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1. Marneros AG, Grossman ME, Silvers DN, Husain S, Nuovo GJ, MacGregor-Cortelli B, Neylon E, Patterson M, O'Connor OA, Zain JM: Pralatrexate-induced tumor cell apoptosis in the epidermis of a patient with HTLV-1 adult T-cell lymphoma/leukemia causing skin erosions. Blood; 2009 Jun 18;113(25):6338-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pralatrexate-induced tumor cell apoptosis in the epidermis of a patient with HTLV-1 adult T-cell lymphoma/leukemia causing skin erosions.
  • Pralatrexate is a novel antifolate, which shows increased antitumor activity in human tumor xenograft studies in mice compared with methotrexate.
  • We investigated the effects of pralatrexate in a patient with adult T-cell lymphoma/leukemia with significant skin involvement.
  • Atypical lymphocytes in epidermal Pautrier microabscesses were positive for HTLV-1.
  • Here we present in vivo evidence that pralatrexate-induced erosions in skin affected by adult T-cell lymphoma/leukemia are a manifestation of apoptosis of tumor cells infiltrating the epidermis and are not the result of cytotoxicity by pralatrexate on keratinocytes.
  • This distinction is critical and may profoundly influence the clinical decision to continue pralatrexate treatment.
  • [MeSH-major] Aminopterin / analogs & derivatives. Antimetabolites, Antineoplastic / pharmacology. Apoptosis / drug effects. Epidermis / drug effects. Exanthema / chemically induced. Folic Acid Antagonists / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Cyclophosphamide / administration & dosage. Diagnosis, Differential. Disease Progression. Doxorubicin / administration & dosage. Drug Eruptions / diagnosis. Etoposide / administration & dosage. Humans. Interferon-alpha / administration & dosage. Male. Prednisone / administration & dosage. Recombinant Proteins. Vincristine / administration & dosage. Zidovudine / administration & dosage

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  • (PMID = 19389878.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 10-propargyl-10-deazaaminopterin; 0 / Antimetabolites, Antineoplastic; 0 / Folic Acid Antagonists; 0 / Interferon-alpha; 0 / Recombinant Proteins; 4B9XT59T7S / Zidovudine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 99210-65-8 / interferon alfa-2b; JYB41CTM2Q / Aminopterin; VB0R961HZT / Prednisone; CHOP protocol; EPOCH protocol
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2. Matsunaga T, Murase K, Yoshida M, Fujimi A, Iyama S, Kuribayashi K, Sato T, Kogawa K, Hirayama Y, Sakamaki S, Kohda K, Niitsu Y: Donor cell derived acute myeloid leukemia after allogeneic cord blood transplantation in a patient with adult T-cell lymphoma. Am J Hematol; 2005 Aug;79(4):294-8
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  • [Title] Donor cell derived acute myeloid leukemia after allogeneic cord blood transplantation in a patient with adult T-cell lymphoma.
  • We report a patient with adult T-cell lymphoma who developed acute myeloid leukemia (AML) after allogeneic cord blood transplantation (CBT).
  • Although 25 cases of donor cell leukemia (DCL) occurring after allogeneic bone marrow transplantation have previously been reported, there have been no reports of DCL after CBT.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Leukemia, Myeloid / etiology. Lymphoma, T-Cell / therapy. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Acute Disease. Chromosomes, Human, X / genetics. Chromosomes, Human, Y / genetics. Fatal Outcome. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Tandem Repeat Sequences. Tissue Donors. Transplantation Chimera. Transplantation, Homologous

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16044441.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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3. Wang SS, Carreon JD, Hanchard B, Chanock S, Hisada M: Common genetic variants and risk for non-Hodgkin lymphoma and adult T-cell lymphoma/leukemia in Jamaica. Int J Cancer; 2009 Sep 15;125(6):1479-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Common genetic variants and risk for non-Hodgkin lymphoma and adult T-cell lymphoma/leukemia in Jamaica.
  • We evaluated whether risk of non-Hodgkin lymphoma (NHL), particularly adult T-cell leukemia/lymphoma (ATL) related to human T-lymphotropic virus (HTLV) infection was associated with 63 single nucleotide polymorphisms (SNPs) from 38 candidate genes.
  • The 395 NHL cases registered in Jamaica were matched by age, sex, calendar-year and HTLV serostatus to 309 controls from the same population.
  • Interleukin 13 (IL13) Ex4+98A>G SNP (rs20541) was associated with decreased NHL risk (OR(AG/AA) = 0.62,95% CI = 0.44-0.87, p = 0.006), as was vascular cell adhesion molecule-1, VCAM1 Ex9+149G>A SNP (rs1041163) (OR(CT) = 0.77, 95% CI = 0.54-1.10, OR(CC) = 0.35, 95% CI = 0.16-0.76, p-trend = 0.007).
  • Both results were stronger in analyses restricted to ATL cases and HTLV-positive controls, suggesting a role for these genes in ATL etiology (IL13 OR(AG/AA) = 0.54, 95% CI = 0.36-0.84, p = 0.005; VCAM1 OR(CT) = 0.65, 95% CI = 0.42-1.01, OR(CC) = 0.20, 95% CI = 0.08-0.54, p-trend = 0.001).
  • [MeSH-major] HTLV-I Infections / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Polymorphism, Single Nucleotide / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Genetic Predisposition to Disease. Human T-lymphotropic virus 1 / immunology. Humans. Interleukin-13 / genetics. Interleukin-5 / genetics. Jamaica / epidemiology. Male. Middle Aged. Vascular Cell Adhesion Molecule-1 / genetics. Young Adult

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  • [Copyright] 2009 UICC
  • (PMID = 19533685.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL5 protein, human; 0 / Interleukin-13; 0 / Interleukin-5; 0 / Vascular Cell Adhesion Molecule-1
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4. Khadilkar UN, Mathai AM, Chakrapani M, Prasad K: Rare association of papillary carcinoma of thyroid with adult T-cell lymphoma/leukemia. Indian J Pathol Microbiol; 2010 Jan-Mar;53(1):125-7
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  • [Title] Rare association of papillary carcinoma of thyroid with adult T-cell lymphoma/leukemia.
  • But the tumor that arises more frequently in thyroiditis is malignant lymphoma.
  • We report a rare association of papillary carcinoma of thyroid in an elderly lady with adult T-cell lymphoma/leukemia.
  • Fine needle aspiration of the thyroid, neck nodes and evaluation of the bone marrow and peripheral blood helped in the diagnosis of papillary cancer coexisting with adult T-cell lymphoma/leukemia.
  • [MeSH-major] Carcinoma, Papillary / complications. Leukemia-Lymphoma, Adult T-Cell / complications. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Thyroid Gland / pathology. Thyroid Neoplasms / complications
  • [MeSH-minor] Adult. Biopsy, Fine-Needle. Bone Marrow / pathology. Female. Histocytochemistry. Humans. Immunohistochemistry. Leukemia. Middle Aged. Neck / radiography. Thyroid Nodule. Tomography

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  • (PMID = 20090241.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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5. Laveaux K, Axiotis CA, Durkin H, Braverman AS: Localized nasal cavity, sinus, and massive bilateral orbital involvement by human T cell leukemia virus 1 adult T cell lymphoma, with epidermal hypertrophy due to mite infestation. Rare Tumors; 2010;2(4):e59

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localized nasal cavity, sinus, and massive bilateral orbital involvement by human T cell leukemia virus 1 adult T cell lymphoma, with epidermal hypertrophy due to mite infestation.
  • HTLV1 adult T cell lymphoma occurs tends to be widely disseminated and aggressive, with only brief responses to chemotherapy.
  • Aside from cervical adenopathy, involvement of head and neck structures is uncommon and orbital involvement rare.We report a case of nasal cavity HTLV lymphoma with massive bilateral orbital involvement and proptosis, resulting in complete left and partial right eye amaurosis.
  • No other sites of disease were found.
  • An associated problem was striking bilateral hypertrophic, hyperkeratotic eyelid and breast lesions due to mite infestation.

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  • (PMID = 21234251.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3019594
  • [Keywords] NOTNLM ; HTLV / lymphoma / oncology
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6. Gallo RC: The discovery of the first human retrovirus: HTLV-1 and HTLV-2. Retrovirology; 2005;2:17
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The discovery of the first human retrovirus: HTLV-1 and HTLV-2.
  • I describe here the history leading up to and including my laboratory's discovery of the first human retrovirus, HTLV-I, and its close relative, HTLV-II.
  • My efforts were inspired by early work showing a retroviral etiology for leukemias in various animals, including non-human primates.
  • These efforts finally yielded success following the discovery of IL-2 and its use to culture adult T cell lymphoma/leukemia cells.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 2 / isolation & purification. Leukemia, T-Cell / history. Lymphoma, T-Cell / history

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  • (PMID = 15743526.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC555587
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7. Nakayama-Ichiyama S, Yokote T, Hiraoka N, Takayama A, Iwaki K, Kobayashi K, Akioka T, Oka S, Miyoshi T, Takubo T, Tsuji M, Hanafusa T: Central nervous system involvement in adult T-cell lymphoma diagnosed with T-cell receptor gene clonality testing of cerebrospinal fluid. Br J Haematol; 2010 Sep;150(5):629-32

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Central nervous system involvement in adult T-cell lymphoma diagnosed with T-cell receptor gene clonality testing of cerebrospinal fluid.
  • [MeSH-major] Central Nervous System / pathology. Gene Rearrangement, T-Lymphocyte / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration / diagnosis

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  • (PMID = 20497173.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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8. Tabata R, Tabata C, Namiuchi S, Terada M, Yasumizu R, Okamoto T, Nagai T: Adult T-cell lymphoma mimicking Henoch-Schönlein purpura. Mod Rheumatol; 2007;17(1):57-62
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  • [Title] Adult T-cell lymphoma mimicking Henoch-Schönlein purpura.
  • We report a male patient with adult T-cell lymphoma, who was initially diagnosed clinically as having Henoch-Schönlein purpura (HSP) with abdominal pain and specific purpura.
  • Adult T-cell lymphoma-like cells were minimal and abdominal lymph nodes were transiently swollen, and the symptoms were improved by supportive management.
  • Although the clinical course was compatible with HSP, the histological examination revealed infiltration of lymphocytes rather than neutrophils.
  • Later he developed lymphoma and was treated with chemotherapy.
  • This rare case suggests the importance of skin biopsies to seek the underlying pathology in adult HSP.

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  • (PMID = 17278024.001).
  • [ISSN] 1439-7595
  • [Journal-full-title] Modern rheumatology
  • [ISO-abbreviation] Mod Rheumatol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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9. Zámecníkova A, Al Bahar S, Elshinnawy SE: Genomic instability and rapid clinical course in adult T-cell lymphoma/leukemia patient. Leuk Res; 2010 Dec;34(12):1617-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic instability and rapid clinical course in adult T-cell lymphoma/leukemia patient.
  • Adult T-cell leukemia/lymphoma is a distinct clinical entity characterized by a clonal proliferation of malignant T-lymphocytes.
  • The etiologic agent of the disease is a Human T-cell lymphotropic virus type I.
  • It occurs almost exclusively in areas where the virus is endemic; however the disease develops only in the minority of patients who are virus carriers.
  • Karyotyping findings and their correlation with clinical features are still limited in T-cell malignancies, complicated by clinical heterogeneity and a plethora of secondary abnormalities.
  • This study describes detailed chromosomal and fluorescence in situ hybridization results observed in a patient with adult T-cell leukemia/lymphoma and correlates them with clinical characteristics.
  • [MeSH-major] Genomic Instability. HTLV-I Infections / genetics. Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell / genetics. T-Lymphocytes
  • [MeSH-minor] Adult. Female. Humans. Karyotyping

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20211490.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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10. Shirdel A, Yazdanpanah MJ, Pezeshkpoor F, Kalantary MR, Soleimani M: Diffuse normolipaemic plane xanthomatosis associated with adult T-cell lymphoma/leukaemia. J Eur Acad Dermatol Venereol; 2008 Nov;22(10):1252-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffuse normolipaemic plane xanthomatosis associated with adult T-cell lymphoma/leukaemia.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Lipids / blood. Xanthomatosis / complications
  • [MeSH-minor] Adult. Humans. Male

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  • (PMID = 18637865.001).
  • [ISSN] 1468-3083
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Lipids
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11. Flower C, Prussia P, Corbin D: Extensive extranodal adult T-cell lymphoma presenting with a lytic arthropathy of the ankle. J Clin Rheumatol; 2007 Dec;13(6):328-30
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  • [Title] Extensive extranodal adult T-cell lymphoma presenting with a lytic arthropathy of the ankle.
  • A case is presented of a 44-year-old human T-cell lymphotropic virus-1 seropositive Afro-Caribbean man whose adult T-cell lymphoma presented with an ankle arthropathy.
  • Over a period of weeks he developed subcutaneous tumor masses, osteolytic lesions, sinonasal involvement, and spinal disease culminating in death 4 months after his diagnosis.
  • The case highlights the extranodal manifestations, generally, and rheumatological complications, specifically, of this very aggressive form of lymphoma with review of the relevant literature.
  • [MeSH-major] Ankle Joint. Arthritis / etiology. Lymphoma, Extranodal NK-T-Cell / complications
  • [MeSH-minor] Adult. Biopsy, Needle. Diagnosis, Differential. Fatal Outcome. Follow-Up Studies. Humans. Male. Photomicrography. Tomography, X-Ray Computed

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  • (PMID = 18176141.001).
  • [ISSN] 1076-1608
  • [Journal-full-title] Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases
  • [ISO-abbreviation] J Clin Rheumatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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12. Karube K, Suzumiya J, Okamoto M, Takeshita M, Maeda K, Sakaguchi M, Inada T, Tsushima H, Kikuchi M, Ohshima K: Adult T-cell lymphoma/leukemia with angioimmunoblastic T-cell lymphomalike features: Report of 11 cases. Am J Surg Pathol; 2007 Feb;31(2):216-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell lymphoma/leukemia with angioimmunoblastic T-cell lymphomalike features: Report of 11 cases.
  • In adult T-cell lymphoma/leukemia (ATLL), the neoplastic lymphoid cells are usually medium-sized to large, often with pronounced nuclear pleomorphism compatible with the diagnosis of diffuse pleomorphic peripheral T-cell lymphoma.
  • We describe here 11 patients with the rare morphologic variant of ATLL, angioimmunoblastic T-cell lymphoma (AILT)-like type.
  • The lymphoma cells were medium-to-large size with clear cytoplasm.
  • However, immunohistochemical features of AILT, namely, CD10 and CXCL13 expression in lymphoma cells and proliferation of CD21-positive follicular dendritic cells, were not detected.
  • Two cases were CXCR3-positive, whereas 9 expressed CCR4, which are usually positive in ATLL.
  • All patients were positive for antiadult T-cell leukemia/lymphoma-associated antigen, which is a specific antibody for human T-cell lymphotropic virus type-I.
  • Southern blot analysis revealed proviral DNA integration in lymphoma cells in 9 patients.
  • Almost all patients showed aggressive clinical course and poor survival (median survival: 5 mo).
  • This is the first report of ATLL with AILT-like morphologic features.
  • [MeSH-major] Immunoblastic Lymphadenopathy / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Lymphoma, T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Antigens, CD / metabolism. Biomarkers, Tumor / metabolism. DNA, Viral / analysis. Female. HTLV-I Infections / virology. Humans. Male. Middle Aged. Survival Rate

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  • (PMID = 17255766.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / DNA, Viral
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13. Beltran BE, Morales D, Quiñones P, Salas R, Castillo J: Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma.
  • : 8575 Background: Adult T-cell leukemia/lymphoma (ATLL) is associated with human T-cell lymphotropic virus type-I (HTLV-1) described in Southern Japan, Europe, Caribbean and South America.
  • Risk-stratification tools for ATLL have not been adequately evaluated.
  • This study attempts to define prognostic factors for patients with ATLL.
  • Diagnosis was based on clinical history and histological findings consistent with ATLL and either positive HTLV-1 serology or evidence of HTLV-1 integration.
  • Clinical types were acute (n=45), lymphomatous (n=43), cutaneous (n=10), smoldering (n=3) and chronic (n=1).
  • Median OS for acute, lymphomatous, smoldering and cutaneous subtype were 2, 11, 17 and 39 months, respectively (log-rank 28.5, p<0.00001).
  • In the univariate analysis, presence of B symptoms, ECOG performance status 2, clinical stage II or higher, elevated LDH level and bone marrow (BM) involvement were independent factors for survival with p<0.05.
  • The prognostic index for T-cell lymphoma (PIT) score was determined in 80 patients; 20 (25%), 17 (21%), 33 (41%) and 10 (13%) patients had scores of 0-1, 2, 3 and 4, respectively.
  • CONCLUSIONS: This retrospective series represents the largest Latin-American experience on ATLL, which is a heterogeneous disease with distinct clinical features and outcomes.
  • The IPI ant PIT scores, used for risk-stratification of aggressive B-cell and peripheral T-cell lymphomas, respectively, appear as good prognostic indicators for ATLL as well.
  • Further research is needed to better risk-stratify this unique lymphoma.

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  • (PMID = 27962272.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Townsend AR, Millward M, Price T, Mainwaring P, Spencer A, Longenecker A, Palladino MA, Lloyd GK, Spear MA, Padrik P: Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm). J Clin Oncol; 2009 May 20;27(15_suppl):3582

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm).
  • Preclinical research suggests improvements in therapeutic ratio and activity in hematologic and solid tumor models, leading to clinical trials in patients with myeloma, lymphomas, leukemias, and solid tumors.
  • METHODS: Patients with solid tumor, lymphoma or leukemia diagnoses without standard treatment options were treated with IV NPI on Days 1, 8 and 15 of 28-day cycles in a 3+3 design dose escalation to a Recommended Phase 2 Dose (RP2D).
  • Enrollment then began in 10 patient lymphoma and CLL RP2D cohorts.
  • Stable disease was induced in 31% of patients, including one each with mantle cell, Hodgkin's lymphoma, follicular lymphoma, sarcoma, prostate carcinoma, and two with melanoma.

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  • (PMID = 27961753.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).
  • Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).
  • Using augmented therapy based on CCG1961 was associated with better outcome.
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Caces DD, Halaas J, Hamlin P, Noy A, Kewalramani T, Portlock CS, Zelenetz AD, O'Connor OA, Gerecitano JF: Therapeutic and palliative benefit from single-agent irinotecan in multiply treated and highly refractory cases of lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19554

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic and palliative benefit from single-agent irinotecan in multiply treated and highly refractory cases of lymphoma.
  • : e19554 Background: Multiple reports corroborate a role for irinotecan in the treatment of lymphoma.
  • This study describes the Memorial Sloan Kettering experience with single-agent irinotecan in the management of heavily pretreated and highly refractory cases of lymphoma.
  • METHODS: Adult patients with histologically diagnosed relapsed or refractory lymphoma treated with irinotecan between 1/2001 and 8/2008 were identified.
  • Treatment responses were evaluated based on the Revised Response Criteria for Malignant Lymphoma.
  • 4 patients had Hodgkin Lymphoma (HL) and 26 had Non-Hodgkin lymphoma (NHL): 17 DLBCL, 6 transformed follicular lymphoma, 1 mantle cell lymphoma, 1 T-cell lymphoma and 1 Burkitt's. 25 patients were evaluable for response.
  • 8 patients (32%) had stable disease and 12 (48%) progressed on treatment.
  • CONCLUSIONS: Irinotecan has utility even in multiply treated and highly refractory cases of lymphoma.
  • It can mitigate symptoms resulting from bulky disease and shows potential as a palliative treatment option.
  • Strategies that limit adverse reactions may enhance the agent's effectiveness in refractory lymphoma.

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  • (PMID = 27961088.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Ming-Tzer L, Chun-Ta H, Shih-Chi K: Pulmonary metastatic calcification in adult T-cell lymphoma/leukemia. Acta Clin Belg; 2009 Sep-Oct;64(5):455-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pulmonary metastatic calcification in adult T-cell lymphoma/leukemia.
  • [MeSH-major] Calcinosis / etiology. Leukemia-Lymphoma, Adult T-Cell / complications. Lung Diseases / etiology
  • [MeSH-minor] Adult. Fatal Outcome. Humans. Male. Multiple Organ Failure / etiology. Radiopharmaceuticals. Technetium Tc 99m Medronate

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  • (PMID = 19999398.001).
  • [ISSN] 1784-3286
  • [Journal-full-title] Acta clinica Belgica
  • [ISO-abbreviation] Acta Clin Belg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; X89XV46R07 / Technetium Tc 99m Medronate
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18. Venkitaraman R, Sagar TG, George MK: Adult T-cell lymphoma with HTLV-I and HTLV-II infection. South Med J; 2007 Nov;100(11):1178-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell lymphoma with HTLV-I and HTLV-II infection.
  • [MeSH-major] HTLV-I Infections / diagnosis. HTLV-II Infections / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Male. Middle Aged

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  • (PMID = 17984755.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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19. Mukhopadhyay A, Gupta P, Mukhopadhyay S, Dey S, Basak J, Pandey R: Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country. J Clin Oncol; 2009 May 20;27(15_suppl):10046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country.
  • : 10046 Background: Acute Lymphatic Leukemia is a curable disease in the range of 80 - 90% in developed countries by aggressive protocol like BFM, St. Judes' but result is much less in adolescence age group (60-70%).
  • Fever 48 (64.0%), lymphadenopathy 35 (46.7%), and haepatosplenomegaly 28 (37.3%) were the major clinical presentation.
  • In a follow-up period of 24 - 88 months (with an average of 54 months) the disease-free survival ( DFS) was 42 (56%) patients with an overall survival of 46 (61.34%) patients.
  • The major cause of the mortality was infection 18% (24.0% patients) followed progressive disease 9 (12.0%) and hemorrhage 2 (2.7%).
  • CONCLUSIONS: The data of acute lymphatic leukemia in adolescent is not satisfactory as compared to other pediatric patients.

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  • (PMID = 27962472.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Jacobsen E, LaCasce A: Update on the therapy of highly aggressive non-Hodgkin's lymphoma. Expert Opin Biol Ther; 2006 Jul;6(7):699-708
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Update on the therapy of highly aggressive non-Hodgkin's lymphoma.
  • This review focuses on the current understanding of the biology of highly aggressive non-Hodgkin's lymphomas, such as Burkitt's lymphoma, lymphoblastic lymphoma and adult T cell lymphoma/leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma. Lymphoma, Non-Hodgkin. Lymphoma, T-Cell. Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adult. Child. Female. Humans. Male

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  • (PMID = 16805709.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 95
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21. Ohtani T, Deguchi M, Aiba S: Erythema multiforme-like lesions associated with lesional infiltration of tumor cells occurring with adult T-cell lymphoma/leukemia. Int J Dermatol; 2008 Apr;47(4):390-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Erythema multiforme-like lesions associated with lesional infiltration of tumor cells occurring with adult T-cell lymphoma/leukemia.
  • [MeSH-major] Erythema Multiforme / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration / pathology. Skin / pathology
  • [MeSH-minor] Aged. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Immunophenotyping

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  • (PMID = 18377607.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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22. Dungerwalla M, Osuji N, Waldman AD, Al Jehani F, Mehta A, Tailor R, Wotherspoon A, Cogill G, Matutes E: Isolated central nervous system involvement in adult T-cell lymphoma/leukaemia. Br J Haematol; 2005 Aug;130(4):511-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolated central nervous system involvement in adult T-cell lymphoma/leukaemia.
  • Central nervous system (CNS) presentation of adult T-cell lymphoma/leukaemia is rare, and almost invariably associated with systemic disease.
  • We report an unusual manifestation of adult T-cell lymphoma/leukaemia, with isolated CNS involvement and unusual imaging findings.
  • [MeSH-major] Brain Neoplasms / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Antiviral Agents / therapeutic use. Disease Progression. Frontal Lobe / surgery. Humans. Interferons / therapeutic use. Magnetic Resonance Imaging. Male. Palliative Care. Tomography, X-Ray Computed

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  • [ErratumIn] Br J Haematol. 2005 Nov;131(4):557. Taylor, R [corrected to Tailor, R]
  • (PMID = 16098064.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 9008-11-1 / Interferons
  • [Number-of-references] 22
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23. Park CW, Kim A, Cha SW, Jung SH, Yang HW, Lee YJ, Lee HIe, Kim SH, Kim YH: A case of phlegmonous gastritis associated with marked gastric distension. Gut Liver; 2010 Sep;4(3):415-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of phlegmonous gastritis associated with marked gastric distension.
  • Phlegmonous gastritis is an acute and severe infectious disease that is occasionally fatal if the diagnosis is delayed.
  • Alcohol consumption, an immunocompromised state (e.g., due to HIV infection, rheumatoid arthritis, diabetes mellitus, or adult T-cell lymphoma), and mucosal injury of the stomach are reported to be predisposing factors.

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  • (PMID = 20981225.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2956360
  • [Keywords] NOTNLM ; Gastric outlet obstruction / Phlegmonous gastritis
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24. Lü SQ, Yang JM, Wang JM: [Effects of proteasome inhibitors on leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):896-900
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of proteasome inhibitors on leukemias].
  • The abnormality of its activity is sign of tumorigenesis.
  • Bortezomib, the first proteasome inhibitor, obtained permission of clinical trial and on sale.
  • A lot of studies on effects of proteasome inhibitors on leukemias, including plasma cell leukemia; chronic lymphocytic leukemia, adult T cell lymphoma/leukemia, chronic myeloid leukemia and acute myeloid leukemia, were reviewed in this article.

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  • (PMID = 17708829.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 27
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25. Tagawa H: [Analysis of genomic copy number alterations of malignant lymphomas and its application for diagnosis]. Gan To Kagaku Ryoho; 2007 Jul;34(7):975-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Analysis of genomic copy number alterations of malignant lymphomas and its application for diagnosis].
  • Using this technique, we were thus able to reveal disease-specific genomic alterations and the candidate target genes in various lymphomas.
  • We herein report the characteristic genomic alterations of malignant lymphomas including diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL) and adult T cell lymphoma/leukemia (ATLL).
  • For instance, we revealed that activated B-cell-like DLBCL is characterized by a gain of chromosome 3, 18q and loss of 9 p21, whereas the germinal center B-cell-like DLBCL is characterized by a gain of 2p15, 7q, and 12q.
  • Comparison of genome profiles between acute type and lymphoma types of adult T cell lymphoma also demonstrated that acute and lymphoma types are genomically distinct subtypes, and thus may develop tumors via distinct genetic pathways.
  • In addition to identifying disease-specific genomic alterations, we also discovered several target genes of the genomic gains and losses.
  • Furthermore,we developed a computer algorithm to classify lymphoma diseases or subtypes on the basis of copy number gains and losses.
  • These results demonstrate that copy number gains and losses detected by array CGH could be used for classifying lymphomas into biologically and clinically distinct diseases or subtypes.
  • The genomic copy number alterations detected by array CGH are therefore considered to have the potential to help diagnose or classify different disease entities and tumor subtypes.
  • [MeSH-major] Gene Dosage. Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Follicular / genetics. Lymphoma, Large B-Cell, Diffuse / genetics
  • [MeSH-minor] Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / genetics. Genome, Human. Humans. Lymphoma, Mantle-Cell / diagnosis. Lymphoma, Mantle-Cell / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Translocation, Genetic

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  • (PMID = 17637530.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 13
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26. Oka S, Yokote T, Akioka T, Hara S, Kobayashi K, Hirata Y, Tuji M, Hanafusa T: [Septic shock induced by Serratia marcescens complicating adult T-cell leukemia (ATL)]. Kansenshogaku Zasshi; 2006 May;80(3):257-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Septic shock induced by Serratia marcescens complicating adult T-cell leukemia (ATL)].
  • Hypercalcemia appeared when of the dose of prednisolone was reduced, and human T-cell lymphotropic virus type-I (HTLV-I) proviral DNA was detected in the leukemic cells by Southern blot analysis, and a diagnosis of acute adult T-cell lymphoma (ATL) was made.
  • [MeSH-major] Leukemia, T-Cell / complications. Serratia Infections / complications. Serratia marcescens. Shock, Septic / complications

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  • (PMID = 16780133.001).
  • [ISSN] 0387-5911
  • [Journal-full-title] Kansenshōgaku zasshi. The Journal of the Japanese Association for Infectious Diseases
  • [ISO-abbreviation] Kansenshogaku Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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27. Liu TY, Chen CY, Tien HF, Lin CW: Loss of CD7, independent of galectin-3 expression, implies a worse prognosis in adult T-cell leukaemia/lymphoma. Histopathology; 2009 Jan;54(2):214-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of CD7, independent of galectin-3 expression, implies a worse prognosis in adult T-cell leukaemia/lymphoma.
  • AIMS: Loss of CD7 is characteristic of adult T-cell lymphoma/leukaemia (ATLL).
  • Galectin-3 (Gal-3) is strongly induced in cultured human T lymphotropic virus-1-infected T lymphocytes, and may cause apoptosis through interaction with CD7.
  • The aim was to investigate the clinical relevance of the Gal-3-CD7 pathway in ATLL.
  • METHODS AND RESULTS: Immunohistochemistry for Gal-3 and CD7 was performed on 22 cases of ATLL in the leukaemic phase.
  • We found that the lymphoma cells were not necessarily Gal-3+, but Gal-3+ stromal cells could always be found.
  • CONCLUSIONS: These data suggest that, by down-regulating CD7, ATLL cells could have escaped Gal-3-induced apoptosis to run a more aggressive clinical course.
  • [MeSH-major] Antigens, CD7 / metabolism. Galectin 3 / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Apoptosis. Cells, Cultured. Chromosome Aberrations. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis

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  • (PMID = 19207946.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Galectin 3
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28. Jost PJ, Ruland J: Aberrant NF-kappaB signaling in lymphoma: mechanisms, consequences, and therapeutic implications. Blood; 2007 Apr 1;109(7):2700-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant NF-kappaB signaling in lymphoma: mechanisms, consequences, and therapeutic implications.
  • The transcription factor NF-kappaB is a tightly regulated positive mediator of T- and B-cell development, proliferation, and survival.
  • However, constitutive NF-kappaB activation can promote continuous lymphocyte proliferation and survival and has recently been recognized as a critical pathogenetic factor in lymphoma.
  • Various molecular events lead to deregulation of NF-kappaB signaling in Hodgkin disease and a variety of T- and B-cell non-Hodgkin lymphomas either up-stream or downstream of the central IkappaB kinase.
  • These alterations are prerequisites for lymphoma cell cycling and blockage of apoptosis.
  • This review provides an overview of the NF-kappaB pathway and discusses the mechanisms of NF-kappaB deregulation in distinct lymphoma entities with defined aberrant pathways: Hodgkin lymphoma (HL), diffuse large B-cell lymphoma (DLBCL), mucosa-associated lymphoid tissue (MALT) lymphoma, primary effusion lymphoma (PEL), and adult T-cell lymphoma/leukemia (ATL).
  • In addition, we summarize recent data that validates the NF-kappaB signaling pathway as an attractive therapeutic target in T- and B-cell malignancies.
  • [MeSH-major] Lymphoma / physiopathology. NF-kappa B / physiology
  • [MeSH-minor] Hodgkin Disease / physiopathology. Humans. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Lymphocytes / physiology. Lymphoma, B-Cell / physiopathology. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / physiopathology. Lymphoma, Large B-Cell, Diffuse / physiopathology. Models, Biological. Oncogene Proteins, Viral / physiology. Prognosis. Signal Transduction / physiology. Translocation, Genetic

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  • (PMID = 17119127.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Oncogene Proteins, Viral
  • [Number-of-references] 96
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29. Zhang H, Zhang L, Wang J, Ma Y, Zhang J, Mo F, Zhang W, Yan S, Yang G, Lin B: Proteomic analysis of bone tissues of patients with osteonecrosis of the femoral head. OMICS; 2009 Dec;13(6):453-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Osteonecrosis of the femoral head (ONFH) is a devastating disease that can result in a femoral head collapse.
  • GSEA (gene set enrichment analysis) revealed that proteins overexpressed in ONFH are enriched for gene sets related to multiple myeloma and adult T-cell lymphoma (ATL), and to JAK2-dependent genes.
  • [MeSH-minor] Adult. Aged. Chromatography, Liquid / methods. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Protein Isoforms / metabolism. Proteomics / methods. Receptors, G-Protein-Coupled / metabolism. Sulfotransferases / metabolism. Tandem Mass Spectrometry / methods

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  • (PMID = 20001860.001).
  • [ISSN] 1557-8100
  • [Journal-full-title] Omics : a journal of integrative biology
  • [ISO-abbreviation] OMICS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Proteome; 0 / Receptors, G-Protein-Coupled; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.- / carbohydrate sulfotransferases
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30. Silverman LR, Phipps AJ, Montgomery A, Fernandez S, Tsukahara T, Ratner L, Lairmore MD: In vivo analysis of replication and immunogenicity of proviral clones of human T-lymphotropic virus type 1 with selective envelope surface-unit mutations. Blood; 2005 Nov 15;106(10):3602-8
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  • [Title] In vivo analysis of replication and immunogenicity of proviral clones of human T-lymphotropic virus type 1 with selective envelope surface-unit mutations.
  • Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell lymphoma/leukemia (ATL).
  • The HTLV-1 envelope gene exhibits limited variability when examined from infected individuals, but has not been tested using infectious clones of the virus in animal models.
  • In vitro assays indicate that HTLV-1 envelope (Env) Ser75Ile, Asn95Asp, and Asn195Asp surface unit (SU) mutants are able to replicate in and immortalize lymphocytes.
  • Herein, we examined the effects of these Env mutants in rabbits inoculated with HTLV-1 immortalized ACH.75, ACH.95, or ACH.195 cell lines (expressing full-length molecular clones with the SU mutations) or the ACH.1 cell line (expressing wild-type SU).
  • However, SU point mutations resulted in decreased antibody responses to viral group-associated antigen (Gag) and Env antigens.
  • ACH.195 rabbits had a selective decreased antibody response to SU, and one ACH.195 rabbit had an antibody response to both HTLV-1 and HTLV-2 SUs.
  • However, peripheral-blood mononuclear cell (PBMC) proviral loads did not correlate with antibody responses.
  • Our data are the first to demonstrate that mutations in critical determinants of HTLV-1 Env SU altered antibody responses and proviral loads, but do not prevent viral replication in vivo.

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  • (PMID = 16046523.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100730-02; United States / NCI NIH HHS / CA / CA-63417; United States / NCI NIH HHS / CA / CA09338; United States / NCI NIH HHS / CA / CA70529
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Gene Products, env; 0 / Gene Products, gag
  • [Other-IDs] NLM/ PMC1895059
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31. Cooper CM, James K, Wilks RJ: HTLV-1 related knowledge, attitude and behaviour patterns among mothers who participated in the Jamaica Breastfeeding Intervention Study (1996-2000). West Indian Med J; 2010 Jan;59(1):35-40
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  • [Title] HTLV-1 related knowledge, attitude and behaviour patterns among mothers who participated in the Jamaica Breastfeeding Intervention Study (1996-2000).
  • Human T-cell Lymphotropic Virus type-1 (HTLV-1), the first human retrovirus associated with a malignant disease, is endemic in Jamaica.
  • Women are at greater risk of contracting the virus as it is more efficiently transmitted from male to female than in the reverse.
  • The study aims to document the knowledge, attitude and behaviour pattern (KABP) of a group of women five years after they had participated in a mother-to-child transmission of HTLV-1 risk reduction study.
  • There were large deficiencies in the knowledge and practice of women at risk of being infected with HTLV-1.
  • Only 58% knew that HTLV-1 is sexually transmitted.
  • A minority was aware of HTLV-1 associated diseases: Adult T-cell lymphoma/leukaemia (ATL) -30.7%; Tropical Spastic Paraparesis (TSP) -42%; Infective dermatitis -42%).
  • Ten (11.4%) believed that HTLV-1 infection can cause HIV/AIDS and only 33% knew that there was no cure for the virus.
  • Controlling HTLV-1 spread must be based on interrupting transmission.
  • In Jamaica, donated blood is screened for HTLV-1 and sharing of infected needle is an insignificant mode of transmission.
  • However although safe practices in breastfeeding and sexual intercourse are proven ways to reduce HTLV-1 transmission, these data show that knowledge and safe practices among those at risk may not be retained and health education will need to be sustained.
  • [MeSH-major] Breast Feeding. HTLV-I Infections / transmission. Health Knowledge, Attitudes, Practice. Human T-lymphotropic virus 1. Mothers
  • [MeSH-minor] Adult. Chi-Square Distribution. Cross-Sectional Studies. Demography. Female. Focus Groups. Health Education. Humans. Infectious Disease Transmission, Vertical. Jamaica / epidemiology. Male. Middle Aged. Regression Analysis. Surveys and Questionnaires

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  • (PMID = 20931911.001).
  • [ISSN] 0043-3144
  • [Journal-full-title] The West Indian medical journal
  • [ISO-abbreviation] West Indian Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Jamaica
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32. Matsuhashi S, Narisawa Y, Ozaki I, Mizuta T: Expression patterns of programmed cell death 4 protein in normal human skin and some representative skin lesions. Exp Dermatol; 2007 Mar;16(3):179-84
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  • [Title] Expression patterns of programmed cell death 4 protein in normal human skin and some representative skin lesions.
  • Expression of a tumor suppressor gene, programmed cell death 4 (PDCD4), was investigated at the protein level in the human skin.
  • Immunohistochemically, PDCD4 protein expressed mainly in suprabasal layers, while PDCD4-positive and -negative areas were observed discontinuously in the basal cell layer of the epidermis.
  • In hair follicles, the suprabulbar area including the hair and inner root sheath was immunoreactive, while the bulbar area, containing germinative cells which were strongly proliferating cell nuclear antigen (PCNA)-positive, was not or less.
  • PDCD4-positive cells were localized in the inside layers while PCNA-positive cells were located in the basal layer in the outer root sheath of hair follicles.
  • The cells of sebaceous glands and sweat glands also were PDCD4-positive.
  • PDCD4 expression was found to be suppressed in the epidermis overlying an adult T-cell lymphoma (ATL), possibly reflecting a paracrine effect of factors produced by ATL cells.
  • PDCD4 expression was suppressed in the keratinocyte cell line HaCaT by exposure of cultures to epidermal growth factor, transforming growth factor-beta1 or hepatocyte growth factor.
  • [MeSH-minor] Cell Line. Cell Nucleus / metabolism. Hair Follicle / immunology. Hair Follicle / metabolism. Humans. Immunohistochemistry. Keratinocytes / cytology. Keratinocytes / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Sebaceous Glands / cytology. Sebaceous Glands / metabolism. Sweat Glands / cytology. Sweat Glands / metabolism

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  • (PMID = 17286809.001).
  • [ISSN] 0906-6705
  • [Journal-full-title] Experimental dermatology
  • [ISO-abbreviation] Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / PDCD4 protein, human; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA-Binding Proteins
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33. Haruki H, Tanaka S, Koga M, Kawai M, Negoro K, Kanda T: [Central nervous system leukemia mimicking rapidly progressive HTLV-1 associated myelopathy]. Nihon Ronen Igakkai Zasshi; 2009 Mar;46(2):184-7
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  • [Title] [Central nervous system leukemia mimicking rapidly progressive HTLV-1 associated myelopathy].
  • After one month, she showed flaccid paraplegia and hyperreflexia in the lower limbs with positive Babinski signs.
  • Anti-HTLV-1 antibody titer was elevated in the serum, but negative in the cerebrospinal fluid (CSF).
  • Adult T cell lymphoma (ATL)-like cells were seen in the CSF.
  • A tentative diagnosis of rapidly progressive HTLV-1 associated myelopathy (HAM) was given, but intravenous methylprednisolone was ineffective.
  • Six months later, she developed pneumonia, and abundant ATL cells were seen in the peripheral blood, suggesting a diagnosis of ATL.
  • Direct infiltration of ATL cells to central nervous system was therefore suggested to have caused neurological abnormalities in this case.
  • One may consider central nervous system leukemia when rapidly progressive HAM-like symptoms and signs are recognized, especially without positive anti-HTLV-1 antibody in the CSF.
  • [MeSH-major] Central Nervous System Neoplasms / diagnosis. HTLV-I Infections / complications. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Spinal Cord Diseases / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans

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  • (PMID = 19491526.001).
  • [ISSN] 0300-9173
  • [Journal-full-title] Nihon Ronen Igakkai zasshi. Japanese journal of geriatrics
  • [ISO-abbreviation] Nihon Ronen Igakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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34. Kamata H, Mitani S, Fujiwara M, Aoki N, Okada S, Mori S: Mutation of the p53 tumour suppressor gene and overexpression of its protein in 62 Japanese non-Hodgkin's lymphomas. Clin Exp Med; 2007 Jun;7(2):39-46
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  • [Title] Mutation of the p53 tumour suppressor gene and overexpression of its protein in 62 Japanese non-Hodgkin's lymphomas.
  • To clarify whether p53 mutation could be involved in the pathogenesis of various subtypes of lymphoma, we investigated 62 Japanese cases of non-Hodgkin's lymphomas (NHLs) for p53 gene mutations and their relationship with the expression of p53 protein.
  • Missense and/or nonsense mutations of p53 were detected in 3 (10.7%) of 28 diffuse large B-cell lymphomas (DLBLs) and 2 (15.4%) of 13 T-cell NHLs (15.4%).
  • A single missense mutation at codon 157 (Val to Phe) in exon 5 and at codon 273 (Arg to Pro) in exon 8 was found respectively in 2 DLBLs and in one peripheral T-cell lymphoma (unspecified).
  • Double transversion mutations comprising of a missense mutation at codon 167 (Gln to His) in exon 5 and a nonsense mutation at codon 183 (Ser to stop codon) in exon 5 were detected in one DLBL that had apparently transformed from follicular lymphoma and in one advanced adult T-cell lymphoma (ATL).
  • In these two cases harbouring p53 nonsense mutation, no cells positive for p53 protein immunostaining were detected, as well as lymphomas without p53 mutation.
  • [MeSH-major] Asian Continental Ancestry Group. Gene Expression Regulation, Neoplastic / genetics. Lymphoma, Non-Hodgkin / genetics. Lymphoma, Non-Hodgkin / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Child. Exons / genetics. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mutation / genetics. Ribonucleases / metabolism

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  • (PMID = 17609875.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 3.1.- / Ribonucleases
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35. Kameoka J, Ichinohasama R, Inoue H, Yamamoto J, Yokoyama H, Tomiya Y, Yamada M, Ishizawa K, Harigae H, Sawai T, Sasaki T: CD26, together with cell surface adenosine deaminase, is selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma. Leuk Lymphoma; 2006 Oct;47(10):2181-8
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  • [Title] CD26, together with cell surface adenosine deaminase, is selectively expressed on ALK-positive, but not on ALK-negative, anaplastic large cell lymphoma and Hodgkin's lymphoma.
  • CD26/dipeptidyl peptidase IV is a cell surface antigen with multiple biological functions.
  • Although its involvement in tumor biology has been suggested, the significance of its expression in malignant lymphoma has not been clarified in detail.
  • This study examined the expression of CD26 and cell surface adenosine deaminase (ADA) in 42 cases of Hodgkin's lymphoma (HL) and T-cell lymphoma by immunohistochemistry on frozen sections.
  • CD26 was expressed in three of 14 cases of HL, in four of eight cases of anaplastic large cell lymphoma (ALCL), in two of nine cases of peripheral T-cell lymphoma, in one of six cases of lymphoblastic lymphoma and in none of three cases of adult T-cell lymphoma/leukemia.
  • Expression of cell surface ADA was fully correlated with the expression of CD26 and expression of CD26/ADA in ALCL and HL was also completely correlated with the expression of p80 and epithelial membrane antigen.
  • Of 10 CD26-positive patients, seven had fever and elevated CRP at initial diagnosis and over a median follow-up of 61 months (range, 7 - 152 months) only three survived.
  • This study suggested that CD26 is selectively expressed on ALK-positive, but not on ALK-negative, ALCL and HL.
  • This is also the first report to demonstrate that ADA is coexpressed with CD26 on the cell surface of malignant neoplasms in vivo.
  • [MeSH-major] Adenosine Deaminase / biosynthesis. Cell Membrane / enzymology. Dipeptidyl Peptidase 4 / biosynthesis. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Hodgkin Disease / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Protein-Tyrosine Kinases / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD3 / biosynthesis. Female. Humans. Jurkat Cells. Male. Middle Aged. Receptor Protein-Tyrosine Kinases

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  • (PMID = 17071493.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.5.4.4 / Adenosine Deaminase
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36. Parrula C, Zimmerman B, Nadella P, Shu S, Rosol T, Fernandez S, Lairmore M, Niewiesk S: Expression of tumor invasion factors determines systemic engraftment and induction of humoral hypercalcemia in a mouse model of adult T-cell leukemia. Vet Pathol; 2009 Sep;46(5):1003-14
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  • [Title] Expression of tumor invasion factors determines systemic engraftment and induction of humoral hypercalcemia in a mouse model of adult T-cell leukemia.
  • Infection with human T-cell leukemia virus type 1 (HTLV-1) leads sometimes to the development of adult T-cell lymphoma/leukemia (ATL), which is invariably fatal and often associated with humoral hypercalcemia of malignancy.
  • The transformation of infected CD4 T cells and the pathogenesis of leukemia have been studied with great limitation in tissue culture and patients.
  • To better understand the pathogenesis and perform preclinical drug studies, animal models of ATL are urgently needed.
  • In mice, inoculation of HTLV-1 cell lines mostly leads to development of localized lymphomas.
  • To develop an ATL animal model with leukemic spread of ATL cells, mouse strains with different well-defined immune deficiencies were inoculated intraperitoneally with different HTLV-1-infected cell lines (ACH.2, C8166, MT-2, MET-1).
  • Inoculation of MET-1 cells into NOD/SCID mice provided the best model system for slowly developing T-cell leukemia with multiple organ involvement.
  • In contrast to the other cell lines that did not spread systemically, MET-1 expressed both the adhesion molecules CD11a (LFA-1alpha) and CD49d (VLA-4alpha) and produced or induced expression of matrix metalloproteinases 1, 2, 3, and 9, thus underlining the importance of these molecules in the spread of adult T-cell leukemia cells.

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  • (PMID = 19429977.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100730-07; United States / NCI NIH HHS / CA / CA100730-07S19003; United States / NCI NIH HHS / CA / P01 CA100730-07S19003; United States / NCI NIH HHS / CA / CA100730-07; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11a; 0 / Bsg protein, mouse; 0 / Parathyroid Hormone-Related Protein; 0 / RANK Ligand; 0 / Receptors, Chemokine; 0 / Tnfsf11 protein, mouse; 0 / macrophage inflammatory protein 1alpha receptor; 136894-56-9 / Antigens, CD147; 143198-26-9 / Integrin alpha4; 63231-63-0 / RNA; EC 3.4.24.- / Mmp9 protein, mouse; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ NIHMS175834; NLM/ PMC2852243
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37. Haynes RA 2nd, Phipps AJ, Yamamoto B, Green P, Lairmore MD: Development of a cytotoxic T-cell assay in rabbits to evaluate early immune response to human T-lymphotropic virus type 1 infection. Viral Immunol; 2009 Dec;22(6):397-405
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of a cytotoxic T-cell assay in rabbits to evaluate early immune response to human T-lymphotropic virus type 1 infection.
  • Human T-lymphotropic virus type 1 (HTLV-1) infection causes adult T-cell lymphoma/leukemia (ATL) following a prolonged clinical incubation period, despite a robust adaptive immune response against the virus.
  • We have developed a cytotoxic T-lymphocyte (CTL) assay to monitor the early events of HTLV-1 infection in rabbits.
  • Rabbit skin fibroblast cell lines were established by transformation with a plasmid expressing simian virus 40 (SV40) large T antigen and used as autochthonous targets (derived from same individual animal) to measure CTL activity against HTLV-1 infection in rabbits.
  • Recombinant vaccinia virus (rVV) constructs expressing either HTLV-1 envelope surface unit (SU) glycoprotein 46 or Tax proteins were used to infect fibroblast targets in a (51)Cr-release CTL assay.
  • Rabbits inoculated with Jurkat T cells or ACH.2 cells (expressing ACH HTLV-1 molecule clone) were monitored at 0, 2, 4, 6, 8, 13, 21, and 34 wk post-infection.
  • Proviral load analysis indicated that rabbits with higher proviral loads had significant CTL activity against HTLV-1 SU as early as 2 wk post-infection, while both low- and high-proviral-load groups had minimal Tax-specific CTL activity throughout the study.
  • This first development of a stringent assay to measure HTLV-1 SU and Tax-specific CTL assay in the rabbit model will enhance immunopathogenesis studies of HTLV-1 infection.
  • Our data suggest that during the early weeks following infection, HTLV-1-specific CTL responses are primarily targeted against Env-SU.

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  • (PMID = 19951176.001).
  • [ISSN] 1557-8976
  • [Journal-full-title] Viral immunology
  • [ISO-abbreviation] Viral Immunol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / RR014324-05; United States / NCI NIH HHS / CA / CA100730-02S1; United States / NCI NIH HHS / CA / P01 CA100730-02S1; United States / NCI NIH HHS / CA / P01 CA100730-07; United States / NCI NIH HHS / CA / CA100730; United States / NCI NIH HHS / CA / CA100730-03S1; United States / NCI NIH HHS / CA / P01 CA100730-04S1; United States / NCRR NIH HHS / RR / R01 RR014324-05; United States / NCI NIH HHS / CA / CA100730-04S1; United States / NCI NIH HHS / CA / P01 CA100730-03S1; United States / NCI NIH HHS / CA / CA100730-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, env; 0 / Gene Products, tax; 0 / Recombinant Fusion Proteins; 0 / Retroviridae Proteins, Oncogenic; 0 / gp46 protein, Human T-cell leukemia virus type I; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Other-IDs] NLM/ NIHMS175831; NLM/ PMC2852241
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38. Birmann BM, Breen EC, Stuver S, Cranston B, Martínez-Maza O, Falk KI, Okayama A, Hanchard B, Mueller N, Hisada M: Population differences in immune marker profiles associated with human T-lymphotropic virus type I infection in Japan and Jamaica. Int J Cancer; 2009 Feb 1;124(3):614-21
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  • [Title] Population differences in immune marker profiles associated with human T-lymphotropic virus type I infection in Japan and Jamaica.
  • The natural history of human T-lymphotropic virus type I (HTLV-I) has been shown to differ markedly by geographic area.
  • The differences include contrasting patterns of risk of adult T-cell lymphoma (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), which may be due in part to differences in host immune response to infection.
  • To characterize variations in host immunity across populations, we compared serologic immune marker patterns in HTLV-I-endemic populations in Japan and Jamaica.
  • We matched 204 participants with archived blood from the Miyazaki Cohort Study (Japan) and the Food Handlers Study (Jamaica)-i.e., 51 HTLV-I-positive ("carriers") and 51 HTLV-I-negative individuals ("noncarriers") from each population-by age, sex and blood collection year.
  • We compared plasma concentrations of markers of T-cell-mediated (antigen-specific) and nonspecific immunity using regression models and correlation coefficients.
  • Compared to Jamaican HTLV-I noncarriers, Japanese noncarriers had higher covariate-adjusted mean levels of T-cell activation markers, including antibody to Epstein-Barr virus nuclear antigen-1 (reciprocal titer 27 vs. 71, respectively, p=0.005), soluble interleukin-2 receptor-alpha (477 vs. 623 pg/mL, p=0.0008) and soluble CD30 (34 vs. 46 U/mL, p=0.0001) and lower levels of C-reactive protein (1.1 vs. 0.43 microg/mL, p=0.0004).
  • HTLV-I infection was associated with activated T-cell immunity in Jamaicans but with diminished T-cell immunity in Japanese persons.
  • The observed population differences in background and HTLV-I-related host immunity correspond closely to the divergent natural histories of infection observed among HTLV-I carriers in Japan and Jamaica and corroborate a role for host immune status in the contrasting patterns of ATL and HAM/TSP risk.

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  • (PMID = 18989900.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA038450-15; United States / NCI NIH HHS / CA / CA115687-01A1; United States / NCI NIH HHS / CA / R01 CA038450-15; United States / NCI NIH HHS / CA / K07 CA115687-01A1; United States / NCI NIH HHS / CA / K07 CA115687; United States / NCI NIH HHS / CA / CA115687-02; United States / NCI NIH HHS / CA / R01 CA038450-14; United States / NCI NIH HHS / CA / K07 CA115687-03; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / CA115687-03; United States / NCI NIH HHS / CA / CA115687; United States / NCI NIH HHS / CA / CA09001; United States / NCI NIH HHS / CA / CA038450-14; United States / NCI NIH HHS / CA / T32 CA009001; United States / NCI NIH HHS / CA / CA38450; United States / NCI NIH HHS / CA / K07 CA115687-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Antigens, Viral
  • [Other-IDs] NLM/ NIHMS99048; NLM/ PMC2701897
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39. Pumfery A, de la Fuente C, Kashanchi F: HTLV-1 Tax: centrosome amplification and cancer. Retrovirology; 2006 Aug 09;3:50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HTLV-1 Tax: centrosome amplification and cancer.
  • During interphase, each cell contains a single centrosome that acts as a microtubule organizing center for cellular functions in interphase and in mitosis.
  • Centrosome amplification during the S phase of the cell cycle is a tightly regulated process to ensure that each daughter cell receives the proper complement of the genome.
  • The controls that ensure that centrosomes are duplicated exactly once in the cell cycle are not well understood.
  • These phenotypes are also observed in cancers induced by viruses, including adult T cell lymphoma which is caused by the human T cell lymphotrophic virus Type 1 (HTLV-1).
  • Several reports have indicated that the HTLV-1 transactivator, Tax, is directly responsible for the centrosomal abnormalities observed in ATL cells.
  • A recent paper in Nature Cell Biology by Ching et al. has shed some new light into how Tax may be inducing centrosome abnormalities.
  • The authors demonstrated that 30% of ATL cells contained more than two centrosomes and expression of Tax alone induced supernumerary centrosomes.
  • These results suggest that Tax1BP2 may be an important block to centrosome re-duplication that is observed in normal cells.
  • Presently, a specific cellular protein that prevents centrosome re-duplication has not been identified.
  • This paper has provided further insight into how Tax induces centrosome abnormalities that lead to ATL.
  • Lastly, additional work on Tax1BP2 will also provide insight into how the cell suppresses centrosome re-duplication during the cell cycle and the role that Tax1BP2 plays in this important cellular pathway.

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  • (PMID = 16899128.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI44357; United States / NIAID NIH HHS / AI / R01 AI043894; United States / PHS HHS / / 13969; United States / NIAID NIH HHS / AI / AI43894; United States / NIAID NIH HHS / AI / R29 AI044357
  • [Publication-type] Editorial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / VAC14 protein, human
  • [Other-IDs] NLM/ PMC1555608
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40. Bouaziz JD, Cordel N, Hickman G, Fieschi C, Ortonne N, Bagot M: Cutaneous tumor lysis syndrome in a patient with HTLV-1 adult T-cell lymphoma/leukemia. Blood; 2009 Nov 5;114(19):4320-1
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  • [Title] Cutaneous tumor lysis syndrome in a patient with HTLV-1 adult T-cell lymphoma/leukemia.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Skin Diseases / pathology. Tumor Lysis Syndrome / pathology

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  • (PMID = 19892727.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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41. Saito Y, Takenaka H, Chin T, Ueda E, Katoh N, Shimazaki C, Inaba R, Kishimoto S: Cytomegalovirus in cutaneous ulcers in a patient with adult T-cell lymphoma. Acta Derm Venereol; 2006;86(2):181-2
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  • [Title] Cytomegalovirus in cutaneous ulcers in a patient with adult T-cell lymphoma.
  • [MeSH-major] Cytomegalovirus / isolation & purification. Cytomegalovirus Infections / complications. Lymphoma, T-Cell / complications. Skin Ulcer / virology

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  • (PMID = 16648934.001).
  • [ISSN] 0001-5555
  • [Journal-full-title] Acta dermato-venereologica
  • [ISO-abbreviation] Acta Derm. Venereol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Norway
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42. Watabe H, Soma Y, Obara W, Murakami N, Kawase A, Mizukami T, Koike M, Shibuya Y, Mizoguchi M: Adult T-cell lymphoma/leukaemia developing in a patient with psoriasis treated with long-term cyclosporine. Acta Derm Venereol; 2006;86(2):184-5
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  • [Title] Adult T-cell lymphoma/leukaemia developing in a patient with psoriasis treated with long-term cyclosporine.
  • [MeSH-major] Cyclosporine / adverse effects. Dermatologic Agents / adverse effects. Leukemia-Lymphoma, Adult T-Cell / chemically induced. Psoriasis / drug therapy

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  • (PMID = 16648935.001).
  • [ISSN] 0001-5555
  • [Journal-full-title] Acta dermato-venereologica
  • [ISO-abbreviation] Acta Derm. Venereol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Dermatologic Agents; 83HN0GTJ6D / Cyclosporine
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43. Demarest RM, Ratti F, Capobianco AJ: It's T-ALL about Notch. Oncogene; 2008 Sep 1;27(38):5082-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL.
  • Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease.
  • In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Proteins / physiology. Receptors, Notch / physiology. T-Lymphocytes / pathology
  • [MeSH-minor] Animals. Apoptosis / physiology. Cell Cycle / physiology. F-Box Proteins / physiology. Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. Humans. Ikaros Transcription Factor / genetics. Ikaros Transcription Factor / physiology. Ligands. Mice. Mice, Transgenic. Oncogenes. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / physiology. Signal Transduction / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology

  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
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  • (PMID = 18758476.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA09171
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / IKZF1 protein, human; 0 / Ligands; 0 / Neoplasm Proteins; 0 / Receptors, Notch; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 148971-36-2 / Ikaros Transcription Factor; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Number-of-references] 84
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44. Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA: WT1 mutations in T-ALL. Blood; 2009 Jul 30;114(5):1038-45
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  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.
  • In addition, we identified deletions and associated mutations in the WT1 tumor suppressor gene in 2 of 9 samples.
  • Subsequent analysis showed WT1 mutations in 28 of 211 (13.2%) of pediatric and 10 of 85 (11.7%) of adult T-ALL cases.
  • Survival analysis demonstrated that WT1 mutations do not confer adverse prognosis in pediatric and adult T-ALL.

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  • (PMID = 19494353.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE15931
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / MC/ U137686861; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2721784
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45. Harashima N, Tanosaki R, Shimizu Y, Kurihara K, Masuda T, Okamura J, Kannagi M: Identification of two new HLA-A*1101-restricted tax epitopes recognized by cytotoxic T lymphocytes in an adult T-cell leukemia patient after hematopoietic stem cell transplantation. J Virol; 2005 Aug;79(15):10088-92
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  • [Title] Identification of two new HLA-A*1101-restricted tax epitopes recognized by cytotoxic T lymphocytes in an adult T-cell leukemia patient after hematopoietic stem cell transplantation.
  • We previously reported that Tax-specific CD8(+) cytotoxic T lymphocytes (CTLs), directed to single epitopes restricted by HLA-A2 or A24, expanded in vitro and in vivo in peripheral blood mononuclear cells (PBMC) from some adult T-cell leukemia (ATL) patients after but not before allogeneic hematopoietic stem cell transplantation (HSCT).
  • Here, we demonstrated similar Tax-specific CTL expansion in PBMC from another post-HSCT ATL patient without HLA-A2 or A24, whose CTLs equally recognized two newly identified epitopes, Tax88-96 and Tax272-280, restricted by HLA-A11, suggesting that these immunodominant Tax epitopes are present in the ATL patient in vivo.
  • [MeSH-major] Epitopes / immunology. Gene Products, tax / immunology. HLA-A Antigens / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / therapy. Stem Cell Transplantation. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Amino Acid Sequence. Coculture Techniques. Human T-lymphotropic virus 1 / immunology. Humans. Leukocytes, Mononuclear. Male. Middle Aged. Molecular Sequence Data. Peptides / genetics. T-Cell Antigen Receptor Specificity. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
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  • (PMID = 16014972.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes; 0 / Gene Products, tax; 0 / HLA-A Antigens; 0 / Peptides
  • [Other-IDs] NLM/ PMC1181560
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46. Clappier E, Cuccuini W, Kalota A, Crinquette A, Cayuela JM, Dik WA, Langerak AW, Montpellier B, Nadel B, Walrafen P, Delattre O, Aurias A, Leblanc T, Dombret H, Gewirtz AM, Baruchel A, Sigaux F, Soulier J: The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children. Blood; 2007 Aug 15;110(4):1251-61
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  • [Title] The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children.
  • The C-Myb transcription factor is essential for hematopoiesis, including in the T-cell lineage.
  • The C-Myb locus is a common site of retroviral insertional mutagenesis, however no recurrent genomic involvement has been reported in human malignancies.
  • Here, we identified 2 types of genomic alterations involving the C-MYB locus at 6q23 in human T-cell acute leukemia (T-ALL).
  • Expression analysis, including allele-specific approaches, showed stronger C-MYB expression in the MYB-rearranged cases compared with other T-ALLs, and a dramatically skewed C-MYB allele expression in the TCRB-MYB cases, which suggests that a translocation-driven deregulated expression may overcome a cellular attempt to down-regulate C-MYB.
  • Strikingly, profiling of the T-ALLs by clinical, genomic, and large-scale gene expression analyses shows that the TCRB-MYB translocation defines a new T-ALL subtype associated with a very young age for T-cell leukemia (median, 2.2 years) and with a proliferation/mitosis expression signature.
  • By contrast, the MYB(dup) alteration was associated with the previously defined T-ALL subtypes.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Proto-Oncogene Proteins c-myb / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Base Sequence. Child. Child, Preschool. Female. Gene Dosage. Gene Expression Profiling. Genome, Human. Humans. Infant. Male. Middle Aged. Molecular Sequence Data. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Sequence Homology, Nucleic Acid

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  • (PMID = 17452517.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA101859
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb
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47. Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP: Cooperative genetic defects in TLX3 rearranged pediatric T-ALL. Leukemia; 2008 Apr;22(4):762-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del(19)(p13.2).
  • From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases.
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

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  • (PMID = 18185524.001).
  • [ISSN] 1476-5551
  • [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 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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48. Matsubar Y, Hori T, Morita R, Sakaguchi S, Uchiyama T: Delineation of immunoregulatory properties of adult T-cell leukemia cells. Int J Hematol; 2006 Jul;84(1):63-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Delineation of immunoregulatory properties of adult T-cell leukemia cells.
  • We characterized leukemic cells from 20 adult T-cell leukemia (ATL) cases and 7 ATL-derived cell lines in terms of Foxp3 messenger RNA (mRNA) expression, cytokine production, cell surface markers associated with regulatory T-cells (Treg), and in vitro immunoregulatory activity and compared the results with those of cells from 3 T-cell-type chronic lymphocytic leukemia (T-CLL) patients and normal CD4+ T-cells.
  • Real-time polymerase chain reaction analysis showed that cells from 10 ATL cases, 1 T-CLL case, and 1 ATL cell line had higher Foxp3 mRNA levels than CD4+ T-cells.
  • In 5 ATL cases, Foxp3 levels were comparable to those of CD4+CD25+ T-cells.
  • Flow cytometric analysis revealed that CTLA-4 expression correlated with Foxp3 mRNA level in ATL cells.
  • The cells of all ATL cases examined produced no interleukin 2 or interferon gamma after iono-mycin and phorbolmyristate acetate stimulation.
  • An in vitro inhibition assay showed that the proliferation of normal CD4+CD25- T-cells stimulated with anti-CD3 monoclonal antibody and autologous dendritic cells was significantly suppressed by coculture with Foxp3-high ATL cells.
  • These results indicate that Foxp3 expression is variable in ATL cases and that Foxp3-high ATL cells, which resemble Treg phenotypically as well as functionally, may be involved in immune suppression in ATL.
  • [MeSH-major] Gene Expression Regulation, Leukemic / immunology. Immune Tolerance. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Aged. Cell Line, Tumor. Coculture Techniques. Female. Humans. Male. Middle Aged. T-Lymphocytes, Regulatory / immunology

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  • (PMID = 16867905.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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49. Ferrando AA: The role of NOTCH1 signaling in T-ALL. Hematology Am Soc Hematol Educ Program; 2009;:353-61
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  • The identification of activating mutations in NOTCH1 in over 50% of T-cell acute lymphoblastic leukemias (T-ALL) has generated major interest in the elucidation of the mechanisms of transformation downstream of oncogenic NOTCH and in the targeting of the NOTCH signaling pathway in this disease.
  • Small molecule gamma-secretase inhibitors (GSIs) block NOTCH1 signaling in T-ALL lymphoblasts, yet the clinical development of GSIs has been held back by the development of gastrointestinal toxicity and their weak antileukemic effects against human T-ALL.
  • This review focuses on the molecular basis of NOTCH1-induced transformation, the mechanisms of action of oncogenic NOTCH1 and clinical significance of NOTCH1 mutations in T-ALL.

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  • (PMID = 20008221.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA129382-02; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01 CA129382-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Number-of-references] 40
  • [Other-IDs] NLM/ NIHMS168983; NLM/ PMC2847371
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50. Sanda T, Asamitsu K, Ogura H, Iida S, Utsunomiya A, Ueda R, Okamoto T: Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor. Leukemia; 2006 Apr;20(4):590-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor.
  • NF-kappaB is constitutively activated in adult T-cell leukemia (ATL) and is considered responsible for cell growth and prevention of cell death.
  • In this study, we demonstrate that NF-kappaB is constitutively activated in various HTLV-1-infected T-cell lines and ATL-derived cell lines irrespectively of Tax expression as evidenced by the phosphorylation of IkappaBalpha and p65 subunit of NF-kappaB, activation of NF-kappaB DNA binding, and upregulation of various target genes including bcl-xL, bcl-2, XIAP, c-IAP1, survivin, cyclinD1, ICAM-1 and VCAM-1.
  • The effects of a novel IkappaB kinase (IKK) inhibitor, 2-amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-piperidin-4-yl nicotinonitrile (ACHP), were examined on cell growth of these cell lines and fresh ATL leukemic cells.
  • We found that ACHP could inhibit the phosphorylation of IkappaBalpha and p65, as well as NF-kappaB DNA-binding, associated with downregulation of the NF-kappaB target genes and induce cell growth arrest and apoptosis in these cells.
  • When Tax-active and Tax-inactive cell lines were compared, ACHP could preferentially inhibit cell growth of Tax-active cells.
  • Moreover, ACHP exhibited strong apoptosis-inducing activity in fresh ATL cells.
  • These findings indicate that ACHP and its derivatives are effective in inducing ATL cell death and thus feasible candidates for the treatment of ATL.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. I-kappa B Kinase / antagonists & inhibitors. Leukemia-Lymphoma, Adult T-Cell / metabolism. Nicotinic Acids / pharmacology. Nitriles / pharmacology. T-Lymphocytes / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Binding Sites. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA / metabolism. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Enzyme Activation / genetics. Enzyme Activation / physiology. Gene Expression Regulation, Enzymologic / drug effects. Human T-lymphotropic virus 1 / metabolism. Humans. In Vitro Techniques. Phosphorylation. Protein Subunits / antagonists & inhibitors. Protein Subunits / genetics. Protein Subunits / metabolism. Structure-Activity Relationship. Transcription Factor RelA / antagonists & inhibitors. Transcription Factor RelA / genetics. Transcription Factor RelA / metabolism

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  • (PMID = 16453001.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-amino-6-(2-(cyclopropylmethoxy)-6-hydroxyphenyl)-4-piperidin-4-yl nicotinonitrile; 0 / Enzyme Inhibitors; 0 / Nicotinic Acids; 0 / Nitriles; 0 / Protein Subunits; 0 / Transcription Factor RelA; 9007-49-2 / DNA; EC 2.7.11.10 / I-kappa B Kinase
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51. Yamasaki M, Fujita S, Ishiyama E, Mukai A, Madhyastha H, Sakakibara Y, Suiko M, Hatakeyama K, Nemoto T, Morishita K, Kataoka H, Tsubouchi H, Nishiyama K: Soy-derived isoflavones inhibit the growth of adult T-cell leukemia cells in vitro and in vivo. Cancer Sci; 2007 Nov;98(11):1740-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Soy-derived isoflavones inhibit the growth of adult T-cell leukemia cells in vitro and in vivo.
  • Adult T-cell leukemia occurs in human T-lymphotropic virus type I-infected individuals and is endemic to the south-western area of Kyushu in Japan.
  • In this communication, we examined the effect of soy isoflavones on the growth of adult T-cell leukemia cells in vitro and in vivo.
  • Among the isoflavones studied, genistein had the highest growth-inhibitory effect; however, genistein did not exert an apparent growth-inhibitory effect on Jurkat and Molt-4 cells, which were non-adult T-cell leukemia cells.
  • The in vivo studies demonstrated that soy-derived isoflavones significantly inhibit ED-40515 cell growth and infiltration into various organs in non-obese diabetic severe combined-immunodeficiency common gamma-chain knockout mice.
  • Taken together, it is evident that soy isoflavones might serve as a promising compound for the treatment of adult T-cell leukemia.
  • [MeSH-major] Isoflavones / pharmacology. Isoflavones / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Soybeans
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Genistein / pharmacology. Humans. Jurkat Cells. Mice. Mice, Knockout. Mice, SCID. Transplantation, Heterologous

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  • (PMID = 17727682.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoflavones; 6287WC5J2L / daidzein; 92M5F28TVF / glycitein; DH2M523P0H / Genistein
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52. Dik WA, Brahim W, Braun C, Asnafi V, Dastugue N, Bernard OA, van Dongen JJ, Langerak AW, Macintyre EA, Delabesse E: CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes. Leukemia; 2005 Nov;19(11):1948-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10.
  • Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL).
  • The overexpression of HOXA genes was associated with overexpression of its cofactor MEIS1 in CALM-AF10+ T-ALL, reaching levels of expression similar to those observed in MLL-t AL.
  • We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.
  • [MeSH-major] Homeodomain Proteins / biosynthesis. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Cell Proliferation. Cell Transformation, Neoplastic. Child. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Polycomb Repressive Complex 1. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation

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  • (PMID = 16107895.001).
  • [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 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
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53. O'Neil J, Calvo J, McKenna K, Krishnamoorthy V, Aster JC, Bassing CH, Alt FW, Kelliher M, Look AT: Activating Notch1 mutations in mouse models of T-ALL. Blood; 2006 Jan 15;107(2):781-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1.
  • We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1.
  • Cell lines derived from these tumors undergo G(0)/G(1) arrest and apoptosis when treated with a gamma-secretase inhibitor.
  • In addition, we found activating Notch1 mutations in 31% of thymic lymphomas that occur in mice deficient for various combinations of the H2AX, Tp53, and Rag2 genes.
  • Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations.
  • [MeSH-major] Disease Models, Animal. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma / genetics. Mutation / genetics. Receptor, Notch1 / genetics. Thymus Neoplasms / genetics

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  • (PMID = 16166587.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / H2AX protein, mouse; 0 / Histones; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse
  • [Other-IDs] NLM/ PMC1895623
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54. Yamasaki M, Mukai A, Ohba M, Mine Y, Sakakibara Y, Suiko M, Morishita K, Nishiyama K: Genistein induced apoptotic cell death in adult T-cell leukemia cells through estrogen receptors. Biosci Biotechnol Biochem; 2010;74(10):2113-5
Hazardous Substances Data Bank. ESTRADIOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genistein induced apoptotic cell death in adult T-cell leukemia cells through estrogen receptors.
  • Adult T-cell leukemia (ATL) occurs in human T-lymphotropic virus type I-infected individuals and is endemic to the southwestern area of Kyushu in Japan.
  • Here, we found that nM levels of genistein and 17β-estradiol had cytotoxic effects on ATL cells and activated caspase-3.
  • In addition, G protein-coupled estrogen receptor agonist G-1 also had a cytotoxic effect on ATL cells.
  • This is the first report suggesting that estrogen receptors are a molecular target for ATL therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Genistein / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology. Receptors, Estrogen / metabolism
  • [MeSH-minor] Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Estradiol / analogs & derivatives. Estradiol / pharmacology. Humans

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  • (PMID = 20944417.001).
  • [ISSN] 1347-6947
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Estrogen; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; DH2M523P0H / Genistein; EC 3.4.22.- / Caspase 3
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55. Nonaka M, Uota S, Saitoh Y, Takahashi M, Sugimoto H, Amet T, Arai A, Miura O, Yamamoto N, Yamaoka S: Role for protein geranylgeranylation in adult T-cell leukemia cell survival. Exp Cell Res; 2009 Jan 15;315(2):141-50
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  • [Title] Role for protein geranylgeranylation in adult T-cell leukemia cell survival.
  • Adult T-cell leukemia (ATL) is a fatal lymphoproliferative disease that develops in human T-cell leukemia virus type I (HTLV-I)-infected individuals.
  • Despite the accumulating knowledge of the molecular biology of HTLV-I-infected cells, effective therapeutic strategies remain to be established.
  • Here, we report that statins hinder the survival of ATL cells and induce apoptotic cell death.
  • Inhibition of protein geranylgeranylation is responsible for these effects, since simultaneous treatment with isoprenoid precursors, geranylgeranyl pyrophosphate or farnesyl pyrophosphate, but not a cholesterol precursor squalene, restored the viability of ATL cells.
  • Simvastatin inhibited geranylgeranylation of small GTPases Rab5B and Rac1 in ATL cells, and a geranylgeranyl transferase inhibitor GGTI-298 reduced ATL cell viability more efficiently than a farnesyl transferase inhibitor FTI-277.
  • These results not only unveil an important role for protein geranylgeranylation in ATL cell survival, but also implicate therapeutic potentials of statins in the treatment of ATL.
  • [MeSH-minor] Adult. Benzamides / pharmacology. Caspase 3 / metabolism. Cell Line, Tumor. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cell Survival / drug effects. Cell Survival / physiology. Enzyme Inhibitors / pharmacology. Humans. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. I-kappa B Proteins / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. Methionine / analogs & derivatives. Methionine / pharmacology. NF-kappa B / metabolism. Phosphorylation / drug effects. Polyisoprenyl Phosphates / pharmacology. Sesquiterpenes / pharmacology. rab5 GTP-Binding Proteins / metabolism. rac1 GTP-Binding Protein / metabolism

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  • (PMID = 18992741.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / FTI 277; 0 / GGTI 298; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Polyisoprenyl Phosphates; 0 / RAC1 protein, human; 0 / Sesquiterpenes; 139874-52-5 / NF-kappaB inhibitor alpha; 6699-20-3 / geranylgeranyl pyrophosphate; 79W6B01D07 / farnesyl pyrophosphate; AE28F7PNPL / Methionine; EC 3.4.22.- / Caspase 3; EC 3.6.5.2 / rab5 GTP-Binding Proteins; EC 3.6.5.2 / rac1 GTP-Binding Protein
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56. Baba M, Okamoto M, Hamasaki T, Horai S, Wang X, Ito Y, Suda Y, Arima N: Highly enhanced expression of CD70 on human T-lymphotropic virus type 1-carrying T-cell lines and adult T-cell leukemia cells. J Virol; 2008 Apr;82(8):3843-52
Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.

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  • [Title] Highly enhanced expression of CD70 on human T-lymphotropic virus type 1-carrying T-cell lines and adult T-cell leukemia cells.
  • Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia (ATL).
  • In Japan, the number of HTLV-1 carriers is estimated to be 1.2 million and more than 700 cases of ATL have been diagnosed every year.
  • Considering the poor prognosis and lack of curative therapy of ATL, it seems mandatory to establish an effective strategy for the treatment of ATL.
  • In this study, we attempted to identify the cell surface molecules that will become suitable targets of antibodies for anti-ATL therapy.
  • The expression levels of approximately 40,000 host genes of three human T-cell lines carrying HTLV-1 genomes were analyzed by oligonucleotide microarray and compared with the expression levels of the genes in an HTLV-1-negative T-cell line.
  • The HTLV-1-carrying T-cell lines used for experiments had totally different expression patterns of viral genome.
  • Among the genes evaluated, the expression levels of 108 genes were found to be enhanced more than 10-fold in all of the T-cell lines examined and 11 of the 108 genes were considered to generate the proteins expressed on the cell surface.
  • In particular, the CD70 gene was upregulated more than 1,000-fold and the enhanced expression of the CD70 molecule was confirmed by laser flow cytometry for various HTLV-1-carrying T-cell lines and primary CD4(+) T cells isolated from acute-type ATL patients.
  • Since CD70 expression is strictly restricted in normal tissues, such as highly activated T and B cells, CD70 appears to be a potential target for effective antibody therapy against ATL.
  • [MeSH-major] Antigens, CD70 / biosynthesis. Human T-lymphotropic virus 1 / immunology. T-Lymphocytes / chemistry. T-Lymphocytes / virology. Up-Regulation
  • [MeSH-minor] Antigens, Surface / biosynthesis. Cell Line, Tumor. Flow Cytometry. Gene Expression Profiling. Gene Expression Regulation, Viral. Humans. Japan. Leukemia-Lymphoma, Adult T-Cell / virology. Oligonucleotide Array Sequence Analysis. Viral Proteins / biosynthesis

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  • (PMID = 18256142.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD70; 0 / Antigens, Surface; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2292990
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57. Díaz Sastre MA, Padilla Parrado M, Morales Puebla JM, Chacón Martínez J, Jiménez Antolín JA, Caro García MA, Galán Morales JT, Menéndez Loras LM, Orradre Romeo JL: [Nasal T lymphoma]. An Otorrinolaringol Ibero Am; 2007;34(4):329-41
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  • [Title] [Nasal T lymphoma].
  • [Transliterated title] Linfoma T nasal.
  • Nasal T lymphoma constitute a type of lymphoproliferative very infrequent symdrome.
  • Only the close cooperation between the otorhinolaryngologist and the anatomopathologist can arrive to obtain a very speedy diagnose and in that way the possibility of a correct treatment, because newly treatments appear, to which this type of disease every day better respond.
  • We present the cases of nasal T lymphomas diagnosticated in the ORL Service of the Toledo area during 15 years, their symptomotology, treatment, evolution and survival.
  • [MeSH-major] Lymphoma, T-Cell / therapy. Nasal Cavity. Nose Neoplasms / therapy
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Disease-Free Survival. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 17844952.001).
  • [ISSN] 0303-8874
  • [Journal-full-title] Anales otorrinolaringológicos ibero-americanos
  • [ISO-abbreviation] An Otorrinolaringol Ibero Am
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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58. Mahieux R, Gessain A: [New human retroviruses: HTLV-3 and HTLV-4]. Med Trop (Mars); 2005 Nov;65(6):525-8
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  • [Title] [New human retroviruses: HTLV-3 and HTLV-4].
  • [Transliterated title] Les nouveaux rétrovirus humains HTLV-3 et HTLV-4.
  • Human T cell leukemia/lymphoma virus Type 1 and 2 (HTLV-1 and HTLV-2), together with their simian counterparts (STLV-1, STLV-2 and STLV-3), belong to the Primate T lymphotropic viruses group (PTLV).
  • HTLV-1 infects 15 to 20 million people worldwide, while STLV-1 is endemic in a number of simian species living in the Old World.
  • Due to the high percentage of homologies between HTLV-1 and STLV-1 strains, it has now been widely accepted that most HTLV-1 subtypes arose from interspecies transmission between monkeys and humans.
  • On the opposite, there is no close human homolog of the two STLV-2 strains that have been discovered in African bonobos chimpanzees.
  • These results suggest that the interspecies transmission that lead to the present day HTLV-2 must have occurred in a distant past.
  • STLV-3 viruses are very divergent, both from HTLV-1 and from HTLV-2.
  • Recently, two laboratories independently reported the discovery of the human homolog (HTLV-3) of STLV-3 in two inhabitants from south Cameroon whose sera exhibited HTLV indeterminate serologies.
  • Together with STLV-3, these two viruses belong therefore to the PTLV-3 group.
  • In addition, a fourth HTLV type (HTLV-4) was also discovered in the same geographical area.
  • Current studies are aimed at determining the molecular characterization of these viruses.
  • In particular, the possible oncogenic properties of their viral transactivator Tax is being investigated, as well as their modes of transmission and their possible association with human diseases.

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  • (PMID = 16555510.001).
  • [ISSN] 0025-682X
  • [Journal-full-title] Médecine tropicale : revue du Corps de santé colonial
  • [ISO-abbreviation] Med Trop (Mars)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 23
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59. Dik WA, Nadel B, Przybylski GK, Asnafi V, Grabarczyk P, Navarro JM, Verhaaf B, Schmidt CA, Macintyre EA, van Dongen JJ, Langerak AW: Different chromosomal breakpoints impact the level of LMO2 expression in T-ALL. Blood; 2007 Jul 1;110(1):388-92

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  • The t(11;14)(p13;q11) is presumed to arise from an erroneous T-cell receptor delta TCRD V(D)J recombination and to result in LMO2 activation.
  • We performed combined in vivo, ex vivo, and in silico analyses on 9 new t(11;14)(p13;q11)-positive T-cell acute lymphoblastic leukemia (T-ALL) as well as normal thymocytes.
  • [MeSH-major] Chromosome Breakage. DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Metalloproteins / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Genes, T-Cell Receptor delta. Humans. LIM Domain Proteins. Proto-Oncogene Proteins / genetics. Translocation, Genetic

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  • (PMID = 17360939.001).
  • [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 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
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60. Braun C, Duffau P, Mahon FX, Rosier E, Leguay T, Etienne G, Michaud M: [Acute pancreatitis due to hypercalcemia revealing adult T-cell leukemia]. Rev Med Interne; 2007 Feb;28(2):116-9
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  • [Title] [Acute pancreatitis due to hypercalcemia revealing adult T-cell leukemia].
  • [Transliterated title] Une pancréatite aiguë révélant une leucémie/lymphome T de l'adulte.
  • INTRODUCTION: Hypercalcemia frequently occurs in the course of Adult T-cell leukemia/lymphoma (ATLL).
  • We report the first case of acute pancreatitis revealing ATLL.
  • EXEGESIS: A 41-year-old woman, without medical history, presented with acute pancreatitis.
  • Biochemical tests showed severe hypercalcemia and the peripheral white blood cell count revealed an atypical lymphocytosis.
  • ATLL was diagnosed by immunophenotypic and morphological analysis of circulating lymphocytes, bone marrow and lymphatic node biopsy.
  • CONCLUSION: In spite of the high prevalence of hypercalcemia in ATLL, acute pancreatitis revealing this pathology is an exceptional condition.

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  • (PMID = 17157965.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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61. Sertöz R, Turhan A, Bozkurt H, Samlıoğlu P, Değirmenci A, Aydınok Y, Erensoy S: [Investigation of anti-HTLV I/II seroprevalence in healthy blood donors in Izmir region, Turkey]. Mikrobiyol Bul; 2010 Oct;44(4):579-84
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  • [Title] [Investigation of anti-HTLV I/II seroprevalence in healthy blood donors in Izmir region, Turkey].
  • [Transliterated title] İzmir bölgesinde sağlıklı kan vericilerinde anti-HTLV-I/II seroprevalansının araştırılması
  • Almost 10-20 million people in the world are thought to be infected by human deltaretroviruses, namely human T-cell lymphotropic virus (HTLV) type I and II, recently.
  • HTLV-I is endemic in southwestern Japan, the Caribbean and sub-Saharan Africa, whereas HTLV-II is more prevalent in intravenous drug addicts, and in American indian populations, endemically.
  • HTLV-I is mainly responsible for adult T-cell leukemia (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), however, HTLVII is not clearly associated with a known clinical disease.
  • Both viruses may be transmitted by sexual contact, parenteral route, whole blood transfusion and breast-feeding.
  • In most of the countries [USA, Canada, South America, Caribbean, Japan, Taiwan and some Europe countries (France, UK, Ireland, Sweden, Denmark, The Netherlands, Portugal, Romania, Greece)] routine screening of anti-HTLV-I/II in blood donors is mandatory, however, there is no such practice in Turkey since seroepidemiologic data on HTLVI/II infections is insufficient.
  • In this study, the seroprevalence of HTLV-I/II in healthy blood donors admitted to the blood bank of Ege University Medical Faculty Hospital, Izmir (located at Aegean region), was investigated to support data on the decision making process on routine screening of anti-HTLV-I/II in blood centers.
  • Serum samples from 10.000 healthy blood donors (mean age: 32.6 years; 87.8% were male), who succeeded the donor history questionnaire, were included to the study, and HTLV-I/II antibodies were screened by a commercial enzyme immunoassay (ELISA) (Murex HTLVI-II, Murex Diagnostics, UK) method.
  • Serum samples which were yielded reactive and borderline results were retested by ELISA, and repeated reactive/borderline results were then confirmed by HTLV-I/II confirmation test (INNO-LIA HTLV-I/II, Innogenetics, Belgium).
  • According to our data HTLV-I/II infections are not endemic in Izmir region, and anti-HTLV-I/II screening of blood donors is not required in our blood center currently.
  • Thus, even its prevalence is very low, much more comprehensive and multi-centered studies are necessary for making the decision of integrating HTLV-I/II in routine blood bank screening tests in Turkey.
  • [MeSH-major] Blood Donors / statistics & numerical data. HTLV-I Antibodies / blood. HTLV-I Infections / epidemiology. HTLV-II Antibodies / blood. HTLV-II Infections / epidemiology
  • [MeSH-minor] Adult. Enzyme-Linked Immunosorbent Assay. Female. Humans. Male. Mandatory Testing. Seroepidemiologic Studies. Turkey / epidemiology

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  • (PMID = 21063970.001).
  • [ISSN] 0374-9096
  • [Journal-full-title] Mikrobiyoloji bülteni
  • [ISO-abbreviation] Mikrobiyol Bul
  • [Language] tur
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / HTLV-I Antibodies; 0 / HTLV-II Antibodies
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62. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
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  • [Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
  • Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder caused by mutations in the NF1 gene.
  • Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).
  • In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.
  • However, our patients lacked clinical NF1 symptoms.
  • Mutation analysis in 4 of these del(17)(q11.2)-positive patients revealed that mutations in the remaining NF1 allele were present in 3 patients, confirming its role as a tumor-suppressor gene in cancer.
  • NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics

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  • (PMID = 18172006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / RNA, Messenger
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63. Sugita K, Shimauchi T, Tokura Y: Chronic actinic dermatitis associated with adult T-cell leukemia. J Am Acad Dermatol; 2005 Feb;52(2 Suppl 1):38-40
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  • [Title] Chronic actinic dermatitis associated with adult T-cell leukemia.
  • We describe a patient with chronic actinic dermatitis that occurred with the progress of adult T-cell leukemia.
  • Immunohistochemically, CD8 + T cells, but not CD4 + cells, predominantly infiltrated the lichenoid lesional skin, indicating that the eruption was induced by reactive, normal CD8 + T cells but not adult T-cell leukemia cells.
  • Our patient suggests that chronic actinic dermatitis may occur in association with the advanced human T-lymphotrophic virus-I infectious disorder.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Photosensitivity Disorders / etiology

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  • (PMID = 15692511.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / Cytokines; 0 / Receptors, CCR4; 0 / Receptors, Chemokine
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64. Mani R, Belcadhi M, Krifa N, Sriha B, Elomri H, Ben Ali M, Abdelkéfi M, Bouzouita K: [NK/T-Cell lymphoma of nasopharynx]. Ann Otolaryngol Chir Cervicofac; 2006 Sep;123(4):189-93
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  • [Title] [NK/T-Cell lymphoma of nasopharynx].
  • [Transliterated title] Lymphomes T/NK du nasopharynx.
  • OBJECTIVE: Discussion of the clinical and paraclinical features of a rare tumor in the nasopharynx, the NK/T-cell lymphoma, with an emphasis on the implications of Epstein Barr Virus (EBV) in its pathogenesis and prognosis.
  • Clinical presentation was non-specific and diagnosis was established with deep biopsies under general anesthesia.
  • Immunochemistry and in situ hybridization were positive for Epstein Barr virus in tumor cells in both cases.
  • He died from acute renal failure during treatment of the second recurrence.
  • CONCLUSION: Diagnosis of NK/T-cell lymphoma may be delayed in the event of non-specific symptoms.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Herpesvirus 4, Human / isolation & purification. Killer Cells, Natural. Lymphoma, T-Cell. Nasopharyngeal Neoplasms
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols. Biopsy. Combined Modality Therapy. Cyclophosphamide. Doxorubicin. Female. Follow-Up Studies. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Nasopharynx / pathology. Neoplasm Recurrence, Local. Prednisolone. Prognosis. Radiotherapy Dosage. Time Factors. Treatment Outcome. Vincristine

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  • (PMID = 17088706.001).
  • [ISSN] 0003-438X
  • [Journal-full-title] Annales d'oto-laryngologie et de chirurgie cervico faciale : bulletin de la Société d'oto-laryngologie des hôpitaux de Paris
  • [ISO-abbreviation] Ann Otolaryngol Chir Cervicofac
  • [Language] fre
  • [Publication-type] Case Reports; Comparative Study; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VAP-cyclo protocol
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65. Shahnaz S, Reich D, Arévalo-Valencia D, Kucinska S, Tulczynska J, Fleischman J: HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia. J Gen Intern Med; 2007 Mar;22(3):420-3
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  • [Title] HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia.
  • BACKGROUND: Since the initial description of human T cell lymphotropic virus (HTLV-1), clusters of this infection have been detected globally.
  • Unlike HIV infection, most patients infected with HTLV-1 remain asymptomatic throughout their lifetime.
  • CASE REPORT: We report the case of a 39-year-old Afro-Caribbean man with HTLV-1 infection presenting as hypercalcemia and granulomatous pneumocystis jiroveci pneumonia.
  • HTLV-1-associated adult T cell leukemia lymphoma (ATLL) was diagnosed in this patient by bone marrow and lymph node biopsy.
  • This is believed to be the first description of this type of reaction to pneumocystis jiroveci in a HTLV-1-infected ATLL patient.
  • [MeSH-major] HTLV-I Infections / diagnosis. Hypercalcemia / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Pneumocystis jirovecii. Pneumonia, Pneumocystis / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans

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  • (PMID = 17356979.001).
  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1824742
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66. Kurihara K, Harashima N, Hanabuchi S, Masuda M, Utsunomiya A, Tanosaki R, Tomonaga M, Ohashi T, Hasegawa A, Masuda T, Okamura J, Tanaka Y, Kannagi M: Potential immunogenicity of adult T cell leukemia cells in vivo. Int J Cancer; 2005 Mar 20;114(2):257-67
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  • [Title] Potential immunogenicity of adult T cell leukemia cells in vivo.
  • Experimental vaccines targeting human T cell leukemia virus type-I (HTLV-I) Tax have been demonstrated in a rat model of HTLV-I-induced lymphomas.
  • However, the scarcity of HTLV-I-expression and the presence of defective HTLV-I-proviruses in adult T cell leukemia (ATL) cells have raised controversy about the therapeutic potential of HTLV-I-targeted immunotherapy in humans.
  • We investigated the expression of HTLV-I antigens in fresh ATL cells by using both in vitro and in vivo assays.
  • In flow cytometric analysis, we found that 3 of 5 acute-type and six of fifteen chronic-type ATL patients tested showed significant induction of HTLV-I Tax and Gag in their ATL cells in a 1-day culture.
  • Concomitantly with HTLV-I-expression, these ATL cells expressed co-stimulatory molecules such as CD80, CD86 and OX40, and showed elevated levels of antigenicity against allogeneic T cells and HTLV-I Tax-specific cytotoxic T-lymphocytes (CTL).
  • Representative CTL epitopes restricted by HLA-A2 or A24 were conserved in 4 of 5 acute-type ATL patients tested.
  • Furthermore, spleen T cells from rats, which had been subcutaneously inoculated with formalin-fixed uncultured ATL cells, exhibited a strong interferon gamma-producing helper T cell responses specific for HTLV-I Tax-expressing cells.
  • Our study indicated that ATL cells from about half the patients tested readily express HTLV-I antigens including Tax in vitro, and that ATL cells express sufficient amounts of Tax or Tax-induced antigens to evoke specific T cell responses in vivo.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification
  • [MeSH-minor] Adult. Aged. Animals. Base Sequence. DNA Primers. Female. Humans. Japan. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemia, Prolymphocytic, T-Cell / virology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology. Male. Middle Aged. Polymerase Chain Reaction. Rats. Rats, Inbred F344. Reference Values. Transplantation, Heterologous / pathology

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551352.001).
  • [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 / DNA Primers
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67. Hernandez CP, Morrow K, Lopez-Barcons LA, Zabaleta J, Sierra R, Velasco C, Cole J, Rodriguez PC: Pegylated arginase I: a potential therapeutic approach in T-ALL. Blood; 2010 Jun 24;115(25):5214-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Adult patients with acute lymphoblastic T cell leukemia (T-ALL) have a very poor prognosis and few effective therapeutic options.
  • In addition, treatment of malignant T-cell lines with peg-Arg I significantly impaired their proliferation, which correlated with a decreased progression into the cell cycle, followed by the induction of apoptosis.
  • The results suggest the potential benefit of L-Arginine depletion by peg-Arg I in the treatment of T-cell malignancies.

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  • (PMID = 20407034.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20RR021970; United States / NCRR NIH HHS / RR / P20 RR021970; United States / NCI NIH HHS / CA / R01 CA082689; United States / NIGMS NIH HHS / GM / P20 GM103501; United States / NCI NIH HHS / CA / R01 CA107974
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCND3 protein, human; 0 / Cyclin D3; 04079A1RDZ / Cytarabine; 30IQX730WE / Polyethylene Glycols; 94ZLA3W45F / Arginine; EC 3.5.3.1 / Arginase
  • [Other-IDs] NLM/ PMC2892956
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68. Dohnal AM, Inthal A, Felzmann T, Glatt S, Sommergruber W, Mann G, Gadner H, Panzer-Grümayer ER: Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL. Int J Cancer; 2006 Dec 15;119(12):2870-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL.
  • The potential immunogenicity of acute lymphoblastic leukemia of the T cell (T-ALL), a small subgroup of childhood leukemia with increased risk for treatment failure and early relapse, was addressed by serological identification of leukemia-derived antigens by recombinant expression cloning (SEREX).
  • Further characterization of the 4 novel isoforms revealed that 3 (HECTD1Delta, CX-ORF-15Delta and hCAP-EDelta) had restricted mRNA expression in more than 70% of T-ALLs (n = 22) and that specific antibodies against these isoforms were detected in up to 30% of patients (n = 16), with the highest frequency for HECTD1Delta.
  • The latter protein was present at high abundance in T-ALLs but not in normal hematopoietic tissues.
  • Given that the leukemia-associated antigens detected in this study have an intracellular localization, the generation of immune effector responses most likely requires antigen presentation.
  • To test this assumption, dendritic cells were loaded with HECTD1Delta protein and used for T cell stimulation.
  • A specific T cell response was induced in vitro in all 3 healthy donors studied, including a former T-ALL patient.
  • [MeSH-major] Antigens, Neoplasm / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Adolescent. Adult. Antibodies / blood. Antibodies / immunology. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. Child. Child, Preschool. Cloning, Molecular / methods. DNA, Complementary / chemistry. DNA, Complementary / genetics. Enzyme-Linked Immunosorbent Assay. Gene Expression Regulation, Neoplastic. Humans. Infant. Interferon-gamma / biosynthesis. Jurkat Cells. Male. Protein Isoforms / genetics. Protein Isoforms / immunology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 17016825.001).
  • [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 / Antibodies; 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / Protein Isoforms; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma
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69. Pamukçuoğlu M, Nasiroğlu N, Yildirim N, Ozçelik O, Oksüzoğlu B, Abali H, Zengin N: [Sinonasal NK/T-cell lymphoma mimicking Wegener's granulomatosis: a case report]. Tuberk Toraks; 2006;54(3):277-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Sinonasal NK/T-cell lymphoma mimicking Wegener's granulomatosis: a case report].
  • In Western population, sinonasal malignant lymphoma is rare and constitutes 1.5% of all non-Hodgkin lymphoma (NHL) and 2.2% of extranodal lymphomas.
  • Herein, we present a typical WG with isolated sinonasal tract involvement with clinical, and radiological findings with the final diagnosis of NK/T-cell angiocentric lymphoma by the repeated biopsies.
  • Since both diseases have same clinical and radiological findings differential diagnosis may be difficult.
  • [MeSH-major] Granulomatosis with Polyangiitis / diagnosis. Lymphoma, T-Cell / diagnosis. Paranasal Sinus Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans

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  • (PMID = 17001547.001).
  • [ISSN] 0494-1373
  • [Journal-full-title] Tüberküloz ve toraks
  • [ISO-abbreviation] Tuberk Toraks
  • [Language] tur
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Turkey
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70. Marçais A, Jeannet R, Hernandez L, Soulier J, Sigaux F, Chan S, Kastner P: Genetic inactivation of Ikaros is a rare event in human T-ALL. Leuk Res; 2010 Apr;34(4):426-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic inactivation of Ikaros is a rare event in human T-ALL.
  • The Ikaros (Ikzf1) gene, encoding a transcription regulator, is a major tumor suppressor in B-cell acute lymphoblastic leukemia (B-ALL).
  • In the mouse, however, loss of Ikaros is primarily associated with T-ALL development.
  • Whether Ikaros is also implicated in human T-ALL remains unclear.
  • We studied Ikaros in 25 human T-ALL samples from diverse molecular subtypes at the mRNA, protein, sequence and genomic copy number level.
  • Thus, inactivation of Ikaros by deletion or mutation is rare in human T-ALL.
  • [MeSH-major] Gene Silencing. Ikaros Transcription Factor / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Cohort Studies. Comparative Genomic Hybridization. Gene Deletion. Gene Expression Regulation, Leukemic. Humans. Infant. Jurkat Cells. Middle Aged. Mutation / physiology. Protein Isoforms / genetics. Young Adult

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • [CommentIn] Leuk Res. 2010 Apr;34(4):416-7 [19892402.001]
  • (PMID = 19796813.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 0 / Protein Isoforms; 148971-36-2 / Ikaros Transcription Factor
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71. Cavazzana-Calvo M, Six E, André-Schmutz I, Coulombel L: [Human hematopoiesis: from CD34 cells to T lymphocytes]. Med Sci (Paris); 2007 Feb;23(2):151-9
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  • [Title] [Human hematopoiesis: from CD34 cells to T lymphocytes].
  • [Transliterated title] Hématopoïèse humaine: des cellules CD34 aux lymphocytes T.
  • Hematopoietic stem cell (HSC) has two key-properties : the self-renewal and the multipotentiality which guarantee the homeostasis of the hematopoietic system all along the lifespan.
  • This implies the migration of an immature progenitor from the fetal liver and later on from the bone marrow to the thymus.
  • Secondly, T cell differentiation is characterized by thymic selection and generation of T lymphocytes with a diverse repertoire able to answer to all foreign antigens one can meet.
  • These complicated mechanisms underlying the T cell differentiation, completely different from those characterizing the myeloid system, at least partially explain our limited knowledge on human T cell lymphopoiesis.
  • Finally, T cell differentiation pathway shows the particularity of profound ontogenic changes with the huge production of lymphoid progenitors during the fetal and the first years of life which declines during the ageing period.
  • Recently, the discovery of new hematopoietic cytokines, the discovery of genes involved in primary immunodeficiencies and the detailed description of the role of Notch receptors have strongly developed our knowledge on T cell lymphopoiesis.
  • [MeSH-minor] Animals. Antigens, CD34 / analysis. Bone Marrow Cells / cytology. Cell Differentiation. Cell Lineage. Cell Movement. Cytokines / physiology. Gene Expression Regulation, Developmental. Gene Rearrangement, T-Lymphocyte. Hematopoietic Stem Cell Transplantation. Humans. Immunologic Deficiency Syndromes / genetics. Immunologic Deficiency Syndromes / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Liver / embryology. Lymphocytes / cytology. Mice. Receptors, Notch / antagonists & inhibitors. Receptors, Notch / genetics. Receptors, Notch / physiology. Thymus Gland / cytology. Thymus Gland / embryology. Transcription Factors / physiology

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  • (PMID = 17291424.001).
  • [ISSN] 0767-0974
  • [Journal-full-title] Médecine sciences : M/S
  • [ISO-abbreviation] Med Sci (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Cytokines; 0 / Receptors, Notch; 0 / Transcription Factors
  • [Number-of-references] 36
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72. Nagasaki A, Taira N, Tomoyose T, Miyagi T, Nakachi S, Shinzato O, Hasegawa H, Takasu N: [Development of acute type, CD 8 positive adult T-cell leukemia in a carrier of hepatitis B virus--possible therapeutic effect of lamivudine combined with chemotherapy]. Gan To Kagaku Ryoho; 2006 May;33(5):683-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Development of acute type, CD 8 positive adult T-cell leukemia in a carrier of hepatitis B virus--possible therapeutic effect of lamivudine combined with chemotherapy].
  • Cases of adult T-cell leukemia (ATL) with aberrant phenotypes have a very poor prognosis.
  • We report the development of acute type, CD 8 positive ATL in a carrier of hepatitis B virus (HBV).
  • He was positive for anti-HTLV-1 antibody and HBV surface antigen.
  • Cytological examination of ascitis revealed numerous atypical lymphoid cells,which were positive for CD 2, CD 5, CD 8, and CD 25.
  • Monoclonal integration of HTLV-1 provirus was detected by Southern blot analysis on DNA extracted from lymphoid cells.
  • A diagnosis of acute type, CD 8 positive ATL was made.
  • He maintained clinical remission during a follow-up of 13 months and then relapsed.
  • It is possible that lamivudine combined with chemotherapy may have had a therapeutic effect on ATL in this case.
  • [MeSH-major] Anti-HIV Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. CD8-Positive T-Lymphocytes / immunology. Carrier State / immunology. Hepatitis B / immunology. Lamivudine / administration & dosage. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Drug Administration Schedule. Etoposide / administration & dosage. HTLV-I Antibodies / immunology. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Nitrosourea Compounds / administration & dosage. Pentostatin / administration & dosage. Prednisone / administration & dosage. Vincristine / administration & dosage

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  • (PMID = 16685173.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / HTLV-I Antibodies; 0 / Nitrosourea Compounds; 2T8Q726O95 / Lamivudine; 395575MZO7 / Pentostatin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7673326042 / irinotecan; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; RYH2T97J77 / ranimustine; VB0R961HZT / Prednisone; XT3Z54Z28A / Camptothecin; CHOP protocol
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73. van Grotel M, Meijerink JP, van Wering ER, Langerak AW, Beverloo HB, Buijs-Gladdines JG, Burger NB, Passier M, van Lieshout EM, Kamps WA, Veerman AJ, van Noesel MM, Pieters R: Prognostic significance of molecular-cytogenetic abnormalities in pediatric T-ALL is not explained by immunophenotypic differences. Leukemia; 2008 Jan;22(1):124-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pediatric T-cell acute lymphoblastic leukemia (T-ALL) is characterized by chromosomal rearrangements possibly enforcing arrest at specific development stages.
  • We studied the relationship between molecular-cytogenetic abnormalities and T-cell development stage to investigate whether arrest at specific stages can explain the prognostic significance of specific abnormalities.
  • HOX11 cases were CD1 positive consistent with a cortical stage, but as 4/5 cases lacked cytoplasmatic-beta expression, developmental arrest may precede beta-selection.
  • TAL1 rearrangements were restricted to the alphabeta-lineage with most cases being TCR-alphabeta positive.
  • CALM-AF10 was associated with early relapse.
  • TAL1 or HOX11L2 rearrangements were associated with trends to good and poor outcomes, respectively.
  • Most cases with lower TAL1 levels were HOX11L2 or CALM-AF10 positive.
  • Classification into T-cell developmental subgroups was not predictive for outcome.
  • [MeSH-major] Gene Rearrangement / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Recurrence, Local / genetics. Receptor, Notch1 / genetics
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Lineage. Child. Female. Homeodomain Proteins / genetics. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Prognosis. Proto-Oncogene Proteins / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17928886.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / TLX3 protein, human; 135471-20-4 / TAL1 protein, human
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74. Burmeister T, Gökbuget N, Reinhardt R, Rieder H, Hoelzer D, Schwartz S: NUP214-ABL1 in adult T-ALL: the GMALL study group experience. Blood; 2006 Nov 15;108(10):3556-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NUP214-ABL1 in adult T-ALL: the GMALL study group experience.
  • The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.
  • We investigated 279 adult patients with T-ALL treated within the framework of the GMALL 5/93 and 6/99 therapy trials for NUP214-ABL1 by using a novel multiplex real-time, quantitative polymerase chain reaction (PCR).
  • Eleven (3.9%) patients were NUP214-ABL1 positive, and 5 different transcripts were observed; 8 patients had a thymic immunophenotype, 1 had an early T-cell immunophenotype, and 2 had a mature T-cell immunophenotype.
  • NUP214-ABL1-positive and -negative patients did not differ significantly in their major clinical features.
  • In contrast to previous reports suggesting an adverse clinical course for NUP214-ABL1-positive patients, no significant difference in overall survival was observed.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-abl / genetics
  • [MeSH-minor] Adolescent. Adult. Benzamides. Female. Humans. Imatinib Mesylate. Immunophenotyping. Male. Piperazines / therapeutic use. Polymerase Chain Reaction. Prognosis. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. RNA, Messenger / analysis. Survival Rate

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  • (PMID = 16873673.001).
  • [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 / Benzamides; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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75. Ikezoe T, Nishioka C, Bandobashi K, Yang Y, Kuwayama Y, Adachi Y, Takeuchi T, Koeffler HP, Taguchi H: Longitudinal inhibition of PI3K/Akt/mTOR signaling by LY294002 and rapamycin induces growth arrest of adult T-cell leukemia cells. Leuk Res; 2007 May;31(5):673-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Longitudinal inhibition of PI3K/Akt/mTOR signaling by LY294002 and rapamycin induces growth arrest of adult T-cell leukemia cells.
  • This study found that phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling was activated in human T-cell lymphotropic virus type I (HTLV-1)-infected leukemia cells.
  • Rapamycin (1-100 nM, 48h), the inhibitor of mTOR and its analog RAD001 (1-100 nM, 48 h)-induced growth inhibition and G0/G1 cell cycle arrest of these cells in association with de-phosphorylation of p70S6K and 4E-BP-1, although IC50 was not achieved.
  • Blockade of Akt signaling by the PI3K inhibitor LY294002 (1-20 microM, 48 h) also resulted in the growth inhibition and G0/G1 cell cycle arrest of HTLV-1-infected cells, with IC50 ranging from 5 to 20muM, and it caused de-phosphorylation of p70S6K and 4E-BP-1.
  • Of note, when rapamycin was combined with LY294002, rapamycin-induced phosphorylation of Akt was blocked, and the ability of rapamycin to induce growth arrest of HTLV-1-infected T-cells and suppress the p-p70S6K and p-4E-BP-1 proteins was potentiated.
  • Moreover, both LY294002 and rapamycin down-regulated the levels of c-Myc and cyclin D1 proteins in these cells, and their combination further decreased levels of these cell cycle-regulating proteins.
  • Taken together, longitudinal inhibition of PI3K/Akt/mTOR signaling represents a promising treatment strategy for individuals with adult T-cell leukemia.
  • [MeSH-major] Chromones / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein Kinases. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Sirolimus / pharmacology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Cell Cycle / drug effects. Cyclin D. Cyclins / metabolism. Enzyme Inhibitors / pharmacology. Human T-lymphotropic virus 1. Humans. Immunosuppressive Agents / pharmacology. Phosphoproteins / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins c-myc / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction / drug effects. T-Lymphocytes / metabolism. T-Lymphocytes / virology. TOR Serine-Threonine Kinases. Tumor Cells, Cultured

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  • (PMID = 17007924.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Chromones; 0 / Cyclin D; 0 / Cyclins; 0 / EIF4EBP1 protein, human; 0 / Enzyme Inhibitors; 0 / Immunosuppressive Agents; 0 / MYC protein, human; 0 / Morpholines; 0 / Phosphoproteins; 0 / Proto-Oncogene Proteins c-myc; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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76. O'Neil J, Tchinda J, Gutierrez A, Moreau L, Maser RS, Wong KK, Li W, McKenna K, Liu XS, Feng B, Neuberg D, Silverman L, DeAngelo DJ, Kutok JL, Rothstein R, DePinho RA, Chin L, Lee C, Look AT: Alu elements mediate MYB gene tandem duplication in human T-ALL. J Exp Med; 2007 Dec 24;204(13):3059-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alu elements mediate MYB gene tandem duplication in human T-ALL.
  • Recent studies have demonstrated that the MYB oncogene is frequently duplicated in human T cell acute lymphoblastic leukemia (T-ALL).
  • We find that the human MYB locus is flanked by 257-bp Alu repeats and that the duplication is mediated somatically by homologous recombination between the flanking Alu elements on sister chromatids.
  • We conclude that Alu-mediated MYB tandem duplication occurs at low frequency during normal thymocyte development and is clonally selected during the molecular pathogenesis of human T-ALL.

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  • (PMID = 18070937.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE7615
  • [Grant] United States / NCI NIH HHS / CA / P01 CA109901; United States / NIGMS NIH HHS / GM / R37 GM050237; United States / NCI NIH HHS / CA / CA11560; United States / NIGMS NIH HHS / GM / GM067055; United States / NIGMS NIH HHS / GM / R01 GM067055; United States / NIGMS NIH HHS / GM / R01 GM050237; United States / NCI NIH HHS / CA / R01 CA111560; United States / NCI NIH HHS / CA / R21 CA115853; United States / NIGMS NIH HHS / GM / GM050237; United States / NCI NIH HHS / CA / CA115853; United States / NCI NIH HHS / CA / CA68484-11; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / CA109901
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb
  • [Other-IDs] NLM/ PMC2150982
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77. Mestiri S, Zeglaoui I, Sriha B, Belcadhi M, Bouzouita K, Korbi S: [Extra-nodal T lymphomas of the nasal cavities and sinuses]. Ann Otolaryngol Chir Cervicofac; 2008 Sep;125(4):188-92
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  • [Title] [Extra-nodal T lymphomas of the nasal cavities and sinuses].
  • [Transliterated title] Les lymphomes T des fosses nasales et des sinus.
  • INTRODUCTION: Extra-nodal T lymphomas of the ear, nose, and throat (ENT) are unusual in Western countries, with differential diagnosis from other destructive and necrotizing lesions of the sino-nasal tract often difficult.
  • MATERIAL AND METHODS: Eleven cases of extra-nodal lymphomas of the upper aerodigestive tract tract managed in the ENT department of F.
  • The aim of our study was to report the clinical and pathological data and the outcome for each patient.
  • Histological examination identified two cases of T/NK lymphoma and nine cases of T-lymphoma not otherwise specified.
  • Immunohistochemistry and in situ hybridization techniques positively detected Epstein-Barr virus in tumoral cells, in seven cases.
  • After a median follow-up of 11-months, clinical outcome consisted in death in seven patients and remission in three patients; one patient was lost of follow-up.
  • CONCLUSION: Extra-nodal lymphomas of the ORL tract are rare in Tunisia.
  • Clinical presentation is not specific, depending on the lymphoma location.
  • Diagnosis relies on clinical presentation and immunophenotypic and molecular characteristics; morphological features are not specific.
  • These are aggressive lymphomas, often requiring multidisciplinary management.
  • [MeSH-major] Lymphoma, T-Cell. Nasal Cavity. Nose Neoplasms
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Paranasal Sinus Neoplasms / diagnosis. Paranasal Sinus Neoplasms / therapy. Retrospective Studies

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  • (PMID = 18707674.001).
  • [ISSN] 0003-438X
  • [Journal-full-title] Annales d'oto-laryngologie et de chirurgie cervico faciale : bulletin de la Société d'oto-laryngologie des hôpitaux de Paris
  • [ISO-abbreviation] Ann Otolaryngol Chir Cervicofac
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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78. Cauwelier B, Dastugue N, Cools J, Poppe B, Herens C, De Paepe A, Hagemeijer A, Speleman F: Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes. Leukemia; 2006 Jul;20(7):1238-44

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes.
  • Chromosomal aberrations of T-cell receptor (TCR) gene loci often involve the TCRalphadelta (14q11) locus and affect various known T-cell oncogenes.
  • Therefore, we initiated a screening of 126 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma cases and 19 T-ALL cell lines using FISH break-apart assays for the different TCR loci.
  • Some of these chromosome aberrations target new putative T-cell oncogenes at chromosome 11q24, 20p12 and 6q22.
  • Five patients and one cell line carried chromosomal rearrangements affecting both TCRbeta and TCRalphadelta loci.
  • In conclusion, this study presents the first inventory of chromosomal rearrangements of TCR loci in T-ALL, revealing an unexpected high number of cryptic chromosomal rearrangements of the TCRbeta locus and further broadening the spectrum of genes putatively implicated in T-cell oncogenesis.
  • [MeSH-major] Gene Rearrangement, T-Lymphocyte / genetics. Genes, T-Cell Receptor beta / genetics. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Genes, T-Cell Receptor alpha / genetics. Genes, T-Cell Receptor delta / genetics. Humans. In Situ Hybridization, Fluorescence. Incidence. Male. Middle Aged. Retrospective Studies. Translocation, Genetic

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  • (PMID = 16673021.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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79. Eguchi-Ishimae M, Eguchi M, Kempski H, Greaves M: NOTCH1 mutation can be an early, prenatal genetic event in T-ALL. Blood; 2008 Jan 1;111(1):376-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • NOTCH1 mutations are common in T-lineage acute lymphoblastic leukemia (T-ALL).
  • Twin studies and retrospective screening of neonatal blood spots provide evidence that fusion genes and other chromosomal abnormalities associated with pediatric leukemias can originate prenatally.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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  • (PMID = 17901244.001).
  • [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 / NOTCH1 protein, human; 0 / Receptor, Notch1
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80. Bellon M, Lepelletier Y, Hermine O, Nicot C: Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia. Blood; 2009 May 14;113(20):4914-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia.
  • Human T-cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T-cell leukemia (ATL), an aggressive lymphoproliferative disease.
  • MicroRNAs (miRNAs) are differentially expressed during hematopoiesis and lineage commitment of hematopoietic stem cell progenitors (HSCPs).
  • Here, we report aberrant expression of hematopoietic-specific miR-223, miR-181a, miR-150, miR-142.3p, and miR-155 in HTLV-I-infected cells in vitro and uncultured ex vivo ATL cells.
  • Our results suggest that HTLV-I-infected cells have an unbalanced expression of miRNA that favors T-cell differentiation.
  • Strikingly, our data also revealed significant differences between ex vivo ATL tumor cells and in vitro HTLV-I cell lines.
  • Specifically, miR-150 and miR-223 were up-regulated in ATL patients but consistently down-regulated in HTLV-I cell lines, suggesting that ATL cells and in vitro-established cells are derived from distinct cellular populations.

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  • (PMID = 19246560.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106258; United States / NCI NIH HHS / CA / R01 CA115398; United States / NCI NIH HHS / CA / R01CA106258; United States / NCI NIH HHS / CA / R01CA115398
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2686141
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81. Beltrán B, Palomino E, Quiñones P, Morales D, Cotrina E: [Gastric adult T cell leukemia/lymphoma: report of four cases and review of literature]. Rev Gastroenterol Peru; 2010 Apr-Jun;30(2):153-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Gastric adult T cell leukemia/lymphoma: report of four cases and review of literature].
  • [Transliterated title] Leucemia/linfoma T del adulto gástrico: reporte de cuatro casos y revisión de la literatura.
  • Adult T-cell leukemia/lymphoma (ATLL) is an aggressive disease associated with human T-cell lymphotropic virus type-I (HTLV-I) with heterogeneous clinical presentation and outcomes.
  • We describe clinical and endoscopic findings of cases and review literature.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell. Stomach Neoplasms
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Fatal Outcome. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Prednisone / administration & dosage. Prevalence. Stomach Ulcer / etiology. Vincristine / administration & dosage

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  • (PMID = 20644608.001).
  • [ISSN] 1609-722X
  • [Journal-full-title] Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú
  • [ISO-abbreviation] Rev Gastroenterol Peru
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Peru
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VB0R961HZT / Prednisone; CHOEP protocol; CHOP protocol
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82. Sakashita A, Ashizawa K, Minami K, Fukuda T, Fukuda M, Abe K, Hayashi T, Uetani M: Localized ground glass opacities with multiple pulmonary small cysts in adult T-cell leukemia or lymphoma: an "alloy wheel" appearance. J Thorac Imaging; 2009 Nov;24(4):321-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localized ground glass opacities with multiple pulmonary small cysts in adult T-cell leukemia or lymphoma: an "alloy wheel" appearance.
  • We herein report a case of adult T-cell leukemia or lymphoma showing multiple lung cysts within a localized ground glass opacity (GGO) on computed tomography scan.
  • [MeSH-major] Cysts / radiography. Leukemia-Lymphoma, Adult T-Cell / radiography. Lung Neoplasms / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Male. Middle Aged

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  • (PMID = 19935228.001).
  • [ISSN] 1536-0237
  • [Journal-full-title] Journal of thoracic imaging
  • [ISO-abbreviation] J Thorac Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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83. Nomura K, Utsunomiya A, Furushou H, Tara M, Hazeki M, Tokunaga M, Uozumi K, Hanada S, Yashiki S, Tajima K, Sonoda S: A family predisposition to adult T-cell leukemia. J Clin Exp Hematop; 2006 Nov;46(2):67-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A family predisposition to adult T-cell leukemia.
  • We report here the rare case of a family predisposed to adult T-cell leukemia (ATL).
  • Six of seven siblings developed ATL with ages of onset of 77, 48, 60, 64, 72, and 62 years old.
  • Although virological tests for human T-lymphotropic virus type 1 were unavailable for two of the six patients, all were diagnosed with ATL based on their clinical, hematological, and histopathological features.
  • Two of the six patients were tested for HLA haplotypes using fresh blood samples, and both were carriers of the HLA-A*26 allele known in the southern Japanese population to be susceptible to ATL.
  • This series of genetic traits may help explain the familial predisposition to ATL.
  • [MeSH-major] Genetic Predisposition to Disease. HLA-A Antigens / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Aged. Female. HTLV-I Infections / complications. Human T-lymphotropic virus 1. Humans. Male. Middle Aged. Pedigree

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  • (PMID = 17142956.001).
  • [ISSN] 1346-4280
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / HLA-A Antigens
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84. Zhang Z, Zhang M, Garmestani K, Talanov VS, Plascjak PS, Beck B, Goldman C, Brechbiel MW, Waldmann TA: Effective treatment of a murine model of adult T-cell leukemia using 211At-7G7/B6 and its combination with unmodified anti-Tac (daclizumab) directed toward CD25. Blood; 2006 Aug 1;108(3):1007-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effective treatment of a murine model of adult T-cell leukemia using 211At-7G7/B6 and its combination with unmodified anti-Tac (daclizumab) directed toward CD25.
  • Adult T-cell leukemia (ATL) consists of an overabundance of T cells, which express CD25.
  • Therapeutic efficacy of astatine-211 ((211)At)-labeled murine monoclonal antibody 7G7/B6 alone and in combination with daclizumab was evaluated in nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice given injections of MET-1 human T-cell leukemia cells.
  • Either a single dose of 12 microCi (0.444 MBq) (211)At-7G7/B6 per mouse given intravenously or receptor-saturating doses of daclizumab given at 100 microg weekly for 4 weeks intravenously inhibited tumor growth as monitored by serum levels of human beta-2 microglobulin (beta(2)mu) and by prolonged survival of leukemia-bearing mice compared with the control groups (P < .001).
  • These results that demonstrate a significantly improved therapeutic efficacy by combining (211)At-7G7/B6 with daclizumab support a clinical trial of this regimen in patients with ATL.

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  • (PMID = 16569769.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Epitopes; 0 / Immunoglobulin G; 0 / Receptors, Interleukin-2; CUJ2MVI71Y / daclizumab; XI595HAL7H / Astatine
  • [Other-IDs] NLM/ PMC1895861
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85. Satou Y, Yasunaga J, Yoshida M, Matsuoka M: HTLV-I basic leucine zipper factor gene mRNA supports proliferation of adult T cell leukemia cells. Proc Natl Acad Sci U S A; 2006 Jan 17;103(3):720-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HTLV-I basic leucine zipper factor gene mRNA supports proliferation of adult T cell leukemia cells.
  • Human T cell leukemia virus type I (HTLV-I) causes adult T cell leukemia (ATL) in 2-5% of carriers after a long latent period.
  • An HTLV-I encoded protein, Tax, induces proliferation and inhibits apoptosis, resulting in clonal proliferation of infected cells.
  • However, tax gene expression in ATL cells is disrupted by several mechanisms, including genetic changes in the tax gene and DNA methylation/deletion of the 5' long terminal repeat (LTR).
  • Because Tax is the major target of cytotoxic T-lymphocytes in vivo, loss of Tax expression should enable ATL cells to escape the host immune system.
  • The 5' LTR of HTLV-I is frequently hypermethylated or deleted in ATL cells, whereas the 3' LTR remains unmethylated and intact, suggesting the involvement of the 3' LTR in leukemogenesis.
  • Here we show that a gene encoded by the minus strand of the HTLV-I proviral genome, HTLV-I basic leucine zipper factor (HBZ), is transcribed from 3'-LTR in all ATL cells.
  • Suppression of HBZ gene transcription by short interfering RNA inhibits proliferation of ATL cells.
  • In addition, HBZ gene expression promotes proliferation of a human T cell line.
  • Analyses of T cell lines transfected with mutated HBZ genes showed that HBZ promotes T cell proliferation in its RNA form, whereas HBZ protein suppresses Tax-mediated viral transcription through the 5' LTR.
  • The growth-promoting activity of HBZ RNA likely plays an important role in oncogenesis by HTLV-I.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / genetics. Cell Proliferation. Human T-lymphotropic virus 1 / genetics. Leucine Zippers / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. RNA, Messenger / physiology. Viral Proteins / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Line, Transformed. Gene Expression Regulation, Neoplastic. Humans. Mice. Mice, Transgenic. Molecular Sequence Data

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  • [ErratumIn] Proc Natl Acad Sci U S A. 2006 Jun 6;103(23):8906
  • (PMID = 16407133.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ273132
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Messenger; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC1334651
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86. Okudaira T, Tomita M, Uchihara JN, Matsuda T, Ishikawa C, Kawakami H, Masuda M, Tanaka Y, Ohshiro K, Takasu N, Mori N: NIK-333 inhibits growth of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells in association with blockade of nuclear factor-kappaB signal pathway. Mol Cancer Ther; 2006 Mar;5(3):704-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NIK-333 inhibits growth of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells in association with blockade of nuclear factor-kappaB signal pathway.
  • Adult T-cell leukemia (ATL) is caused by human T-cell leukemia virus type I (HTLV-I) and remains incurable.
  • NIK-333, a novel synthetic retinoid, prevents the recurrence of human hepatoma after surgical resection of primary tumors.
  • We explored the effects of NIK-333 on HTLV-I-infected T-cell lines and ATL cells.
  • NIK-333 inhibited cell proliferation, induced G1 arrest, and resulted in massive apoptosis in all tested HTLV-I-infected T-cell lines and ATL cells, whereas little effect was observed on normal peripheral blood mononuclear cells.
  • Further analysis showed that NIK-333 inactivated nuclear factor-kappaB in HTLV-I-infected T-cell lines.
  • In animal studies, treatment with NIK-333 (100 mg/kg given orally every other day) produced partial inhibition of growth of tumors of a HTLV-I-infected T-cell line transplanted s.c. in severe combined immunodeficient mice.
  • Our results indicate that NIK-333 is a potentially useful therapeutic agent for patients with ATL.
  • [MeSH-major] HTLV-I Infections / drug therapy. Human T-lymphotropic virus 1. Leukemia, T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. NF-kappa B / antagonists & inhibitors. Retinoids / therapeutic use
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Transformed. Cell Line, Tumor. Cyclin D1 / metabolism. Cyclin D2. Cyclins / metabolism. Down-Regulation. Female. Humans. Inhibitor of Apoptosis Proteins / metabolism. Mice. Mice, Inbred Strains. Signal Transduction. T-Lymphocytes / virology. X-Linked Inhibitor of Apoptosis Protein / metabolism

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  • (PMID = 16546985.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Inhibitor of Apoptosis Proteins; 0 / NF-kappa B; 0 / Retinoids; 0 / X-Linked Inhibitor of Apoptosis Protein; 11ALM7A4RV / (2E,4E,6E,10E)-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid; 136601-57-5 / Cyclin D1
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87. Kannagi M: Immunologic control of human T-cell leukemia virus type I and adult T-cell leukemia. Int J Hematol; 2007 Aug;86(2):113-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunologic control of human T-cell leukemia virus type I and adult T-cell leukemia.
  • Host T-cell responses to human T-cell leukemia virus type I (HTLV-I) control the expansion of HTLV-I-infected cells and are determinants of the equilibrium proviral load in vivo.
  • Insufficient T-cell responses are regarded as an immunologic risk factor for adult T-cell leukemia (ATL) because they allow increased proviral loads, which represent an epidemiologic risk factor for ATL.
  • ATL cells from approximately half of ATL cases retain the ability to express HTLV-I Tax, a major target antigen of HTLV-I-specific cytotoxic T-lymphocytes (CTL), whereas Tax-specific CTL in ATL patients are inactive.
  • Tax-specific CTL responses are strongly activated after hematopoietic stem cell transplantation in some ATL patients in long-term remission, indicating that HTLV-I Tax is expressed in vivo rather than being silent, and that the donor-derived T-cell system can recognize it.
  • These findings strongly suggest that reactivation of Tax-specific CTL by vaccines may be promising for prophylaxis of ATL in the high-risk group of HTLV-I carriers and for therapy of ATL in patients whose tumor cells are capable of expressing Tax.
  • [MeSH-major] Human T-lymphotropic virus 1 / immunology. Immunity. Leukemia-Lymphoma, Adult T-Cell / immunology

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  • (PMID = 17875523.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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88. Miura H, Maeda M, Yamamoto N, Yamaoka S: Distinct IkappaB kinase regulation in adult T cell leukemia and HTLV-I-transformed cells. Exp Cell Res; 2005 Aug 1;308(1):29-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct IkappaB kinase regulation in adult T cell leukemia and HTLV-I-transformed cells.
  • We have recently shown constitutive IkappaB kinase (IKK) activation and aberrant p52 expression in adult T cell leukemia (ATL) cells that do not express human T cell leukemia virus type I (HTLV-I) Tax, but the mechanism of IKK activation in these cells has remained unknown.
  • Here, we demonstrate distinct regulation of IKK activity in ATL and HTLV-I-transformed T cells in response to protein synthesis inhibition or arsenite treatment.
  • Protein synthesis inhibition for 4 h by cycloheximide (CHX) barely affects IKK activity in Tax-positive HTLV-I-transformed cells, while it diminishes IKK activity in Tax-negative ATL cells.
  • Treatment of ATL cells with a proteasome inhibitor MG132 prior to protein synthesis inhibition reverses the inhibitory effect of CHX, and MG132 alone greatly enhances IKK activity.
  • In addition, treatment of HTLV-I-transformed cells with arsenite for 1 h results in down-regulation of IKK activity without affecting Tax expression, while 8 h of arsenite treatment does not impair IKK activity in ATL cells.
  • These results indicate that a labile protein sensitive to proteasome-dependent degradation governs IKK activation in ATL cells, and suggest a molecular mechanism of IKK activation in ATL cells distinct from that in HTLV-I-transformed T cells.
  • [MeSH-major] Cell Transformation, Viral / physiology. Leukemia-Lymphoma, Adult T-Cell / metabolism. Protein-Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Arsenites / pharmacology. Cell Line, Transformed. Cell Line, Tumor. Cycloheximide / antagonists & inhibitors. Cycloheximide / pharmacology. Enzyme Inhibitors / pharmacology. Human T-lymphotropic virus 1 / physiology. Humans. I-kappa B Kinase. Leupeptins / pharmacology. Proteasome Endopeptidase Complex / metabolism. Protein Synthesis Inhibitors / pharmacology. T-Lymphocytes / drug effects. T-Lymphocytes / metabolism

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  • (PMID = 15878527.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenites; 0 / Enzyme Inhibitors; 0 / Leupeptins; 0 / Protein Synthesis Inhibitors; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 98600C0908 / Cycloheximide; EC 2.7.1.- / IKBKE protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.10 / CHUK protein, human; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / IKBKB protein, human; EC 3.4.25.1 / Proteasome Endopeptidase Complex; N5509X556J / arsenite
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89. Maeda Y, Yamaguchi T, Hijikata Y, Tanaka M, Hirase C, Takai S, Morita Y, Sano T, Miyatake J, Tatsumi Y, Kanamaru A: Clinical efficacy of all-trans retinoic acid for treating adult T cell leukemia. J Cancer Res Clin Oncol; 2008 Jun;134(6):673-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical efficacy of all-trans retinoic acid for treating adult T cell leukemia.
  • PURPOSE: We previously reported that all-trans retinoic acid (ATRA) inhibited growth in human T-cell leukemia virus type I (HTLV-I)-positive T-cell lines and in fresh cells from patients with adult T cell leukemia (ATL).
  • Here, we confirmed the clinical effects of ATRA in 20 patients with ATL.
  • MATERIALS AND METHODS: The 20 patients (n = 20) with a median age of 56 (range 35-73) years who were diagnosed with ATL received ATRA orally.
  • RESULTS: The efficacy of treatment was as follows: no complete response (CR), a partial response (PR) in 40% of the patients, no change (NC) in 45% of the patients, and a progressive disease (PD) in 15% of the patients.
  • In seven acute-type ATL patients, a PR was achieved in two (28.5%), NC was observed in two (28.5%), and a PD was observed in three (42.8%).
  • In three lymphoma-type ATL patients, a PR (100%) was achieved.
  • Among four chronic-type ATL patients, a PR was achieved in one (25%) and NC was observed in the remaining three (75%).
  • In six smoldering-type ATL patients, a PR was achieved in two (33.3%) and NC was observed in four (66.6%).
  • CONCLUSION: These results indicated that ATRA might be a useful agent for the safe treatment of ATL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged

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  • (PMID = 18008086.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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90. Yamaguchi T, Maeda Y, Ueda S, Hijikata Y, Morita Y, Miyatake JI, Matsuda M, Kanamaru A: Dichotomy of all-trans retinoic acid inducing signals for adult T-cell leukemia. Leukemia; 2005 Jun;19(6):1010-7
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dichotomy of all-trans retinoic acid inducing signals for adult T-cell leukemia.
  • We previously reported that all-trans retinoic acid (ATRA) inhibits growth in human T-cell leukemia virus type 1 (HTLV-1)-positive T-cell lines and fresh cells from patients with adult T-cell leukemia.
  • In the present study, we observed that NF-kappaB transcriptional activity as well as cell growth decreased significantly in HTLV-1-positive T-cell lines in the presence of ATRA.
  • Furthermore, we observed that ATRA reduced HTLV-1 proviral DNA, HTLV-1 genes (gag, tax, or pol mRNA) using the real-time quantitative polymerase chain reaction.
  • SIL-2R was reduced by ATRA in both protein level (culture supernantant) and mRNA level in HTLV-1-positive T-cell lines.
  • Interestingly, ATRA significantly inhibited RT activity similar to azidothimidine (AZT) in HTLV-1-positive T-cell lines.
  • Moreover, AZT inhibited proviral DNA but not NF-kappaB transcriptional activity, and sIL-2R on HTLV-1; however, ATRA inhibited of NF-kappaB, proviral DNA and sIL-2R on HTLV-1.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, T-Cell / drug therapy. Leukemia, T-Cell / metabolism. Signal Transduction / drug effects. Tretinoin / pharmacology
  • [MeSH-minor] Adult. Cell Division / drug effects. Deltaretrovirus Infections / drug therapy. Deltaretrovirus Infections / metabolism. Deltaretrovirus Infections / physiopathology. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Viral / drug effects. Gene Products, gag / genetics. Gene Products, pol / genetics. Genes, pX / genetics. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / growth & development. Humans. In Vitro Techniques. Jurkat Cells. NF-kappa B / metabolism. Proviruses / genetics. Receptors, Interleukin-2 / metabolism. Solubility. Transcriptional Activation / drug effects. Viral Load

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  • (PMID = 15843825.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Gene Products, gag; 0 / Gene Products, pol; 0 / NF-kappa B; 0 / Receptors, Interleukin-2; 5688UTC01R / Tretinoin
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91. Przybylski GK, Dik WA, Wanzeck J, Grabarczyk P, Majunke S, Martin-Subero JI, Siebert R, Dölken G, Ludwig WD, Verhaaf B, van Dongen JJ, Schmidt CA, Langerak AW: Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL. Leukemia; 2005 Feb;19(2):201-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with chromosomal aberrations characterized by juxtaposition of proto-oncogenes to T-cell receptor gene loci (TCR), resulting in the deregulated transcription of these proto-oncogenes.
  • The TRDV1-BCL11B joining region was 1344 bp long and contained fragments derived from 20q11.22, 3p21.33 and from 11p12, indicating the complex character of this aberration.
  • Screening of 37 other T-ALLs revealed one additional case with expression of the BCL11B-TRDC fusion transcript.
  • As BCL11B appears to play a key role in T-cell differentiation, BCL11B disruption and disturbed expression may contribute to the development of T-cell malignancies in man.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic

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  • (PMID = 15668700.001).
  • [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 / BCL11B protein, human; 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins
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92. Watters KM, Dean J, Gautier V, Hall WW, Sheehy N: Tax 1-independent induction of vascular endothelial growth factor in adult T-cell leukemia caused by human T-cell leukemia virus type 1. J Virol; 2010 May;84(10):5222-8
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  • [Title] Tax 1-independent induction of vascular endothelial growth factor in adult T-cell leukemia caused by human T-cell leukemia virus type 1.
  • Adult T-cell leukemia (ATL) is caused by human T-cell leukemia virus type 1 (HTLV-1).
  • Elevated expression of vascular endothelial growth factor (VEGF) in ATL patients is associated with leukemic cell invasion and infiltration in different organs.
  • The regulatory protein Tax 1 encoded by HTLV-1 plays a pivotal role in T-cell transformation by deregulating the function and expression of several cellular factors.
  • We showed that VEGF was secreted by HTLV-1-transformed and nontransformed cells, irrespective of Tax 1 expression.
  • Overall our data indicate that, contrary to a previous report, Tax 1 downregulates VEGF expression and suggest there are Tax 1-independent mechanisms of VEGF activation in ATL.
  • [MeSH-major] Cell Adhesion Molecules, Neuronal / physiology. Down-Regulation. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / virology. Up-Regulation. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 20237090.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CNTN2 protein, human; 0 / Cell Adhesion Molecules, Neuronal; 0 / Contactin 2; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2863836
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93. Cauwelier B, Cavé H, Gervais C, Lessard M, Barin C, Perot C, Van den Akker J, Mugneret F, Charrin C, Pagès MP, Grégoire MJ, Jonveaux P, Lafage-Pochitaloff M, Mozzicconacci MJ, Terré C, Luquet I, Cornillet-Lefebvre P, Laurence B, Plessis G, Lefebvre C, Leroux D, Antoine-Poirel H, Graux C, Mauvieux L, Heimann P, Chalas C, Clappier E, Verhasselt B, Benoit Y, Moerloose BD, Poppe B, Van Roy N, Keersmaecker KD, Cools J, Sigaux F, Soulier J, Hagemeijer A, Paepe AD, Dastugue N, Berger R, Speleman F: Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique. Leukemia; 2007 Jan;21(1):121-8
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  • [Title] Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique.
  • Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34) and t(7;7)(p15;q34) involving the T-cell receptor beta (TCRbeta) (7q34) and the HOXA gene locus (7p15) in 5% of T-cell acute lymphoblastic leukemia (T-ALL) patients leading to transcriptional activation of especially HOXA10.
  • To further address the clinical, immunophenotypical and molecular genetic findings of this chromosomal aberration, we studied 330 additional T-ALLs.
  • In conclusion, this study defines TCRbeta-HOXA rearranged T-ALLs as a distinct cytogenetic subgroup by clinical, immunophenotypical and molecular genetic characteristics.
  • [MeSH-major] Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Chromosome Deletion. Chromosome Inversion. Female. Gene Rearrangement, T-Lymphocyte. Humans. Immunophenotyping. Male. Middle Aged. Receptor, Notch1 / genetics. Transcriptional Activation. Translocation, Genetic

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  • (PMID = 17039236.001).
  • [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 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 140441-81-2 / HOXA10 protein, human
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94. Furukawa Y, Tara M, Izumo S, Arimura K, Osame M: HTLV-I viral escape and host genetic changes in the development of adult T cell leukemia. Int J Cancer; 2006 Jan 15;118(2):381-7
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  • [Title] HTLV-I viral escape and host genetic changes in the development of adult T cell leukemia.
  • In the pathogenesis of adult T cell leukemia (ATL), an oncogenetic role of the human T cell lymphotropic virus type I (HTLV-I) Tax protein, viral escape from the host immune system, and host genetic changes have been proposed as contributory factors.
  • We examined the premature stop codons in tax gene as one of the mutations that may lead to escape of HTLV-I from the cytotoxic T lymphocyte (CTL) response in HTLV-I carriers, to test whether a putative CTL escape mutant can emerge in the early stage of ATL development and whether HTLV-I infected cells with such a mutation can proliferate subsequently.
  • We also examined deletion of cyclin-dependent kinase inhibitor 4 (INK4) genes and mutation of p53 gene in combination with changes in the HTLV-I genome in acute type ATL to test whether host genetic changes promoted the malignant transformation of ATL cells that carry putative CTL escape mutations.
  • The premature stop codon in tax gene existed in many non-ATL HTLV-I carriers as a minor population but not in the commonest HTLV-I sequence of the individual.
  • There were cases who had a mutation or deletion in HTLV-I who also have either deletion of INK4 genes or mutation in p53 gene.
  • Our findings suggest that CTL escape mutation can occur at an early stage of ATL development, and that certain host genetic changes favor the development of the aggressive form of ATL.
  • [MeSH-major] Codon, Nonsense. Genes, pX / genetics. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Cell Proliferation. Cell Survival. Cyclin-Dependent Kinase Inhibitor Proteins / genetics. Cyclin-Dependent Kinase Inhibitor Proteins / physiology. Genes, p53. HTLV-I Infections / complications. Humans. Prognosis

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16052518.001).
  • [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 / Codon, Nonsense; 0 / Cyclin-Dependent Kinase Inhibitor Proteins
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95. Nakamura M, Hamasaki T, Tokitou M, Baba M, Hashimoto Y, Aoyama H: Discovery of tetrahydrotetramethylnaphthalene analogs as adult T-cell leukemia cell-selective proliferation inhibitors in a small chemical library constructed based on multi-template hypothesis. Bioorg Med Chem; 2009 Jul 1;17(13):4740-6
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  • [Title] Discovery of tetrahydrotetramethylnaphthalene analogs as adult T-cell leukemia cell-selective proliferation inhibitors in a small chemical library constructed based on multi-template hypothesis.
  • Adult T cell leukemia (ATL), caused by infection of human T-lymphotropic virus type 1 (HTLV-1), has a poor prognosis and curative therapy is unavailable, so it is important to find or design superior lead compounds for the drug treatment of ATL.
  • We used our micro-reversed fragment-based drug design hypothesis and multi-template hypothesis to extract the tetrahydrotetramethylnaphthalene (TMN) skeleton from tamibarotene, a useful medicament for the treatment of acute promyelocytic leukemia (APL).
  • Structural development of TMN yielded highly ATL cell-selective growth inhibitors, including 2-acetyl-3-hydroxy-5,6,7,8-tetrahydro-5,5,8,8-tetramethylnaphthalene (6).
  • Structure-activity relationship analysis suggests the existence of a specific target molecule for ATL cell-selective inhibition of proliferation through G2 arrest.
  • [MeSH-major] Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Tetrahydronaphthalenes / chemistry. Tetrahydronaphthalenes / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Drug Design. Human T-lymphotropic virus 1 / isolation & purification. Humans. Models, Molecular. Molecular Structure. Retinoids. Small Molecule Libraries. Structure-Activity Relationship. T-Lymphocytes / cytology. T-Lymphocytes / virology

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  • (PMID = 19443225.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Retinoids; 0 / Small Molecule Libraries; 0 / Tetrahydronaphthalenes
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96. Chadwick N, Zeef L, Portillo V, Boros J, Hoyle S, van Doesburg JC, Buckle AM: Notch protection against apoptosis in T-ALL cells mediated by GIMAP5. Blood Cells Mol Dis; 2010 Oct 15;45(3):201-9

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  • Recent studies have highlighted the role of Notch signalling in the development of T cell acute lymphoblasic leukaemia (T-ALL).
  • The aims of this study were to determine the effect of Notch signalling on apoptosis in human T-ALL cell lines and to identify targets of Notch signalling that may mediate this effect.
  • Microarray analysis revealed that GIMAP5, a gene coding for an anti-apoptotic intracellular protein, is upregulated by Notch in T-ALL cell lines.
  • [MeSH-major] Apoptosis. GTP-Binding Proteins / biosynthesis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. Receptors, Notch / metabolism. Signal Transduction

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20817506.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GIMAP5 protein, human; 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / NOTCH3 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Receptors, Notch; EC 3.6.1.- / GTP-Binding Proteins
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97. Estes DA, Lovato DM, Khawaja HM, Winter SS, Larson RS: Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples. Br J Haematol; 2007 Oct;139(1):20-30
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  • [Title] Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples.
  • Acquired drug resistance eventually leads to treatment failure in T-cell acute lymphoblastic leukaemia (T-ALL).
  • Immunophenotypic and cytogenetic heterogeneities within T-ALL influence susceptibility to cytotoxic therapy, and little is known about the mechanisms of drug resistance at specific stages of T-cell ontogeny.
  • We developed tolerance to therapeutic concentrations of daunorubicin (DNR) and L-asparaginase (L-asp) in Jurkat (CD1a(-), sCD3(+)) and Sup T1 (CD1a(+), sCD3(-)) cell lines, having respective 'mature' and 'cortical' stages of developmental arrest.
  • Microarray analysis identified upregulation of asparagine synthetase (ASNS) and argininosuccinate synthase 1 (ASS1) to cell lines with acquired resistance to L-asp, and in the case of DNR, upregulation of ATP-binding cassette B1 (ABCB1).
  • This study expands the pool of available drug resistant cell lines having cortical and mature stages of developmental arrest, introduces three new drug resistant T-ALL cell lines, and identifies gene interactions leading to L-asp and DNR resistance.
  • [MeSH-major] Cell Line, Tumor. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Genes, MDR. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 17854304.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 R01 CA114589; United States / NCI NIH HHS / CA / U10 CA98543-03-14305
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Glycoprotein; 0 / RNA, Small Interfering; 5J49Q6B70F / Vincristine; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase; EC 6.3.4.5 / Argininosuccinate Synthase; ZS7284E0ZP / Daunorubicin
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98. Malan R, Berini CA, Eirin ME, Delfino CM, Pedrozo W, Krupp R, García Plichta A, Biglione MM: [Seroprevalence of HTLV-1/2 in blood donors from Misiones Province]. Medicina (B Aires); 2010;70(1):71-4
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  • [Title] [Seroprevalence of HTLV-1/2 in blood donors from Misiones Province].
  • [Transliterated title] Seroprevalencia de HTLV-1/2 en donantes de sangre de la Provincia de Misiones.
  • Human T-cell Lymphotropic viruses type 1 (HTLV-1), the first human oncoretrovirus to be discovered, is the etiologic agent of Adult T-cell Leukemia (ATL) and HTLV-1 Associated Mielopathy or Tropical Spastic Paraparesis (HAM/TSP).
  • It is endemic worldwide, including the North of Argentina where both associated diseases have also been detected.
  • No etiologic role has been described for HTLV-2, although it has been associated with HAM/TSP-like neurologic syndromes.
  • The aim of this study was to estimate the seroprevalence of HTLV-1/2 in a blood donor population from Misiones province.
  • HTLV-1/2 screening was performed with ELISA and particle agglutination, and reactive samples were confirmed by Western Blot.
  • Out of the 5 positive samples, one was an HTLV, three HTLV-1 and one HTLV-2.
  • This study demonstrates the presence of HTLV-1/2 in a population of Misiones with a prevalence rate similar to those reported among blood donors from non-endemic areas.
  • [MeSH-major] Blood Donors / statistics & numerical data. HTLV-I Infections / epidemiology. HTLV-II Infections / epidemiology
  • [MeSH-minor] Adult. Argentina / epidemiology. Enzyme-Linked Immunosorbent Assay. Female. Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 2 / isolation & purification. Humans. Male. Seroepidemiologic Studies

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  • (PMID = 20228028.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Argentina
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99. Ashworth TD, Pear WS, Chiang MY, Blacklow SC, Mastio J, Xu L, Kelliher M, Kastner P, Chan S, Aster JC: Deletion-based mechanisms of Notch1 activation in T-ALL: key roles for RAG recombinase and a conserved internal translational start site in Notch1. Blood; 2010 Dec 16;116(25):5455-64
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  • Point mutations that trigger ligand-independent proteolysis of the Notch1 ectodomain occur frequently in human T-cell acute lymphoblastic leukemia (T-ALL) but are rare in murine T-ALL, suggesting that other mechanisms account for Notch1 activation in murine tumors.
  • Here we show that most murine T-ALLs harbor Notch1 deletions that fall into 2 types, both leading to ligand-independent Notch1 activation.
  • Type 1 deletions remove exon 1 and the proximal promoter, appear to be RAG-mediated, and are associated with mRNA transcripts that initiate from 3' regions of Notch1.
  • Type 2 deletions remove sequences between exon 1 and exons 26 to 28 of Notch1, appear to be RAG-independent, and are associated with transcripts in which exon 1 is spliced out of frame to 3' Notch1 exons.
  • Thus, like human T-ALL, murine T-ALL is often associated with acquired mutations that cause ligand-independent Notch1 activation.
  • [MeSH-major] Homeodomain Proteins / physiology. Peptide Chain Initiation, Translational / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology

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  • (PMID = 20852131.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Notch1 protein, mouse; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Zfpn1a1 protein, mouse; 128559-51-3 / RAG-1 protein; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC3031398
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100. Khosravi Shahi P, Díaz Muñoz de la Espada VM: [Extranodal T/NK-cell lymphoma, nasal type: a case report and review of the literature]. An Med Interna; 2005 Dec;22(12):597-600
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  • [Title] [Extranodal T/NK-cell lymphoma, nasal type: a case report and review of the literature].
  • [Transliterated title] Linfoma T/NK extraganglionar tipo nasal: caso clínico y revisión de la literatura.
  • Extranodal T/NK-cell lymphoma, nasal type: a case report and review of the literature.
  • Extranodal NK/T-cell lymphoma, nasal type, is an extranodal lymphoma, usually with an NK-cell phenotype and EBV positive, with a broad morphologic spectrum, frequent necrosis and angioinvasion, and most commonly presenting in the midfacial region, but also in other extranodal sites.
  • The diagnosis of the case was Extranodal T/NK-cell lymphoma, nasal type.
  • There was not disseminated disease in the extent studies.
  • With the diagnosis of localized extranodal T/NK-cell lymphoma and reactive thrombocytosis, the patient was treated with chemotherapy and sequential radiotherapy, followed by bone marrow transplantation.
  • [MeSH-major] Killer Cells, Natural. Lymphoma, T-Cell / pathology. Nose Neoplasms / pathology
  • [MeSH-minor] Adult. Humans. Immunophenotyping. Male

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  • (PMID = 16454602.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 16
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