 2007 Feb;85(2):105-7
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  • [Title] Successful allogeneic stem cell transplantation for an adult with refractory anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK) expression exists in approximately 60% of anaplastic large cell lymphoma (ALCL) cases.
  • Compared with the ALK-negative cases, ALK-positive cases are usually characterized by a good response to chemotherapy and a good prognosis.
  • In the relapsed or refractory ALCL cases, high-dose chemotherapy followed by autologous stem cell transplantation has been widely used as a salvage therapy.
  • However, 40% of patients who received transplants after more than 2 complete remissions eventually experienced disease progression, despite receiving autologous stem cell transplantation.
  • Allogeneic stem cell transplantation has been proposed as a therapeutic option in refractory ALCL cases, but clinical reports of adult patients are rare.
  • Herein, we report the case of an adult with refractory ALK-positive ALCL who was successfully treated with salvage high-dose chemotherapy followed by allogeneic stem cell transplantation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, Large-Cell, Anaplastic / therapy. Stem Cell Transplantation

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  • (PMID = 17321986.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CEOP protocol 1; CVAD protocol
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65. Asano N, Suzuki R, Matsuo K, Kagami Y, Ishida F, Tamaru JI, Jin GS, Sato Y, Shimoyama Y, Yoshino T, Morishima Y, Nakamura S: Cytotoxic molecule expression is predictive of prognosis in Hodgkin's-like anaplastic large cell lymphoma. Histopathology; 2007 May;50(6):705-15
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  • [Title] Cytotoxic molecule expression is predictive of prognosis in Hodgkin's-like anaplastic large cell lymphoma.
  • AIMS: The Revised European American Lymphoma classification uses the term Hodgkin's-like anaplastic large cell lymphoma (HD-like ALCL) for borderline cases with features of both anaplastic large cell lymphoma (ALCL) and classical Hodgkin's lymphoma (HL).
  • The aim of this study was to clarify the association between cytotoxic molecule (CM) expression and clinical outcome in HD-like ALCL.
  • METHODS AND RESULTS: Subjects were 59 patients with HD-like ALCL, defined by nodal presentation without mediastinal bulky lesions, T- or null-cell phenotype, CD30+ anaplastic lymphoma kinase (ALK)- phenotype and by confluent sheets or nodules of large cells mimicking classic Hodgkin and Reed-Sternberg cells.
  • We evaluated the presenting features and prognosis of subjects on categorization into two defined groups, namely CM (TIA1 and/or granzyme B)-positive (n = 21) and CM-negative (n = 38).
  • Multivariate analysis confirmed that CM expression was an independent prognostic factor, in contrast to phenotypic categorization (T-cell vs. null-cell group), which had no prognostic impact on disease-specific survival.
  • CONCLUSION: CM expression is predictive of prognosis in HD-like ALCL.
  • [MeSH-major] Granzymes / metabolism. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / metabolism. Poly(A)-Binding Proteins / metabolism

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  • [ErratumIn] Histopathology. 2007 Jun;50(7):962
  • (PMID = 17493234.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Poly(A)-Binding Proteins; 0 / TIA1 protein, human; EC 3.4.21.- / Granzymes
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66. Kotoula V, Bobos M, Kostopoulos I, Kaloutsi V, Koletsa T, Karayannopoulou G, Papadimitriou CS: In situ detection of hTERT variants in anaplastic large cell lymphoma. Leuk Lymphoma; 2006 Aug;47(8):1639-50
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  • [Title] In situ detection of hTERT variants in anaplastic large cell lymphoma.
  • The expression of hTERT and its isoforms is difficult to assess in lymphoma tissues with the commonly used reverse transcription-polymerase chain reaction (RT-PCR) methods, because non-neoplastic lymphocytes expressing hTERT are always present in the lymphomatous infiltrates.
  • The present study aimed to investigate hTERT mRNA variants in anaplastic large cell lymphoma (ALCL) (n = 38) with in situ hybridization (ISH), along with the immunodetection of hTERT protein.
  • Although all ALCL examined were found positive for hTERT expression with RT-PCR, hTERT mRNAs were identified in 68% of these tumors with ISH, with a higher incidence in the group bearing ALK translocations (10 out of 11; 90.9%) compared to the ALK negative group (17 out of 27; 59.3%) (PPearson's = 0.002).
  • In approximately 50% of cases, only Bplus positive cells were identified, again with a higher incidence in the ALK positive compared to the ALK negative group (PPearson's = 0.016).
  • Aberrations in hTERT variant profiles and a decline in the expression of the B deleted isoform may be associated with the pathogenesis of ALCL, especially with respect to ALK positive tumors.
  • [MeSH-major] Genetic Variation. In Situ Hybridization / methods. Lymphoma, Large-Cell, Anaplastic / genetics. Telomerase / genetics

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  • (PMID = 16966278.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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67. Beltran B, Castillo J, Salas R, Quiñones P, Morales D, Hurtado F, Riva L, Winer E: ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature. J Hematol Oncol; 2009;2:11
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature.
  • BACKGROUND: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma (ALK-DLBCL) is a rare lymphoma with several clinicopathological differences from ALK-positive anaplastic large cell lymphoma (ALCL).
  • The latest WHO classification of lymphomas recognizes ALK-DLBCL as a separate entity.
  • By immunohistochemistry, cases were positive for cytoplasmic ALK, MUM1, CD45, and EMA; they marked negative for CD3, CD30 and CD20.
  • Studies for EBV and HHV-8 were negative.
  • CONCLUSION: ALK-DLBCL is a distinct variant of DLBCL with plasmacytic differentiation, which is characterized by a bimodal age incidence curve, primarily nodal involvement, plasmablastic morphology, lack of expression of CD20, aggressive behavior and poor response to standard therapies, although some cases can have prolonged survival as the cases reported in this study.
  • ALK-DLBCL does not seem associated to immunosuppression or the presence of EBV or HHV8.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / metabolism

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  • [Cites] Hum Pathol. 2009 Jan;40(1):75-82 [18755494.001]
  • [Cites] Am J Hematol. 2008 Oct;83(10):804-9 [18756521.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Am J Clin Pathol. 2001 Mar;115(3):396-403 [11242796.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3370-9 [11369626.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Mod Pathol. 2003 Aug;16(8):828-32 [12920229.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2638-41 [12750159.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2568-73 [12763927.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2642-4 [12816858.001]
  • [Cites] Am J Surg Pathol. 2003 Nov;27(11):1473-6 [14576483.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Am J Surg Pathol. 2004 Jun;28(6):736-47 [15166665.001]
  • [Cites] Hum Pathol. 2004 Oct;35(10):1285-8 [15492998.001]
  • [Cites] N Engl J Med. 1993 Sep 30;329(14):987-94 [8141877.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] Blood. 1997 Mar 1;89(5):1483-90 [9057627.001]
  • [Cites] N Engl J Med. 1997 Oct 30;337(18):1259-66 [9345074.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3913-21 [10339500.001]
  • [Cites] J Mol Diagn. 2005 Feb;7(1):17-27 [15681470.001]
  • [Cites] Pol J Pathol. 2005;56(1):37-45 [15921012.001]
  • [Cites] Curr Oncol Rep. 2005 Sep;7(5):357-63 [16091196.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1839-40 [16107887.001]
  • [Cites] Pediatr Blood Cancer. 2006 Mar;46(3):390-1 [16086416.001]
  • [Cites] Rinsho Ketsueki. 2005 Jul;46(7):501-6 [16440742.001]
  • [Cites] Pediatr Blood Cancer. 2006 May 1;46(5):649-53 [15852431.001]
  • [Cites] Nat Rev Cancer. 2006 Jul;6(7):493-505 [16794633.001]
  • [Cites] Zhonghua Bing Li Xue Za Zhi. 2006 Sep;35(9):529-34 [17134546.001]
  • [Cites] Mod Pathol. 2007 Mar;20(3):310-9 [17277765.001]
  • [Cites] Blood. 2007 Apr 1;109(7):2773-80 [17132719.001]
  • [Cites] Hum Pathol. 2007 Jun;38(6):940-5 [17509395.001]
  • [Cites] Eur J Haematol. 2007 Aug;79(2):166-9 [17635242.001]
  • [Cites] Cancer. 2007 Aug 25;111(4):224-33 [17554754.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2573-80 [18089849.001]
  • [Cites] J Cell Mol Med. 2008 Jan-Feb;12(1):126-44 [18039352.001]
  • [Cites] Korean J Lab Med. 2008 Apr;28(2):89-94 [18458503.001]
  • [Cites] Biochem J. 2008 Jun 15;412(3):415-23 [18498251.001]
  • [Cites] Hematol Oncol. 2008 Jun;26(2):108-13 [18220322.001]
  • (PMID = 19250532.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 39
  • [Other-IDs] NLM/ PMC2651189
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68. de Jong D, Vasmel WL, de Boer JP, Verhave G, Barbé E, Casparie MK, van Leeuwen FE: Anaplastic large-cell lymphoma in women with breast implants. JAMA; 2008 Nov 5;300(17):2030-5
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  • [Title] Anaplastic large-cell lymphoma in women with breast implants.
  • CONTEXT: Recently, we identified 2 patients with anaplastic large T-cell lymphoma (ALCL) negative for tyrosine kinase anaplastic lymphoma kinase (ALK-negative) in the fibrous capsule of silicone breast prostheses, placed for cosmetic reasons.
  • Although an increased risk of ALCL in patients with breast prostheses has been speculated, no studies have been conducted so far.
  • OBJECTIVE: To determine whether ALCL risk is associated with breast prostheses.
  • DESIGN: A search for all patients with lymphoma in the breast diagnosed in The Netherlands between 1990 and 2006 was performed through the population-based nationwide pathology database.
  • Conditional logistic regression analysis was performed to estimate the relative risk of ALCL associated with breast prostheses.
  • SETTING AND PATIENTS: Eleven patients with breast ALCL were identified in the registry.
  • For each case patient with ALCL in the breast, we selected 1 to 5 controls with other lymphomas in the breast, matched on age and year of diagnosis.
  • MAIN OUTCOME MEASURE: Association between breast implants and ALCL of the breast.
  • RESULTS: The 11 patients with ALCL of the breast were diagnosed between 1994 and 2006 at a median age of 40 years (range, 24-68 years).
  • In 5 of these patients, bilateral silicone breast prostheses had been placed 1 to 23 years before diagnosis.
  • Lymphoma classes of 35 eligible control patients were 12 diffuse large B-cell lymphomas, including 1 T-cell rich B-cell lymphoma; 5 Burkitt lymphomas; 10 mucosa-associated lymphoid tissue-type lymphoma; 3 follicular lymphomas; 3 peripheral T-cell lymphomas; and 2 indolent B-cell lymphomas, unclassified.
  • One of 35 control patients had a breast implant placed before diagnosis of lymphoma.
  • The odds ratio for ALCL associated with breast prostheses was 18.2 (95% confidence interval, 2.1-156.8).
  • CONCLUSIONS: These preliminary findings suggest an association between silicone breast prostheses and ALCL, although the absolute risk is exceedingly low due to the rare occurrence of ALCL of the breast (11 cases in The Netherlands in 17 years).


69. 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

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  • (PMID = 15621840.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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70. Tokura Y, Sugita K, Yagi H, Shimauchi T, Kabashima K, Takigawa M: Primary cutaneous anaplastic large cell lymphoma with fatal leukemic outcome in association with CLA and CCR4-negative conversion. J Am Acad Dermatol; 2007 Nov;57(5 Suppl):S92-6
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  • [Title] Primary cutaneous anaplastic large cell lymphoma with fatal leukemic outcome in association with CLA and CCR4-negative conversion.
  • A 70-year-old Japanese male presented with a 1-year history of skin tumors, which were diagnosed as primary cutaneous anaplastic large cell lymphoma (ALCL) because of the CD3(low+), CD4(+), CD25(+), CD30(+), CD45RO(+), CD71(+), HLA-DR(+), CD8(-), CD56(-), and NPM/ALK(-) phenotype and monoclonal T-cell receptor-rearranged property of tumor cells as well as the absence of systemic involvement.
  • At this time, the tumor cell was positive for cutaneous lymphocyte-associated antigen (CLA) and TH(2) chemokine receptor CCR4.
  • The eruption had repeatedly appeared and spontaneously regressed or regressed by virtue of several therapeutic modalities, including radiotherapy, interferon-alpha and chemotherapy, until the tumor cell invaded the gastric mucosa and spread to the peripheral blood 5 years later.
  • Flow cytometric monitoring of the phenotype of peripheral blood and skin-infiltrating lymphocytes disclosed that the expression of CLA and CCR4 on the tumor cells was converted from positive to negative in association with the leukemic change.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Leukemia / etiology. Lymphoma, Large B-Cell, Diffuse / complications. Lymphoma, Large B-Cell, Diffuse / metabolism. Membrane Glycoproteins / metabolism. Receptors, Chemokine / metabolism

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  • (PMID = 17938033.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / CCR4 protein, human; 0 / CTAGE1 protein, human; 0 / Membrane Glycoproteins; 0 / Receptors, CCR4; 0 / Receptors, Chemokine
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71. Rudzki Z, Rucińska M, Jurczak W, Skotnicki AB, Maramorosz-Kurianowicz M, Mruk A, Piróg K, Utych G, Bodzioch P, Srebro-Stariczyk M, Włodarska I, Stachura J: ALK-positive diffuse large B-cell lymphoma: two more cases and a brief literature review. Pol J Pathol; 2005;56(1):37-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ALK-positive diffuse large B-cell lymphoma: two more cases and a brief literature review.
  • Anaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma (DLBCL) is a rare, recently defined tumor distinct in many aspects from ALK-positive anaplastic large cell lymphoma (ALCL).
  • We present two additional cases of ALK+DLBCL recently diagnosed in our department and a review of literature.
  • A 48-year old man presented with a large upper neck mass growing slowly over 18 months.
  • Histologically the tumor was diagnosed as an ALK-positive diffuse large B-cell lymphoma. with plasmablastic features.
  • Large, frequently intrasinusoidal tumor cells expressed CD138, EMA, weakly IgA and kappa, but were negative for other B-cell markers, T-cell markers and CD30.
  • The ALK staining was cytoplasmic with the increased intensity in the Golgi area.
  • At the diagnosis the patient manifested with the stage IIIB.
  • The patient died of massive bleeding from his decomposing tumor 3 months after the diagnosis.
  • The tumor showed immunoblastic/anaplastic morphology, with some Reed-Sternberg-like cells positive for ALK.
  • ALK immunostaining was cytoplasmic, weak in a routine immunostain, enhanced with double (proteinase + pressure cooker) antigen retrieval.
  • FISH was consistent with the t(2;5)/nucleophosmin(NPM)-ALK rearrangement.
  • ALK-positive DLBCL affects mostly middle-aged men, shows generally poor but stage-dependent prognosis (at least 60% mortality rate), presents typically as a lymph node-based disseminated disease, and very rarely involves the bone marrow.
  • Genetic studies showed that the majority of ALK+DLBCL cases are characterized by the clathrin (CLTC)-ALK fusion and in a few cases the NPM-ALK rearrangement has been found.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 15921012.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
  • [Number-of-references] 17
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72. Shi Y, Chen G, Zhou XG, Gong LP, Yu R, Zheng YY, Xie JL, Jin Y: [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study]. Zhonghua Bing Li Xue Za Zhi; 2010 Apr;39(4):235-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinicopathologic features of 66 cases of anaplastic lymphoma kinase positive and negative systemic anaplastic large cell lymphoma: a comparative study].
  • OBJECTIVE: To study the clinicopathologic features of 66 cases of primary systemic anaplastic large cell lymphoma (ALCL), with emphasis on the differences between ALK-positive and ALK-negative cases.
  • METHODS: The clinical data of 66 cases of ALCL was analyzed.
  • Immunohistochemical study for CD30, ALK protein, epithelial membrane antigen, CD2, CD3, granzyme B and TIA-1 was carried out.
  • The differences between ALK-positive and ALK-negative cases were statistically analyzed.
  • RESULTS: There were 48 cases of ALK-positive ALCL and 18 cases of ALK-negative ALCL.
  • The patients with ALK-positive ALCL were younger than those with ALK-negative ALCL (P < 0.05), with the median age being 18 years and 36 years, respectively.
  • Fever, especially hyperpyrexia, was more commonly observed in ALK-positive ALCL patients than in ALK-negative ALCL patients (33 cases versus 4 cases, P < 0.05).
  • The overall survival rate and median duration of survival in patients with ALK-positive ALCL were higher and longer than those in patients with ALK-negative ALCL (80% versus 71%; 21 months versus 12.5 months, P > 0.05).
  • There were however no significant differences in histology between ALK-positive ALCL and ALK-negative ALCL.
  • "Hallmark" cells were seen in most of the ALCL cases.
  • Most ALK-positive cases belonged to the common variant (35 cases).
  • Small cell variant and sarcomatoid subtype were found only in few cases (3 cases and 2 cases, respectively).On the other hand, common variant (17 cases) constituted the majority of ALK-negative ALCL.
  • Immunohistochemical study showed that ALK-positive ALCL always expressed CD30 and epithelial membrane antigen.
  • ALK-positive ALCL more often expressed epithelial membrane antigen (100% versus 72%; P < 0.05) but less so for T-cell markers (including CD2, CD3, CD43 and CD45RO).
  • Cytotoxic molecules were more commonly expressed in ALK-positive ALCL (P > 0.05).
  • EBER was negative in all cases studied.
  • FISH showed that in ALK-positive ALCL, 1 case had normal ALK gene, 1 had deletion and multicopy and 2 had deletion.
  • On the other hand, 1 case of ALK-negative ALCL had normal ALK gene.
  • CONCLUSIONS: While there are no significant morphologic differences between ALK-positive ALCL and ALK-negative ALCL, the clinical features, immunophenotypes and genetic features of both groups vary.
  • These differences are helpful in guiding the differential diagnosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antigens, CD30 / metabolism. Child. Child, Preschool. Diagnosis, Differential. Female. Follow-Up Studies. Gene Deletion. Humans. Male. Malignant Hyperthermia / etiology. Middle Aged. Mucin-1 / metabolism. Neoplasm Recurrence, Local. Receptor Protein-Tyrosine Kinases. Survival Rate. Young Adult

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  • (PMID = 20654121.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Mucin-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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73. Kansal R, Sait SN, Block AW, Ward PM, Kelly FL, Cheney RT, Czuczman M, Brecher ML, Barcos M: Extra copies of chromosome 2 are a recurring aberration in ALK-negative lymphomas with anaplastic morphology. Mod Pathol; 2005 Feb;18(2):235-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extra copies of chromosome 2 are a recurring aberration in ALK-negative lymphomas with anaplastic morphology.
  • The purpose of this study was to evaluate fluorescence in situ hybridization abnormalities of the 2p23 anaplastic lymphoma kinase (ALK) gene loci in lymphomas with anaplastic morphology.
  • We studied 24 anaplastic large cell lymphomas (ALCL) classified by World Health Organization criteria [17 primary nodal/systemic (10 ALK+, 7 ALK-), seven primary cutaneous], and 17 additional non-Hodgkin's lymphomas [one ALK+ B-lineage lymphoma, 14 ALK- diffuse large B-cell lymphomas (seven anaplastic variants, five nonanaplastic, two secondary CD30+), two follicular lymphomas].
  • ALK- lymphomas with anaplastic morphology showed extra nonrearranged anaplastic lymphoma kinase gene loci (P=0.004) due to trisomy 2 irrespective of the following factors: B or T/null phenotype (P=0.315), diagnostic categories of systemic or cutaneous ALCL or the above-mentioned B-cell lymphomas (P=0.131), and CD30 positivity by immunohistochemistry (P=1.000).
  • Trisomy 2 was absent in all ALK+ lymphomas (P=0.009), which showed rearranged ALK gene loci (P<0.001).
  • Whether trisomy 2 is a primary or secondary event that leads to ALK- lymphomas cannot be determined from this study.
  • Its presence in secondary B-cell lymphomas suggests that trisomy 2 may be a secondary cytogenetic aberration in lymphomas in general.
  • Further investigation of this finding is necessary to further our understanding of the heterogeneous group of ALK- lymphomas.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 2 / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Antigens, CD15 / analysis. Antigens, CD30 / analysis. Child. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology. Male. Mucin-1 / analysis. Receptor Protein-Tyrosine Kinases. Statistics as Topic

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  • (PMID = 15475930.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD15; 0 / Antigens, CD30; 0 / Mucin-1; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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74. Querfeld C, Khan I, Mahon B, Nelson BP, Rosen ST, Evens AM: Primary cutaneous and systemic anaplastic large cell lymphoma: clinicopathologic aspects and therapeutic options. Oncology (Williston Park); 2010 Jun;24(7):574-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary cutaneous and systemic anaplastic large cell lymphoma: clinicopathologic aspects and therapeutic options.
  • Anaplastic large cell lymphoma (ALCL) is a biologic and clinically heterogenous subtype of T-cell lymphoma.
  • Clinically, ALCL may present as localized (primary) cutaneous disease or widespread systemic disease.
  • These two forms of ALCL are distinct entities with different clinical and biologic features.
  • Both types share similar histology, however, with cohesive sheets of large lymphoid cells expressing the Ki-1 (CD30) molecule.
  • Primary cutaneous ALCL (C-ALCL) is part of the spectrum of CD30+ lymphoproliferative diseases of the skin including lymphomatoid papulosis.
  • The systemic ALCL type is an aggressive lymphoma that may secondarily involve the skin, in addition to other extranodal sites.
  • Further, systemic ALCL may be divided based on the expression of anaplastic lymphoma kinase (ALK) protein, which is activated most frequently through the nonrandom t(2;5) chromosome translocation, causing the fusion of the nucleophosmin (NPM) gene located at 5q35 to 2p23 encoding the receptor tyrosine kinase ALK.
  • Systemic ALK+ ALCLs have improved prognosis compared with ALK-negative ALCL, although both subtypes warrant treatment with polychemotherapy.
  • Allogeneic and, to a lesser extent, autologous stem cell transplantation play a role in relapsed disease, while the benefit of upfront transplant is not clearly defined.
  • In addition, a multitude of novel therapeutics are being studied, including anti-CD30 antibodies, histone deacetylase inhibitors, immunomodulatory drugs, proteasome inhibitors, and inhibitors of ALK and its downstream signaling pathways.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / pathology. Lymphoma, Large-Cell, Anaplastic / therapy. Lymphoma, Primary Cutaneous Anaplastic Large Cell / pathology. Lymphoma, Primary Cutaneous Anaplastic Large Cell / therapy. Skin Neoplasms / pathology. Skin Neoplasms / therapy

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  • [CommentIn] Oncology (Williston Park). 2010 Jun;24(7):587, 592-3 [20669795.001]
  • [CommentIn] Oncology (Williston Park). 2010 Jun;24(7):594 [20669796.001]
  • (PMID = 20669794.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Number-of-references] 118
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75. 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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76. Rapkiewicz A, Wen H, Sen F, Das K: Cytomorphologic examination of anaplastic large cell lymphoma by fine-needle aspiration cytology. Cancer; 2007 Dec 25;111(6):499-507
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytomorphologic examination of anaplastic large cell lymphoma by fine-needle aspiration cytology.
  • BACKGROUND: The cytomorphology of anaplastic large cell lymphoma (ALCL) is distinctive yet variable.
  • To the authors' knowledge, to date only small case series have described the cytologic findings noted in patients with ALCL.
  • The current series is the largest case series presented to date to retrospectively review the cytomorpholgic findings noted in patients with ALCL, with specific attention paid to those with anaplastic lymphoma kinase (ALK)-negative ALCL.
  • METHODS: Over a 13-year period, the available Diff-Quik cytology smears and surgical excision specimens taken from patients with ALCL were evaluated.
  • Different clinical and morphologic parameters were evaluated, including ALK status.
  • ALK-negative ALCL cytology smears were found to have a high number of anaplastic cells compared with ALK-positive cases.
  • The hallmark cells in the ALK-negative cases were not classic.
  • CONCLUSIONS: ALCL can be diagnosed accurately by fine-needle aspiration cytology (FNAC) alone when aided by immunocytochemistry in ALK-positive cases.
  • Ancillary studies should be anticipated such that material for cell block preparation and molecular studies is taken at the time of FNAC.
  • The results of the current study demonstrate the varied FNAC morphology of ALCL.
  • The presence of severe pleomorphism and anaplasia was found to correlate with ALK-negative status.
  • [MeSH-major] Biopsy, Fine-Needle. Lymphoma, Large-Cell, Anaplastic / pathology

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  • [Copyright] 2007 American Cancer Society
  • (PMID = 17941004.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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77. Piva R, Agnelli L, Pellegrino E, Todoerti K, Grosso V, Tamagno I, Fornari A, Martinoglio B, Medico E, Zamò A, Facchetti F, Ponzoni M, Geissinger E, Rosenwald A, Müller-Hermelink HK, De Wolf-Peeters C, Piccaluga PP, Pileri S, Neri A, Inghirami G: Gene expression profiling uncovers molecular classifiers for the recognition of anaplastic large-cell lymphoma within peripheral T-cell neoplasms. J Clin Oncol; 2010 Mar 20;28(9):1583-90
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  • [Title] Gene expression profiling uncovers molecular classifiers for the recognition of anaplastic large-cell lymphoma within peripheral T-cell neoplasms.
  • PURPOSE: To unravel the regulatory network underlying nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) -mediated lymphomagenesis of anaplastic large-cell lymphoma (ALCL) and to discover diagnostic genomic classifiers for the recognition of patients with ALK-positive and ALK-negative ALCL among T-cell non-Hodgkin's lymphoma (T-NHL).
  • PATIENTS AND METHODS: The transcriptome of NPM-ALK-positive ALCL cell lines was characterized by silencing the expression of ALK or STAT3, a major effector of ALK oncogenic activity.
  • Gene expression profiling (GEP) was performed in a series of systemic primary T-NHL (n = 70), including a set of ALK-positive and ALK-negative ALCL (n = 36).
  • Genomic classifiers for ALK-positive and ALK-negative ALCL were generated by prediction analyses and validated by quantitative reverse-transcriptase polymerase chain reaction and/or immunohistochemistry.
  • RESULTS: In ALCL cell lines, two thirds of ALK-regulated genes were concordantly dependent on STAT3 expression.
  • GEP of systemic primary T-NHL significantly clustered ALK-positive ALCL samples in a separate subgroup, underscoring the relevance of in vitro ALK/STAT3 signatures.
  • A set of genomic classifiers for ALK-positive ALCL and for ALCL were identified by prediction analyses.
  • These gene clusters were instrumental for the distinction of ALK-negative ALCL from peripheral T-cell lymphomas not otherwise specified (PTCLs-NOS) and angioimmunoblastic lymphomas.
  • CONCLUSION: We proved that experimentally controlled GEP in ALCL cell lines represents a powerful tool to identify meaningful signaling networks for the recognition of systemic primary T-NHL.
  • The identification of a molecular signature specific for ALCL suggests that these T-NHLs may represent a unique entity discernible from other PTCLs, and that a restricted number of genes can be instrumental for clinical stratification and, possibly, therapy of T-NHL.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Expression Profiling. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, T-Cell, Peripheral / genetics
  • [MeSH-minor] Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Humans. Nuclear Proteins / genetics. Protein-Tyrosine Kinases / genetics. Receptor Protein-Tyrosine Kinases. Signal Transduction

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  • (PMID = 20159827.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 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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78. Matsumoto N, Ohki H, Mukae S, Amano Y, Harada D, Nishimura S, Komiyama K: Anaplastic large cell lymphoma in gingiva: case report and literature review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2008 Oct;106(4):e29-34
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  • [Title] Anaplastic large cell lymphoma in gingiva: case report and literature review.
  • We report an unusual case of gingival anaplastic large-cell lymphoma (ALCL) that occurred in a 76-year-old Japanese woman who showed marked gingival swelling in both the maxilla and mandible.
  • The specimens showed proliferation of large atypical and amphophilic epithelioid cells beneath the covering epithelium.
  • Immunohistochemical analysis of the proliferating cells revealed positivity for CD30 and T-cell markers, such as CD45RB, as well as CD45RO antibodies, and they were weakly positive for the granzyme B antibody.
  • In contrast, the tumor cells were negative for all B-cell markers as well as for CD3, CD56, S-100 protein, epithelial membrane antigen, and p80(NPM/ALK) antibodies.
  • Based on the clinical and histopathologic features, the lesion was diagnosed as an ALCL in both the upper and the lower gingiva.
  • This is an extremely rare case, in which a specific subtype of T-cell lymphoma appeared in the oral cavity.
  • [MeSH-major] Gingival Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 18656392.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 3.1.3.48 / Antigens, CD45
  • [Number-of-references] 30
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79. 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


80. Lagmay J, Termuhlen A, Fung B, Ranalli M: Primary testicular presentation of ALK-1-negative anaplastic large cell lymphoma in a pediatric patient. J Pediatr Hematol Oncol; 2009 May;31(5):330-2
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  • [Title] Primary testicular presentation of ALK-1-negative anaplastic large cell lymphoma in a pediatric patient.
  • Anaplastic large cell lymphoma is a heterogeneous group of malignant non-Hodgkin lymphomas that occurs in up to 15% of all pediatric non-Hodgkin lymphomas.
  • This brief report describes first reported case of pediatric primary testicular anaplastic large cell lymphoma in a 14-year-old boy.
  • [MeSH-major] Activin Receptors, Type II / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / pathology. Testicular Neoplasms / metabolism. Testicular Neoplasms / pathology
  • [MeSH-minor] Adolescent. Antigens, CD30 / metabolism. Biomarkers, Tumor / metabolism. Biopsy. Cell Nucleus / metabolism. Cell Nucleus / pathology. Golgi Apparatus / metabolism. Golgi Apparatus / pathology. Humans. Male. Orchiectomy. Testis / pathology. Testis / surgery

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  • (PMID = 19415011.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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81. Laurent C, Do C, Gascoyne RD, Lamant L, Ysebaert L, Laurent G, Delsol G, Brousset P: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis. J Clin Oncol; 2009 Sep 1;27(25):4211-6
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  • [Title] Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis.
  • PURPOSE: Anaplastic lymphoma kinase (ALK) -positive diffuse large B-cell lymphoma (DLBCL) is a rare variant of DLBCL that has been described only in small case reports.
  • PATIENTS AND METHODS: We retrospectively analyzed 38 patients with ALK-positive DLBCL treated with cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP) or CHOP-like regimens from different institutions to better define the presenting features, clinical course, and response to treatment.
  • All patients expressed ALK fusion proteins, but virtually all were CD30 and CD20 negative.
  • Most patients (60%) followed an aggressive clinical course with advanced stage at diagnosis, frequent marrow infiltration, and poor outcome.
  • CONCLUSION: ALK-positive DLBCLs display clinicopathologic features that distinguish them from common DLBCL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / enzymology. Protein-Tyrosine Kinases / analysis

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  • [ErratumIn] J Clin Oncol. 2010 Jan 1;28(1):182
  • (PMID = 19636007.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, CD30; 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / oncoprotein CLTCL-ALK; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
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82. 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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  • [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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83. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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84. Szomor A, Al Saati T, Delsol G, Kereskai L, Szijártó Z, Losonczy H: Primary bone marrow T-cell anaplastic large cell lymphoma with triple M gradient. Pathol Oncol Res; 2007;13(3):260-2
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  • [Title] Primary bone marrow T-cell anaplastic large cell lymphoma with triple M gradient.
  • We present a case of a 60-year-old male patient with primary bone marrow anaplastic large cell lymphoma.
  • Bone marrow biopsy showed massive CD30-positive, ALK-negative large lymphoid cell infiltration of T-cell origin with anaplastic morphology.
  • PCR analysis of lymphoid cells separated from the bone marrow demonstrated the presence of a B/T hybrid genotype disorder with no evidence of the t(2;5), nor t(1;2) translocations.
  • [MeSH-major] Bone Marrow Neoplasms / diagnosis. Bone Marrow Neoplasms / immunology. Lymphoma, Large-Cell, Anaplastic / diagnosis. Lymphoma, Large-Cell, Anaplastic / immunology. T-Lymphocytes / immunology

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  • (PMID = 17922057.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Immunoglobulin M
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85. Plaza JA, Ortega P, Lynott J, Mullane M, Kroft S, Olteanu H: CD8-positive primary cutaneous anaplastic large T-cell lymphoma (PCALCL): case report and review of this unusual variant of PCALCL. Am J Dermatopathol; 2010 Jul;32(5):489-91
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  • [Title] CD8-positive primary cutaneous anaplastic large T-cell lymphoma (PCALCL): case report and review of this unusual variant of PCALCL.
  • Primary cutaneous anaplastic large T-cell lymphoma (PCALCL) is a well-defined CD30-positive lymphoproliferative disorder with relatively good prognosis and response to treatment.
  • The large cohesive atypical cells were admixed with a reactive infiltrate composed of neutrophils, eosinophils, and small lymphocytes.
  • Immunohistochemical studies showed the tumor cells to be strongly positive for CD8, CD30, and TIA-1, focally positive for CD3, and negative for CD4, CD20, CD56, Anaplastic Lymphoma Kinase (ALK-1), and HSV.
  • Epstein-Barr virus by in situ hybridization was negative.
  • The diagnosis of a CD8+ PCALCL was confirmed.
  • [MeSH-major] CD8-Positive T-Lymphocytes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Skin Neoplasms / pathology


86. 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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87. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


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

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16114011.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes, B-Lymphocyte; 0 / Epitopes, T-Lymphocyte; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Peptide Fragments; 82115-62-6 / Interferon-gamma; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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89. 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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90. 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

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  • (PMID = 16596703.001).
  • [ISSN] 1615-9853
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 0 / Proteome; 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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91. Wang TT, Wang L, Tang ZR, Cheng JR, Li W, Li FY, Wang WY, Li GD: [Primary cutaneous anaplastic large cell lymphoma: a clinicopathologic analysis of 8 cases]. Zhonghua Bing Li Xue Za Zhi; 2009 Nov;38(11):749-53
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  • [Title] [Primary cutaneous anaplastic large cell lymphoma: a clinicopathologic analysis of 8 cases].
  • OBJECTIVE: To study the clinicopathologic features, immunophenotype and prognosis of primary cutaneous anaplastic large cell lymphoma (C-ALCL).
  • METHODS: Eight cases of C-ALCL were enrolled into the study.
  • C-ALCL often presented with solitary skin nodule, without systemic symptoms.
  • Histologically, the lymphoma cells infiltrated the dermis and subcutis in a sheet-like pattern.
  • They were of large size and showed conspicuous nuclear atypia.
  • Immunohistochemical study showed that more than 75% of the lymphoma cells were positive for CD30.
  • All cases expressed one to three T cell markers (CD3, CD5 or CD45RO) and cytotoxic granule-associated antigens (TIA-1, granzyme B or perforin).
  • The staining for leukocyte common antigen was positive in all cases, while the expression of CD5, CD8, ALK-1 and epithelial membrane antigen was noted in 5, 1, 1 and 3 cases, respectively.
  • The staining for CD15, CD20, CK and HMB45 was negative.
  • In-situ hybridization for EBER 1/2 was also negative in all the cases studied.
  • CONCLUSIONS: C-ALCL has distinctive clinicopathologic and immunophenotypic features.
  • [MeSH-major] Antigens, CD30 / metabolism. Lymphoma, Primary Cutaneous Anaplastic Large Cell / pathology. Skin Neoplasms / pathology

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  • (PMID = 20079014.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antigens, CD5; 0 / Epstein-Barr virus encoded RNA 1; 0 / RNA, Viral; EC 3.1.3.48 / Antigens, CD45
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92. Chao-Lo MP, King-Ismael D, Lopez RA: Primary cutaneous CD30+ anaplastic large cell lymphoma: report of a rare case. J Dermatol Case Rep; 2008 Oct 11;2(3):31-4
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  • [Title] Primary cutaneous CD30+ anaplastic large cell lymphoma: report of a rare case.
  • Primary cutaneous anaplastic large cell lymphoma (PCALCL) is a rare type of non-Hodgkin's lymphoma comprising approximately 0.9-9.0% of all cutaneous lymphomas.
  • Skin punch biopsy revealed dense infiltrates of non-epidermotropic, large, irregularly-shaped lymphocytes with hyperchromatic and pyknotic nuclei.
  • Immunohistochemistry revealed that these atypical cells are anaplastic lymphoma kinase (ALK) positive, CD30+, CD3-, CD20- and epithelial membrane antigen (EMA) negative.

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  • [Cites] J Am Acad Dermatol. 1999 May;40(5 Pt 2):857-61 [10321635.001]
  • [Cites] Eur J Pediatr. 2008 Jan;167(1):111-3 [17219127.001]
  • [Cites] J Am Acad Dermatol. 2000 Nov;43(5 Pt 1):793-6 [11050582.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3681-95 [11090048.001]
  • [Cites] Am J Dermatopathol. 2003 Apr;25(2):142-7 [12652196.001]
  • [Cites] J Am Acad Dermatol. 2003 Dec;49(6):1049-58 [14639383.001]
  • [Cites] Blood. 2005 May 15;105(10):3768-85 [15692063.001]
  • [Cites] Pediatr Dev Pathol. 2005 Jan-Feb;8(1):52-60 [15719203.001]
  • [Cites] Indian J Dermatol Venereol Leprol. 2004 May-Jun;70(3):168-71 [17642599.001]
  • [Cites] Blood. 2007 Jul 15;110(2):479-84 [17339420.001]
  • [Cites] Hematol Oncol Clin North Am. 2003 Dec;17(6):1319-32, vii-viii [14710887.001]
  • [Cites] Pediatr Dermatol. 2004 May-Jun;21(3):212-7 [15165197.001]
  • [Cites] Br J Dermatol. 2004 Jun;150(6):1202-7 [15214912.001]
  • [Cites] J Am Acad Dermatol. 2004 Jul;51(1):103-10 [15243534.001]
  • [Cites] Eur J Haematol. 2005 Sep;75(3):221-6 [16104878.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:323-30, 513 [17124079.001]
  • [Cites] Am J Dermatopathol. 2000 Oct;22(5):422-8 [11048978.001]
  • (PMID = 21886709.001).
  • [ISSN] 1898-7249
  • [Journal-full-title] Journal of dermatological case reports
  • [ISO-abbreviation] J Dermatol Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Other-IDs] NLM/ PMC3157779
  • [Keywords] NOTNLM ; lymphomatoid papulosis / lymphoproliferative disorders / mycosis fungoides / primary cutaneous CD30 positive large T cell lymphoma / primary cutaneous anaplastic large cell lymphoma
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93. Wang FH, Li YH, Zeng J, Rao HL, Xia ZJ, Sun XF, Huang HQ, Lin TY, Jiang WQ, Guan ZZ: Clinical analysis of primary systemic anaplastic large cell lymphoma: a report of 57 cases. Ai Zheng; 2009 Jan;28(1):49-53
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  • [Title] Clinical analysis of primary systemic anaplastic large cell lymphoma: a report of 57 cases.
  • BACKGROUND AND OBJECTIVE: The clinical characteristics and prognosis of primary systemic anaplastic large cell lymphoma (ALCL) are various according to different reports.
  • Anaplastic lymphoma kinase (ALK), a specific marker of primary systemic ALCL, is related with its clinical characteristics and prognosis.
  • This study was to investigate the clinical characteristics and prognosis of primary systemic ALCL, and to explore the expression and clinical significance of ALK.
  • METHODS: Clinical data of 57 primary systemic ALCL patients, treated in Cancer Center of Sun Yat-sen University from January 1997 to January 2006, were reviewed.
  • The expression of ALK in 46 tumor specimens was detected by SP immunohisochemistry.
  • Of the 57 patients, 33 (57.9%) had B symptoms, 23 (40.4%) had Ann Arbor stage III-IV tumors, and 23 (40.4%) had extranodal disease at diagnosis.
  • The positive rate of ALK was 63.0% in the 46 cases detected.
  • Compared with ALK-negative patients, ALK-positive patients were younger (p = 0.001) and had higher expected 5-year survival rate (p < 0.01).
  • Multivariate analysis confirmed the independent prognostic values of ALK expression, primary disease site and lactate dehydrogenase (LDH) level.
  • CONCLUSIONS: Primary systemic ALCL usually occurs in young patients, with good response to chemotherapy and good prognosis.
  • No ALK expression, high-intermediate/high IPI, extranodal disease and elevated LDH level are correlated to unfavorable prognosis.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / drug therapy. Protein-Tyrosine Kinases / analysis

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  • (PMID = 19448428.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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94. Yamamoto H, Kohashi K, Oda Y, Tamiya S, Takahashi Y, Kinoshita Y, Ishizawa S, Kubota M, Tsuneyoshi M: Absence of human herpesvirus-8 and Epstein-Barr virus in inflammatory myofibroblastic tumor with anaplastic large cell lymphoma kinase fusion gene. Pathol Int; 2006 Oct;56(10):584-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Absence of human herpesvirus-8 and Epstein-Barr virus in inflammatory myofibroblastic tumor with anaplastic large cell lymphoma kinase fusion gene.
  • Some populations of IMT have anaplastic large cell lymphoma kinase (ALK) gene rearrangements.
  • Infection with Epstein-Barr virus (EBV) and human herpesvirus-8 (HHV-8) in tumor cells of IMT has been reported; these reports, however, have been limited to ALK-negative IMT.
  • Immunohistochemically, 15 cases were ALK positive and six were negative.
  • Of eight cases analyzed using reverse transcription-polymerase chain reaction, tropomyosin 3 (TPM3)-ALK, TPM4-ALK and clathrin heavy chain-ALK fusion genes were detected in one, two and two cases, respectively.
  • All 21 IMT, irrespective of ALK expression, were negative for EBV by in situ hybridization for EBV-encoded RNA and immunohistochemical stain for latent membrane antigen-1.
  • HHV-8 was also negative in all IMT by PCR for HHV-8 DNA sequence (KS330/233) and immunohistochemical stain for latent nuclear antigen.
  • These results suggest that IMT may be a heterogeneous group in terms of pathogenesis, and EBV and HHV-8 do not play a major role in the pathogenesis of ALK-positive tumor.

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  • (PMID = 16984614.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / TPM3 protein, human; 0 / TPM4 protein, human; 0 / Tropomyosin; 0 / latency-associated nuclear antigen; 114899-12-6 / Clathrin Heavy Chains; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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95. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


96. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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97. Feldman AL, Law ME, Inwards DJ, Dogan A, McClure RF, Macon WR: PAX5-positive T-cell anaplastic large cell lymphomas associated with extra copies of the PAX5 gene locus. Mod Pathol; 2010 Apr;23(4):593-602

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PAX5-positive T-cell anaplastic large cell lymphomas associated with extra copies of the PAX5 gene locus.
  • Cell lineage is the major criterion by which lymphomas are classified.
  • Immunohistochemistry has greatly facilitated lymphoma diagnosis by detecting expression of lineage-associated antigens.
  • Anaplastic large cell lymphoma is a T-cell lymphoma that shows morphologic and phenotypic overlap with classical Hodgkin's lymphoma, which is a tumor of B-cell derivation.
  • Staining for the B-cell transcription factor, paired box 5 (PAX5), has been suggested to be helpful in this differential, as it is positive in most classical Hodgkin's lymphomas, but absent in anaplastic large cell lymphomas.
  • In this study we report four systemic T-cell anaplastic large cell lymphomas that were positive for PAX5 by immunohistochemistry, with weak staining intensity similar to that observed in classical Hodgkin's lymphoma.
  • Three cases were anaplastic lymphoma kinase (ALK) negative and one was ALK positive.
  • PAX5 immunohistochemistry was negative in 198 additional peripheral T-cell lymphomas, including 66 anaplastic large cell lymphomas.
  • Unexpectedly, although PAX5 translocations were absent, all evaluable PAX5-positive anaplastic large cell lymphomas showed extra copies of the PAX5 gene locus by fluorescence in situ hybridization (FISH).
  • In contrast, only 4% of PAX5-negative peripheral T-cell lymphomas had extra copies of PAX5.
  • We conclude that aberrant expression of PAX5 occurs rarely in T-cell anaplastic large cell lymphomas, and may be associated with extra copies of the PAX5 gene.
  • PAX5-positive lymphomas with morphologic features overlapping different lymphoma types should be evaluated with an extensive immunohistochemical panel and/or molecular studies to avoid diagnostic errors that could lead to inappropriate treatment.
  • As PAX5 overexpression causes T-cell neoplasms in experimental models, PAX5 may have contributed to lymphomagenesis in our cases.

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  • [Cites] Br J Haematol. 1994 Mar;86(3):513-23 [7519036.001]
  • [Cites] Hum Pathol. 2009 Sep;40(9):1252-61 [19368954.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2321-8 [7662979.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):6129-34 [8650231.001]
  • [Cites] Blood. 1996 Nov 15;88(10):4005-11 [8916967.001]
  • [Cites] Blood. 1998 Mar 15;91(6):2076-84 [9490693.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1308-16 [9694719.001]
  • [Cites] Hum Pathol. 1999 Feb;30(2):228-36 [10029454.001]
  • [Cites] Am J Clin Pathol. 1999 Sep;112(3):319-29 [10478136.001]
  • [Cites] Nature. 1999 Oct 7;401(6753):556-62 [10524622.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3358-60 [15297316.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Oct;44(2):218-23 [15942942.001]
  • [Cites] Mod Pathol. 2005 Dec;18(12):1542-9 [16056244.001]
  • [Cites] Am J Surg Pathol. 2006 Feb;30(2):223-9 [16434897.001]
  • [Cites] Am J Clin Pathol. 2006 Mar;125(3):364-74 [16613339.001]
  • [Cites] Leukemia. 2006 Jan;20(1):176-9 [16307010.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2472-9 [16636342.001]
  • [Cites] J Clin Oncol. 2006 Oct 1;24(28):4626-33 [16954517.001]
  • [Cites] Blood. 2007 Jan 1;109(1):281-9 [16968900.001]
  • [Cites] Mod Pathol. 2007 Jun;20(6):632-7 [17431414.001]
  • [Cites] Blood. 1999 Nov 1;94(9):3108-13 [10556196.001]
  • [Cites] Mod Pathol. 2000 Jul;13(7):766-72 [10912936.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3681-95 [11090048.001]
  • [Cites] Mod Pathol. 2001 Feb;14(2):105-10 [11235901.001]
  • [Cites] Mod Pathol. 2001 Mar;14(3):219-28 [11266530.001]
  • [Cites] Science. 2002 Jul 5;297(5578):110-3 [12098702.001]
  • [Cites] Am J Surg Pathol. 2002 Oct;26(10):1343-50 [12360049.001]
  • [Cites] Int J Oncol. 2003 Feb;22(2):319-24 [12527929.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):176-85 [12696066.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4620-5 [12907641.001]
  • [Cites] Am J Surg Pathol. 2003 Dec;27(12):1513-22 [14657710.001]
  • [Cites] J Pathol. 2004 Jan;202(1):60-9 [14694522.001]
  • [Cites] Am J Pathol. 2004 May;164(5):1837-48 [15111330.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7399-404 [15492262.001]
  • [Cites] Am J Pathol. 1990 Nov;137(5):1047-57 [2173409.001]
  • [Cites] Genomics. 1991 Oct;11(2):424-34 [1685142.001]
  • [Cites] Arch Pathol Lab Med. 1992 Nov;116(11):1192-6 [1359849.001]
  • [Cites] J Clin Pathol. 2007 Jun;60(6):709-14 [16837628.001]
  • [Cites] Leuk Lymphoma. 2007 Jun;48(6):1127-38 [17577776.001]
  • [Cites] Adv Anat Pathol. 2007 Sep;14(5):323-34 [17717432.001]
  • [Cites] Nature. 2007 Sep 27;449(7161):473-7 [17851532.001]
  • [Cites] Hematol Oncol Clin North Am. 2007 Oct;21(5):897-914 [17908627.001]
  • [Cites] Br J Haematol. 2008 Mar;140(5):516-26 [18275429.001]
  • [Cites] J Cutan Pathol. 2008 Apr;35(4):398-403 [18261116.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5496-504 [18385450.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1268-72 [17989713.001]
  • [Cites] Am J Clin Pathol. 2008 Aug;130(2):178-85 [18628085.001]
  • [Cites] J Clin Oncol. 2008 Sep 1;26(25):4124-30 [18626005.001]
  • [Cites] J Mol Diagn. 2008 Nov;10(6):502-12 [18832464.001]
  • [Cites] Am J Clin Pathol. 1994 Oct;102(4):483-9 [7524302.001]
  • (PMID = 20118907.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA097274-08; United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / P50 CA097274-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ NIHMS167829; NLM/ PMC2848697
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98. 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


99. 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
MedlinePlus Health Information. consumer health - Breast Reconstruction.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Anaplastic Large Cell Lymphoma.
  • Genetic Alliance. consumer health - Lymphoma, large-cell.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
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  • (PMID = 18594466.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Immunoglobulin Heavy Chains; 0 / Silicone Gels
  • [Number-of-references] 24
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100. Cerimagić Z, Guska S, Banjanović B: A case of T/null anaplastic large cell lymphoma arising in lung. Bosn J Basic Med Sci; 2006 Aug;6(3):34-7
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of T/null anaplastic large cell lymphoma arising in lung.
  • Anaplastic large cell lymphoma (ALCL) is a rare non-Hodgkin, T-cell lymphoma, representing only 2-3% of all lymphoid neoplasm's in adults according to World Health Organization (WHO).
  • CD30 antigen-positive, large neoplastic cells characterize ALCL.
  • We present here a 46-year-old male with pulmonary ALCL previously diagnosed with Hodgkin disease.
  • The neoplastic cells were large and had clear cytoplasm, large vesicular nuclei, and prominent nucleoli.
  • ALK immunostaining was negative.
  • Immunohistochemical profile was consistent with ALK negative ALCL.
  • The progression of Hodgkin lymphoma to aggressive non-Hodgkin lymphoma (ALCL in this case) is well known entity.
  • After the diagnosis was established, our patient immediately had been referred to the Department of Hematology in order to get appropriate chemotherapy, necessary in such cases.






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