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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • [MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

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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 / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; 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; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [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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2. 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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3. 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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4. 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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  • 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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5. 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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6. 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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  • 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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7. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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8. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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10. 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

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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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11. 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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12. 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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13. 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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14. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

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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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15. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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16. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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17. 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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18. 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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  • 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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19. 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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20. 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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21. 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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  • [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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22. 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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23. 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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24. 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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25. 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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26. 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
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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27. 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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28. 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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  • [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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29. 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
The Lens. Cited by Patents in .

  • [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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  • (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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30. 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 .

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  • [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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31. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [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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32. 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
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

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  • [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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33. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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34. 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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35. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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36. 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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  • [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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37. 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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38. 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] Japan
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39. 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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  • [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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40. 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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41. 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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42. Jeannet R, Mastio J, Macias-Garcia A, Oravecz A, Ashworth T, Geimer Le Lay AS, Jost B, Le Gras S, Ghysdael J, Gridley T, Honjo T, Radtke F, Aster JC, Chan S, Kastner P: Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient T-ALL. Blood; 2010 Dec 16;116(25):5443-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Notch pathway is frequently activated in T-cell acute lymphoblastic leukemias (T-ALLs).
  • Of the Notch receptors, Notch1 is a recurrent target of gain-of-function mutations and Notch3 is expressed in all T-ALLs, but it is currently unclear how these receptors contribute to T-cell transformation in vivo.
  • While deletion of Notch3 has little effect, T cell-specific deletion of floxed Notch1 promoter/exon 1 sequences significantly accelerates leukemogenesis.
  • Further, spontaneous deletion of 5' Notch1 sequences occurs in approximately 75% of Ikaros-deficient T-ALLs.
  • [MeSH-major] Ikaros Transcription Factor / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Transformation, Neoplastic. DNA Primers / chemistry. DNA Primers / genetics. Flow Cytometry. Gene Expression Regulation, Neoplastic. Immunoglobulin J Recombination Signal Sequence-Binding Protein / physiology. Mice. Mice, Knockout. Mutation / genetics. RNA, Messenger / genetics. Receptors, Notch / physiology. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Survival Rate

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  • (PMID = 20829372.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD034883
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / Notch1 protein, mouse; 0 / Notch3 protein, mouse; 0 / RNA, Messenger; 0 / Rbpj protein, mouse; 0 / Receptor, Notch1; 0 / Receptors, Notch; 0 / Zfpn1a1 protein, mouse; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC3100247
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43. 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] Japan
  • [Number-of-references] 39
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44. Rodig SJ, Payne EG, Degar BA, Rollins B, Feldman AL, Jaffe ES, Androkites A, Silverman LB, Longtine JA, Kutok JL, Fleming MD, Aster JC: Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1. Am J Hematol; 2008 Feb;83(2):116-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1.
  • Langerhans cell histiocytosis (LCH) and related entities are neoplasms of unknown pathogenesis.
  • Here, we describe studies assessing the role of NOTCH1 mutations in LCH, which were based on a case of fatal Langerhans cell tumor after T-cell acute lymphoblastic leukemia (T-ALL).
  • Although the two types of neoplasm in this patient were temporally and pathologically distinct, molecular analyses showed that they harbored the same T-cell receptor gene rearrangements and two activating NOTCH1 mutations involving exons 27 and 34.
  • Analysis of cDNA prepared from the aggressive Langerhans cell tumor showed that the NOTCH1 mutations were aligned in cis, a configuration that caused synergistic increases in NOTCH1 signal strength in reporter gene assays.
  • Immunohistochemistry confirmed that the Langerhans cell tumor also expressed NOTCH1 protein.
  • Although these data suggested that NOTCH1 mutations might contribute to the pathogenesis of typical sporadic LCH and related neoplasms occurring in the absence of T-ALL, an analysis of 24 cases of LCH and Rosai-Dorfman Disease occurring in patients without an antecedent history of T-ALL revealed no mutations.
  • Thus, activating NOTCH1 mutations appear to be unique to aggressive Langerhans cell tumors occurring after T-ALL.

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  • (PMID = 17874453.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI050225; United States / NCI NIH HHS / CA / CA082308; United States / NCI NIH HHS / CA / CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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45. Indraccolo S, Minuzzo S, Masiero M, Amadori A: Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)? Cell Cycle; 2010 Jan 1;9(1):80-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)?
  • The Notch pathway is an evolutionally conserved cell-cell interaction signalling system involved in several key aspects of cell life, ranging from differentiation and proliferation to apoptosis.
  • The clearest example of oncogenic Notch signalling is observed in T acute lymphoblastic leukemia (T-ALL), an aggressive neoplasm of immature T-cells, due to genetic alterations leading to ligand-independent increased Notch1 receptor signalling.
  • In solid tumors, however, extrinsic regulation through canonical cell-cell interactions appears to drive activation of the pathway.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Notch / metabolism
  • [MeSH-minor] Animals. Humans. Intracellular Signaling Peptides and Proteins. Leukemia / metabolism. Membrane Proteins / metabolism. Models, Biological. Neovascularization, Pathologic / metabolism. Signal Transduction / genetics. Signal Transduction / physiology

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  • (PMID = 20016278.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Receptors, Notch; 0 / delta protein
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46. 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
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  • [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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47. 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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48. 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
The Lens. Cited by Patents in .

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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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49. Yasunaga J, Matsuoka M: Human T-cell leukemia virus type I induces adult T-cell leukemia: from clinical aspects to molecular mechanisms. Cancer Control; 2007 Apr;14(2):133-40
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  • [Title] Human T-cell leukemia virus type I induces adult T-cell leukemia: from clinical aspects to molecular mechanisms.
  • BACKGROUND: Human T-cell leukemia virus type I (HTLV-I) is a causative virus of adult T-cell leukemia (ATL), HTLV-I-associated myelopathy/tropical spastic paraparesis, and HTLV-I-associated uveitis.
  • ATL is a neoplastic disease of CD4-positive T lymphocytes that is characterized by pleomorphic tumor cells with hypersegmented nuclei, termed "flower cells."
  • METHODS: The authors reviewed the virological, clinical, and immunological features of HTLV-I and ATL and summarized recent findings on the oncogenic mechanisms of ATL and therapeutic advances.
  • RESULTS: Multiple factors, such as viral genes, genetic and epigenetic alterations, and the host immune system, may be implicated in the leukemogenesis of ATL.
  • The prognosis of aggressive-type ATL remains poor, regardless of intensive chemotherapy.
  • Effectiveness of allogeneic stem cell transplantation for ATL has been recently reported.
  • CONCLUSIONS: Although the precise mechanism of leukemogenesis of ATL remains unclear, recent progress provides important clues in oncogenesis by HTLV-I.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Adult. Anti-Retroviral Agents / therapeutic use. Antibodies, Monoclonal / therapeutic use. Gene Expression Regulation, Viral. Genes, pX. Humans. NF-kappa B / antagonists & inhibitors. Viral Proteins / genetics

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  • (PMID = 17387298.001).
  • [ISSN] 1073-2748
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Retroviral Agents; 0 / Antibodies, Monoclonal; 0 / NF-kappa B; 0 / Viral Proteins
  • [Number-of-references] 79
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50. 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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  • [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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51. Pancewicz J, Taylor JM, Datta A, Baydoun HH, Waldmann TA, Hermine O, Nicot C: Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1-associated adult T-cell leukemia. Proc Natl Acad Sci U S A; 2010 Sep 21;107(38):16619-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1-associated adult T-cell leukemia.
  • Human T-cell leukemia virus type 1 (HTLV-I) is the etiological agent of adult T-cell leukemia (ATL).
  • The disease has a dismal prognosis and is invariably fatal.
  • In this study, we report a high frequency of constitutively activated Notch in ATL patients.
  • We found activating mutations in Notch in more than 30% of ATL patients.
  • These activating mutations are phenotypically different from those previously reported in T-ALL leukemias and may represent polymorphisms for activated Notch in human cancers.
  • Compared with the exclusive activating frameshift mutations in the proline, glutamic acid, serine, and threonine (PEST) domain in T-ALLs, those in ATLs have, in addition, single-substitution mutations in this domain leading to reduced CDC4/Fbw7-mediated degradation and stabilization of the intracellular cleaved form of Notch1 (ICN1).
  • Finally, we demonstrated that inhibition of Notch signaling by γ-secretase inhibitors reduced tumor cell proliferation and tumor formation in ATL-engrafted mice.
  • These data suggest that activated Notch may be important to ATL pathogenesis and reveal Notch1 as a target for therapeutic intervention in ATL patients.

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  • (PMID = 20823234.001).
  • [ISSN] 1091-6490
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106258; United States / NCI NIH HHS / CA / R01 CA115398; United States / NCI NIH HHS / CA / CA106258; United States / NCI NIH HHS / CA / CA115398
  • [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 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2944748
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52. Fujiwara H, Ozaki A, Yoshimitsu M, Hamada H, Masamoto I, Matsushita K, Yasukawa M, Tei C: Allogeneic stem cell transplantation for refractory adult T-cell leukemia using a non-T-cell-depleted HLA-incompatible family donor graft, with reference to the grown-up child donor to parent recipient setting: report of a pilot study. Int J Hematol; 2008 Apr;87(3):319-26
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  • [Title] Allogeneic stem cell transplantation for refractory adult T-cell leukemia using a non-T-cell-depleted HLA-incompatible family donor graft, with reference to the grown-up child donor to parent recipient setting: report of a pilot study.
  • To increase the availability of alternative stem-cell donors for patients with adult T-cell leukemia (ATL), we examined the feasibility of HLA-incompatible family transplantation, especially from a grown-up child (donor) to a parent (recipient).
  • Since January 2004, seven patients with advanced-phase ATL (three males and four females, median age 59 years), for whom a timely HLA-compatible donor was unavailable, were enrolled.
  • All patients received allografts from their HLA-incompatible sons with reduced-intensity conditioning stem cell transplantation (RIST).
  • Combined graft-versus-host disease (GVHD) prophylaxis involved cyclosporine A or tacrolimus, mycophenolate mofetil or corticosteroid, and short-term methotrexate.
  • Only one patient had grade-IV acute-GVHD, but this was resolved.
  • Four patients died, with causes of death being relapse (n = 2), transplantation-associated microangiopathy (n = 1), and septicemia (n = 1).
  • Three are currently alive: two are in complete remission and one has stable disease.
  • Despite a high rate of relapse, RIST using an allograft from an HLA-incompatible grown-up child donor may be feasible for patients with advanced-phase ATL, and may prolong survival.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, T-Cell / therapy. Lymphocyte Transfusion. Transplantation Conditioning

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  • (PMID = 18288565.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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53. Asnafi V, Buzyn A, Le Noir S, Baleydier F, Simon A, Beldjord K, Reman O, Witz F, Fagot T, Tavernier E, Turlure P, Leguay T, Huguet F, Vernant JP, Daniel F, Béné MC, Ifrah N, Thomas X, Dombret H, Macintyre E: NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study. Blood; 2009 Apr 23;113(17):3918-24
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  • [Title] NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study.
  • Many somatic genetic abnormalities have been identified in T-cell acute lymphoblastic leukemia (T-ALL) but each individual abnormality accounts for a small proportion of cases; therapeutic stratification consequently still relies on classical clinical markers.
  • We screened 141 adult diagnostic T-ALL samples from patients treated on either the Lymphoblastic Acute Leukemia in Adults (LALA)-94 (n = 87) or the GRAALL-2003 (n = 54) trials.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics
  • [MeSH-minor] Adult. Genotype. Humans. Mutation / genetics. Phenotype. Prognosis. Societies, Medical. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 19109228.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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54. Duc Dodon M, Mesnard JM, Barbeau B: [Adult T-cell leukemia induced by HTLV-1: before and after HBZ]. Med Sci (Paris); 2010 Apr;26(4):391-6
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  • [Title] [Adult T-cell leukemia induced by HTLV-1: before and after HBZ].
  • [Transliterated title] Leucémies T induites par HTLV-1 : y a-t-il un avant et un après HBZ ?
  • Adult T-cell leukemia (ATL) is an often fatal leukemia of CD4+ T lymphocytes associated with a complex retrovirus, human T-cell leukemia virus type 1 (HTLV-1).
  • In 2002, we described the characterization of a novel viral protein that we have termed HBZ for HTLV-1 bZIP factor.
  • This viral factor is encoded on the antisense strand of HTLV-1 proviral DNA, demonstrating the existence of antisense transcription from a promoter located in the 3' LTR.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / physiology. Cell Transformation, Viral / genetics. Gene Expression Regulation, Viral. Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / virology. Viral Proteins / physiology
  • [MeSH-minor] Activating Transcription Factors / metabolism. Animals. Cell Division. Cyclic AMP Response Element-Binding Protein / metabolism. Gene Products, tax / metabolism. Genes, pX. Humans. Leucine Zippers / genetics. Leucine Zippers / physiology. Models, Genetic. Promoter Regions, Genetic / genetics. Proviruses / genetics. RNA, Small Interfering / pharmacology. Rabbits. Terminal Repeat Sequences / genetics. Transcription, Genetic / drug effects. Transcription, Genetic / genetics. p300-CBP Transcription Factors / metabolism

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  • (PMID = 20412744.001).
  • [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 / Activating Transcription Factors; 0 / Basic-Leucine Zipper Transcription Factors; 0 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Small Interfering; 0 / Viral Proteins; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.3.1.48 / p300-CBP Transcription Factors
  • [Number-of-references] 31
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55. 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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56. Takizawa J, Aoki S, Kurasaki T, Higashimura M, Honma K, Kitajima T, Momoi A, Takahashi H, Nakamura N, Furukawa T, Aizawa Y: Successful treatment of adult T-cell leukemia with unrelated cord blood transplantation. Am J Hematol; 2007 Dec;82(12):1113-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of adult T-cell leukemia with unrelated cord blood transplantation.
  • This study reports the first well-documented case of adult T-cell leukemia (ATL) successfully treated with unrelated cord blood transplantation (UCBT).
  • A 49-year-old woman was diagnosed with acute-type of ATL.
  • Chemotherapy induced complete remission, but the human T-cell leukemia virus type 1 (HTLV-1) proviral load was detected in mononuclear cells of her peripheral blood.
  • She remains in remission 30 months after UCBT and the HTLV-1 proviral load has fallen to undetectable levels.
  • This result suggests that UCBT should be a therapeutic option for ATL patients who do not have suitable donors and those who urgently require treatment.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / methods. Leukemia-Lymphoma, Adult T-Cell / therapy

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  • (PMID = 17696205.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
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57. Kawahara M, Hori T, Matsubara Y, Okawa K, Uchiyama T: Cyclin-dependent kinaselike 5 is a novel target of immunotherapy in adult T-cell leukemia. J Immunother; 2007 Jul-Aug;30(5):499-505
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclin-dependent kinaselike 5 is a novel target of immunotherapy in adult T-cell leukemia.
  • In the present study, we attempted a comprehensive analysis of human leukocyte antigen (HLA) class I-bound peptides presented on adult T-cell leukemia (ATL) cells by the latest technology of mass spectrometry combined with reversed phase liquid chromatography (LC/MS) to identify novel tumor-associated antigens.
  • Then, we narrowed down the candidate peptides according to the differential expression of their source proteins between ATL cells and normal CD4 T cells.
  • Among these candidates, we focused on cyclin-dependent kinaselike 5 (CDKL5) because it was highly expressed in several ATL cell lines and some ATL clinical samples but not in normal CD4 T cells.
  • To examine its immunogenicity, we stimulated CD8 T cells from an HLA-B62 healthy donor several times with autologous monocyte-derived dendritic cells loaded with HLA-B*62-restricted CDKL5 peptide1012-1021 QVNQAALLTY that we identified.
  • CDKL5-stimulated bulk CD8 T cells exerted higher cytotoxicity against CDKL5 peptide-loaded autologous Epstein Barr virus-transformed B cell line (LCL) than against unloaded LCL.
  • Furthermore these T cells had strong cytotoxic activity against HLA-B*62-positive CDKL5-positive but not HLA-B*62-negative CDKL5-positive ATL cells.
  • These results demonstrate that CDKL5 is a novel tumor (leukemia) antigen in ATL and that the HLA-B*62-restricted CDKL5 peptide can be used for cytotoxic T-lymphocyte-mediated immunotherapy.
  • Identification of tumor-associated antigens by LC/MS is an eligible and efficient method suitable for future taylor-made immunotherapy of hematologic malignancies.
  • [MeSH-major] Antigens, Neoplasm / immunology. Histocompatibility Antigens Class I / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. Peptides / analysis. Protein-Serine-Threonine Kinases / immunology
  • [MeSH-minor] B-Lymphocytes. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / immunology. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Chromatography, Liquid. Cytotoxicity, Immunologic. Dendritic Cells / immunology. HLA-B Antigens / immunology. Herpesvirus 4, Human. Humans. Immunotherapy. Mass Spectrometry. Oligopeptides / immunology

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  • (PMID = 17589290.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HLA-B Antigens; 0 / Histocompatibility Antigens Class I; 0 / Oligopeptides; 0 / Peptides; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDKL5 protein, human
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58. 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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  • 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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59. Calzavara E, Chiaramonte R, Cesana D, Basile A, Sherbet GV, Comi P: Reciprocal regulation of Notch and PI3K/Akt signalling in T-ALL cells in vitro. J Cell Biochem; 2008 Apr 1;103(5):1405-12
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  • Our analyses indicate that the PI3K/Akt pathway is constitutively active in the four T-ALL cell lines tested.
  • PTEN expression was not detected in 3/4 cell lines tested, suggesting the loss of PTEN-mediated Akt activation.
  • We analysed the relationship between Notch-1 and the PI3K/Akt signalling and show that inhibition of the Akt pathway changes Notch expression; Notch-1 protein decreased in all the cell lines upon treatment with the inhibitor.
  • [MeSH-major] Phosphatidylinositol 3-Kinases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / metabolism. Signal Transduction
  • [MeSH-minor] Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Leukemic / drug effects. Humans. Jurkat Cells. PTEN Phosphohydrolase / metabolism. bcl-2-Associated X Protein / metabolism. ras Proteins / antagonists & inhibitors. ras Proteins / metabolism

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  • [Copyright] 2007 Wiley-Liss, Inc.
  • (PMID = 17849443.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / bcl-2-Associated X Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / ras Proteins
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60. Gu L, Zhou C, Liu H, Gao J, Li Q, Mu D, Ma Z: Rapamycin sensitizes T-ALL cells to dexamethasone-induced apoptosis. J Exp Clin Cancer Res; 2010;29:150
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Glucocorticoid (GC) resistance is frequently seen in acute lymphoblastic leukemia of T-cell lineage (T-ALL).
  • METHODS: Cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay.
  • Fluorescence-activated cell sorting (FACS) analysis was used to analyze apoptosis and cell cycles.
  • Western blot analysis was performed to test the expression of the downstream effector proteins of mammalian target of rapamycin (mTOR), the cell cycle regulatory proteins, and apoptosis associated proteins.
  • Cell cycle arrest was associated with modulation of G1-S phase regulators.
  • CONCLUSION: Our data suggests that rapamycin can effectively reverse GC resistance in T-ALL and this effect is achieved by inducing cell cycles arrested at G0/G1 phase and activating the intrinsic apoptotic program.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sirolimus / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Separation. Drug Synergism. Flow Cytometry. Humans

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  • (PMID = 21083937.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7S5I7G3JQL / Dexamethasone; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2998469
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61. Matsuoka M: Human T-cell leukemia virus type I (HTLV-I) infection and the onset of adult T-cell leukemia (ATL). Retrovirology; 2005;2:27

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-cell leukemia virus type I (HTLV-I) infection and the onset of adult T-cell leukemia (ATL).
  • The clinical entity of adult T-cell leukemia (ATL) was established around 1977, and human T-cell leukemia virus type 1 (HTLV-I) was subsequently identified in 1980.
  • In the 25 years since the discovery of HTLV-I, HTLV-I infection and its associated diseases have been extensively studied, and many of their aspects have been clarified.
  • However, the detailed mechanism of leukemogenesis remains unsolved yet, and the prognosis of ATL patients still poor because of its resistance to chemotherapy and immunodeficiency.
  • In this review, I highlight the recent progress and remaining enigmas in HTLV-I infection and its associated diseases, especially ATL.
  • [MeSH-major] Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell
  • [MeSH-minor] Adult. Female. Humans. Infant, Newborn. Virus Replication

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  • (PMID = 15854229.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 129
  • [Other-IDs] NLM/ PMC1131926
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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. Sulis ML, Williams O, Palomero T, Tosello V, Pallikuppam S, Real PJ, Barnes K, Zuurbier L, Meijerink JP, Ferrando AA: NOTCH1 extracellular juxtamembrane expansion mutations in T-ALL. Blood; 2008 Aug 1;112(3):733-40
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  • Heterodimerization domain (HD) mutations in NOTCH1 induce ligand-independent activation of the receptor and contribute to the pathogenesis of one-third of human T-cell lymphoblastic leukemias (T-ALLs).
  • Here we report a novel class of activating mutations in NOTCH1 leading to aberrant activation of NOTCH1 signaling in T-cell lymphoblasts.
  • Notably, structure-function analysis of leukemia-derived and synthetic JME mutants demonstrated that the aberrant activation of NOTCH1 signaling is dependent on the number of residues introduced in the extracellular juxtamembrane region of the receptor and not on the specific amino acid sequence of these insertions.

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  • (PMID = 18411416.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / CA120196; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [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 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2481531
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64. Kubuki Y, Suzuki M, Sasaki H, Toyama T, Yamashita K, Maeda K, Ido A, Matsuoka H, Okayama A, Nakanishi T, Tsubouchi H: Telomerase activity and telomere length as prognostic factors of adult T-cell leukemia. Leuk Lymphoma; 2005 Mar;46(3):393-9

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  • [Title] Telomerase activity and telomere length as prognostic factors of adult T-cell leukemia.
  • In this study, clinical data and disease outcomes were analyzed in conjunction with the telomerase activity (TA) and telomere length (TL) of peripheral blood mononuclear cells.
  • The study was carried out in 22 patients with adult T-cell leukemia (ATL) (7 chronic and 15 acute types) and in 13 asymptomatic human T-lymphotropic virus type 1 (HTLV-1) carriers.
  • The mean values of TA in acute and chronic type patients were 13.8 and 1.6 total product generated (TPG) units, respectively, as determined by telomeric repeat amplification assays.
  • The mean TA values in HTLV-1 carriers and healthy volunteers were 1.8 and 0.7 TPG, respectively.
  • The mean TA value in acute type patients was significantly higher than in the three other subject groups.
  • The mean TL values in patients with acute and chronic types were 5.39 and 4.38 Kb, respectively, while the mean TL values in HTLV-1 carriers and healthy volunteers were 7.69 and 7.06 Kb, respectively.
  • The mean TL values in all ATL patients and in non-ATL subjects were 5.2 and 7.3 Kb, respectively.
  • Neither TA nor TL of ATL cells showed any significant association with the number of ATL cells, serum soluble interleukin-2 receptor, or serum lactate dehydrogenase in the peripheral blood of acute type patients.
  • This suggests that the levels of TA and TL did not reflect the ATL tumor load.
  • The median survival period of acute ATL patients with high TA and shortened TL was 0.47 years, however, which was significantly shorter than that of acute ATL patients with low TA and normal TL (4.21 years) (p < 0.002).
  • These data suggest that high TA and shortened TL were associated with poorer prognosis, and that TA and TL may be novel markers for the prognosis of ATL patients.
  • [MeSH-major] HTLV-I Infections / enzymology. Leukemia-Lymphoma, Adult T-Cell / enzymology. Telomerase / metabolism. Telomere / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Leukocytes, Mononuclear / chemistry. Leukocytes, Mononuclear / enzymology. Male. Middle Aged. Prognosis. Prospective Studies. Restriction Mapping. Serologic Tests. Survival Analysis

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  • (PMID = 15621829.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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65. Xu SN, Chen JP: [Research advance on the pathogenesis of T-ALL induced by notch 1 activating mutations]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):242-5
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  • T-cell acute lymphoblastic leukemia (T-ALL) is the hematological malignancy of bone marrow characterized by the rapid proliferation and subsequent accumulation of immature T lymphocyte and mainly occurs in children and adolescents.
  • This review briefly discusses the four main subtypes of Notch 1 activating mutations, also focuses on how these mutations change the normal signaling pathways and genes expression during their participation in the pathogenesis of T-ALL, and how these insights will promote the development of newly targeting therapies for patients with this aggressive form of leukemia.

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  • (PMID = 20137156.001).
  • [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 / Receptor, Notch1
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66. Rüdiger T, Zettl A, Adam P, Bonzheim I, Geissinger E, Müller-Hermelink HK: [Peripheral NK/T-cell lymphoma]. Pathologe; 2007 Feb;28(1):55-8
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  • [Title] [Peripheral NK/T-cell lymphoma].
  • [Transliterated title] Periphere NK/T-Zell-Lymphome.
  • Peripheral T-cell lymphomas comprise 8% of the malignant lymphomas in Germany.
  • Such localizations are typical for the respective disease and form the basis for the classification of extranodal peripheral T-cell lymphoma.
  • Extranodal NK/T-cell lymphomas of the nasal type are characterized by an angiocentric growth pattern and large confluent areas of necrosis.
  • In addition, there is a clonal infection by Epstein-Barr virus in the T-lymphocytes.
  • In the differential diagnosis, B-cell lymphomas are more frequent at all localizations than T- or NK-cell lymphomas.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoma, T-Cell / pathology. T-Lymphocytes / immunology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunophenotyping. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / pathology

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  • (PMID = 17195040.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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67. Kozako T, Arima N, Toji S, Masamoto I, Akimoto M, Hamada H, Che XF, Fujiwara H, Matsushita K, Tokunaga M, Haraguchi K, Uozumi K, Suzuki S, Takezaki T, Sonoda S: Reduced frequency, diversity, and function of human T cell leukemia virus type 1-specific CD8+ T cell in adult T cell leukemia patients. J Immunol; 2006 Oct 15;177(8):5718-26
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  • [Title] Reduced frequency, diversity, and function of human T cell leukemia virus type 1-specific CD8+ T cell in adult T cell leukemia patients.
  • Human T cell lymphotropic virus type 1 (HTLV-1)-specific CTL are thought to be immune effectors that reduce the risk of adult T cell leukemia (ATL).
  • However, in vivo conditions of anti-HTLV-1 CTL before and after ATL development have yet to be determined.
  • To characterize anti-HTLV-1 CTL in asymptomatic HTLV-1 carriers (AC) and ATL patients, we analyzed the frequency and diversity of HTLV-1-specific CD8+ T cells in PBMC of 35 AC and 32 ATL patients using 16 distinct epitopes of HTLV-1 Tax or Env/HLA tetramers along with intracellular cytolytic effector molecules (IFN-gamma, perforin, and granzyme B).
  • Overall frequency of subjects possessing Tax-specific CD8+ T cells was significantly lower in ATL than AC (53 vs 90%; p = 0.001), whereas the difference in Env-specific CD8+ T cells was not statistically significant.
  • In contrast, ATL recognized only Tax11-19 with HLA-A*0201 and Tax301-309 with HLA-A*2402 at frequencies of 30 and 55%.
  • There were also significant differences in percentage of cells binding Tax11-19/HLA-A*0201 and Tax301-309/HLA-A*2402 tetramers between AC and ATL.
  • Anti-HTLV-1 Tax CD8+ T cells in AC and ATL produced IFN-gamma in response to Tax.
  • In contrast, perforin and granzyme B expression in anti-HTLV-1 CD8+ T cells of ATL was significant lower than that of AC.
  • These results suggest that decreased frequency, diversity, and function of anti-HTLV-1 Tax CD8+ T cell clones may be one of the risks of ATL development.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Cell Antigen Receptor Specificity
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Clone Cells. Female. Gene Products, tax / immunology. HLA Antigens / immunology. Humans. Interferon-gamma / biosynthesis. Male. Middle Aged. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 17015761.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / HLA Antigens; 82115-62-6 / Interferon-gamma
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68. Guo D, Ye J, Dai J, Li L, Chen F, Ma D, Ji C: Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines. Leuk Res; 2009 May;33(5):678-85
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  • [Title] Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines.
  • Gain-of-function mutations in Notch-1 are common in T-cell lymphoblastic leukemia (T-ALL), making this receptor a promising target for drugs such as gamma-secretase inhibitors (GSIs).
  • However, GSIs seem to be active in only a small fraction of T-ALL cell lines with constitutive Notch-1 activity and the downstream response of Notch signaling is only partially understood.
  • To further investigate the molecular mechanisms underlying proliferation suppression and apoptosis and explore effective downstream target genes, we used RNA interference (RNAi) technology to down-regulate the expression of Notch-1 in GSIs-resistant T-ALL cell lines.
  • Results showed that down-regulation of Notch-1 by transfection of a small interfering RNA (siRNA) could cause SupT1 cells proliferation inhibition by inducing G(0)/G(1) cell cycle arrest and apoptosis.
  • The proliferation inhibitory and apoptotic effects resulting from down-regulation of Notch-1 may be mediated through regulating the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 and the activity of Akt signaling.
  • Taken together, cell cycle regulatory proteins and Akt signaling may be attractive targets in T-ALL.
  • [MeSH-major] CDC2 Protein Kinase / genetics. Cyclin D1 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / physiology. Signal Transduction / physiology
  • [MeSH-minor] Apoptosis. Base Sequence. Cell Cycle. Cell Line, Tumor. Cell Proliferation. Down-Regulation / physiology. Humans. Mutation. RNA Interference. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19091404.001).
  • [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 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NOTCH1 protein, human; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.22 / CDC2 Protein Kinase
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69. Liu S, Breit S, Danckwardt S, Muckenthaler MU, Kulozik AE: Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines. Ann Hematol; 2009 Jul;88(7):613-21
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  • [Title] Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines.
  • Activation of Notch1 signaling plays an important role in the pathogenesis of precursor T-cell lymphoblastic leukemia (T-ALL).
  • In this study, we analyzed the response of four T-ALL cell lines to compound E, a potent gamma-secretase inhibitor, and to the combination of compound E with vincristine, daunorubicin, L-asparaginase (L-ASP), and dexamethasone (DEX).
  • We identified two distinct types of responses: In type 1 cell lines, represented by TALL1 and HSB2, GSI-induced apoptosis followed cell cycle arrest and enhanced the induction of apoptosis caused by DEX and L-ASP.
  • In type 2 cell lines, represented by CEM and Jurkat J6, GSI caused neither cell cycle block nor cell death.
  • In conclusion, the data presented here caution against clinical use of a combination treatment of GSI and chemotherapy in T-ALL.
  • [MeSH-major] Amyloid Precursor Protein Secretases / physiology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / antagonists & inhibitors
  • [MeSH-minor] Asparaginase / pharmacology. Benzodiazepinones / pharmacology. Cell Line, Tumor. Daunorubicin / pharmacology. Dexamethasone / pharmacology. Down-Regulation. Humans. Signal Transduction. Vincristine / pharmacology

  • Hazardous Substances Data Bank. DAUNORUBICIN .
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  • (PMID = 19057901.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Benzodiazepinones; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin
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70. Tomita M, Kawakami H, Uchihara JN, Okudaira T, Masuda M, Matsuda T, Tanaka Y, Ohshiro K, Mori N: Inhibition of constitutively active Jak-Stat pathway suppresses cell growth of human T-cell leukemia virus type 1-infected T-cell lines and primary adult T-cell leukemia cells. Retrovirology; 2006;3:22
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  • [Title] Inhibition of constitutively active Jak-Stat pathway suppresses cell growth of human T-cell leukemia virus type 1-infected T-cell lines and primary adult T-cell leukemia cells.
  • BACKGROUND: Human T-cell leukemia virus type 1 (HTLV-1), the etiologic agent for adult T-cell leukemia (ATL), induces cytokine-independent proliferation of T-cells, associated with the acquisition of constitutive activation of Janus kinases (Jak) and signal transducers and activators of transcription (Stat) proteins.
  • Our purposes in this study were to determine whether activation of Jak-Stat pathway is responsible for the proliferation and survival of ATL cells, and to explore mechanisms by which inhibition of Jak-Stat pathway kills ATL cells.
  • RESULTS: Constitutive activation of Stat3 and Stat5 was observed in HTLV-1-infected T-cell lines and primary ATL cells, but not in HTLV-1-negative T-cell lines.
  • AG490 inhibited the growth of HTLV-1-infected T-cell lines and primary ATL cells by inducing G1 cell-cycle arrest mediated by altering the expression of cyclin D2, Cdk4, p53, p21, Pim-1 and c-Myc, and by apoptosis mediated by the reduced expression of c-IAP2, XIAP, survivin and Bcl-2.
  • CONCLUSION: Our results indicate that activation of Jak-Stat pathway is responsible for the proliferation and survival of ATL cells.
  • Inhibition of this pathway may provide a new approach for the treatment of ATL.
  • [MeSH-major] Human T-lymphotropic virus 1 / genetics. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism. T-Lymphocytes / virology
  • [MeSH-minor] Base Sequence. Cell Line. Cell Line, Tumor. DNA Primers. Enzyme Inhibitors / pharmacology. Humans. Leukemia-Lymphoma, Adult T-Cell. Phosphorylation. Protein-Tyrosine Kinases / metabolism. STAT Transcription Factors / metabolism. Signal Transduction. Tyrphostins / pharmacology

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  • [RetractionIn] Tomita M, Kawakami H, Uchihara JN, Okudaira T, Masuda M, Matsuda T, Tanaka Y, Ohshiro K, Mori N. Retrovirology. 2011;8:1 [21210996.001]
  • (PMID = 16603085.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Enzyme Inhibitors; 0 / STAT Transcription Factors; 0 / STAT3 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ PMC1483830
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71. 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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72. Cullion K, Draheim KM, Hermance N, Tammam J, Sharma VM, Ware C, Nikov G, Krishnamoorthy V, Majumder PK, Kelliher MA: Targeting the Notch1 and mTOR pathways in a mouse T-ALL model. Blood; 2009 Jun 11;113(24):6172-81
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  • Mutations in NOTCH1 are frequently detected in patients with T-cell acute lymphoblastic leukemia (T-ALL) and in mouse T-ALL models.
  • Treatment of mouse or human T-ALL cell lines in vitro with gamma-secretase inhibitors (GSIs) results in growth arrest and/or apoptosis.
  • T-ALL cell lines also exhibit PI3K/mTOR pathway activation, indicating that rapamycin may also have therapeutic benefit.
  • Moreover, GSI and rapamycin treatment inhibits human T-ALL growth and extends survival in a mouse xenograft model.

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  • (PMID = 19246562.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA096899; United States / NIDDK NIH HHS / DK / P30DK32529
  • [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 / Carrier Proteins; 0 / Cyclic S-Oxides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / MRK 003; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Thiadiazoles; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2699237
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73. Masuda M, Maruyama T, Ohta T, Ito A, Hayashi T, Tsukasaki K, Kamihira S, Yamaoka S, Hoshino H, Yoshida T, Watanabe T, Stanbridge EJ, Murakami Y: CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells. J Biol Chem; 2010 May 14;285(20):15511-22
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  • [Title] CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells.
  • CADM1 encodes a multifunctional immunoglobulin-like cell adhesion molecule whose cytoplasmic domain contains a type II PSD95/Dlg/ZO-1 (PDZ)-binding motif (BM) for associating with other intracellular proteins.
  • Although CADM1 lacks expression in T lymphocytes of healthy individuals, it is overexpressed in adult T-cell leukemia-lymphoma (ATL) cells.
  • It has been suggested that the expression of CADM1 protein promotes infiltration of leukemic cells into various organs and tissues, which is one of the frequent clinical manifestations of ATL.
  • Amino acid sequence alignment revealed that Tiam1 (T-lymphoma invasion and metastasis 1), a Rac-specific guanine nucleotide exchange factor, has a type II PDZ domain similar to those of membrane-associated guanylate kinase homologs (MAGUKs) that are known to bind to the PDZ-BM of CADM1.
  • In this study, we demonstrated that the cytoplasmic domain of CADM1 directly interacted with the PDZ domain of Tiam1 and induced formation of lamellipodia through Rac activation in HTLV-I-transformed cell lines as well as ATL cell lines.
  • Our results indicate that Tiam1 integrates signals from CADM1 to regulate the actin cytoskeleton through Rac activation, which may lead to tissue infiltration of leukemic cells in ATL patients.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Human T-lymphotropic virus 1 / pathogenicity. Immunoglobulins / metabolism. Leukemia, T-Cell / pathology. Membrane Proteins / metabolism. Neoplasm Invasiveness. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Cell Adhesion Molecules. Cell Line, Tumor. Humans. Immunohistochemistry. Microscopy, Confocal. Molecular Sequence Data. Protein Binding. RNA Interference. RNA, Small Interfering. Sequence Homology, Amino Acid

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  • (PMID = 20215110.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Guanine Nucleotide Exchange Factors; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / TIAM1 protein, human; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2865322
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74. Castro-Costa CM, Araújo AQ, Menna-Barreto M, Penalva-de-Oliveira AC: [Guide of clinical management of HTLV patient: neurological aspects]. Arq Neuropsiquiatr; 2005 Jun;63(2B):548-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Guide of clinical management of HTLV patient: neurological aspects].
  • [Transliterated title] Guia de manejo clínico do paciente com HTLV: aspectos neurológicos.
  • The Brazilian Ministry of Health (STD and Aids Program) invited specialists to make up an informative guide to deal with HTLV patients.
  • Among the different topics, the neurological aspects associated to HTLV were contemplated.
  • [MeSH-minor] Brazil. Humans. Paraparesis, Tropical Spastic / diagnosis. Paraparesis, Tropical Spastic / therapy. Paraparesis, Tropical Spastic / virology

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  • (PMID = 16059617.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Practice Guideline
  • [Publication-country] Brazil
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75. 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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76. Frey O, Kamradt T: [Effector function plasticity of T helper lymphocytes]. Z Rheumatol; 2009 Dec;68(10):834-5
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  • However, a number of recent findings show a much higher degree of Th cell plasticity and interconvertibility than previously assumed.

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  • [Cites] Immunity. 2009 Jan 16;30(1):155-67 [19144320.001]
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  • (PMID = 19847446.001).
  • [ISSN] 1435-1250
  • [Journal-full-title] Zeitschrift fur Rheumatologie
  • [ISO-abbreviation] Z Rheumatol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-2; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; 207137-56-2 / Interleukin-4
  • [Number-of-references] 12
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77. Rajnics P, Krenács L, Kenéz A, Járay Z, Bagdi E, Demeter J: [Long-term survival after nasal NK/T cell lymphoma]. Orv Hetil; 2008 Apr 27;149(17):801-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Long-term survival after nasal NK/T cell lymphoma].
  • [Transliterated title] Nazális NK/T-sejtes lymphoma hosszú túlélése.
  • The nasal NK/T cell lymphoma is a rare, extranodal non-Hodgkin lymphoma in western civilizations, which has poor prognosis.
  • The Epstein-Barr virus can be detected in tumor cells in nearly all cases.
  • [MeSH-major] Killer Cells, Natural. Lymphoma, T-Cell, Peripheral / diagnosis. Lymphoma, T-Cell, Peripheral / therapy. Nose Neoplasms / diagnosis. Nose Neoplasms / therapy
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Female. Herpesvirus 4, Human / isolation & purification. Humans. Prednisone / therapeutic use. Tomography, X-Ray Computed. Vincristine / therapeutic use

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  • (PMID = 18426762.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  • [Number-of-references] 10
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78. Gieryńska M, Schollenberger A, Cespedes IS, Pawlak E: [Dendritic epidermal T cells: sentinels of the skin]. Postepy Hig Med Dosw (Online); 2009 Mar 23;63:114-22

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These cells are in intimate contact with neighboring cells and, through their unique antigen recognition, can immediately react to incoming signals and secrete a variety of cytokines, growth factors, and chemokines that have been implicated in tissue repair and cell survival, proliferation, migration, and recruitment.

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  • (PMID = 19373192.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Number-of-references] 65
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79. Arimura K, Arima N, Kukita T, Inoue H, Arai A, Matsushita K, Taguchi S, Yoshida H, Ozaki A, Kawada H, Akimoto M, Tei C: Fatal splenic rupture caused by infiltration of adult T cell leukemia cells. Acta Haematol; 2005;113(4):255-7
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  • [Title] Fatal splenic rupture caused by infiltration of adult T cell leukemia cells.
  • The present report describes a fatal case of splenic rupture caused by infiltration of adult T cell leukemia cells and reports the mechanism of splenic rupture.
  • The importance of rapid diagnosis and surgery is emphasized.
  • [MeSH-major] Leukemia, T-Cell / complications. Splenic Rupture / etiology
  • [MeSH-minor] Fatal Outcome. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Middle Aged

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel
  • (PMID = 15983432.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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80. Matsui H, Udaka F, Kubori T, Oda M, Nishinaka K, Oka N: HTLV-I-associated peripheral neuropathy with smoldering-type adult T-cell leukemia. Neurologist; 2006 Mar;12(2):109-13
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  • [Title] HTLV-I-associated peripheral neuropathy with smoldering-type adult T-cell leukemia.
  • BACKGROUND: Peripheral neuropathy with adult T-cell leukemia/lymphoma (ATLL) has seldom been reported.
  • REVIEW SUMMARY: A 69-year-old woman with smoldering-type ATLL presented with pain and muscle weakness of the bilateral upper and lower limbs and gait disturbance.
  • Anti-human T lymphotropic virus type I antibody was positive in the serum but negative in the cerebrospinal fluid.
  • CONCLUSIONS: This is the first reported case of ATLL and peripheral neuropathy in which a nerve biopsy was performed.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Peripheral Nervous System Diseases / pathology

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  • (PMID = 16534449.001).
  • [ISSN] 1074-7931
  • [Journal-full-title] The neurologist
  • [ISO-abbreviation] Neurologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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81. Li X, Gounari F, Protopopov A, Khazaie K, von Boehmer H: Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1. J Exp Med; 2008 Nov 24;205(12):2851-61
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  • Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed in human T cell acute lymphoblastic leukemia (T-ALL).
  • Early consequences are the generation of polyclonal nontumorigenic CD4(+)8(+) T cell receptor (TCR)-alphabeta(+) cells that do not qualify as tumor precursors despite the observation that they overexpress Notch 1 and c-Myc and degrade the tumor suppressor E2A by posttranslational modification.

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  • (PMID = 18981238.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE12948
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA109901; United States / NCI NIH HHS / CA / T32 CA070083; United States / NCI NIH HHS / CA / T32-CA70083; United States / NIAID NIH HHS / AI / R01 AI45846; 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 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2585834
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82. Kamihira S, Sugahara K, Tsuruda K, Minami S, Uemura A, Akamatsu N, Nagai H, Murata K, Hasegawa H, Hirakata Y, Takasaki Y, Tsukasaki K, Yamada Y: Proviral status of HTLV-1 integrated into the host genomic DNA of adult T-cell leukemia cells. Clin Lab Haematol; 2005 Aug;27(4):235-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proviral status of HTLV-1 integrated into the host genomic DNA of adult T-cell leukemia cells.
  • Human T-cell leukemia virus type-1 (HTLV-1) is the etiological agent of adult T-cell leukemia (ATL), and leukemic cells always carry the proviral genome monoclonally integrated into their host genomes at the same sequence site, designated as the monoclonal integration.
  • Using Southern blot hybridization (SBH) and sequenced tagged site polymerase chain reaction assays, we examined the proviral status in 558 clinical specimens from 350 patients who are suspected to have ATL.
  • A total of 321 specimens (57.5%) from 241 patients showed positive results for the monoclonal integration according to SBH, using EcoR1 and Pst1.
  • The incidence of the D- and M-types were in the order of smoldering, chronic, and acute subtypes of ATL, suggesting that such an aberrant proviral status is generated on the way to multistep carcinogenesis and is subsequently clinically important for the malignant behavior of the disease.
  • These results suggest that analysis of the proviral status provides useful diagnostic and virologic-oncological information about ATL and HTLV-1 pathology, especially the important role of pX gene in tumorigenesis.
  • [MeSH-major] DNA, Viral / genetics. Genes, Viral. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / virology. Proviruses / genetics
  • [MeSH-minor] Adult. Blotting, Southern. Cell Line, Tumor. Follow-Up Studies. Humans. In Situ Hybridization / methods. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity

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  • (PMID = 16048490.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral
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83. Nitta T, Kanai M, Sugihara E, Tanaka M, Sun B, Nagasawa T, Sonoda S, Saya H, Miwa M: Centrosome amplification in adult T-cell leukemia and human T-cell leukemia virus type 1 Tax-induced human T cells. Cancer Sci; 2006 Sep;97(9):836-41
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  • [Title] Centrosome amplification in adult T-cell leukemia and human T-cell leukemia virus type 1 Tax-induced human T cells.
  • Centrosomes play pivotal roles in cell polarity, regulation of the cell cycle and chromosomal segregation.
  • Centrosome amplification was recently described as a possible cause of aneuploidy in certain solid tumors and leukemias.
  • ATL is a T-cell malignancy caused by HTLV-1.
  • Although the precise mechanism of cell transformation is unclear, the HTLV-1-encoded protein, Tax, is thought to play a crucial role in leukemogenesis.
  • Here we demonstrate that lymphocytes isolated from patients with ATL show centrosome amplification and that a human T cell line shows centrosome amplification after induction of Tax, which was suppressed by CDK inhibitors.
  • Micronuclei formation was also observed after centrosome amplification in Tax-induced human T cells.
  • These findings suggest that Tax deregulates CDK activity and induces centrosome amplification, which might be associated with cellular transformation by HTLV-1 and chromosomal instability in HTLV-1-infected human T cells.
  • [MeSH-major] Cell Transformation, Viral / genetics. Centrosome / physiology. Gene Products, tax / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. T-Lymphocytes / virology

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  • (PMID = 16805820.001).
  • [ISSN] 1347-9032
  • [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 / Gene Products, tax
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84. de Bree GJ, van Leeuwen EM, ten Berge RJ: [Immunological defense to viral infections: focus on virus-specific T cells]. Ned Tijdschr Geneeskd; 2007 Nov 3;151(44):2440-4
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  • [Title] [Immunological defense to viral infections: focus on virus-specific T cells].
  • The T cell population consists ofa diversity ofvirus-specific memory T cells.
  • The characteristics of these T cells seem to depend largely on the type of virus for which they are specific.
  • T cells directed against latent viruses, such as cytomegalovirus, are cytotoxic cells.
  • T cells directed against viruses that after the initial infection are completely removed by the immune system, such as the influenza virus, are non-cytotoxic cells.
  • The development of new immunological techniques, such as the detection of virus-specific cells with HLA-peptide tetrameric complexes, enables the characterization of the properties of virus-specific T cells in the blood and organs.
  • [MeSH-major] Immunologic Memory. T-Lymphocytes / immunology. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / virology. Virus Diseases / immunology

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  • (PMID = 18064863.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 15
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85. Gordon WR, Roy M, Vardar-Ulu D, Garfinkel M, Mansour MR, Aster JC, Blacklow SC: Structure of the Notch1-negative regulatory region: implications for normal activation and pathogenic signaling in T-ALL. Blood; 2009 Apr 30;113(18):4381-90
The Lens. Cited by Patents in .

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  • The NRR includes the 3 Lin12/Notch repeats and the juxtamembrane heterodimerization domain, the region of Notch1 most frequently mutated in T-cell acute lymphoblastic leukemia lymphoma (T-ALL).
  • The majority of known T-ALL-associated point mutations map to residues in the hydrophobic interior of the Notch1 NRR.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / chemistry. Receptor, Notch1 / metabolism. Regulatory Sequences, Nucleic Acid. Signal Transduction

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  • (PMID = 19075186.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R56 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-030003; United States / NCI NIH HHS / CA / R01 CA092433-05S1; United States / NCI NIH HHS / CA / CA092433; United States / NCI NIH HHS / CA / R56 CA092433-06A1; United States / NCI NIH HHS / CA / R01 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-03; United States / NCI NIH HHS / CA / P01 CA119070-039001; United States / NCI NIH HHS / CA / P01 CA119070-029001; United States / NCI NIH HHS / CA / P01 CA119070-020003; United States / NCI NIH HHS / CA / R01 CA092433-05; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01 CA092433-04; United States / NCI NIH HHS / CA / P01 CA119070
  • [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 / NOTCH1 protein, human; 0 / NOTCH2 protein, human; 0 / Receptor, Notch1; 0 / Receptor, Notch2; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC2676092
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86. Ravandi F, Faderl S: Complete response in a patient with adult T-cell leukemia (ATL) treated with combination of alemtuzumab and pentostatin. Leuk Res; 2006 Jan;30(1):103-5
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  • [Title] Complete response in a patient with adult T-cell leukemia (ATL) treated with combination of alemtuzumab and pentostatin.
  • Treatment of adult T-cell leukemia (ATL) remains difficult.
  • However, the associated immunosuppression is a concern in patients with viral-mediated disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia-Lymphoma, Adult T-Cell / drug therapy

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  • (PMID = 15979704.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab
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87. Chen S, Ishii N, Ine S, Ikeda S, Fujimura T, Ndhlovu LC, Soroosh P, Tada K, Harigae H, Kameoka J, Kasai N, Sasaki T, Sugamura K: Regulatory T cell-like activity of Foxp3+ adult T cell leukemia cells. Int Immunol; 2006 Feb;18(2):269-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulatory T cell-like activity of Foxp3+ adult T cell leukemia cells.
  • Adult T cell leukemia (ATL) is an aggressive neoplastic disease, in which a quarter of the patients develop opportunistic infections due to cellular immunodeficiency.
  • Recent studies have demonstrated that the leukemia cells from a subset of patients with ATL express Foxp3, a specific marker for CD25+CD4+ regulatory T (Treg) cells, which regulate the immune response by suppressing CD4+ T cell functions.
  • However, whether there is a functional resemblance between ATL cells that have Foxp3 expression and Treg cells is still unknown.
  • In this report, we confirmed the high expression of Foxp3 in leukemia cells from 5 of 12 ATL patients and demonstrated that ATL cells from 3 patients suppressed the proliferation of CD4+ T cells.
  • Similarly, one of six HTLV-I-infected cell lines showed both high Foxp3 expression and suppressive activity.
  • Like Treg cells, the suppression induced by the ATL cells from two patients and the HTLV-infected cell line appeared to be mediated by a cell-cell contact-dependent mechanism.
  • Nevertheless, among the ATL cells that strongly expressed Foxp3, those from two of the five patients showed no apparent suppressive activity.
  • Furthermore, retroviral transfection of Foxp3 did not confer any suppressive function on low Foxp3-expressing HTLV-I-infected cell lines.
  • These results indicate that Foxp3 may be essential but is not sufficient for the Treg-cell-like suppressive activity of ATL cells and HTLV-I-infected cell lines.
  • [MeSH-major] Forkhead Transcription Factors / metabolism. Leukemia, T-Cell / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Female. Gene Products, tax / biosynthesis. Human T-lymphotropic virus 1 / immunology. Humans. Immunocompromised Host. Lymphocyte Activation. Male. Middle Aged. Phenotype

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  • (PMID = 16361311.001).
  • [ISSN] 0953-8178
  • [Journal-full-title] International immunology
  • [ISO-abbreviation] Int. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Gene Products, tax
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88. 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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  • [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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89. 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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90. Yoshie O: Expression of CCR4 in adult T-cell leukemia. Leuk Lymphoma; 2005 Feb;46(2):185-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of CCR4 in adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a malignancy of mature T cells that is etiologically associated with human T-cell leukemia virus type 1 (HTLV-1).
  • The frequent manifestation of ATL is infiltration of leukemic cells into various organs.
  • Besides certain cell adhesion molecules and matrix metalloproteineses, chemokine receptors may play important roles in tissue infiltration of ATL.
  • Identification of a unique set of chemokine receptors expressed by ATL would thus provide valuable information about the molecular mechanism of tissue infiltration of ATL.
  • This may also reveal that ATL frequently develops from a certain subset of T cells that express a particular set of chemokine receptors.
  • Since HTLV-1 encodes a potent viral transcriptional activator Tax, which is known to induce various cellular genes, expression of some chemokine receptors may be affected by Tax.
  • This, however, may relate more to HTLV-1-infected T cells, since ATL cells usually do not express Tax.
  • Finally, identification of a unique set of chemokine receptors expressed by ATL may also provide a new therapeutic target.
  • These considerations prompted us to examine the chemokine receptor expression in ATL.
  • We found that in the majority of ATL cases, leukemic cells consistently express CCR4.
  • Since CCR4 is known to be involved in T cell migration into skin, this may in part explain the frequent skin infiltration in ATL.
  • Thus, the majority of ATL may predominantly originate from either Th2 or regulatory T cells.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Receptors, Chemokine / analysis

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  • (PMID = 15621800.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / Receptors, Chemokine
  • [Number-of-references] 44
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91. Ishida Y, Yamashita K, Sasaki H, Takajou I, Kubuki Y, Morishita K, Tsubouchi H, Okayama A: Activation of complement system in adult T-cell leukemia (ATL) occurs mainly through lectin pathway: a serum proteomic approach using mass spectrometry. Cancer Lett; 2008 Nov 18;271(1):167-77
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  • [Title] Activation of complement system in adult T-cell leukemia (ATL) occurs mainly through lectin pathway: a serum proteomic approach using mass spectrometry.
  • Adult T-cell leukemia (ATL) is a fatal malignancy caused by infection with human T lymphotropic virus type-1 (HTLV-1).
  • To search for a new biomarker of ATL, we analyzed sera from ATL patients using ProteinChip arrays.
  • The spectral comparison of ATL patients with HTLV-1 carriers and healthy volunteers showed that the intensities of five peaks (1779, 1866, 2022, 4467, and 8930 m/z) were significantly increased in ATL, while those of four peaks (4067, 4151, 8130, and 8597 m/z) were decreased.
  • From these differentially expressed peaks, we chose peaks of 1779, 1866, and 2022 m/z as biomarker candidates of ATL.
  • MS/MS ion search using tandem mass spectrometry and immunoprecipitation assay using anti-C3 antibody showed that factors derived from these candidate peaks were identified as C3f, which is a component of the complement system and a fragment of complement C3.
  • These results indicate that the complement system was activated in ATL.
  • Further analysis of markers specific to the activation pathways (classical, alternative, and lectin pathways) in the complement system showed that the serum concentration of the marker of the lectin pathway was significantly higher in ATL patients.
  • These results suggest that activation of the complement system in ATL occurs mainly through the lectin pathway.
  • [MeSH-major] Complement Activation. Lectins / metabolism. Leukemia, T-Cell / metabolism. Proteomics. Tandem Mass Spectrometry / methods
  • [MeSH-minor] Adult. Case-Control Studies. Gene Expression Profiling. Humans. Immunoprecipitation. Neoplasm Proteins / blood. Neoplasm Proteins / genetics

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  • (PMID = 18691810.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Lectins; 0 / Neoplasm Proteins
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92. Ryba M, Myśliwska J: [CD4+CD25+Foxp3+ T lymphocytes: naturally occuring regulatory T cells]. Pediatr Endocrinol Diabetes Metab; 2010;16(4):289-94

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  • [Title] [CD4+CD25+Foxp3+ T lymphocytes: naturally occuring regulatory T cells].
  • [Transliterated title] Limfocyty T CD4+CD25+Foxp3+: naturalnie występujące limfocyty T regulatorowe.
  • The mechanism that plays an essential role in immunosuppression and regulation is the presence of naturally occurring regulatory T cells (Tregs), which comprise 5-10% of peripheral CD4+ lymphocytes.
  • They are characterized by the constant and high expression of the α subunit of IL-2 receptor (CD25), which makes them different from conventional, CD4+ and CD8+ lymphocytes, which express this molecule at lower level only during the activation state.
  • The function of regulatory T cells is to inhibit proliferation as well as cytokine production by effector CD4+CD25- lymphocytes.
  • They are also able to suppress CD8+ T cells, monocytes, NK cells, dendritic cells and B cells.
  • The transcription factor Foxp3 is the key regulatory gene for the development and function of regulatory T lymphocytes.
  • Its expression is limited to CD4+CD25high T cells at both mRNA and protein levels.
  • Foxp3 is a specific indicator of suppressive activity of Tregs and it acts as repressor as well as activator of transcription.
  • [MeSH-major] Forkhead Transcription Factors / metabolism. Interleukin-2 Receptor alpha Subunit / metabolism. T-Lymphocytes, Regulatory / immunology. Transcription, Genetic / genetics
  • [MeSH-minor] Animals. Humans

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  • (PMID = 21447271.001).
  • [ISSN] 2081-237X
  • [Journal-full-title] Pediatric endocrinology, diabetes, and metabolism
  • [ISO-abbreviation] Pediatr Endocrinol Diabetes Metab
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit
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93. Fassbender M, Rothenbacher G, Weschler C, Müller CA, Pfister U: [Minimally invasive T-plating at the proximal humerus]. Z Orthop Unfall; 2008 May-Jun;146(3):318-24
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  • According to the general surgical trend to minimally invasive techniques, the object of this study was to conduct follow-up examinations of the technique of minimally invasive T-plating at the proximal humerus developed at our hospital and to compare the results with those of other osteosynthetic techniques, especially concerning the complications of the surgical approach and the clinical outcome.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Equipment Failure. Female. Follow-Up Studies. Humans. Male. Middle Aged. Osteonecrosis / etiology. Osteonecrosis / radiography. Patient Satisfaction. Range of Motion, Articular / physiology. Retrospective Studies

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  • (PMID = 18561076.001).
  • [ISSN] 1864-6697
  • [Journal-full-title] Zeitschrift für Orthopädie und Unfallchirurgie
  • [ISO-abbreviation] Z Orthop Unfall
  • [Language] ger
  • [Publication-type] Case Reports; Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
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94. Persiani R, D'Ugo D, Biondi A, Rausei S, Vigorita V, Zoccali M, Picciocchi A: [T-downstaging after neoadjuvant chemotherapy in locally advanced gastric carcinoma]. Suppl Tumori; 2005 May-Jun;4(3):S88
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  • Aim of this study is to evaluate the clinical significance and the possible impact on survival of tumor downstaging after neoadjuvant chemotherapy followed by D2-gastrectomy in an accurately staged and thoroughly selected group of 30 locally advanced gastric cancer patients, with a complete follow-up of at least 3 years.
  • In our series, T-downstaging was observed in 43.3% of patients; this parameter, along with other known prognostic factors, was found to be significantly associated with survival (p <0.05).
  • Moreover, T-downstaging induced by preoperative chemotherapy was significantly associated with absence of residual tumor (R0) and no lymph node metastases (ypN0) (p <0.05).

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  • (PMID = 16437922.001).
  • [ISSN] 2283-5423
  • [Journal-full-title] I supplementi di Tumori : official journal of Società italiana di cancerologia ... [et al.]
  • [ISO-abbreviation] Suppl Tumori
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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95. Kchour G, Tarhini M, Sharifi N, Farid R, Khooei AR, Shirdel A, Afshari JT, Sadeghian A, Otrock Z, Hermine O, El-Sabban M, Bazarbachi A: Increased microvessel density in involved organs from patients with HTLV-I associated adult T cell leukemia lymphoma. Leuk Lymphoma; 2008 Feb;49(2):265-70

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  • [Title] Increased microvessel density in involved organs from patients with HTLV-I associated adult T cell leukemia lymphoma.
  • Adult T-cell leukemia-lymphoma (ATLL) is a rapidly progressive lymphoproliferative disorder secondary to infection with the human T cell lymphotropic virus type I (HTLV-I).
  • We have previously shown that ATLL derived cells secrete high levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (b-FGF), induce endothelial tube formation in vitro and establish functional gap junction-mediated communication with endothelial cells.
  • We also demonstrated that plasma from ATLL and tropical spastic paraparesis/HTLV-I associated myelopathy patients exhibit very high levels of VEGF and b-FGF.
  • Recently, we showed that treatment with the combination of zidovudine and interferon alpha reduced both HTLV-I proviral load and importantly VEGF plasma levels suggesting a potential anti-angiogenic effect of this therapy.
  • In this report, we evaluated microvessel density (MVD) in involved organs from 20 patients with ATLL, as compared to normal organs from matched controls.
  • We show evidence of significantly increased MVD in all tested involved organs from ATLL patients, suggesting that angiogenesis plays an important role in the development or organ invasion of ATLL, and could represent a potentially interesting target for anti-angiogenic therapy of ATLL.
  • [MeSH-major] Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell / etiology. Leukemia-Lymphoma, Adult T-Cell / pathology. Neovascularization, Pathologic
  • [MeSH-minor] Adult. Aged. Bone Marrow / blood supply. Capillaries. Case-Control Studies. Female. Humans. Immunohistochemistry. Lymph Nodes / blood supply. Male. Middle Aged. Skin / blood supply. Testis / blood supply

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  • (PMID = 18231912.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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96. Kuk S: [CD8+ and CD4+ T lymphocyte responses against malaria]. Mikrobiyol Bul; 2007 Apr;41(2):329-39
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  • Host response against malaria is multifactorial, including complicated mechanisms of humoral and cell-mediated immunity.
  • Hence, many vaccine strategies are focused on CD8+ T cell response.
  • The development and maintenance of memory CD8+ T cell response are closely related to the CD4+ T cells together with interleukin (IL)-4, IL-7, IL-15 and IL-2.
  • CD4+ T cells also play a triple role in the immune response to malaria parasites; by activating B cells to produce high level of antimalarial antibodies, by enhancing the induction of CD8+ T cell responses, and by inhibiting the development of liver stage parasites.
  • Although it has been known much about CD8+ T and CD4+ T cell responses, cross-talking mechanisms of these cells, and other factors which contribute to this response during malaria so far, many questions also need to be answered in the future.
  • In this review article, CD8+ T and CD4+ T cell responses to malaria infection have been discussed in the light of current literature.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Malaria / immunology. Plasmodium / immunology

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  • (PMID = 17682721.001).
  • [ISSN] 0374-9096
  • [Journal-full-title] Mikrobiyoloji bülteni
  • [ISO-abbreviation] Mikrobiyol Bul
  • [Language] tur
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Malaria Vaccines
  • [Number-of-references] 35
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97. Callens C, Moura IC, Lepelletier Y, Coulon S, Renand A, Dussiot M, Ghez D, Benhamou M, Monteiro RC, Bazarbachi A, Hermine O: Recent advances in adult T-cell leukemia therapy: focus on a new anti-transferrin receptor monoclonal antibody. Leukemia; 2008 Jan;22(1):42-8
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  • [Title] Recent advances in adult T-cell leukemia therapy: focus on a new anti-transferrin receptor monoclonal antibody.
  • HTLV-I is an endemic retrovirus responsible for the adult T-cell leukemia/lymphoma (ATLL).
  • This aggressive lymphoid proliferation is associated with a bad prognosis due to the resistance of HTLV-I-infected cells to most classical chemotherapeutic agents.
  • Here we review recent advances in ATLL immunotherapy.
  • We particularly focus on promising data from our group, characterizing a new mouse monoclonal antibody (mAb A24) against the human transferrin receptor (TfR-1).
  • Monoclonal antibodies to target cell differentiation markers on ATLL cells have already been proposed as therapeutic agents.
  • However, in clinical trials acute forms of ATLL were resistant to these immunotherapies.
  • It blocks the proliferation of malignant cells (TfR-1(high)), such as HTLV-I-infected T cells but not of resting cells.
  • In HTLV-I-infected cells, A24 targets and induces apoptosis of both chronic and acute ATLL forms, independent of antibody aggregation, antibody-dependent cellular cytotoxicity and/or complement addition.
  • We are currently developing strategies to use A24 in clinical trials.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, T-Cell / therapy. Receptors, Transferrin / immunology
  • [MeSH-minor] Adult. Humans. Immunotherapy. T-Lymphocytes / immunology

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  • (PMID = 17898788.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Receptors, Transferrin
  • [Number-of-references] 53
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98. Miyara M, Amoura Z, Piette JC, Gorochov G: [Systemic lupus erythematosus and regulatory T cells]. Rev Med Interne; 2008 Sep;29(9):691-5
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  • [Transliterated title] Cellules T régulatrices et lupus érythémateux systémique.
  • A global depletion of FoxP3+ CD25(bright) CD4+ regulatory T cell is observed during lupus flares.

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  • (PMID = 18538896.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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99. Dewan MZ, Takamatsu N, Hidaka T, Hatakeyama K, Nakahata S, Fujisawa J, Katano H, Yamamoto N, Morishita K: Critical role for TSLC1 expression in the growth and organ infiltration of adult T-cell leukemia cells in vivo. J Virol; 2008 Dec;82(23):11958-63
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  • [Title] Critical role for TSLC1 expression in the growth and organ infiltration of adult T-cell leukemia cells in vivo.
  • Adult T-cell leukemia (ATL) is associated with human T-cell leukemia virus type 1 infection.
  • The tumor suppressor lung cancer 1 (TSLC1) gene was previously identified as a novel cell surface marker for ATL, and this study demonstrated the involvement of TSLC1 expression in tumor growth and organ infiltration of ATL cells.
  • In experiments using NOD/SCID/gamma c(null) mice, both leukemia cell lines and primary ATL cells with high TSLC1 expression caused more tumor formation and aggressive infiltration of various organs of mice.
  • Our results suggest that TSLC1 expression in ATL cells plays an important role in the growth and organ infiltration of ATL cells.
  • [MeSH-major] Immunoglobulins / physiology. Leukemia-Lymphoma, Adult T-Cell / pathology. Membrane Proteins / physiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Adult. Aged. Animals. Cell Adhesion Molecules. Female. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Inbred NOD. Mice, SCID. Middle Aged

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  • (PMID = 18922876.001).
  • [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 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / Tumor Suppressor Proteins; 0 / cell adhesion molecule 1, mouse
  • [Other-IDs] NLM/ PMC2583669
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100. Kiniş V, Naiboğlu B, Habeşoğlu TE, Toros SZ, Eriman M, Habeşoğlu M, Egeli E: [Efficacy of clinical examination and computed tomography at T-staging of laryngeal carcinoma]. Kulak Burun Bogaz Ihtis Derg; 2010 Jan-Feb;20(1):1-6
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  • [Title] [Efficacy of clinical examination and computed tomography at T-staging of laryngeal carcinoma].
  • T-staging of the tumors were separately determined according to their clinical examination, computed tomography (CT) findings, and their correlation between these methods.
  • The rates of accuracy in determining histopathologic T-stage of tumors were 40% by clinical examination; 66% by CT; and 76% when both methods were used together.
  • Among the patients whose tumors had been staged inaccurately by clinical examination, 71% were underestimated while 29% were overestimated.