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

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  • (PMID = 18755494.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Clathrin; 0 / Oncogene Proteins, Fusion; 0 / STAT3 Transcription Factor; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
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2. Reimer P, Hentrich M: [Peripheral T-cell lymphoma: diagnosis and treatment]. Dtsch Med Wochenschr; 2006 Mar 31;131(13):685-90
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  • [Title] [Peripheral T-cell lymphoma: diagnosis and treatment].
  • Peripheral T/NK-cell lymphomas (PTCL) comprise a heterogeneous group of rare diseases accounting for approximately 10-15% of all non-Hodgkin"s lymphomas.
  • Compared to B-cell lymphomas, PTCL more frequently involve extranodal sites and have a worse prognosis.
  • Because of their usually indolent course, primary cutaneous T/NK-cell lymphomas should be distinguished from the other PTCL.
  • The International Prognostic Index, established for aggressive B-cell lymphomas, has also proved relevant for PTCL.
  • Apart from (ALK-positive) anaplastic large cell lymphoma it thus gives poorer results than those obtained in patients with aggressive B-cell lymphomas.
  • Data for high-dosage therapy with autologous stem cell transplantation (autoSCT) for relapsing and refractory PTCL are similar to those reported for aggressive B-cell lymphomas.
  • Allogeneic stem cell transplantation following reduced conditioning regimens has also given promising results in patients with relapse.
  • [MeSH-major] Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / therapy
  • [MeSH-minor] Humans. Stem Cell Transplantation. Survival Analysis. Transplantation, Homologous

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  • [CommentIn] Dtsch Med Wochenschr. 2006 Aug 25;131(34-35):1884; author reply 1884 [16915558.001]
  • (PMID = 16555177.001).
  • [ISSN] 0012-0472
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 56
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3. Rudzki Z, Rucińska M, Jurczak W, Skotnicki AB, Maramorosz-Kurianowicz M, Mruk A, Piróg K, Utych G, Bodzioch P, Srebro-Stariczyk M, Włodarska I, Stachura J: ALK-positive diffuse large B-cell lymphoma: two more cases and a brief literature review. Pol J Pathol; 2005;56(1):37-45
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  • [Title] ALK-positive diffuse large B-cell lymphoma: two more cases and a brief literature review.
  • Anaplastic lymphoma kinase (ALK)-positive diffuse large B-cell lymphoma (DLBCL) is a rare, recently defined tumor distinct in many aspects from ALK-positive anaplastic large cell lymphoma (ALCL).
  • We present two additional cases of ALK+DLBCL recently diagnosed in our department and a review of literature.
  • A 48-year old man presented with a large upper neck mass growing slowly over 18 months.
  • Histologically the tumor was diagnosed as an ALK-positive diffuse large B-cell lymphoma. with plasmablastic features.
  • Large, frequently intrasinusoidal tumor cells expressed CD138, EMA, weakly IgA and kappa, but were negative for other B-cell markers, T-cell markers and CD30.
  • The ALK staining was cytoplasmic with the increased intensity in the Golgi area.
  • At the diagnosis the patient manifested with the stage IIIB.
  • The patient died of massive bleeding from his decomposing tumor 3 months after the diagnosis.
  • The tumor showed immunoblastic/anaplastic morphology, with some Reed-Sternberg-like cells positive for ALK.
  • ALK immunostaining was cytoplasmic, weak in a routine immunostain, enhanced with double (proteinase + pressure cooker) antigen retrieval.
  • FISH was consistent with the t(2;5)/nucleophosmin(NPM)-ALK rearrangement.
  • ALK-positive DLBCL affects mostly middle-aged men, shows generally poor but stage-dependent prognosis (at least 60% mortality rate), presents typically as a lymph node-based disseminated disease, and very rarely involves the bone marrow.
  • Genetic studies showed that the majority of ALK+DLBCL cases are characterized by the clathrin (CLTC)-ALK fusion and in a few cases the NPM-ALK rearrangement has been found.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 15921012.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; VB0R961HZT / Prednisone; CHOP protocol
  • [Number-of-references] 17
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4. Yang J, Zhang F, Fang H, Ye Z, Lin S, Han A: Clinicopathologic features of primary lymphoma in soft tissue. Leuk Lymphoma; 2010 Nov;51(11):2039-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathologic features of primary lymphoma in soft tissue.
  • By reviewing 3725 lymphomas diagnosed in our institution from 1999 to 2010, we found eight cases (0.21%) of primary lymphoma in soft tissue with comprehensive histologic and immunohistochemical studies.
  • Of the eight cases of primary lymphoma in soft tissue, two patients were male and six were female.
  • Six cases were diffuse large B-cell lymphoma (DLBCL), subclassified as three DLBCL non-germinal center B-cell phenotype, one DLBCL germinal center B-cell phenotype, and two (Epstein-Barr Virus) EBV-positive DLBCL of the elderly; one case was anaplastic large cell lymphoma, ALK-positive; and one case was peripheral T cell lymphoma, not otherwise specified.
  • One patient who refused further therapy died of the disease at 2 months after diagnosis.
  • [MeSH-major] Lymphoma / pathology. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Immunophenotyping. Male. Middle Aged. Retrospective Studies. Young Adult

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  • (PMID = 20929318.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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5. Alsop S, Sanger WG, Elenitoba-Johnson KS, Lim MS: Chronic myeloid leukemia as a secondary malignancy after ALK-positive anaplastic large cell lymphoma. Hum Pathol; 2007 Oct;38(10):1576-80
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  • [Title] Chronic myeloid leukemia as a secondary malignancy after ALK-positive anaplastic large cell lymphoma.
  • The development of Philadelphia chromosome-positive chronic myelogenous leukemia (CML) in the adolescent population is very rare.
  • CML occurring as a secondary malignancy in individuals treated for anaplastic large cell lymphoma (ALCL) is also rare.
  • We present the case of a 16-year-old adolescent boy who developed a right orbital mass that was diagnosed as ALCL with the t(2;5)(p23;q25) chromosomal aberration.
  • Four years after receiving treatment for ALCL, he presented with a swollen leg and a white cell count of 431,000.
  • We present the histopathologic, molecular, and cytogenetic findings of this patient's initial presentation with systemic ALCL as well as his secondary presentation with CML 4 years later.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Neoplasms, Second Primary / pathology. Protein-Tyrosine Kinases / metabolism


6. Cluzeau T, Pécuchet N, Mounier N, Vignot S: [Implications of ALK (anaplastic lymphoma kinase) in oncohematology]. Bull Cancer; 2010 Aug;97(8):991-6
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  • [Title] [Implications of ALK (anaplastic lymphoma kinase) in oncohematology].
  • [Transliterated title] Implications d'ALK (anaplastic lymphoma kinase) en oncohématologie.
  • The anaplastic lymphoma kinase gene (ALK) code for a receptor tyrosine-kinase.
  • The fusion proteins from the ALK gene have been identified in oncohaematology malignancies including ALK positive anaplastic lymphoma large cell and non small cells lung cancer with EML4-ALK fusion gene.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / enzymology. Lung Neoplasms / enzymology. Lymphoma, Large-Cell, Anaplastic / enzymology. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics

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  • (PMID = 20483705.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Neoplasm Proteins; 0 / Nucleoplasmins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 27
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7. Driss M, Abbes I, Mrad K, Sassi S, Oubich F, Barsaoui S, Romdhane KB: Primary CD30/ALK-1 positive anaplastic large cell lymphoma of the skeletal muscle in a child. Pathologica; 2009 Apr;101(2):97-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary CD30/ALK-1 positive anaplastic large cell lymphoma of the skeletal muscle in a child.
  • Anaplastic large cell lymphoma (ALCL) represents approximately 10 to 30% of all childhood non-Hodgkin lymphomas.
  • Biopsy of the lesion showed large anaplastic cells with voluminous and abundant cytoplasm as well as folded nuclei.
  • The tumour cells were positive for CD30, CD3, EMA and ALK-1.
  • This case emphasizes the occurrence of anaplastic large cell lymphoma in the soft tissue and the favourable outcome of ALK-positive anaplastic large cell lymphoma.
  • [MeSH-major] Activin Receptors, Type II / biosynthesis. Antigens, CD30 / biosynthesis. Lymphoma, Large-Cell, Anaplastic / pathology. Muscle Neoplasms / pathology. Muscle, Skeletal / pathology

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  • (PMID = 19886557.001).
  • [ISSN] 0031-2983
  • [Journal-full-title] Pathologica
  • [ISO-abbreviation] Pathologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type II
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8. Bordon V, De Paepe P, Dhooge C, Vandecruys E, Benoit Y, Laureys G: Successful treatment with allogeneic bone marrow transplantation of an early relapse of ALK-positive anaplastic large cell lymphoma. Haematologica; 2005 Mar;90(3):ECR19
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  • [Title] Successful treatment with allogeneic bone marrow transplantation of an early relapse of ALK-positive anaplastic large cell lymphoma.
  • [MeSH-major] Bone Marrow Transplantation. Lymphoma, Large-Cell, Anaplastic / therapy


9. Beltran B, Castillo J, Salas R, Quiñones P, Morales D, Hurtado F, Riva L, Winer E: ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature. J Hematol Oncol; 2009;2:11
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  • [Title] ALK-positive diffuse large B-cell lymphoma: report of four cases and review of the literature.
  • BACKGROUND: Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma (ALK-DLBCL) is a rare lymphoma with several clinicopathological differences from ALK-positive anaplastic large cell lymphoma (ALCL).
  • The latest WHO classification of lymphomas recognizes ALK-DLBCL as a separate entity.
  • By immunohistochemistry, cases were positive for cytoplasmic ALK, MUM1, CD45, and EMA; they marked negative for CD3, CD30 and CD20.
  • CONCLUSION: ALK-DLBCL is a distinct variant of DLBCL with plasmacytic differentiation, which is characterized by a bimodal age incidence curve, primarily nodal involvement, plasmablastic morphology, lack of expression of CD20, aggressive behavior and poor response to standard therapies, although some cases can have prolonged survival as the cases reported in this study.
  • ALK-DLBCL does not seem associated to immunosuppression or the presence of EBV or HHV8.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 19250532.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 39
  • [Other-IDs] NLM/ PMC2651189
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10. Corradini P, Tarella C, Zallio F, Dodero A, Zanni M, Valagussa P, Gianni AM, Rambaldi A, Barbui T, Cortelazzo S: Long-term follow-up of patients with peripheral T-cell lymphomas treated up-front with high-dose chemotherapy followed by autologous stem cell transplantation. Leukemia; 2006 Sep;20(9):1533-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term follow-up of patients with peripheral T-cell lymphomas treated up-front with high-dose chemotherapy followed by autologous stem cell transplantation.
  • We report the results of two prospective phase II studies investigating the role of high-dose sequential chemotherapy, followed by autologous stem cell transplantation (ASCT) in 62 patients with advanced stage peripheral T-cell lymphomas (PTCLs) at diagnosis.
  • Conditioning regimen consisted of mitoxantrone (60 mg/m2) and melphalan (180 mg/m2) or carmustine, etoposide, Ara-C and melphalan followed by peripheral blood stem cell autografting.
  • OS and EFS were significantly better in patients with anaplastic lymphoma-kinase (ALK)-positive anaplastic large-cell lymphoma (ALCL), as compared with the remaining PTCL.
  • In conclusion, our findings indicate (1) up-front high-dose therapy and ASCT are feasible, but could induce a high rate of long-term CR only in patients with ALK-positive ALCL and (2) the achievement of CR before autografting is a strong predictor of better survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, T-Cell / drug therapy. Lymphoma, T-Cell / surgery. Stem Cell Transplantation

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  • (PMID = 16871285.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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11. Vega F, Medeiros LJ, Leventaki V, Atwell C, Cho-Vega JH, Tian L, Claret FX, Rassidakis GZ: Activation of mammalian target of rapamycin signaling pathway contributes to tumor cell survival in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma. Cancer Res; 2006 Jul 1;66(13):6589-97
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  • [Title] Activation of mammalian target of rapamycin signaling pathway contributes to tumor cell survival in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) frequently carries the t(2;5)(p23;q35) resulting in aberrant expression of chimeric nucleophosmin-ALK.
  • Previously, nucleophosmin-ALK has been shown to activate phosphatidylinositol 3-kinase (PI3K) and its downstream effector, the serine/threonine kinase AKT.
  • In this study, we hypothesized that the mammalian target of rapamycin (mTOR) pathway, which functions downstream of AKT, mediates the oncogenic effects of activated PI3K/AKT in ALK+ ALCL.
  • Here, we provide evidence that mTOR signaling phosphoproteins, including mTOR, eukaryotic initiation factor 4E-binding protein-1, p70S6K, and ribosomal protein S6, are highly phosphorylated in ALK+ ALCL cell lines and tumors.
  • We also show that inhibition of mTOR with rapamycin, as well as silencing mTOR gene product expression using mTOR-specific small interfering RNA, decreased phosphorylation of mTOR signaling proteins and induced cell cycle arrest and apoptosis in ALK+ ALCL cells.
  • Cell cycle arrest was associated with modulation of G(1)-S-phase regulators, including the cyclin-dependent kinase inhibitors p21(waf1) and p27(kip1).
  • These findings suggest that the mTOR pathway contributes to nucleophosmin-ALK/PI3K/AKT-mediated tumorigenesis and that inhibition of mTOR represents a potential therapeutic strategy in ALK+ ALCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Kinases / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / physiology. Chromones / pharmacology. Down-Regulation. Enzyme Activation. Humans. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / genetics. Receptor Protein-Tyrosine Kinases. Signal Transduction. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Transfection


12. Anastasov N, Bonzheim I, Rudelius M, Klier M, Dau T, Angermeier D, Duyster J, Pittaluga S, Fend F, Raffeld M, Quintanilla-Martinez L: C/EBPβ expression in ALK-positive anaplastic large cell lymphomas is required for cell proliferation and is induced by the STAT3 signaling pathway. Haematologica; 2010 May;95(5):760-7
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  • [Title] C/EBPβ expression in ALK-positive anaplastic large cell lymphomas is required for cell proliferation and is induced by the STAT3 signaling pathway.
  • BACKGROUND: Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma is characterized by the t(2;5) chromosomal translocation, resulting in the expression of a fusion protein formed of nucleophosmin (NPM) and ALK.
  • Recently, we reported the abnormal expression of the transcription factor CCAAT/enhancer binding protein-beta (C/EBPbeta) in ALK-positive anaplastic large cell lymphomas, and demonstrated its dependence on NPM-ALK activity.
  • DESIGN AND METHODS: In this study, the role of C/EBPbeta in proliferation and survival of ALK-positive anaplastic large cell lymphomas was investigated, as well as the mechanism of its expression and activity.
  • RESULTS: Interference with C/EBPbeta expression resulted in a dramatic decrease in cell proliferation in ALK-positive anaplastic large cell lymphomas, with a mild induction of apoptosis after 6 days.
  • Down-regulation of STAT3 resulted in a marked decrease in C/EBPbeta mRNA and protein levels with impairment in cell proliferation and viability, underscoring the important role of these two proteins in ALK-mediated oncogenesis.
  • CONCLUSIONS: These findings reveal the convergence of STAT3 and ERK1/2 signaling pathways activated by NPM-ALK in mediating the regulation of C/EBPbeta expression, a transcription factor central to NPM-ALK transformation.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / biosynthesis. Cell Proliferation. Gene Expression Regulation, Neoplastic. Lymphoma, Large-Cell, Anaplastic / enzymology. Receptor Protein-Tyrosine Kinases / biosynthesis. STAT3 Transcription Factor / physiology. Signal Transduction
  • [MeSH-minor] Animals. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Cell Survival / genetics. Down-Regulation / genetics. Humans. Mice


13. Patel P, Godwin J, Velankar M, Alkan S: Nodal ALK positive anaplastic large cell lymphoma of the axilla with spontaneous regression. Leuk Lymphoma; 2007 Jun;48(6):1250-2
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  • [Title] Nodal ALK positive anaplastic large cell lymphoma of the axilla with spontaneous regression.
  • [MeSH-major] Axilla. Lymph Nodes / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Neoplasm Regression, Spontaneous. Protein-Tyrosine Kinases / genetics

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  • (PMID = 17577798.001).
  • [ISSN] 1042-8194
  • [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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14. Han Y, Amin HM, Frantz C, Franko B, Lee J, Lin Q, Lai R: Restoration of shp1 expression by 5-AZA-2'-deoxycytidine is associated with downregulation of JAK3/STAT3 signaling in ALK-positive anaplastic large cell lymphoma. Leukemia; 2006 Sep;20(9):1602-9
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  • [Title] Restoration of shp1 expression by 5-AZA-2'-deoxycytidine is associated with downregulation of JAK3/STAT3 signaling in ALK-positive anaplastic large cell lymphoma.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALK+ ALCL) is characterized by constitutive activation of the Janus kinase (JAK)3/signal transducers and activators of transcription 3 (STAT3) signaling pathway.
  • SHP1, a tyrosine phosphatase that negatively regulates JAK/STAT, is frequently absent in ALK+ ALCL owing to gene methylation.
  • To test the hypothesis that loss of SHP1 contributes to JAK3/STAT3 activation in ALK+ ALCL cells, we induced SHP1 expression using 5-aza-2'-deoxycytidine (5-AZA), an inhibitor of DNA methyltransferase, in ALK+ ALCL cell lines, and correlated with changes in the JAK3/STAT3 pathway.
  • 5-AZA induced no significant increase in apoptosis but it sensitized ALCL cells to doxorubicin-induced apoptosis.
  • Our findings support the concept that loss of SHP1 contributes to the constitutive activation of JAK3/STAT3 in ALK+ ALCL cells.
  • [MeSH-major] Azacitidine / analogs & derivatives. Down-Regulation / drug effects. Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein Tyrosine Phosphatases / metabolism. Protein-Tyrosine Kinases / metabolism. STAT3 Transcription Factor / metabolism. Signal Transduction
  • [MeSH-minor] Apoptosis / drug effects. Base Sequence. Blotting, Western. Cell Cycle. Cell Line. DNA Primers. Doxorubicin / pharmacology. Humans. Janus Kinase 3. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Receptor Protein-Tyrosine Kinases

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  • (PMID = 16871283.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Intracellular Signaling Peptides and Proteins; 0 / JAK3 protein, human; 0 / STAT3 Transcription Factor; 776B62CQ27 / decitabine; 80168379AG / Doxorubicin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.48 / Protein Tyrosine Phosphatases; M801H13NRU / Azacitidine
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15. Youssif C, Goldenbogen J, Hamoudi R, Carreras J, Viskaduraki M, Cui YX, Bacon CM, Burke GA, Turner SD: Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: a Children's Cancer and Leukaemia Group Study. Genes Chromosomes Cancer; 2009 Nov;48(11):1018-26
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  • [Title] Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: a Children's Cancer and Leukaemia Group Study.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) is a T-cell malignancy in which ALK expression is a consequence of the t(2;5) or a variant translocation involving Chromosome 2.
  • Although the t(2;5) product nucleophosmin-ALK has been extensively studied for its transforming properties, very little is known regarding cooperative genetic mutations that may contribute to lymphomagenesis and may predict survival outcome, specifically in a purely pediatric population.
  • We collected biopsy material from 15 UK-resident children with ALK-expressing ALCL.
  • A range of genomic imbalances exist in ALK-expressing ALCL of a pediatric origin, with a greater number associated with poorer overall survival.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / enzymology. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / genetics

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19691112.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / DDB1 protein, human; 0 / DNA-Binding Proteins; 0 / HOXB1 homeodomain protein; 0 / Homeodomain Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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16. 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.


17. Vose J, Armitage J, Weisenburger D, International T-Cell Lymphoma Project: International peripheral T-cell and natural killer/T-cell lymphoma study: pathology findings and clinical outcomes. J Clin Oncol; 2008 Sep 1;26(25):4124-30
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  • [Title] International peripheral T-cell and natural killer/T-cell lymphoma study: pathology findings and clinical outcomes.
  • PURPOSE: Peripheral T-cell lymphoma (PTCL) and natural killer/T-cell lymphoma (NKTCL) are rare and heterogeneous forms of non-Hodgkin's lymphoma (NHL) that, in general, are associated with a poor clinical outcome.
  • RESULTS: A diagnosis of PTCL or NKTCL was confirmed in 1,153 (87.8%) of the cases.
  • The most common subtypes were PTCL not otherwise specified (NOS; 25.9%), angioimmunoblastic type (18.5%), NKTCL (10.4%), and adult T-cell leukemia/lymphoma (ATLL; 9.6%).
  • Misclassification occurred in 10.4% of the cases including Hodgkin's lymphoma (3%), B-cell lymphoma (1.4%), unclassifiable lymphoma (2.8%), or a diagnosis other than lymphoma (2.3%).
  • The use of an anthracycline-containing regimen was not associated with an improved outcome in PTCL-NOS or angioimmunoblastic type, but was associated with an improved outcome in anaplastic large-cell lymphoma, ALK positive.
  • However, expert hematopathology review is important for accurate diagnosis.
  • The clinical outcome for patients with most of these lymphoma subtypes is poor with standard therapies, and novel agents and new modalities are needed to improve survival.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoma, T-Cell / diagnosis. Lymphoma, T-Cell / mortality. T-Lymphocytes / pathology

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  • (PMID = 18626005.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Investigator] Savage K; Connors J; Gascoyne R; Chhanabhai M; Wilson W; Jaffe E; Armitage J; Vose J; Weisenburger D; Anderson J; Ullrich F; Bast M; Hochberg E; Harris N; Levine A; Nathwani B; Miller T; Rimsza L; Montserrat E; Lopez-Guillermo A; Campo E; Cuadros M; Alvarez Ferreira J; Martinez Delgado B; Holte H; Delabie J; Rüdiger T; Müller-Hermelink K; Reimer P; Adam P; Wilhelm M; Schmitz N; Nerl C; Lister A; Norton A; MacLennan KA; Luigi Zinzani P; Pileri S; Federico M; Bellei M; Coiffier B; Berger F; Tanin I; Wannakrairot P; Au W; Liang R; Loong F; Rajan S; Sng I; Tobinai K; Matsuno Y; Morishima Y; Nakamura S; Seto M; Tanimoto M; Yoshino T; Suzumiya J; Ohshima K; Kim WS; Ko YH
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18. Li C, Takino H, Eimoto T, Ishida T, Inagaki A, Ueda R, Suzuki R, Yoshino T, Nakagawa A, Nakamura S, Inagaki H: Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma. Mod Pathol; 2007 Jun;20(6):648-55
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  • [Title] Prognostic significance of NPM-ALK fusion transcript overexpression in ALK-positive anaplastic large-cell lymphoma.
  • In anaplastic large-cell lymphomas positive for anaplastic lymphoma kinase (ALK) protein, the ALK gene is most commonly fused to the NPM gene, and less commonly to TPM3, TFG, ATIC, and other rare genes.
  • Although this lymphoma is generally associated with a favorable clinical outcome, 25% of the patients die of the disease within 5 years.
  • (1) a sensitive reverse transcription-polymerase chain reaction (RT-PCR) assay for various X-ALK fusion genes, (2) a 5' rapid amplification of cDNA ends (RACE) assay to identify unknown fusion partners, and (3) a real-time RT-PCR assay to quantify the amount of the NPM-ALK fusion transcript.
  • In 26 cases of ALK(+) anaplastic large-cell lymphoma, the RT-PCR assay showed that the ALK was fused to NPM in 21 cases, to TPM3 in three, and to TFG in one.
  • The 5' RACE assay detected ATIC-ALK fusion in the remaining case.
  • The real-time quantitative RT-PCR assay showed that the NPM-ALK transcript was over expressed in four of 20 quantifiable cases.
  • Patients with NPM-ALK overexpression showed a significantly unfavorable overall survival compared with those with a low expression of this transcript.
  • The RT-PCR and 5' RACE assays developed here may be useful for identification of known and unknown gene partners fused to the ALK gene.
  • Overexpression of the NPM-ALK fusion transcript may be associated with a poor prognosis of the patients with ALK(+) anaplastic large-cell lymphomas.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / metabolism. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Protein-Tyrosine Kinases / biosynthesis

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  • (PMID = 17464320.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Fixatives; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; 1HG84L3525 / Formaldehyde; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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19. Bakshi NA, Ross CW, Finn WG, Valdez R, Ruiz R, Koujok K, Schnitzer B: ALK-positive anaplastic large cell lymphoma with primary bone involvement in children. Am J Clin Pathol; 2006 Jan;125(1):57-63
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  • [Title] ALK-positive anaplastic large cell lymphoma with primary bone involvement in children.
  • We describe the clinical, radiologic, and pathologic features of primary bone anaplastic large cell lymphoma (ALCL) in 3 boys.
  • Differential diagnoses included osteomyelitis and small round cell tumors of childhood, particularly Ewing sarcoma.
  • Preoperatively, ALCL was not a diagnostic consideration in any case.
  • Two cases showed classic large pleomorphic cells; 1 showed a composite pattern with a distinct small cell component and the more typical large cell type.
  • Neoplastic cells in all cases showed strong CD30 and anaplastic lymphoma kinase expression with relatively weak epithelial membrane antigen positivity.
  • Two patients were disease-free at last follow-up (15 months and 11 years); 1 patient died of disseminated disease within a year of diagnosis.
  • ALCL should be considered a diagnostic possibility when evaluating neoplastic bone lesions in children.
  • Although expression of NSE in ALCL has not been emphasized in the literature, it is worth noting because it may pose a diagnostic pitfall.
  • [MeSH-major] Bone Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / analysis

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  • (PMID = 16482992.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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20. Hosoi M, Ichikawa M, Imai Y, Kurokawa M: A case of anaplastic large cell lymphoma, ALK positive, primary presented in the skin and relapsed with systemic involvement and leukocytosis after years of follow-up period. Int J Hematol; 2010 Nov;92(4):667-8
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  • [Title] A case of anaplastic large cell lymphoma, ALK positive, primary presented in the skin and relapsed with systemic involvement and leukocytosis after years of follow-up period.
  • [MeSH-major] Leukocytosis. Lymphoma, Large-Cell, Anaplastic. Lymphoma, Primary Cutaneous Anaplastic Large Cell. Neoplasm Recurrence, Local. Protein-Tyrosine Kinases / metabolism. Skin Neoplasms

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  • [Cites] Blood. 1996 Apr 15;87(8):3437-41 [8605362.001]
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  • (PMID = 20976631.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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21. Ait-Tahar K, Cerundolo V, Banham AH, Hatton C, Blanchard T, Kusec R, Becker M, Smith GL, Pulford K: B and CTL responses to the ALK protein in patients with ALK-positive ALCL. Int J Cancer; 2006 Feb 1;118(3):688-95
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  • [Title] B and CTL responses to the ALK protein in patients with ALK-positive ALCL.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) has a good prognosis compared to ALK-negative ALCL, possibly as a result of the immune recognition of the ALK proteins.
  • The aim of our study was to investigate the presence of both a B and cytotoxic T cell (CTL) response to ALK in ALK-positive ALCL.
  • We confirmed the presence of an antibody response to ALK in all 9 ALK-positive ALCL patients investigated.
  • An ELISpot assay was used to detect a gamma-interferon (IFN) T cell response after short term culture of mononuclear blood cells with 2 ALK-derived HLA-A*0201 restricted peptides: ALKa and ALKb.
  • A significant gamma-IFN response was identified in all 7 HLA-A*0201-positive ALK-positive ALCL patients but not in ALK-negative ALCL patients (n = 2) or normal subjects (n = 6).
  • CTL lines (>95% CD8-positive) raised from 2 ALK-positive ALCL patients lysed ALK-positive ALCL derived cell lines in a MHC-Class I restricted manner.
  • This is the first report of both a B cell and CTL response to ALK in patients with ALK-positive ALCL.
  • The use of modified vaccinia virus Ankara (MVA) to express ALK is also described.
  • Our findings are of potential prognostic value and open up therapeutic options for those ALK-positive patients who do not respond to conventional treatment.
  • [MeSH-major] Epitopes, B-Lymphocyte / immunology. Epitopes, T-Lymphocyte / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Protein-Tyrosine Kinases / immunology. Protein-Tyrosine Kinases / metabolism. T-Lymphocytes, Cytotoxic / immunology

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16114011.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes, B-Lymphocyte; 0 / Epitopes, T-Lymphocyte; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Peptide Fragments; 82115-62-6 / Interferon-gamma; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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22. Matsubara K, Tanaka T, Taki T, Nakagawa A, Nigami H, Tamura A, Fukaya T: [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature]. Rinsho Ketsueki; 2008 May;49(5):325-30
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  • [Title] [ATIC-ALK-positive anaplastic large cell lymphoma: a case report and review of the literature].
  • We report a 10-year-old girl with ATIC-anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • Pathological findings showed that staining of ALK was restricted to the cytoplasm of ALCL cells.
  • ATIC-ALK chimeric transcripts were detected by reverse transcriptase polymerase chain reaction.
  • The patient was assigned to the standard risk group proposed by the international multicenter study for pediatric ALCL, ALCL99.
  • To date, 7 genes have been identified as a fusion partner of ALK, with the highest frequency in nucleophosmin (NPM).
  • Little is known about the clinical implications of subtypes of ALCL harboring each of the 7 fusion genes, especially those of variant fusion genes other than NPM-ALK.
  • In this paper, we review 9 patients with ATIC-ALK-positive ALCL in the literature in addition to discussing our patient.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Oncogene Proteins, Fusion / analysis

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  • (PMID = 18572809.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / ATIC-ALK fusion protein, human; 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 18
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23. Liu T, He M, Carlson DL, Hedvat C, Teruya-Feldstein J: ALK-positive anaplastic large cell lymphoma in a patient with chronic lymphocytic leukemia. Int J Surg Pathol; 2010 Oct;18(5):424-8
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  • [Title] ALK-positive anaplastic large cell lymphoma in a patient with chronic lymphocytic leukemia.
  • This article reports the case of a 59-year-old patient with an 8-year history of chronic lymphocytic leukemia (CLL), prostate carcinoma, and squamous cell carcinoma who developed an ALK-positive anaplastic large cell lymphoma (ALCL).
  • Lymph node and bone marrow biopsies showed 2 distinct morphologic populations: (a) the CLL component showing a diffuse monomorphous infiltrate of small lymphocytes with the typical immunophenotype showing positive CD20, CD5, CD23, and κ light chain restriction and (b) the ALCL component showing large anaplastic pleomorphic cells positive for CD30, CD45, ALK, CD45Ro, CD4, and vimentin.
  • Polymerase chain reaction performed on the lymph node for immunoglobulin heavy chain and T-cell receptor γ and β showed gene rearrangements after macrodissection of morphologically distinct populations, indicating confirmed genetically distinct populations.
  • This case represents the rare occurrence of an ALK-positive ALCL developing in a patient with CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasms, Multiple Primary. Protein-Tyrosine Kinases / metabolism


24. Hwang YY, Liang RH: An update in management of noncutaneous T-cell lymphomas. Adv Hematol; 2010;2010:424786
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  • [Title] An update in management of noncutaneous T-cell lymphomas.
  • T-cell lymphoma is a heterogeneous group of diseases.
  • Except for ALK positive anaplastic large cell lymphoma, T-cell lymphoma responds to conventional chemotherapy unfavourably, and most patients carry poor prognosis.
  • In recent years, efforts have been made to improve the outcome of T-cell lymphoma patients.
  • Novel agents, high-dose therapy, and allogeneic stem cell transplantation are studied, and various results are reported in literature.
  • This paper looks into the prognostication and treatment approach of different entities of noncutaneous T-cell lymphoma and would focus on the latest updates in its management.

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  • (PMID = 21188274.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3003949
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25. de Leval L, Bisig B, Thielen C, Boniver J, Gaulard P: Molecular classification of T-cell lymphomas. Crit Rev Oncol Hematol; 2009 Nov;72(2):125-43
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  • [Title] Molecular classification of T-cell lymphomas.
  • T-cell neoplasms encompass a heterogeneous group of relatively rare disease entities.
  • This review, focused on lymphoblastic tumors (T-ALL/LBL) and nodal-based peripheral T-cell lymphomas (PTCL), summarizes recent advances in the molecular characterization of these diseases.
  • Angioimmunoblastic T-cell lymphoma (AITL), one of the most common PTCL entities, comprises neoplastic cells with a molecular signature similar to normal follicular helper T cells, and this cellular derivation might account for several of the peculiar aspects of this disease.
  • Except in ALK-positive anaplastic large cell lymphoma, defined by ALK gene fusions, chromosomal translocations are otherwise rare in PTCLs, but some recurrent rearrangements might be associated with distinct lymphoma subtypes.
  • [MeSH-major] Biomarkers, Tumor / genetics. Lymphoma, T-Cell / classification. Lymphoma, T-Cell / genetics

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  • (PMID = 19233683.001).
  • [ISSN] 1879-0461
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 111
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26. Lamant L, Pileri S, Sabattini E, Brugières L, Jaffe ES, Delsol G: Cutaneous presentation of ALK-positive anaplastic large cell lymphoma following insect bites: evidence for an association in five cases. Haematologica; 2010 Mar;95(3):449-55
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  • [Title] Cutaneous presentation of ALK-positive anaplastic large cell lymphoma following insect bites: evidence for an association in five cases.
  • BACKGROUND: Skin involvement is frequent in ALK-positive anaplastic large cell lymphomas.
  • DESIGN AND METHODS: We retrospectively investigated five cases of ALK-positive anaplastic large cell lymphoma who presented with skin lesions occurring after an insect bite.
  • Biopsies were immunostained with antibodies against CD30, ALK, T- and B-cell antigens.
  • In four cases the correct diagnosis was delayed due to misinterpretation of the findings as a reactive infiltrate in the skin (n=2) or lymph nodes (n=2); all cases subsequently showed small numbers of cells with nuclear and cytoplasmic staining for ALK.
  • The final diagnoses were lymphohistiocytic variant (n=3) and composite common/small cell type (n=2) anaplastic large cell lymphoma.
  • CONCLUSIONS: In these cases the sequence of events between the insect bites and the occurrence of both skin lesions and satellite lymphadenopathy suggest a direct relationship between the bite and the presentation with anaplastic large cell lymphoma.
  • The subsequent release of cytokines at the site of the bite could act as a 'second hit', eliciting activation of the latter cells, which would then express the oncogenic NPM-ALK protein and undergo uncontrolled proliferation.

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  • (PMID = 19951975.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2833075
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27. Shi X, Franko B, Frantz C, Amin HM, Lai R: JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells. Br J Haematol; 2006 Oct;135(1):26-32
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  • [Title] JSI-124 (cucurbitacin I) inhibits Janus kinase-3/signal transducer and activator of transcription-3 signalling, downregulates nucleophosmin-anaplastic lymphoma kinase (ALK), and induces apoptosis in ALK-positive anaplastic large cell lymphoma cells.
  • As STAT3 activation is pathogenetically important in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ ALCL), we investigated whether JSI-124 can mediate significant inhibitory effects in this cell type.
  • In two ALK+ ALCL cell lines (Karpas 299 and SU-DHL-1), JSI-124 significantly reduced the number of viable cells to 50% of that of negative controls at a dose of 5-10 micromol/l at 24 h and 1-1.25 micromol/l at 48 h.
  • 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


28. Singh RR, Cho-Vega JH, Davuluri Y, Ma S, Kasbidi F, Milito C, Lennon PA, Drakos E, Medeiros LJ, Luthra R, Vega F: Sonic hedgehog signaling pathway is activated in ALK-positive anaplastic large cell lymphoma. Cancer Res; 2009 Mar 15;69(6):2550-8
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  • [Title] Sonic hedgehog signaling pathway is activated in ALK-positive anaplastic large cell lymphoma.
  • Deregulation of the sonic hedgehog (SHH) signaling pathway has been implicated in several cancers but has not been explored in T-cell lymphomas.
  • Here, we report that the SHH/GLI1 signaling pathway is activated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL).
  • We show that SHH, but not its transcriptional effector GLI1, is amplified in ALK+ ALCL tumors and cell lines, and that SHH and GLI1 proteins are highly expressed in ALK+ ALCL tumors and cell lines.
  • We also show that inhibition of SHH/GLI1 signaling with cyclopamine-KAAD, as well as silencing GLI1 gene expression by small interfering (si)RNA, decreased cell viability and clonogenicity of ALK+ ALCL cells.
  • Transfection of wild-type or mutant NPM-ALK into 293T cells showed that only wild-type NPM-ALK increased GLI1 protein levels and activated SHH/GLI1 signaling as shown by increase of CCND2 mRNA levels.
  • Inhibition of ALK tyrosine kinase and phosphatidylinositol 3-kinase (PI3K)/AKT or forced expression of pAKT down-regulated or up-regulated SHH/GLI1 signaling, respectively.
  • In conclusion, the SHH/GLI1 signaling pathway is activated in ALK+ ALCL.
  • SHH/GLI1 activation is the result of SHH gene amplification and is further mediated by NPM-ALK through activation of PI3K/AKT and stabilization of GLI1 protein.
  • There is a positive synergistic effect between the SHH/GLI1 and PI3K/AKT pathways that contributes to the lymphomagenic effect of NPM-ALK.
  • [MeSH-major] Hedgehog Proteins / metabolism. Lymphoma, Large-Cell, Anaplastic / metabolism
  • [MeSH-minor] Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / physiology. Enzyme Activation. Gene Amplification. Humans. Immunohistochemistry. Jurkat Cells. Phosphatidylinositol 3-Kinases / metabolism. Protein-Tyrosine Kinases / biosynthesis. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptor Protein-Tyrosine Kinases. Signal Transduction. Transcription Factors / antagonists & inhibitors. Transcription Factors / biosynthesis. Transcription Factors / genetics. Transcription Factors / metabolism. Transcription, Genetic. Transfection

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  • (PMID = 19244133.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / SHH protein, human; 0 / Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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29. Ait-Tahar K, Damm-Welk C, Burkhardt B, Zimmermann M, Klapper W, Reiter A, Pulford K, Woessmann W: Correlation of the autoantibody response to the ALK oncoantigen in pediatric anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor dissemination and relapse risk. Blood; 2010 Apr 22;115(16):3314-9
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  • [Title] Correlation of the autoantibody response to the ALK oncoantigen in pediatric anaplastic lymphoma kinase-positive anaplastic large cell lymphoma with tumor dissemination and relapse risk.
  • Anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) constitutes an ideal model disease to study tumor-specific immune responses.
  • All the tumor cells express oncogenic ALK resulting from a chromosomal translocation involved in lymphomagenesis.
  • Although antibodies and T-cell responses to ALK have previously been detected in ALK-positive ALCL patients, their prognostic significance is unknown.
  • We investigated a large cohort of uniformly treated ALK-positive pediatric ALCL patients to ascertain whether the titers of preexisting ALK autoantibodies correlated with clinical and histologic characteristics, tumor dissemination, and patient outcome.
  • ALK autoantibodies were analyzed in pretherapeutic serum samples from 95 patients enrolled into 2 therapy studies between 1996 and 2007.
  • ALK autoantibodies were detected in 87/95 patients.
  • Our results provide the first clinical evidence that a robust preexisting immune response to an oncoantigen resulting from an oncogenic chromosomal translocation inhibits lymphoma dissemination and decreases the risk of relapse.
  • [MeSH-major] Autoantibodies / immunology. Lymphoma, Large-Cell, Anaplastic / immunology. Lymphoma, Large-Cell, Anaplastic / pathology. Neoplasm Recurrence, Local / immunology. Protein-Tyrosine Kinases / immunology

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  • (PMID = 20185586.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Autoantigens; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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30. Krishnan C, Moline S, Anders K, Warnke RA: Intravascular ALK-positive anaplastic large-cell lymphoma mimicking inflammatory breast carcinoma. J Clin Oncol; 2009 May 20;27(15):2563-5
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  • [Title] Intravascular ALK-positive anaplastic large-cell lymphoma mimicking inflammatory breast carcinoma.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Adult. Antigens, CD30 / biosynthesis. Biomarkers, Tumor / metabolism. Cellulitis / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Inflammation / pathology. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19364961.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers, Tumor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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31. Lim ZY, Grace R, Salisbury JR, Creamer D, Jayaprakasam A, Ho AY, Devereux S, Mufti GJ, Pagliuca A: Cardiac presentation of ALK positive anaplastic large cell lymphoma. Eur J Haematol; 2005 Dec;75(6):511-4
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  • [Title] Cardiac presentation of ALK positive anaplastic large cell lymphoma.
  • Cardiac involvement as an initial presentation of malignant lymphoma is a rare occurrence.
  • Transcutaneous cardiac biopsy was non-diagnostic, therefore an open cardiac biopsy was performed from which a provisional diagnosis of a cardiac inflammatory pseudotumour was made.
  • Histological and immunophenotypic review of the initial cardiac biopsy revealed features consistent with a diagnosis of CD30, ALK1 positive anaplastic large cell lymphoma (ALCL).
  • Despite intensive treatment with combination chemotherapy, there was significant progression of disease, and he died 11 months after diagnosis.
  • The overall prognosis of cardiac lymphoma remains poor, which may be due to the often late presentation of the tumour.
  • To our knowledge, this is the first reported case of a cardiac ALK positive ALCL.
  • Although rare, cardiac presentation of ALCL should be added to the list of differential diagnoses of cardiac lymphomas.
  • [MeSH-major] Activin Receptors, Type I. Heart Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology

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  • (PMID = 16313264.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 2.7.11.30 / ACVRL1 protein, human; EC 2.7.11.30 / Activin Receptors, Type I; EC 2.7.11.30 / Activin Receptors, Type II
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32. Quintanilla-Martinez L, Pittaluga S, Miething C, Klier M, Rudelius M, Davies-Hill T, Anastasov N, Martinez A, Vivero A, Duyster J, Jaffe ES, Fend F, Raffeld M: NPM-ALK-dependent expression of the transcription factor CCAAT/enhancer binding protein beta in ALK-positive anaplastic large cell lymphoma. Blood; 2006 Sep 15;108(6):2029-36
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  • [Title] NPM-ALK-dependent expression of the transcription factor CCAAT/enhancer binding protein beta in ALK-positive anaplastic large cell lymphoma.
  • Although C/EBPbeta has important functions in B- and T-cell differentiation, its expression has not been well studied in lymphoid tissues.
  • We, therefore, analyzed its expression by immunohistochemistry and Western blot in normal lymphoid tissues and in 248 well-characterized lymphomas and lymphoma cell lines.
  • Nonneoplastic lymphoid tissues and most B-cell, T-cell, and Hodgkin lymphomas lacked detectable levels of C/EBPbeta.
  • In contrast, most (40 of 45; 88%) cases of ALK-positive anaplastic large cell lymphoma (ALCL) strongly expressed C/EBPbeta.
  • Western blot analysis confirmed C/EBPbeta expression in the ALK-positive ALCLs and demonstrated elevated levels of the LIP isoform, which has been associated with increased proliferation and aggressiveness in carcinomas.
  • Transfection of Ba/F3 and 32D cells with NPM-ALK and a kinase-inhibitable modified NPM-ALK resulted in the induction of C/EBPbeta and demonstrated dependence on NPM-ALK kinase activity.
  • In conclusion, we report the constitutive expression of C/EBPbeta in ALK-positive ALCL and show its relationship to NPM-ALK.
  • We suggest that C/EBPbeta is likely to play an important role in the pathogenesis and unique phenotype of this lymphoma.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-beta / genetics. CCAAT-Enhancer-Binding Protein-beta / metabolism. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Cell Line, Tumor. Gene Expression. Humans. Immunohistochemistry. Lymphoid Tissue / metabolism. Receptor Protein-Tyrosine Kinases. Transfection

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  • (PMID = 16709933.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-beta; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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33. Wang C, Zhang WM, Zhang ZH, Li BZ: [ALK-positive anaplastic large cell lymphoma with obvious nodular growth pattern: report of a case]. Zhonghua Bing Li Xue Za Zhi; 2010 Nov;39(11):779-80
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  • [Title] [ALK-positive anaplastic large cell lymphoma with obvious nodular growth pattern: report of a case].
  • [MeSH-major] Lymph Nodes / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Receptor Protein-Tyrosine Kinases / metabolism

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  • (PMID = 21215175.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD30; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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34. Savage KJ: Aggressive peripheral T-cell lymphomas (specified and unspecified types). Hematology Am Soc Hematol Educ Program; 2005;:267-77
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  • [Title] Aggressive peripheral T-cell lymphomas (specified and unspecified types).
  • Peripheral T-cell lymphomas (PTCLs) are a biologically diverse and uncommon group of diseases.
  • Compared to their B-cell counterparts, PTCLs remain largely unexplored and the optimal treatment ill-defined due to disease rarity and biological heterogeneity.
  • For the majority of PTCL subtypes, prognosis is poor with a 5-year overall survival of approximately 30% in most series.The notable exception is ALK-positive anaplastic large-cell lymphoma (ALK-pos ALCL), which has a superior outcome.

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  • [ErratumIn] Hematology Am Soc Hematol Educ Program. 2006;()
  • (PMID = 16304391.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Matsushita H, Nakamura N, Asai S, Yabe M, Hayama N, Kondo Y, Urano T, Miyachi H: A leukemic change as an initial manifestation of the common variant type of ALK-positive anaplastic large cell lymphoma in a patient with lung adenocarcinoma. Intern Med; 2008;47(23):2057-62
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  • [Title] A leukemic change as an initial manifestation of the common variant type of ALK-positive anaplastic large cell lymphoma in a patient with lung adenocarcinoma.
  • We report an 81-year-old man who had leukemic presentation of ALK-positive anaplastic large cell lymphoma (ALCL) as an initial manifestation.
  • The peripheral blood smear and bone marrow aspiration revealed the infiltration of atypical large cells with horseshoe-shaped or lobulated nuclei.
  • The detection of CD30 expression and the t (2;5) (p23;q35) translocation in these cells was confirmatory of a diagnosis of common variant ALK-positive ALCL in a leukemic phase.
  • An adequate, prompt diagnosis is necessary for this rare disease status in oncologic emergency to improve the disease management.
  • [MeSH-major] Adenocarcinoma / diagnosis. Genetic Variation / genetics. Lung Neoplasms / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis
  • [MeSH-minor] Aged, 80 and over. Antigens, CD30 / genetics. Diagnosis, Differential. Humans. Male

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  • (PMID = 19043261.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Number-of-references] 20
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36. Gualco G, Klumb CE, Barber GN, Weiss LM, Bacchi CE: Pediatric lymphomas in Brazil. Clinics (Sao Paulo); 2010;65(12):1267-77
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  • METHODS: A retrospective analyses of diagnosed pediatric lymphoma cases in a 10-year period was performed.
  • RESULTS: Non-Hodgkin lymphomas represented 68% of the cases, including those of precursor (36%) and mature (64%) cell origin.
  • Mature cell lymphomas comprised 81% of the B-cell phenotype and 19% of the T-cell phenotype.
  • Among mature B-cell lymphomas, most of the cases were Burkitt lymphomas (65%), followed by diffuse large B-cell lymphomas (24%).
  • In the mature T-cell group, anaplastic large cell lymphoma, ALK-positive was the most prevalent (57%), followed by peripheral T-cell lymphoma, then not otherwise specified (25%).
  • [MeSH-major] Lymphoma / epidemiology

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  • (PMID = 21340214.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / P30 AI073961
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Other-IDs] NLM/ PMC3020336
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37. Drakos E, Atsaves V, Schlette E, Li J, Papanastasi I, Rassidakis GZ, Medeiros LJ: The therapeutic potential of p53 reactivation by nutlin-3a in ALK+ anaplastic large cell lymphoma with wild-type or mutated p53. Leukemia; 2009 Dec;23(12):2290-9
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  • [Title] The therapeutic potential of p53 reactivation by nutlin-3a in ALK+ anaplastic large cell lymphoma with wild-type or mutated p53.
  • p53 is expressed frequently, but is rarely mutated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) tumours.
  • We show that nutlin-3a activates p53 in ALK+ ALCL cells carrying a wild type (wt) or mutated but partially functional p53 gene resulting in p53-dependent cell-cycle arrest and apoptosis.
  • Cell-cycle arrest was associated with upregulation of the cyclin-dependent kinase inhibitor p21.
  • Nutlin-3a-induced apoptotic cell death was accompanied by Bax and Puma upregulation, downregulation of Bcl-xl, survivin, and caspase-3 cleavage, and this was reduced when p53-dependent transactivation activity was inhibited by pifithrin-alpha, or when pifithrin-mu was used to inhibit direct p53 targeting of mitochondria.
  • Nutlin-3a sensitized the activation of the extrinsic apoptotic pathway in wt-p53 ALK+ ALCL cells, in part, through upregulation of DR-5 and downregulation of c-Flip(S/L), and was synergistic with TRAIL in cell death induction.
  • In addition, nutlin-3a treatment enhanced doxorubicin cytotoxicity against ALK+ ALCL cells harbouring mt p53, and this was associated with p73 upregulation.
  • These data suggest that disruption of the p53-mdm2 interaction by nutlin-3a offers a novel therapeutic approach for ALK+ ALCL patients.
  • [MeSH-major] Imidazoles / pharmacology. Lymphoma, Large-Cell, Anaplastic / drug therapy. Mutation. Piperazines / pharmacology. Tumor Suppressor Protein p53 / drug effects
  • [MeSH-minor] Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. Cell Cycle. Cell Line, Tumor. Doxorubicin / pharmacology. Drug Synergism. Humans. TNF-Related Apoptosis-Inducing Ligand / pharmacology


38. Hughes M, Morrison A, Jackson R: Primary bladder lymphoma: management and outcome of 12 patients with a review of the literature. Leuk Lymphoma; 2005 Jun;46(6):873-7
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  • [Title] Primary bladder lymphoma: management and outcome of 12 patients with a review of the literature.
  • Primary bladder non-Hodgkin's lymphoma (NHL) is rare.
  • Using the Scotland and Newcastle lymphoma group database, 12 patients with primary bladder lymphoma were identified between 1980 and 2001, the largest single group of patients available to date.
  • Six cases were low-grade extranodal marginal zone lymphoma, 4 diffuse large B-cell lymphoma, one an ALK 1 positive anaplastic large cell lymphoma (ALKoma) and one a low-grade lymphoma unspecified.
  • A review of 88 additional cases in the literature support the findings that primary bladder lymphoma is associated with a good prognosis.
  • Patients with low-grade extranodal marginal zone lymphoma may respond well to simple therapies.
  • Patients with diffuse large B-cell lymphoma respond well to first-line chemotherapy regimens.
  • [MeSH-major] Lymphoma, B-Cell / diagnosis. Lymphoma, B-Cell / therapy. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / therapy. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / therapy. Urinary Bladder Neoplasms / diagnosis. Urinary Bladder Neoplasms / therapy

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  • (PMID = 16019532.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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39. 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


40. Sung CO, Ko YH, Park S, Kim K, Kim W: Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma. J Korean Med Sci; 2005 Dec;20(6):952-6
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  • [Title] Immunoreactivity of CD99 in non-Hodgkin's lymphoma: unexpected frequent expression in ALK-positive anaplastic large cell lymphoma.
  • To verify the spectrum of CD99-expressing lymphoid malignancy, an immunohistochemical study for CD99 was carried out in 182 cases of non-Hodgkin's lymphoma, including 21 lymphoblastic lymphomas, 11 small lymphocytic lymphomas, 9 mantle cell lymphomas, 12 follicular lymphomas, 37 diffuse large B cell lymphomas, 18 Burkitt's lymphomas, 28 NK/T-cell lymphomas, 8 angioimmunoblastic T-cell lymphomas, 23 peripheral T-cell lymphomas, unspecified, and 15 systemic anaplastic large cell lymphomas.
  • CD99 was positive in all T-lymphoblastic lymphomas and in 60% of B-lymphoblastic lymphomas.
  • Majority of T and NK cell lymphomas were negative for CD99, except anaplastic large cell lymphomas (ALCLs).
  • Seven of 10 (70%) ALK positive ALCLs expressed CD99, whereas only 1 of 5 (20%) ALK negative ALCLs were positive.
  • Of the mature B-cell lymphomas, 5.4% (2/37) of diffuse large B cell lymphomas and 11.1% (2/18) of Burkitt's lymphomas expressed CD99.
  • In conclusion, CD99 is infrequently expressed in mature B and T cell lymphomas, except ALK-positive ALCL.
  • High expression of CD99 in ALK-positive ALCL is unexpected finding and its biologic and clinical significances have yet to be clarified.
  • [MeSH-major] Antigens, CD / metabolism. Cell Adhesion Molecules / metabolism. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Non-Hodgkin / immunology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 16361803.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2779325
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41. Dien Bard J, Gelebart P, Anand M, Zak Z, Hegazy SA, Amin HM, Lai R: IL-21 contributes to JAK3/STAT3 activation and promotes cell growth in ALK-positive anaplastic large cell lymphoma. Am J Pathol; 2009 Aug;175(2):825-34
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  • [Title] IL-21 contributes to JAK3/STAT3 activation and promotes cell growth in ALK-positive anaplastic large cell lymphoma.
  • Interleukin (IL)-21 has been reported to both stimulate cell growth and promote survival in benign lymphoid cells and several types of hematopoietic neoplasms.
  • It induces JAK3/STAT3 signaling, a biologically important cellular pathway activated in most cases of anaplastic lymphoma kinase (ALK)-expressing anaplastic large cell lymphoma (ALK(+)ALCL).
  • Therefore, we hypothesize that IL-21 may contribute to JAK3/STAT3 activation and cell growth in ALK(+)ALCL.
  • By reverse transcription-PCR, we found consistent expression of IL-21 receptor (IL-21R) in all ALK(+)ALCL cell lines and frozen tumors examined.
  • IL-21 was also consistently expressed in ALK(+)ALCL tumors, although its mRNA was detectable in only one of three cell lines tested.
  • By immunohistochemistry, we examined 10 paraffin-embedded ALK(+)ALCL tumors; all cases were positive for both IL-21 and IL-21R in these neoplastic cells.
  • IL-21 signaling is biologically significant in ALK(+)ALCL since the addition of recombinant IL-21 enhanced the activation of JAK3/STAT3 and significantly increased cell growth in ALK(+)ALCL cell lines.
  • However, small interfering RNA down-regulation of IL-21R significantly decreased both STAT3 activation and cell growth.
  • IL-21R expression is not linked to nucleophosmin-ALK since forced expression of nucleophosmin-ALK and small interfering RNA down-regulation of nucleophosmin-ALK did not significantly change the expression of either IL-21R or IL-21.
  • Our findings thus support the enhancement of JAK3/STAT3 activation and cell growth in ALK(+)ALCL via IL-21 signaling.
  • [MeSH-major] Interleukins / metabolism. Janus Kinase 3 / biosynthesis. Lymphoma, Large-Cell, Anaplastic / pathology. STAT3 Transcription Factor / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Protein-Tyrosine Kinases / analysis. RNA, Small Interfering / genetics. Receptor Protein-Tyrosine Kinases. Receptors, Interleukin-21 / metabolism

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  • (PMID = 19608866.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukins; 0 / JAK3 protein, human; 0 / RNA, Small Interfering; 0 / Receptors, Interleukin-21; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / interleukin-21; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 2.7.10.2 / Janus Kinase 3
  • [Other-IDs] NLM/ PMC2716977
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42. Niitsu N, Kohri M, Hayama M, Tamaru J, Miura I: ALK-positive anaplastic large cell lymphoma with dic(2;4)(p23;q33). Leuk Res; 2009 Jun;33(6):e23-5
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  • [Title] ALK-positive anaplastic large cell lymphoma with dic(2;4)(p23;q33).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 4. Lymphoma, Large-Cell, Anaplastic / genetics. Protein-Tyrosine Kinases / metabolism. Translocation, Genetic

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  • (PMID = 19036440.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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43. Daneshbod Y, Oryan A, Khojasteh HN, Rasekhi A, Ahmadi N, Mohammadianpanah M: Primary ALK-positive anaplastic large cell lymphoma of the breast: a case report and review of the literature. J Pediatr Hematol Oncol; 2010 Mar;32(2):e75-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary ALK-positive anaplastic large cell lymphoma of the breast: a case report and review of the literature.
  • BACKGROUND: Non-Hodgkin lymphomas of the breast are uncommon, which represent less than 1% of all breast malignancies and predominantly are of B-cell origin.
  • OBSERVATION: In this report, a rare case of anaplastic lymphoma kinase (ALK)-positive anaplastic large T-cell lymphoma in the breast of a 16-year-old female without breast implant is described.
  • The immunohistochemical profile showed positivity for CD30 and ALK and confirmed the diagnosis of ALK-positive anaplastic large T-cell lymphoma of the breast.
  • CONCLUSION: Anaplastic large T-cell lymphoma of the breast is rare, and can clinically mimic inflammatory breast carcinoma in adolescence.
  • [MeSH-major] Breast Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / analysis


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

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20451371.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GSK 1838705A; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase
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45. 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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46. Delsol G: [Molecular abnormalities in lymphomas]. Bull Cancer; 2010 Nov;97(11):1347-64
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  • In the present review, molecular abnormalities observed in the most frequent B, T or NK cell lymphomas are discussed.
  • In the broad spectrum of diffuse large B-cell lymphomas microarray analysis shows mostly two subgroups of tumors, one with gene expression signature corresponding to germinal center B-cell-like (GCB: CD10+, BCL6 [B-Cell Lymphoma 6]+, centerine+, MUM1-) and a subgroup expressing an activated B-cell-like signature (ABC: CD10-, BCL6-, centerine-, MUM1+).
  • Among other B-cell lymphomas with well characterized molecular abnormalies are follicular lymphoma (BCL2 deregulation), MALT lymphoma (Mucosa Associated Lymphoid Tissue) [API2-MALT1 (mucosa-associated-lymphoid-tissue-lymphoma-translocation-gene1) fusion protein or deregulation BCL10, MALT1, FOXP1.
  • MALT1 transcription factors], mantle cell lymphoma (cycline D1 [CCND1] overexpression) and Burkitt lymphoma (c-Myc expression).
  • Except for ALK (anaplastic lymphoma kinase)-positive anaplastic large cell lymphoma, well characterized molecular anomalies are rare in lymphomas developed from T or NK cells.
  • Peripheral T cell lymphomas not otherwise specified are a heterogeneous group of tumors with frequent but not recurrent molecular abnormalities.
  • In angio-immunoblastic T-cell lymphomas molecular abnormalities are found in follicular helper T-cell (TFH) that express some distinctive markers such as CD10, PD-1, CXCR5 and the CXCL13 chemokine.
  • ALK-positive anaplastic large cell lymphoma is a paradigme of T-cell lymphoma since it is associated with an X-ALK oncogenic fusion protein due to a translocation involving ALK gene at 2p23.
  • ALK tyrosine kinase activates downstream pathways (Stat3/5b, Src kinases, PLCγ, PI3 kinase) implicated in lymphomagenesis, proliferation and protection against apoptosis.
  • Specific ALK inhibitors are currently in clinical evaluation.
  • Helicobacter pylori in MALT lymphoma) in lymphomagenesis.
  • [MeSH-major] Gene Amplification / genetics. Genes, Tumor Suppressor. Lymphoma / genetics. Mutation / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Gene Deletion. Gene Expression Regulation, Neoplastic / genetics. Genetic Techniques. Humans. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / metabolism. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell / metabolism. Neoplasm Proteins / metabolism


47. Grewal JS, Smith LB, Winegarden JD 3rd, Krauss JC, Tworek JA, Schnitzer B: Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature. Ann Hematol; 2007 Jul;86(7):499-508
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  • [Title] Highly aggressive ALK-positive anaplastic large cell lymphoma with a leukemic phase and multi-organ involvement: a report of three cases and a review of the literature.
  • Anaplastic large cell lymphoma (ALCL) is an aggressive neoplasm of T- or null cell phenotype and is recognized as a distinct clinicopathologic subtype of non-Hodgkin lymphoma (NHL) in the revised World Health Organization (WHO) classification of hematopoietic neoplasms.
  • Most cases with leukemic involvement are the small cell variant of ALCL.
  • These cases often lack the pleomorphism seen in the common variant of ALCL and may be misdiagnosed.
  • We report a series of three patients who presented with leukemic phase ALCL.
  • The patients in our case series with leukemic phase ALCL exhibited rare clinical features.
  • Two of the patients had small cell variant and the third patient had common type ALCL.
  • The neoplastic cells in all three patients were ALK positive; however these patients died within months of diagnosis.
  • Leukemic phase ALCL is rare, and behaves in an aggressive manner.
  • Some, but not all, cases in the literature presenting with peripheral blood involvement had small cell variant ALCL, as seen in two of our cases.
  • The leukemic phase of ALCL should be considered when a T-cell leukemia with unusual morphologic features is encountered.
  • [MeSH-major] Leukemia / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Protein-Tyrosine Kinases / metabolism

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  • (PMID = 17396261.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 91
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48. Osoegawa A, Nosaki K, Miyamoto H, Kometani T, Hirai F, Ondo K, Seto T, Sugio K, Choi YL, Soda M, Mano H, Ichinose Y: Incidentally proven pulmonary "ALKoma". Intern Med; 2010;49(6):603-6
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  • [Title] Incidentally proven pulmonary "ALKoma".
  • Genetic alterations of echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) inversion were recently found in lung cancer.
  • Biopsy from her supraclavicular lymph nodes was performed to differentiate the diagnosis between lymphoma and lung cancer.
  • On the other hand, the commercially available chromosomal fluorescent in situ hybridization (FISH) analysis showed split signals of ALK, which was confirmed to be the EML4-ALK inversion.
  • The commercial-based ALK FISH is useful for screening pulmonary ALKoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / genetics. Cell Cycle Proteins / genetics. Chromosome Inversion / genetics. Lung Neoplasms / diagnosis. Lung Neoplasms / genetics. Microtubule-Associated Proteins / genetics. Protein-Tyrosine Kinases / genetics. Serine Endopeptidases / genetics
  • [MeSH-minor] Adult. Biopsy. Diagnosis, Differential. Female. Humans. In Situ Hybridization, Fluorescence. Lymph Nodes / pathology. Lymphoma / diagnosis. Lymphoma / pathology. Receptor Protein-Tyrosine Kinases

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  • (PMID = 20228600.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Microtubule-Associated Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.21.- / EML4 protein, human; EC 3.4.21.- / Serine Endopeptidases
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