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The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.

This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.

In addition, we identified deletions and associated mutations in the WT1 tumor suppressor gene in 2 of 9 samples.

Subsequent analysis showed WT1 mutations in 28 of 211 (13.2%) of pediatric and 10 of 85 (11.7%) of adult T-ALL cases.

Survival analysis demonstrated that WT1 mutations do not confer adverse prognosis in pediatric and adult T-ALL.

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(PMID = 19494353.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Databank-accession-numbers] GEO/ GSE15931

[Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / MC/ U137686861; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins

[Other-IDs] NLM/ PMC2721784

   

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

[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

   

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

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

Recent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1.

We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1.

Cell lines derived from these tumors undergo G(0)/G(1) arrest and apoptosis when treated with a gamma-secretase inhibitor.

In addition, we found activating Notch1 mutations in 31% of thymic lymphomas that occur in mice deficient for various combinations of the H2AX, Tp53, and Rag2 genes.

Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations.

[MeSH-major] Disease Models, Animal. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma / genetics. Mutation / genetics. Receptor, Notch1 / genetics. Thymus Neoplasms / genetics

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(PMID = 16166587.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA096899

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / H2AX protein, mouse; 0 / Histones; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse

[Other-IDs] NLM/ PMC1895623

   

[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

Hazardous Substances Data Bank. (L)-Methionine .

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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

   

[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

   

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

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.

Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del(19)(p13.2).

From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases.

[MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion

[MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

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(PMID = 18185524.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

[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

   

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

[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

   

[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

MedlinePlus Health Information. consumer health - Blood Transfusion and Donation.

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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

   

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

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL.

Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease.

In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Proteins / physiology. Receptors, Notch / physiology. T-Lymphocytes / pathology

[MeSH-minor] Animals. Apoptosis / physiology. Cell Cycle / physiology. F-Box Proteins / physiology. Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. Humans. Ikaros Transcription Factor / genetics. Ikaros Transcription Factor / physiology. Ligands. Mice. Mice, Transgenic. Oncogenes. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / physiology. Signal Transduction / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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(PMID = 18758476.001).

[ISSN] 1476-5594

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Grant] United States / NCI NIH HHS / CA / T32 CA09171

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] England

[Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / IKZF1 protein, human; 0 / Ligands; 0 / Neoplasm Proteins; 0 / Receptors, Notch; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 148971-36-2 / Ikaros Transcription Factor; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / Ubiquitin-Protein Ligases

[Number-of-references] 84

   

[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

   

[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

   

[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

   

[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

   

[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

   

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

[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

   

[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

   

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

Adult patients with acute lymphoblastic T cell leukemia (T-ALL) have a very poor prognosis and few effective therapeutic options.

In addition, treatment of malignant T-cell lines with peg-Arg I significantly impaired their proliferation, which correlated with a decreased progression into the cell cycle, followed by the induction of apoptosis.

The results suggest the potential benefit of L-Arginine depletion by peg-Arg I in the treatment of T-cell malignancies.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. CYTARABINE .

Hazardous Substances Data Bank. (L)-ARGININE .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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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

   

[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

   

[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

   

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

[Title] NUP214-ABL1 in adult T-ALL: the GMALL study group experience.

The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.

We investigated 279 adult patients with T-ALL treated within the framework of the GMALL 5/93 and 6/99 therapy trials for NUP214-ABL1 by using a novel multiplex real-time, quantitative polymerase chain reaction (PCR).

Eleven (3.9%) patients were NUP214-ABL1 positive, and 5 different transcripts were observed; 8 patients had a thymic immunophenotype, 1 had an early T-cell immunophenotype, and 2 had a mature T-cell immunophenotype.

NUP214-ABL1-positive and -negative patients did not differ significantly in their major clinical features.

In contrast to previous reports suggesting an adverse clinical course for NUP214-ABL1-positive patients, no significant difference in overall survival was observed.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-abl / genetics

[MeSH-minor] Adolescent. Adult. Benzamides. Female. Humans. Imatinib Mesylate. Immunophenotyping. Male. Piperazines / therapeutic use. Polymerase Chain Reaction. Prognosis. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. RNA, Messenger / analysis. Survival Rate

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(PMID = 16873673.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Benzamides; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl

   

[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

   

[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

   

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

[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

   

[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

   

[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

   

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

[Title] [Gastric adult T cell leukemia/lymphoma: report of four cases and review of literature].

[Transliterated title] Leucemia/linfoma T del adulto gástrico: reporte de cuatro casos y revisión de la literatura.

Adult T-cell leukemia/lymphoma (ATLL) is an aggressive disease associated with human T-cell lymphotropic virus type-I (HTLV-I) with heterogeneous clinical presentation and outcomes.

We describe clinical and endoscopic findings of cases and review literature.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell. Stomach Neoplasms

[MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Fatal Outcome. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Prednisone / administration & dosage. Prevalence. Stomach Ulcer / etiology. Vincristine / administration & dosage

Genetic Alliance. consumer health - Gastric Lymphoma.

MedlinePlus Health Information. consumer health - Stomach Cancer.

Hazardous Substances Data Bank. DOXORUBICIN .

Hazardous Substances Data Bank. ETOPOSIDE .

Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

Hazardous Substances Data Bank. PREDNISOLONE .

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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

   

[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

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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[ErratumIn] Proc Natl Acad Sci U S A. 2006 Jun 6;103(23):8906

(PMID = 16407133.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] eng

[Databank-accession-numbers] GENBANK/ DQ273132

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Messenger; 0 / Viral Proteins

[Other-IDs] NLM/ PMC1334651

   

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

[Title] Dichotomy of all-trans retinoic acid inducing signals for adult T-cell leukemia.

We previously reported that all-trans retinoic acid (ATRA) inhibits growth in human T-cell leukemia virus type 1 (HTLV-1)-positive T-cell lines and fresh cells from patients with adult T-cell leukemia.

In the present study, we observed that NF-kappaB transcriptional activity as well as cell growth decreased significantly in HTLV-1-positive T-cell lines in the presence of ATRA.

Furthermore, we observed that ATRA reduced HTLV-1 proviral DNA, HTLV-1 genes (gag, tax, or pol mRNA) using the real-time quantitative polymerase chain reaction.

SIL-2R was reduced by ATRA in both protein level (culture supernantant) and mRNA level in HTLV-1-positive T-cell lines.

Interestingly, ATRA significantly inhibited RT activity similar to azidothimidine (AZT) in HTLV-1-positive T-cell lines.

Moreover, AZT inhibited proviral DNA but not NF-kappaB transcriptional activity, and sIL-2R on HTLV-1; however, ATRA inhibited of NF-kappaB, proviral DNA and sIL-2R on HTLV-1.

[MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, T-Cell / drug therapy. Leukemia, T-Cell / metabolism. Signal Transduction / drug effects. Tretinoin / pharmacology

[MeSH-minor] Adult. Cell Division / drug effects. Deltaretrovirus Infections / drug therapy. Deltaretrovirus Infections / metabolism. Deltaretrovirus Infections / physiopathology. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Viral / drug effects. Gene Products, gag / genetics. Gene Products, pol / genetics. Genes, pX / genetics. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / growth & development. Humans. In Vitro Techniques. Jurkat Cells. NF-kappa B / metabolism. Proviruses / genetics. Receptors, Interleukin-2 / metabolism. Solubility. Transcriptional Activation / drug effects. Viral Load

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(PMID = 15843825.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Gene Products, gag; 0 / Gene Products, pol; 0 / NF-kappa B; 0 / Receptors, Interleukin-2; 5688UTC01R / Tretinoin

   

[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

MedlinePlus Health Information. consumer health - Blood Transfusion and Donation.

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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

   

[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

   

[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

   

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

[Title] Clinical efficacy of all-trans retinoic acid for treating adult T cell leukemia.

PURPOSE: We previously reported that all-trans retinoic acid (ATRA) inhibited growth in human T-cell leukemia virus type I (HTLV-I)-positive T-cell lines and in fresh cells from patients with adult T cell leukemia (ATL).

Here, we confirmed the clinical effects of ATRA in 20 patients with ATL.

MATERIALS AND METHODS: The 20 patients (n = 20) with a median age of 56 (range 35-73) years who were diagnosed with ATL received ATRA orally.

RESULTS: The efficacy of treatment was as follows: no complete response (CR), a partial response (PR) in 40% of the patients, no change (NC) in 45% of the patients, and a progressive disease (PD) in 15% of the patients.

In seven acute-type ATL patients, a PR was achieved in two (28.5%), NC was observed in two (28.5%), and a PD was observed in three (42.8%).

In three lymphoma-type ATL patients, a PR (100%) was achieved.

Among four chronic-type ATL patients, a PR was achieved in one (25%) and NC was observed in the remaining three (75%).

In six smoldering-type ATL patients, a PR was achieved in two (33.3%) and NC was observed in four (66.6%).

CONCLUSION: These results indicated that ATRA might be a useful agent for the safe treatment of ATL.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Tretinoin / therapeutic use

[MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged

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(PMID = 18008086.001).

[ISSN] 0171-5216

[Journal-full-title] Journal of cancer research and clinical oncology

[ISO-abbreviation] J. Cancer Res. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin

   

[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

   

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

[Title] Localized ground glass opacities with multiple pulmonary small cysts in adult T-cell leukemia or lymphoma: an "alloy wheel" appearance.

We herein report a case of adult T-cell leukemia or lymphoma showing multiple lung cysts within a localized ground glass opacity (GGO) on computed tomography scan.

[MeSH-major] Cysts / radiography. Leukemia-Lymphoma, Adult T-Cell / radiography. Lung Neoplasms / radiography. Tomography, X-Ray Computed

[MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Male. Middle Aged

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(PMID = 19935228.001).

[ISSN] 1536-0237

[Journal-full-title] Journal of thoracic imaging

[ISO-abbreviation] J Thorac Imaging

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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

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

   

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

[Title] Longitudinal inhibition of PI3K/Akt/mTOR signaling by LY294002 and rapamycin induces growth arrest of adult T-cell leukemia cells.

This study found that phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling was activated in human T-cell lymphotropic virus type I (HTLV-1)-infected leukemia cells.

Rapamycin (1-100 nM, 48h), the inhibitor of mTOR and its analog RAD001 (1-100 nM, 48 h)-induced growth inhibition and G0/G1 cell cycle arrest of these cells in association with de-phosphorylation of p70S6K and 4E-BP-1, although IC50 was not achieved.

Blockade of Akt signaling by the PI3K inhibitor LY294002 (1-20 microM, 48 h) also resulted in the growth inhibition and G0/G1 cell cycle arrest of HTLV-1-infected cells, with IC50 ranging from 5 to 20muM, and it caused de-phosphorylation of p70S6K and 4E-BP-1.

Of note, when rapamycin was combined with LY294002, rapamycin-induced phosphorylation of Akt was blocked, and the ability of rapamycin to induce growth arrest of HTLV-1-infected T-cells and suppress the p-p70S6K and p-4E-BP-1 proteins was potentiated.

Moreover, both LY294002 and rapamycin down-regulated the levels of c-Myc and cyclin D1 proteins in these cells, and their combination further decreased levels of these cell cycle-regulating proteins.

Taken together, longitudinal inhibition of PI3K/Akt/mTOR signaling represents a promising treatment strategy for individuals with adult T-cell leukemia.

[MeSH-major] Chromones / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein Kinases. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Sirolimus / pharmacology

[MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Cell Cycle / drug effects. Cyclin D. Cyclins / metabolism. Enzyme Inhibitors / pharmacology. Human T-lymphotropic virus 1. Humans. Immunosuppressive Agents / pharmacology. Phosphoproteins / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins c-myc / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction / drug effects. T-Lymphocytes / metabolism. T-Lymphocytes / virology. TOR Serine-Threonine Kinases. Tumor Cells, Cultured

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

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NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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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

   

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

[Title] Delineation of immunoregulatory properties of adult T-cell leukemia cells.

We characterized leukemic cells from 20 adult T-cell leukemia (ATL) cases and 7 ATL-derived cell lines in terms of Foxp3 messenger RNA (mRNA) expression, cytokine production, cell surface markers associated with regulatory T-cells (Treg), and in vitro immunoregulatory activity and compared the results with those of cells from 3 T-cell-type chronic lymphocytic leukemia (T-CLL) patients and normal CD4+ T-cells.

Real-time polymerase chain reaction analysis showed that cells from 10 ATL cases, 1 T-CLL case, and 1 ATL cell line had higher Foxp3 mRNA levels than CD4+ T-cells.

In 5 ATL cases, Foxp3 levels were comparable to those of CD4+CD25+ T-cells.

Flow cytometric analysis revealed that CTLA-4 expression correlated with Foxp3 mRNA level in ATL cells.

The cells of all ATL cases examined produced no interleukin 2 or interferon gamma after iono-mycin and phorbolmyristate acetate stimulation.

An in vitro inhibition assay showed that the proliferation of normal CD4+CD25- T-cells stimulated with anti-CD3 monoclonal antibody and autologous dendritic cells was significantly suppressed by coculture with Foxp3-high ATL cells.

These results indicate that Foxp3 expression is variable in ATL cases and that Foxp3-high ATL cells, which resemble Treg phenotypically as well as functionally, may be involved in immune suppression in ATL.

[MeSH-major] Gene Expression Regulation, Leukemic / immunology. Immune Tolerance. Leukemia-Lymphoma, Adult T-Cell / immunology

[MeSH-minor] Aged. Cell Line, Tumor. Coculture Techniques. Female. Humans. Male. Middle Aged. T-Lymphocytes, Regulatory / immunology

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(PMID = 16867905.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[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

   

[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

   

[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

   

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

[Title] Immunologic control of human T-cell leukemia virus type I and adult T-cell leukemia.

Host T-cell responses to human T-cell leukemia virus type I (HTLV-I) control the expansion of HTLV-I-infected cells and are determinants of the equilibrium proviral load in vivo.

Insufficient T-cell responses are regarded as an immunologic risk factor for adult T-cell leukemia (ATL) because they allow increased proviral loads, which represent an epidemiologic risk factor for ATL.

ATL cells from approximately half of ATL cases retain the ability to express HTLV-I Tax, a major target antigen of HTLV-I-specific cytotoxic T-lymphocytes (CTL), whereas Tax-specific CTL in ATL patients are inactive.

Tax-specific CTL responses are strongly activated after hematopoietic stem cell transplantation in some ATL patients in long-term remission, indicating that HTLV-I Tax is expressed in vivo rather than being silent, and that the donor-derived T-cell system can recognize it.

These findings strongly suggest that reactivation of Tax-specific CTL by vaccines may be promising for prophylaxis of ATL in the high-risk group of HTLV-I carriers and for therapy of ATL in patients whose tumor cells are capable of expressing Tax.

[MeSH-major] Human T-lymphotropic virus 1 / immunology. Immunity. Leukemia-Lymphoma, Adult T-Cell / immunology

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(PMID = 17875523.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 39

   

[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

   

[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

   

[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

   

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

[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

   

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

[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

   

[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 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