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[Title] CD26/DPPIV expression and 8-azaguanine response in T-acute lymphoblastic leukaemia cell lines in culture.

Dipeptidyl peptidase IV, a cell membrane surface protease also known as CD26 (CD26/DPPIV), is known to play multiple functions in human organism, where it is largely expressed, for instance, in the development of human cancer and metastasis as well as in chemotherapy response.

The objective of this work was to study the CD26 membrane expression and DPPIV activity in T-acute leukaemia cell lines (CEM and MOLT3) in culture, in order to observe the modification of its expression under the 8-azaguanine treatment.

Cell line samples were incubated, some without different azaguanine concentration and others with, ranging from 10 to 100muM.

Cell surface CD26 expression has been identified by flow cytometry and DPPIV activity, in cultured medium, was fluorimetrically measured.

Results we have observed showed that 8-azaguanine induced a decrease in cell viability in a dose, time and cell type dependent manner with MOLT3 cells being the most sensitive to 8-azaguanine citotoxic effects (24h IC50: +/-10muM) when compared with CEM cells (24h IC50: +/-100muM).

In the same experimental conditions, MOLT3 cell treated with 8-azaguanine shows an increase in CD26 expression (MIF) compared with that of CEM cell submitted to the same conditions (65.4+/-1.3 versus 18.7+/-1.7).

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(PMID = 17055708.001).

[ISSN] 0928-4680

[Journal-full-title] Pathophysiology : the official journal of the International Society for Pathophysiology

[ISO-abbreviation] Pathophysiology

[Language] ENG

[Publication-type] Journal Article

[Publication-country] Netherlands

   

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[Title] Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica.

In Central America, nearly 70% of pediatric cancer is related to hemato-oncologic disorders, especially acute lymphoblastic leukemia (ALL).

Preliminary studies have described a high incidence of childhood leukemia in these countries; however, no molecular analyses of these malignancies have yet been carried out.

We studied diagnostic samples from 84 patients from the National Children's Hospital in San Jose, Costa Rica (65 precursor B-ALL, 5 T-cell ALL, and 14 acute myeloblastic leukemia).

The observed rate of leukemia was 52.2 cases per million children per year.

Twelve out of 65 (18.4%) precursor B-ALL tested positive for TEL-AML1 and 3 cases for BCR-ABL (4.6%).

None of the T-cell ALL cases were positive for either SIL-TAL1 or HOX11L2.

Within 14 acute myeloblastic leukemia patients, we confirmed 2 cases with FLT3-internal tandem duplication+, 1 patient with AML1-ETO, and only 1 case carrying a PML-RARalpha rearrangement.

The present study confirms the relatively high incidence of pediatric leukemia in Costa Rica and constitutes the first report regarding the incidence of the main molecular alterations of childhood leukemia in our region.

[MeSH-major] Leukemia / epidemiology. Leukemia / genetics

[MeSH-minor] Acute Disease. Child. Costa Rica / epidemiology. Cytogenetic Analysis. Gene Rearrangement. Humans. Mutation. Oncogene Proteins, Fusion / analysis

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(PMID = 19194200.001).

[ISSN] 1536-3678

[Journal-full-title] Journal of pediatric hematology/oncology

[ISO-abbreviation] J. Pediatr. Hematol. Oncol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Oncogene Proteins, Fusion

   

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[Title] Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia.

[MeSH-major] Genes, Homeobox / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Recombination, Genetic / genetics

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[CommentOn] Haematologica. 2006 Mar;91(3):317-21 [16531254.001]

(PMID = 16531247.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comment; Journal Article

[Publication-country] Italy

   

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[Title] A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia.

Fanconi anemia (FA) is an autosomal recessive disease characterized by pancitopenia, congenital malformations, predisposition to cancers and chromosomal instability.

We report the clinical and molecular features of a patient initially identified as a potential FA case only because of chemotherapy toxicity during the treatment of a T-lineage acute lymphoblastic leukemia (ALL).

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fanconi Anemia Complementation Group D2 Protein / genetics. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation

[MeSH-minor] Amino Acid Substitution. Antigens, CD. Antigens, CD13. Antigens, Differentiation, Myelomonocytic. Child. Chromosomal Instability. Disease Progression. Fanconi Anemia / genetics. Humans. Infection / etiology. Infection / genetics. Male. Pancytopenia / chemically induced. Pancytopenia / genetics. Remission Induction. Sialic Acid Binding Ig-like Lectin 3

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(PMID = 17096012.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Grant] Italy / Telethon / / TGM06S01

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

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FANCD2 protein, human; 0 / Fanconi Anemia Complementation Group D2 Protein; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13

   

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[Title] Combinatorial targeting of the macropinocytotic pathway in leukemia and lymphoma cells.

Ligand-directed delivery of agents to leukemia and lymphoma cells has the potential to yield new mechanistic disease insights and targeted therapies.

From the screening of acute T-lymphoblastic leukemia Molt-4 cells with a random phage-display peptide library, we isolated a phage displaying the sequence CAYHRLRRC.

This peptide contains a lymph node-homing motif (Cys-Ala-Tyr) and a cell-penetrating motif (Arg-Leu-Arg-Arg).

Binding of this ligand-directed phage to a large panel of leukemia/lymphoma cells and to patient-derived samples was much higher than to non-leukemia control cells.

Flow cytometry with fluorescein-labeled peptide and endocytosis blocking with specific inhibitors revealed that CAYHRLRRC is indeed taken up through macropinocytosis in Molt-4 and K562 human leukemia cells.

Unexpectedly, the cell surface receptor for the CAYHRLRRC peptide is not a heparan sulfate proteoglycan as it would be predicted for other cell-penetrating peptides.

Confirming this interpretation, a CAYHRLRRC-directed peptidomimetic-induced cell death in all the leukemia and lymphoma cells was evaluated, whereas a control transactivator of transcription protein (tat)-directed proapoptotic peptidomimetic was non-selective.

In summary, the targeting peptide CAYHRLRRC is selectively internalized through macropinocytosis in leukemia and lymphoma cells and has potential as a drug lead for ligand-directed anti-leukemia therapies.

[MeSH-major] Antineoplastic Agents / pharmacology. Gene Expression Regulation, Leukemic. Leukemia / metabolism. Lymphoma / metabolism

[MeSH-minor] Catalysis. Cell Line, Tumor. Cell Survival. Chemistry, Pharmaceutical / methods. Drug Design. Humans. K562 Cells. Ligands. Peptide Library. Peptides / chemistry. Pinocytosis

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[Cites] Pharmacol Rev. 2006 Mar;58(1):32-45 [16507881.001]

[Cites] Nat Rev Drug Discov. 2007 Oct;6(10):834-48 [17853901.001]

[Cites] Exp Hematol. 2006 Apr;34(4):443-52 [16569591.001]

[Cites] Mol Biol Cell. 2000 Oct;11(10):3341-52 [11029040.001]

[Cites] Cancer Res. 2000 Dec 1;60(23):6551-6 [11118031.001]

[Cites] J Biol Chem. 2001 Feb 23;276(8):5836-40 [11084031.001]

[Cites] J Cell Biol. 2001 May 28;153(5):905-16 [11381078.001]

[Cites] Curr Opin Chem Biol. 2001 Jun;5(3):308-13 [11479123.001]

[Cites] Nat Med. 2001 Nov;7(11):1249-53 [11689892.001]

[Cites] Cancer Res. 2001 Nov 15;61(22):8110-2 [11719437.001]

[Cites] Nat Med. 2002 Feb;8(2):121-7 [11821895.001]

[Cites] Cancer Res. 2002 Feb 1;62(3):867-74 [11830545.001]

[Cites] J Cell Sci. 2002 Jul 15;115(Pt 14):2953-62 [12082155.001]

[Cites] Nat Rev Cancer. 2002 Jul;2(7):521-8 [12094238.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13055-60 [12242328.001]

[Cites] J Biol Chem. 2003 Jan 3;278(1):585-90 [12411431.001]

[Cites] Int J Med Microbiol. 2002 Feb;291(6-7):487-94 [11890548.001]

[Cites] Nat Rev Immunol. 2003 Jan;3(1):23-35 [12511873.001]

[Cites] Nature. 2003 Mar 6;422(6927):37-44 [12621426.001]

[Cites] J Urol. 2003 Apr;169(4):1535-40 [12629410.001]

[Cites] J Control Release. 2003 Aug 28;91(1-2):45-51 [12932636.001]

[Cites] Nat Biotechnol. 2003 Sep;21(9):1040-6 [12897791.001]

[Cites] Cancer Res. 2003 Sep 1;63(17):5213-7 [14500347.001]

[Cites] Cancer Res. 2004 Jan 15;64(2):435-9 [14744752.001]

[Cites] Nat Med. 2004 Mar;10(3):310-5 [14770178.001]

[Cites] Cancer Cell. 2004 Feb;5(2):151-62 [14998491.001]

[Cites] Nature. 2004 May 20;429(6989):309-14 [15152255.001]

[Cites] Nat Med. 2004 Jun;10(6):625-32 [15133506.001]

[Cites] Cancer Cell. 2004 Sep;6(3):275-84 [15380518.001]

[Cites] J Cell Biol. 1986 Apr;102(4):1312-9 [3485637.001]

[Cites] J Cell Biol. 1994 Mar;124(5):689-703 [8120092.001]

[Cites] J Biol Chem. 1994 Dec 9;269(49):30745-8 [7982998.001]

[Cites] J Cell Biol. 1996 Dec;135(5):1249-60 [8947549.001]

[Cites] J Biol Chem. 1997 Jun 20;272(25):16010-7 [9188504.001]

[Cites] Science. 1998 Jan 16;279(5349):377-80 [9430587.001]

[Cites] Nat Biotechnol. 1999 Aug;17(8):768-74 [10429241.001]

[Cites] Nat Med. 1999 Sep;5(9):1032-8 [10470080.001]

[Cites] Mol Ther. 2004 Dec;10(6):1011-22 [15564133.001]

[Cites] J Control Release. 2005 Jan 20;102(1):247-53 [15653149.001]

[Cites] Adv Drug Deliv Rev. 2005 Feb 28;57(4):579-96 [15722165.001]

[Cites] J Biol Chem. 2005 Apr 15;280(15):15300-6 [15687490.001]

[Cites] Blood. 2005 Aug 15;106(4):1154-63 [15870183.001]

[Cites] Cancer Res. 2006 Jan 1;66(1):34-40 [16397212.001]

[Cites] Biochemistry. 2006 Jan 31;45(4):1116-27 [16430208.001]

[Cites] J Biol Chem. 2006 Feb 10;281(6):3544-51 [16326716.001]

[Cites] Cell. 2006 Apr 21;125(2):385-98 [16630824.001]

[Cites] J Biol Chem. 2006 Jun 9;281(23):15757-62 [16606620.001]

[Cites] Blood. 2006 Jun 15;107(12):4930-7 [16497970.001]

[Cites] Lancet. 2006 Nov 25;368(9550):1894-907 [17126723.001]

[Cites] Adv Drug Deliv Rev. 2006 Dec 30;58(15):1622-54 [17123658.001]

[Cites] Methods Mol Biol. 2007;357:385-406 [17172704.001]

[Cites] Biochemistry. 2007 Jan 16;46(2):492-501 [17209559.001]

[Cites] Nat Rev Drug Discov. 2007 Feb;6(2):149-65 [17268486.001]

[Cites] Leukemia. 2007 Mar;21(3):411-20 [17252013.001]

[Cites] Biochem J. 2007 Apr 15;403(2):335-42 [17217340.001]

[Cites] Adv Drug Deliv Rev. 2007 Mar 30;59(2-3):134-40 [17451840.001]

[Cites] Mol Pharm. 2007 May-Jun;4(3):435-47 [17373820.001]

[Cites] Biochem Soc Trans. 2007 Aug;35(Pt 4):784-7 [17635148.001]

[Cites] Biochem Soc Trans. 2007 Aug;35(Pt 4):788-93 [17635149.001]

[Cites] Trends Cardiovasc Med. 2006 Apr;16(3):80-8 [16546688.001]

(PMID = 18292083.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[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 / Ligands; 0 / Peptide Library; 0 / Peptides

[Other-IDs] NLM/ PMC3762554

   

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[Title] Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.

A significant proportion of children with T-cell acute lymphoblastic leukemia (T-ALL) continue to fail therapy.

Consequently, characterization of the cells that proliferate to maintain the disease should provide valuable information on the most relevant therapeutic targets.

The majority of cells capable of long-term proliferation in vitro were derived from the CD34+/CD4- and CD34+/CD7- subfractions.

The immunophenotype and genotype of the original leukemia cells were preserved with serial passage in the NOD/SCID mice.

These data demonstrate the long-term repopulating ability of the CD34+/CD4- and CD34+/CD7- subfractions in T-ALL and suggest that a cell with a more primitive phenotype was the target for leukemic transformation in these cases.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Stem Cells / immunology. Stem Cells / pathology

[MeSH-minor] Adolescent. Animals. Cell Culture Techniques. Cell Proliferation. Cell Separation. Cells, Cultured. Child. Child, Preschool. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Genotype. Humans. Immunophenotyping. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. Xenograft Model Antitumor Assays

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(PMID = 17003368.001).

[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

   

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[Title] T-lymphocyte reconstitution following rigorously T-cell-depleted versus unmodified autologous stem cell transplants.

We compared the kinetics of T-cell recovery after extensive ex vivo and in vivo T-cell depleted autologous stem cell transplantation (SCT) for multiple sclerosis (MS; n=8) with unmodified SCT for hematological malignancies (HM; n=39).

Unexpectedly, the kinetics of T-cell recovery between 3 and 12 months post transplant was similar in T-depleted and unmodified SCT.

Before SCT, the HM patients showed lymphopenia of all T-cell subsets, upregulated HLA-DR and CD95 expression and increased cytokine responses.

We suggest that the similar kinetics of T-cell recovery in the two patient groups may be explained by the susceptibility to apoptosis of the activated CD4(+) T-cells in the autografts of the HM patients.

This susceptibility to apoptosis would interfere with a swift and sustained CD4(+) T-cell regeneration post SCT.

[MeSH-major] Multiple Sclerosis / blood. Multiple Sclerosis / therapy. Stem Cell Transplantation / methods. T-Lymphocytes / metabolism. Transplantation, Autologous / methods

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(PMID = 16518423.001).

[ISSN] 0268-3369

[Journal-full-title] Bone marrow transplantation

[ISO-abbreviation] Bone Marrow Transplant.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD27; 0 / Antigens, CD3; 0 / Antigens, CD4; 0 / Antigens, CD95; 0 / Cytokines; 0 / Interleukin-2; 126880-86-2 / L-Selectin; 82115-62-6 / Interferon-gamma; EC 3.1.3.48 / Antigens, CD45

   

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[Title] Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of acute leukemias.

BACKGROUND: Multiparametric flow cytometry has become an indispensable but complex tool for the diagnosis of acute leukemias.

METHODS: Eight laboratories participated in the study and recruited a total of 151 individuals including 29 patients with B-cell precursor acute lymphoblastic leukemia (BCP-ALL), 77 with acute myeloid leukemia (AML), 10 with T-cell precursor acute lymphoblastic leukemia (T-ALL), and 35 normal bone marrow donors.

CONCLUSION: Residual normal lymphocytes can serve as internal quality control for studies addressing fluorescence intensity in the setting of immunophenotyping of acute leukemias.

[MeSH-major] Flow Cytometry / methods. Immunophenotyping / methods. Leukemia. Lymphocytes / cytology. Lymphocytes / metabolism

[MeSH-minor] Acute Disease. Case-Control Studies. Fluorescence. Humans. Quality Control. Reference Standards

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[Copyright] Copyright (c) 2005 Wiley-Liss, Inc.

(PMID = 16278833.001).

[ISSN] 1552-4949

[Journal-full-title] Cytometry. Part B, Clinical cytometry

[ISO-abbreviation] Cytometry B Clin Cytom

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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Fifteen patients had a cytotoxic T-cell and seven patients had an NK-cell phenotype.

All T-cell expansions were clonal.

Responses to dasatinib were good and included complete, unexpectedly long-lasting remissions in patients with advanced leukemia.

In a phase II clinical study on 46 Philadelphia chromosome-positive acute lymphoblastic leukemia, patients with lymphocytosis had superior survival compared with patients without lymphocytosis.

[MeSH-major] Antineoplastic Agents / pharmacology. Killer Cells, Natural / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lymphocytosis / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. T-Lymphocyte Subsets / drug effects. T-Lymphocytes, Cytotoxic / drug effects. Thiazoles / pharmacology

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[CommentIn] Acta Haematol. 2016;136(4):219-228 [27656875.001]

(PMID = 19295545.001).

[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 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib

   

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[Title] Impact of TCR status and genotype on outcome in adult T-cell acute lymphoblastic leukemia: a LALA-94 study.

Patients with T-cell acute lymphoblastic leukemias (T-ALLs) within the Leucemies Aigues Lymphoblastiques de l'Adulte-94 (LALA-94) prospective trial were treated with a 4-drug per 4-week induction, with intermediate-dose cytarabine and mitoxantrone salvage treatment for patients not achieving complete remission (CR) in 1 course.

Representative patients with T-ALL (91 patients) were classified into surface T-cell receptor (TCR)-expressing T-ALL patients (TCRalphabeta+ or TCRgammadelta+), pre-alphabeta T-ALL patients (cTCRbeta+, TCR-), and immature (IM) cTCRbeta-, TCR- T-ALL patients; 81 patients underwent genotyping for SIL-TAL1, CALM-AF10, HOX11, and HOX11L2.

Once CR was obtained, cumulative relapse rates were similar for IM, pre-alphabeta, and TCR+ T-ALL patients (P = .51), but were higher in HOX11L2 (83%) and SIL-TAL1 (82%) T-ALL patients compared with other genetic subgroups (48%; P = .05).

This was associated with an inferior OS for HOX11L2 T-ALLs (13% vs 47% in HOX11L2-T-ALLs; P = .009).

Both TCR and genotypic stratification can therefore contribute to risk-adapted management of adult T-ALLs.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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(PMID = 15637138.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Receptors, Antigen, T-Cell; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone

   

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[Title] Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia.

T-cell large granular lymphocyte leukemia (T-LGL) also known as T-cell chronic lymphocytic leukemia is rare and comprises a small minority of all small lymphocytic leukemias.

The concomitant presentation of T-LGL with acute myeloid leukemia (AML) has not been previously reported.

We present an elderly gentleman with concomitant T-LGL and AML (non-M3) diagnosed by a combination of morphologic evaluation, immunophenotyping by flow cytometry, and T-cell gene rearrangement studies.

He remains alive and well seven months after initial diagnosis.

[MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Prolymphocytic, T-Cell / diagnosis

[MeSH-minor] Acute Disease. Aged, 80 and over. Antigens, CD / analysis. Flow Cytometry. Humans. Male

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(PMID = 17453377.001).

[ISSN] 0284-186X

[Journal-full-title] Acta oncologica (Stockholm, Sweden)

[ISO-abbreviation] Acta Oncol

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] Norway

[Chemical-registry-number] 0 / Antigens, CD

[Number-of-references] 17

   

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[Title] Management of poor peripheral blood stem cell mobilization: incidence, predictive factors, alternative strategies and outcome. A retrospective analysis on 2177 patients from three major Italian institutions.

Patients' characteristics, including age, sex, stage of the underlying disease (complete or partial remission), diagnosis, previously administered radio/chemotherapy regimens, time-lapse from last chemotherapy before mobilization and mobilization schedule (including dose of GF) were considered as possibly predictive of poor or failed mobilization.

Therefore, a patient who fails a first mobilization (and when an HLA-compatible related on unrelated donor is not available) could undergo a second attempt either with different mobilization schedule or by using different GF, such as stem cell factor, growth hormone (GH), or more recently newly introduced drugs such as AMD3100, alone or in combination with rHuG- or -rHuGM-CSF.

[MeSH-major] Neoplasms / surgery. Peripheral Blood Stem Cell Transplantation / methods

[MeSH-minor] Adult. Antigens, CD34 / blood. Follow-Up Studies. Hematopoiesis. Hematopoietic Stem Cell Mobilization / methods. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / surgery. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukemia, Myeloid, Acute / surgery. Lymphoma, Non-Hodgkin / surgery. Multiple Myeloma / surgery. Retrospective Studies. Survival Analysis

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(PMID = 19540167.001).

[ISSN] 1473-0502

[Journal-full-title] Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis

[ISO-abbreviation] Transfus. Apher. Sci.

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD34

   

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[Title] Shb promotes blood vessel formation in embryoid bodies by augmenting vascular endothelial growth factor receptor-2 and platelet-derived growth factor receptor-beta signaling.

To elucidate a possible role of Shb in embryonic vascular development, wild-type and SH2 domain mutated (R522K) Shb were overexpressed in murine embryonic stem (ES) cells.

This response may be the consequence of an increased number of VEGFR-2 positive cells at an early stage of EB development, a finding corroborated by both immunostaining and real-time RT-PCR.

The findings suggest that Shb may play a crucial role during early ES cell differentiation to vascular structures by transducing VEGFR-2 and PDGFR-beta signals.

[MeSH-major] Blood Vessels / embryology. Blood Vessels / metabolism. Neovascularization, Physiologic / physiology. Pluripotent Stem Cells / metabolism. Proto-Oncogene Proteins / metabolism. Receptor, Platelet-Derived Growth Factor beta / metabolism. Up-Regulation / physiology. Vascular Endothelial Growth Factor Receptor-2 / metabolism

[MeSH-minor] Animals. Antigens, CD31 / metabolism. Basic Helix-Loop-Helix Transcription Factors. Cell Differentiation / physiology. Cell Line. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Embryo Culture Techniques. Endothelial Cells / cytology. Endothelial Cells / metabolism. Gene Expression Profiling. Gene Expression Regulation, Developmental / physiology. Mice. Mutation / genetics. Oligonucleotide Array Sequence Analysis. Phenotype. Platelet Membrane Glycoprotein IIb / genetics. Platelet Membrane Glycoprotein IIb / metabolism. RNA, Messenger / metabolism. Signal Transduction / physiology. Transcription Factors / genetics. Transcription Factors / metabolism

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(PMID = 15919073.001).

[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 / Antigens, CD31; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Platelet Membrane Glycoprotein IIb; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Shb protein, mouse; 0 / Tal1 protein, mouse; 0 / Transcription Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2

   

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[Title] Activation of the JNK pathway promotes phosphorylation and degradation of BimEL--a novel mechanism of chemoresistance in T-cell acute lymphoblastic leukemia.

T-cell acute lymphoblastic leukemias (T-ALLs) are highly malignant tumors with 20% of patients continues to fail therapy, in part due to chemoresistance of T-ALL cells via largely unknown mechanisms.

Here, we showed that lack of Bcl-2-interacting mediator of cell death (Bim)(EL) protein expression, a BH3-only member of the Bcl-2 family proteins, conferred resistance of a T-ALL cell line, Sup-T1, to etoposide-induced apoptosis.

[MeSH-major] Apoptosis Regulatory Proteins / metabolism. Drug Resistance, Neoplasm. Leukemia-Lymphoma, Adult T-Cell / metabolism. MAP Kinase Kinase 4 / metabolism. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism

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(PMID = 18174237.001).

[ISSN] 1460-2180

[Journal-full-title] Carcinogenesis

[ISO-abbreviation] Carcinogenesis

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 6PLQ3CP4P3 / Etoposide; EC 2.7.12.2 / MAP Kinase Kinase 4

   

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

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

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

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(PMID = 18185524.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

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

[Publication-country] England

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

   

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[Title] Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia.

Morphologic distinction of leukemic lymphoblasts in B acute lymphoblastic leukemia (B-ALL) from their nonneoplastic counterparts in bone marrow (hematogones) can be difficult.

Thus, the presence of aberrant antigen expression detectable by flow cytometry may be critical for diagnosis of B-ALL and detection of minimal residual disease.

Of 200 cases, 9.0% aberrantly expressed T cell-associated antigens.

[MeSH-major] Bone Marrow Cells / pathology. Immunophenotyping / methods. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Precursor Cells, B-Lymphoid / pathology

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(PMID = 19926587.001).

[ISSN] 1943-7722

[Journal-full-title] American journal of clinical pathology

[ISO-abbreviation] Am. J. Clin. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

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[Title] Plerixafor (AMD3100) and granulocyte colony-stimulating factor (G-CSF) mobilize different CD34+ cell populations based on global gene and microRNA expression signatures.

Three peripheral blood stem cell concentrates were collected from 3 macaques treated with G-CSF, plerixafor, or plerixafor plus G-CSF.

Plerixafor-mobilized cells were enriched for B cells, T cells, and mast cell genes, and G-CSF-mobilized cells were enriched for neutrophils and mononuclear phagocyte genes.

Two hematopoietic progenitor cell miR, miR-10 and miR-126, and a dendritic cell miR, miR-155, were up-regulated in G-CSF-mobilized CD34(+) cells.

A pre-B-cell acute lymphocytic leukemia miR, miR-143-3p, and a T-cell miR, miR-143-5p, were up-regulated in plerixafor plus G-CSF-mobilized cells.

Plerixafor-mobilized CD34(+) cells include more B-, T-, and mast cell precursors, whereas G-CSF-mobilized cells have more neutrophil and mononuclear phagocyte precursors.

[MeSH-major] Antigens, CD34 / metabolism. Gene Expression Profiling. Gene Expression Regulation / drug effects. Granulocyte Colony-Stimulating Factor / pharmacology. Hematopoietic Stem Cell Mobilization. Heterocyclic Compounds / pharmacology. MicroRNAs / genetics

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[Cites] Exp Hematol. 2006 Aug;34(8):1052-9 [16863911.001]

[Cites] Blood. 2006 May 1;107(9):3772-8 [16439684.001]

[Cites] Biol Blood Marrow Transplant. 2007 Apr;13(4):398-411 [17382247.001]

[Cites] Nature. 2007 Jun 21;447(7147):1007-11 [17581586.001]

[Cites] PLoS One. 2007;2(10):e1020 [17925868.001]

[Cites] J Immunol. 2008 Jun 1;180(11):7358-67 [18490735.001]

[Cites] Blood. 2008 Aug 15;112(4):990-8 [18426988.001]

[Cites] J Transl Med. 2008;6:39 [18647411.001]

[Cites] Blood. 2008 Sep 1;112(5):2092-100 [18523146.001]

[Cites] Sci Signal. 2009 Jan 6;2(52):pe1 [19126861.001]

[Cites] Cell Stem Cell. 2009 Jan 9;4(1):62-72 [19128793.001]

[Cites] Pediatr Hematol Oncol. 2009 Jan;26(1):1-10 [19206004.001]

[Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2735-40 [19193853.001]

[Cites] J Cell Biochem. 2006 Oct 15;99(3):690-705 [16888804.001]

[Cites] J Clin Invest. 2000 Dec;106(11):1331-9 [11104786.001]

[Cites] Genome Biol. 2003;4(5):P3 [12734009.001]

[Cites] Blood. 2003 Oct 15;102(8):2728-30 [12855591.001]

[Cites] J Clin Oncol. 2004 Mar 15;22(6):1095-102 [15020611.001]

[Cites] Blood. 1996 Feb 15;87(4):1644-53 [8608259.001]

[Cites] Blood. 1997 May 15;89(10):3522-8 [9160656.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]

[Cites] Science. 1999 Feb 5;283(5403):845-8 [9933168.001]

[Cites] Transfus Apher Sci. 2004 Dec;31(3):233-43 [15556471.001]

[Cites] Transfusion. 2005 Mar;45(3):295-300 [15752146.001]

[Cites] J Exp Med. 2005 Apr 18;201(8):1307-18 [15837815.001]

[Cites] Blood. 2005 Sep 1;106(5):1867-74 [15890685.001]

[Cites] Blood. 2005 Dec 1;106(12):4002-8 [16105977.001]

[Cites] Blood. 2006 Feb 1;107(3):870-9 [16204315.001]

[Cites] Bone. 2006 Apr;38(4):497-508 [16337237.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5078-83 [16549775.001]

[CommentIn] Blood. 2010 Jan 28;115(4):916-7 [20110438.001]

(PMID = 19602709.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Antigens, CD34; 0 / Biomarkers; 0 / Drug Combinations; 0 / Heterocyclic Compounds; 0 / MicroRNAs; 0 / RNA, Messenger; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 155148-31-5 / JM 3100

[Other-IDs] NLM/ PMC2746476

   

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[Title] Genetic aberrations in paediatric acute leukaemias and implications for management of patients.

The process of malignant transformation in paediatric acute leukaemias is complex, requiring at least two deleterious events resulting in DNA damage.

In this review we summarise the most common genetic aberrations for the three main subtypes of paediatric acute leukaemia: B-cell-precursor acute lymphoblastic leukaemia, T-cell acute lymphoblastic leukaemia and acute myeloid leukaemia.

Some genetic aberrations represent sensitive targets for molecular detection of minimal residual disease.

[MeSH-major] Cell Transformation, Neoplastic / genetics. Chromosome Aberrations. Leukemia / genetics

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[Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.

(PMID = 20435517.001).

[ISSN] 1474-5488

[Journal-full-title] The Lancet. Oncology

[ISO-abbreviation] Lancet Oncol.

[Language] eng

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

[Publication-country] England

[Number-of-references] 76

   

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BACKGROUND: Nelarabine was approved by the US Food and Drug Administration (FDA) in October 2005 for the treatment of T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) that has not responded to or has relapsed after treatment with at least 2 chemotherapy regimens.

Nelarabine has activity in T-cell malignancies, as evaluated in 2 Phase I and 5 Phase II studies.

In PGAA 2001, patients with T-ALL in first relapse (n = 33) had an objective response rate of 55% (16 with a complete response [CR] and 2 with a partial response [PR]), and those with T-ALL in second relapse (n = 30) had an objective response rate of 27% (7 CR and 1 PR).

Among patients with central nervous system-positive T-ALL or T-cell non-Hodgkins lymphoma (T-NHL) (n = 21), 33% had an objective response (5 CR and 2 PR); among patients with T-ALL or T-NHL with extramedullary relapse (n = 22), 14% had a PR.

CALGB 19801 included 39 adult patients with T-cell malignancies, of whom 7 (18%) had a CR and an additional 2 (5%) had a CR without full hematologic recovery.

[MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Arabinonucleosides / therapeutic use. Hematologic Neoplasms / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Purine Nucleosides / therapeutic use

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(PMID = 18035189.001).

[ISSN] 0149-2918

[Journal-full-title] Clinical therapeutics

[ISO-abbreviation] Clin Ther

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Arabinonucleosides; 0 / Purine Nucleosides; 60158CV180 / nelarabine

[Number-of-references] 29

   

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[Title] Quantitation of Human herpes virus 6 genome in children with acute lymphoblastic leukemia.

Acute lymphoblastic leukemia is the main type of leukemia in children.

The potential role of HHV-6 in the pathogenesis of pediatric acute lymphoblastic leukemia was investigated.

HHV-6 genome copy number was measured by quantitative real-time PCR (RQ-PCR) in bone marrow or peripheral blood samples obtained from 36 children (median age = 4 years) with B acute lymphoblastic leukemia (n = 31) and T acute lymphoblastic leukemia (n = 5) at diagnosis and during complete remission.

A total of 24.7% of samples were positive for HHV-6 genome: 13.9% were leukemia samples and 34.1% were complete remission samples.

Viral load was low with values lower at diagnosis (median viral copy number = 22.9) than at complete remission (median copy number = 60.1).

These results argue against a role of HHV6 infection in the development of pediatric acute lymphoblastic leukemia.

[MeSH-major] DNA, Viral / analysis. Herpesvirus 6, Human / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / virology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / virology. Roseolovirus Infections / complications. Roseolovirus Infections / virology

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(PMID = 18297709.001).

[ISSN] 0146-6615

[Journal-full-title] Journal of medical virology

[ISO-abbreviation] J. Med. Virol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Viral

   

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[Title] A small molecule inhibitor of Pim protein kinases blocks the growth of precursor T-cell lymphoblastic leukemia/lymphoma.

We demonstrate that SMI-4a, a novel benzylidene-thiazolidine-2, 4-dione small molecule inhibitor of the Pim kinases, kills a wide range of both myeloid and lymphoid cell lines with precursor T-cell lymphoblastic leukemia/lymphoma (pre-T-LBL/T-ALL) being highly sensitive.

Incubation of pre-T-LBL cells with SMI-4a induced G1 phase cell-cycle arrest secondary to a dose-dependent induction of p27(Kip1), apoptosis through the mitochondrial pathway, and inhibition of the mammalian target of rapamycin C1 (mTORC1) pathway based on decreases in phospho-p70 S6K and phospho-4E-BP1, 2 substrates of this enzyme.

In addition, treatment of these cells with SMI-4a was found to induce phosphorylation of extracellular signal-related kinase1/2 (ERK1/2), and the combination of SMI-4a and a mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor was highly synergistic in killing pre-T-LBL cells.

In immunodeficient mice carrying subcutaneous pre-T-LBL tumors, treatment twice daily with SMI-4a caused a significant delay in the tumor growth without any change in the weight, blood counts, or chemistries.

Our data suggest that inhibition of the Pim protein kinases may be developed as a therapeutic strategy for the treatment of pre-T-LBL.

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[Cites] Nature. 2001 Aug 23;412(6849):822-6 [11518967.001]

[Cites] Leukemia. 2002 Sep;16(9):1713-24 [12200686.001]

[Cites] Genes Dev. 2003 Aug 1;17(15):1841-54 [12869584.001]

[Cites] J Biol Chem. 2003 Nov 14;278(46):45358-67 [12954615.001]

[Cites] Mol Cell Biol. 2004 Jul;24(13):6104-15 [15199164.001]

[Cites] FEBS Lett. 2004 Jul 30;571(1-3):43-9 [15280015.001]

[Cites] Leuk Lymphoma. 2004 May;45(5):951-5 [15291354.001]

[Cites] Cancer Res. 2004 Sep 1;64(17):6082-90 [15342391.001]

[Cites] Cell. 1984 May;37(1):141-50 [6327049.001]

[Cites] Br J Haematol. 2006 Sep;134(5):500-9 [16869825.001]

[Cites] Cancer Cell. 2007 Dec;12(6):501-13 [18068628.001]

[Cites] Blood. 2008 Jan 1;111(1):379-82 [17878402.001]

[Cites] Cancer Res. 2008 Jul 1;68(13):5076-85 [18593906.001]

[Cites] Toxicology. 2008 Sep 4;250(2-3):100-8 [18621092.001]

[Cites] J Clin Invest. 2008 Sep;118(9):3065-74 [18725988.001]

[Cites] J Clin Invest. 2008 Sep;118(9):3051-64 [18725989.001]

[Cites] J Clin Invest. 2008 Nov;118(11):3762-74 [18830414.001]

[Cites] Eur J Cancer. 2008 Oct;44(15):2144-51 [18715779.001]

[Cites] Leuk Lymphoma. 2008 Nov;49(11):2081-90 [19021050.001]

[Cites] J Med Chem. 2009 Jan 8;52(1):74-86 [19072652.001]

[Cites] Cancer Biol Ther. 2009 May;8(9):846-53 [19276681.001]

[Cites] Cancer Res. 2009 Jun 1;69(11):4577-81 [19458076.001]

[Cites] Mol Cancer Ther. 2009 Jun;8(6):1473-83 [19509254.001]

[Cites] Blood. 2009 Aug 20;114(8):1618-27 [19458359.001]

[Cites] Oncogene. 1999 Dec 23;18(56):7994-9 [10637510.001]

[Cites] Mol Cell Biol. 2000 Sep;20(18):6945-57 [10958690.001]

[Cites] Blood. 2000 Oct 15;96(8):2655-63 [11023495.001]

[Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]

[Cites] EMBO J. 1985 Jul;4(7):1793-8 [2992942.001]

[Cites] Cell. 1989 Feb 24;56(4):673-82 [2537153.001]

[Cites] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8857-61 [2682662.001]

[Cites] Cancer Res. 1991 Feb 1;51(3):958-63 [1988138.001]

[Cites] Mol Cell Biol. 1991 Feb;11(2):1176-9 [1990273.001]

[Cites] Oncogene. 1991 Nov;6(11):1941-8 [1658705.001]

[Cites] Curr Top Microbiol Immunol. 1992;182:293-8 [1337029.001]

[Cites] J Exp Med. 1993 Nov 1;178(5):1665-73 [8228813.001]

[Cites] Cancer Res. 1997 Jan 1;57(1):62-7 [8988042.001]

[Cites] Biochem J. 1997 Aug 15;326 ( Pt 1):1-16 [9337844.001]

[Cites] Oncogene. 1997 Nov 27;15(22):2735-42 [9401000.001]

[Cites] Cell Growth Differ. 1997 Dec;8(12):1371-80 [9419425.001]

[Cites] Blood. 1998 Nov 1;92(9):3410-5 [9787181.001]

[Cites] Cancer Res. 1999 Feb 15;59(4):886-94 [10029080.001]

[Cites] J Exp Med. 1999 Oct 18;190(8):1059-68 [10523604.001]

[Cites] Blood. 2005 Feb 15;105(4):1759-67 [15498859.001]

[Cites] Cancer Res. 2006 Apr 1;66(7):3828-35 [16585210.001]

[Cites] Nature. 2006 May 25;441(7092):424-30 [16724053.001]

(PMID = 19965690.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P30 CA138313; United States / NCRR NIH HHS / RR / UL1 RR029882; United States / NCI NIH HHS / CA / P30 CA 138313

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

[Publication-country] United States

[Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / MYC protein, human; 0 / PIM2 protein, human; 0 / Pim2 protein, mouse; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / PIM1 protein, human; EC 2.7.11.1 / PIM3 protein, human; EC 2.7.11.1 / Pim1 protein, mouse; EC 2.7.11.1 / Pim3 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases

[Other-IDs] NLM/ PMC2941996

   

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[Title] Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance.

T-cell acute lymphoblastic leukemia (T-ALL) is associated with a significant risk of disease relapse, but the biological basis for relapse is poorly understood.

Here, we identify leukemiainitiating cells (L-ICs) on the basis of functional assays and prospective isolation and report a role for L-ICs in T-ALL disease and relapse.

Long-term proliferation in response to NOTCH1 activating signals in OP9-DL1 coculture system or capacity to initiate leukemia in xenografts by the CD7(+)CD1a(-) subset of primary T-ALL samples was superior to other subsets, refining the identity of T-ALL L-ICs.

T-ALL engraftment was improved in nonobese diabetic/severe combined immunodeficiency (NOD/scid)IL2Rγ(null) (NSG) mice compared with NOD/scid with anti-CD122 treatment (NS122), but both showed changes in leukemia immunophenotype.

Our results establish that primary CD1a(-) T-ALL cells are functionally distinct from CD1a(+) cells and that the CD7(+)CD1a(-) subset is enriched for L-IC activity that may be involved in mediating disease relapse after therapy.

[MeSH-minor] Animals. Antigens, CD1. Antigens, CD7. Antineoplastic Agents, Hormonal / pharmacology. Cell Proliferation. Clone Cells / pathology. Coculture Techniques. Dexamethasone / pharmacology. Humans. Immunophenotyping. Mice. Mice, SCID. Receptor, Notch1 / metabolism. Recurrence. Transplantation, Heterologous

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(PMID = 20810926.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD7; 0 / Antineoplastic Agents, Hormonal; 0 / CD1a antigen; 0 / Glucocorticoids; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 7S5I7G3JQL / Dexamethasone

   

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[Title] Efficacy of low dose clofarabine in refractory precursor T- acute lymphoblastic leukemia.

Refractory T-lymphoblastic leukemia in adults has a poor prognosis in patients who relapse after allogeneic stem cell transplantation, and relatively few new agents have demonstrated activity.

We used low dose clofarabine and induced a remission in a patient who relapsed in the skin and marrow after allogeneic transplant and was refractory to nelarabine and report a near complete response, suggesting significant activity for low intermittent dose clofarabine in patients with relapsed T-cell leukemias.

[MeSH-major] Adenine Nucleotides / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy

[MeSH-minor] Adult. Bone Marrow Neoplasms / drug therapy. Bone Marrow Neoplasms / secondary. Clinical Trials as Topic. Drug Administration Schedule. Drug Resistance, Neoplasm. Humans. Immunophenotyping. Male. Recurrence. Skin Neoplasms / drug therapy. Skin Neoplasms / secondary. Stem Cell Transplantation. Transplantation, Homologous. Treatment Outcome

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[Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]

[Cites] Nat Rev Drug Discov. 2006 Oct;5(10):855-63 [17016426.001]

[Cites] J Clin Oncol. 2005 May 20;23(15):3396-403 [15908652.001]

[Cites] Mol Pharmacol. 2006 Jan;69(1):346-53 [16234483.001]

[Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]

[Cites] J Clin Oncol. 2006 Apr 20;24(12):1917-23 [16622268.001]

[Cites] Cancer Res. 1991 May 1;51(9):2386-94 [1707752.001]

[Cites] J Clin Oncol. 2003 Mar 15;21(6):1167-73 [12637486.001]

[Cites] Blood. 2003 Oct 1;102(7):2379-86 [12791647.001]

[Cites] Blood. 2004 Feb 1;103(3):784-9 [14551141.001]

(PMID = 17940627.001).

[ISSN] 1551-4056

[Journal-full-title] The Yale journal of biology and medicine

[ISO-abbreviation] Yale J Biol Med

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 60158CV180 / nelarabine; 762RDY0Y2H / clofarabine

[Other-IDs] NLM/ PMC1994805

   

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[Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].

OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.

METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.

The cell cycle was examined by flow cytometric analysis.

(1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).

CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.

Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.

[MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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(PMID = 16029562.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger

   

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[Title] Immunology: Egocentric pre-T-cell receptors.

[MeSH-major] Protein Multimerization. Receptors, Antigen, T-Cell, alpha-beta / chemistry. Receptors, Antigen, T-Cell, alpha-beta / metabolism

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[CommentOn] Nature. 2010 Oct 14;467(7317):844-8 [20944746.001]

(PMID = 20944732.001).

[ISSN] 1476-4687

[Journal-full-title] Nature

[ISO-abbreviation] Nature

[Language] eng

[Publication-type] Comment; News

[Publication-country] England

[Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta

   

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This study found that oridonin, a natural diterpenoid purified from Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266, RPMI8226), acute lymphoblastic T-cell leukemia (Jurkat), and adult T-cell leukemia (MT-1) cells with an effective dose that inhibited 50% of target cells (ED50) ranging from 0.75 to 2.7 microg/mL.

Of note, oridonin decreased survival of freshly isolated adult T-cell leukemia (three samples), acute lymphoblastic leukemia (one sample), chronic lymphocytic leukemia (one sample), non-Hodgkin's lymphoma (three samples), and MM (four samples) cells from patients in association with inhibition of NF-kappa B DNA-binding activity.

Taken together, oridonin might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia.

[MeSH-major] Cell Proliferation / drug effects. Diterpenes / pharmacology. Isodon / metabolism. NF-kappa B / metabolism. Phytotherapy / methods. Plant Extracts / pharmacology

[MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Apoptosis. Blotting, Western. Cell Line. Cell Line, Tumor. Diterpenes, Kaurane. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Genes, Reporter. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. In Situ Nick-End Labeling. Jurkat Cells. Leukemia / drug therapy. Leukemia / pathology. Lipopolysaccharides / metabolism. Male. Mice. Middle Aged. Models, Chemical. Multiple Myeloma / drug therapy. Multiple Myeloma / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction. T-Lymphocytes / metabolism. T-Lymphocytes / virology. Thymidine / chemistry. Thymidine / metabolism. Time Factors. Transfection. Trypan Blue / pharmacology. bcl-X Protein

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(PMID = 15827331.001).

[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; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Diterpenes; 0 / Diterpenes, Kaurane; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 0APJ98UCLQ / oridonin; I2ZWO3LS3M / Trypan Blue; VC2W18DGKR / Thymidine

   

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[Title] Large granular lymphocytic leukaemia complicated with histiocytic sarcoma in a dog.

Based on these findings this case was diagnosed as LGL leukaemia.

Shortly after diagnosis, the dog developed sudden onset of central nervous system signs and died on day 270.

A common outcome of canine LGL is the development of acute blast crisis or lymphoma.

[MeSH-major] Antineoplastic Agents / administration & dosage. Histiocytic Sarcoma / veterinary. Leukemia, Large Granular Lymphocytic / veterinary

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(PMID = 20458870.001).

[ISSN] 1019-9128

[Journal-full-title] Journal of the South African Veterinary Association

[ISO-abbreviation] J S Afr Vet Assoc

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] South Africa

[Chemical-registry-number] 0 / Antineoplastic Agents

   

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[Title] High rate of centrosome aberrations and correlation with proliferative activity in patients with untreated B-cell chronic lymphocytic leukemia.

B-cell chronic lymphocytic leukemia (CLL) is characterized by a high rate of clonal genomic alterations and a low proliferative activity with cell cycle arrest in G(0)/G(1) phase.

To investigate whether centrosome aberrations do occur in CLL and whether they correlate with common prognostic factors and disease activity, we examined peripheral blood mononuclear cells (PBMC) from 70 patients with previously untreated CLL using an antibody to gamma-tubulin.

Accordingly, more centrosome aberrations were found in PHA-stimulated T lymphocytes from healthy individuals as well as in B cells from surgically removed tonsil tissue of patients with acute tonsillitis as compared to the peripheral blood B lymphocytes from the control group.

[MeSH-major] Cell Proliferation. Centrosome. Leukemia, Lymphocytic, Chronic, B-Cell / pathology

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[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 17417785.001).

[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

   

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[Title] Acute abdomen as initial manifestation of M4 - acute non-lymphocytic leukemia.

Visceral involvement in acute non-lymphocytic leukemia (ANLL) seldom precedes hematological manifestation.

We report on a patient with M4 - ANLL presenting with acute abdomen without any evidence of blood disorder.

We discuss the contrast between histology and short disease duration, the unusual presentation and the bad prognosis, and attempt to correlate the clinical course with the coexpression of markers.

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(PMID = 17343343.001).

[ISSN] 1107-0625

[Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology

[ISO-abbreviation] J BUON

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

   

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To identify target cell populations affected, a differentiating primary liquid erythroid culture system using sca-1(+)cells from mouse bone marrow was developed and challenged with p38is SB-203580, SB-226882, and SB-267030.

Drug-related alterations in genes involved at different stages of erythropoiesis, cell-surface antigen expression (CSAE), burst-forming unit erythroid (BFU-E) colony formation, and cellular morphology (CM), growth (CG), and viability were evaluated.

[MeSH-minor] Animals. Antigens, Ly / metabolism. Basic Helix-Loop-Helix Transcription Factors / metabolism. Bone Marrow Cells / drug effects. Cell Culture Techniques. Cell Survival / drug effects. Cells, Cultured. Colony-Forming Units Assay. Erythroid Precursor Cells / drug effects. GATA2 Transcription Factor / metabolism. Immunophenotyping. Male. Membrane Proteins / metabolism. Mice. Proto-Oncogene Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 19126791.001).

[ISSN] 1533-1601

[Journal-full-title] Toxicologic pathology

[ISO-abbreviation] Toxicol Pathol

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Ly; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / GATA2 Transcription Factor; 0 / Gata2 protein, mouse; 0 / Imidazoles; 0 / Ly6a protein, mouse; 0 / Membrane Proteins; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 0 / SB 203580; 0 / Tal1 protein, mouse; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases

   

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Accelerated maturation is observed in mice injected with anti-CD3 to mimic pre-T-cell receptor stimulation, and also in mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide to induce EAE.

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[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

[Cites] Nature. 2003 Feb 13;421(6924):744-8 [12610626.001]

[Cites] Nat Immunol. 2003 Mar;4(3):255-60 [12577054.001]

[Cites] J Immunol. 1999 Oct 15;163(8):4349-59 [10510375.001]

[Cites] J Immunol. 2005 Jan 1;174(1):261-9 [15611248.001]

[Cites] J Immunol. 2005 Mar 1;174(5):2796-804 [15728489.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13574-9 [16174747.001]

[Cites] Semin Immunol. 2005 Dec;17(6):411-20 [16256363.001]

[Cites] J Immunol. 2006 Apr 1;176(7):4029-41 [16547238.001]

[Cites] J Immunol. 2006 Apr 1;176(7):4066-74 [16547242.001]

[Cites] J Immunol. 2006 Apr 15;176(8):4818-25 [16585576.001]

[Cites] Drug News Perspect. 2006 Mar;19(2):77-83 [16628262.001]

[Cites] Curr Med Chem. 2006;13(10):1149-56 [16719776.001]

[Cites] J Neuroimmunol. 2007 Apr;185(1-2):75-86 [17320975.001]

[Cites] Methods Mol Biol. 2007;380:377-90 [17876107.001]

[Cites] Mol Immunol. 2008 Feb;45(3):599-606 [17920446.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):2987-92 [18287049.001]

[Cites] Immunol Lett. 2008 Mar 15;116(2):104-10 [18243340.001]

[Cites] Prog Histochem Cytochem. 2008;43(2):73-120 [18555891.001]

[Cites] J Immunol. 2008 Jul 1;181(1):320-8 [18566397.001]

[Cites] Biochem Biophys Res Commun. 2008 Aug 8;372(4):509-12 [18503756.001]

[Cites] Annu Rev Immunol. 2003;21:139-76 [12414722.001]

[Cites] J Exp Med. 2003 Jul 21;198(2):349-60 [12860933.001]

[Cites] J Exp Med. 2003 Sep 1;198(5):757-69 [12953095.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13453-8 [14597717.001]

[Cites] Immunity. 2003 Nov;19(5):641-4 [14614851.001]

[Cites] J Exp Med. 2003 Dec 15;198(12):1951-7 [14662908.001]

[Cites] Cell Mol Life Sci. 2004 Feb;61(3):263-80 [14770292.001]

[Cites] J Immunol. 2004 Mar 1;172(5):2909-16 [14978093.001]

[Cites] Blood. 2004 Mar 15;103(6):1985-94 [14592827.001]

[Cites] Nat Immunol. 2004 Apr;5(4):418-25 [14991052.001]

[Cites] Proc Natl Acad Sci U S A. 2004 May 4;101(18):7058-63 [15118099.001]

[Cites] J Neuroimmunol. 2004 Nov;156(1-2):123-31 [15465603.001]

[Cites] J Immunol. 1990 Dec 15;145(12):4167-73 [2124236.001]

[Cites] Proc Natl Acad Sci U S A. 1991 Jul 15;88(14):6323-7 [2068112.001]

[Cites] Cell Immunol. 1993 Jan;146(1):52-61 [8425230.001]

[Cites] J Immunol. 1994 Mar 15;152(6):2729-35 [7511624.001]

[Cites] Annu Rev Immunol. 1995;13:93-126 [7612239.001]

[Cites] J Exp Med. 1995 Oct 1;182(4):961-71 [7561699.001]

[Cites] J Exp Med. 1995 Nov 1;182(5):1377-88 [7595208.001]

[Cites] Immunity. 1997 Mar;6(3):245-55 [9075925.001]

[Cites] Annu Rev Immunol. 1998;16:495-521 [9597139.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1707-12 [10677522.001]

[Cites] J Immunol. 2000 Dec 1;165(11):6221-8 [11086056.001]

[Cites] Immunity. 2000 Nov;13(5):715-25 [11114383.001]

[Cites] Int Immunol. 2002 Aug;14(8):943-51 [12147631.001]

[Cites] J Clin Invest. 2002 Aug;110(4):493-7 [12189243.001]

[Cites] J Immunol. 2002 Dec 15;169(12):7104-10 [12471147.001]

[Cites] J Immunol. 2003 Feb 15;170(4):2153-60 [12574388.001]

[Cites] Eur J Immunol. 1999 Aug;29(8):2476-83 [10458761.001]

(PMID = 20599940.001).

[ISSN] 1096-0945

[Journal-full-title] Experimental and molecular pathology

[ISO-abbreviation] Exp. Mol. Pathol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / R01 AI061818; United States / NINDS NIH HHS / NS / R01 NS048435; United States / NIAID NIH HHS / AI / U19 AI082726

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antigens, CD3; 0 / Mog protein, mouse; 0 / Myelin Proteins; 0 / Myelin-Associated Glycoprotein; 0 / Myelin-Oligodendrocyte Glycoprotein; 187348-17-0 / Interleukin-12

[Other-IDs] NLM/ NIHMS218212; NLM/ PMC2939283

   

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[Title] Molecular basis for pre-TCR-mediated autonomous signaling.

The pre-T-cell receptor (pre-TCR) is a multimeric complex composed of a nascent TCRbeta chain, an invariant pre-TCRalpha (pTalpha) chain and CD3 molecules, and is crucial for early T-cell development.

Despite its structural similarity to the mature alphabetaTCR, which requires MHC-antigen for receptor triggering, the pre-TCR is proposed to initiate signals in a ligand-independent manner.

In this review, we summarize current data relating to the molecular mechanism underlying the initiation of pre-TCR-mediated autonomous signaling.

[MeSH-major] Lymphoma / immunology. Membrane Glycoproteins / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology. Signal Transduction / immunology

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(PMID = 17126602.001).

[ISSN] 1471-4906

[Journal-full-title] Trends in immunology

[ISO-abbreviation] Trends Immunol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / pre-T cell receptor alpha

[Number-of-references] 48

   

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The acquired activation of stem cell leukemia (SCL) during T lymphopoiesis is a common event in T-cell acute lymphoblastic leukemia (T-ALL).

Here, we generated tamoxifen (TAM)-inducible transgenic mice (lck-ER(T2)-SCL) to study the consequences of acquired SCL activation during T-cell development.

Aberrant activation of SCL in thymocytes resulted in the accumulation of immature CD4(+)CD8(+) (double-positive, DP) cells by preventing normal surface expression of the T-cell receptor alphabeta (TCRalphabeta) complex.

[MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / metabolism. Leukemia, T-Cell / genetics. Proto-Oncogene Proteins / genetics. Receptor, Notch1 / metabolism

[MeSH-minor] Animals. CD4-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / cytology. Cell Survival. Genes, T-Cell Receptor beta. Mice. Mice, Transgenic. Models, Biological. Organ Culture Techniques. Signal Transduction / physiology. Thymus Gland / cytology. Thymus Gland / embryology

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(PMID = 17698635.001).

[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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse

   

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Chromosome 6q deletions are also commonly found in lymphoid malignancies such as acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), non-Hodgkins lymphoma (NHL), multiple myeloma (MM), mantle zone lymphoma (MZL), and Waldenström's macroglobulinemia (WM).

In childhood B- and T-cell ALL a deletion of 6q is the hallmark of a neutral prognosis; however, it may be cytogenetically obscure or cryptic, requiring interphase FISH analysis.

In adult ALL it indicates a favorable prognosis, but in CLL, B-cell small lymphocytic lymphoma (SLL), WM, and MM it has a poor prognosis.

Since the deletion of 6q has prognostic implications and may be used to monitor residual disease, FISH analysis remains a valuable tool in treatment of these disorders.

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(PMID = 19952391.001).

[ISSN] 1523-7834

[Journal-full-title] Journal of the Association of Genetic Technologists

[ISO-abbreviation] J Assoc Genet Technol

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Differential upregulation of CD38 on different T-cell subsets may influence the ability to reconstitute CD4+ T cells under successful highly active antiretroviral therapy.

BACKGROUND: Immune activation is an independent surrogate marker of CD4 T-cell depletion in HIV-infected patients.

Highly active antiretroviral therapy (HAART) reduces disease progression as a direct consequence of suppressing HIV replication.

So far, it is unclear to what extent immune activation may influence the evolution of CD4 T-cell counts in patients on HAART.

In patients on successful HAART, immune activation declined in all T-cell subsets, particularly among memory CD8+ cells.

There was a significant correlation between the CD8+ T-cell activation decay and the increase of CD4+ T cells on HAART.

Patients with the highest decline in CD8 activation were those showing the highest CD4 T-cell gains after 12 months of therapy.

CONCLUSIONS: The level of CD38 expression on different T-cell subsets is differentially upregulated in drug-naive HIV-infected patients.

After successful HAART, immune activation decreases in all T-cell subsets, although it still remains elevated in most cases after 12 months of HAART.

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(PMID = 15764953.001).

[ISSN] 1525-4135

[Journal-full-title] Journal of acquired immune deficiency syndromes (1999)

[ISO-abbreviation] J. Acquir. Immune Defic. Syndr.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Membrane Glycoproteins; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human

   

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[Title] Deregulation of the telomerase reverse transcriptase (TERT) gene by chromosomal translocations in B-cell malignancies.

Here we show that this locus including the gene encoding the telomerase reverse-transcriptase TERT at 5p13.33 is rarely but recurrently targeted by somatic chromosomal translocations to IGH and non-IG loci in B-cell neoplasms, including acute lymphoblastic leukemia, chronic lymphocytic leukemia, mantle cell lymphoma and splenic marginal zone lymphoma.

These data suggest that deregulation of TERT gene by chromosomal abnormalities leading to increased telomerase activity might contribute to B-cell lymphomagenesis.

[MeSH-major] Leukemia, B-Cell / genetics. Lymphoma, B-Cell / genetics. Telomerase / genetics. Translocation, Genetic

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(PMID = 20460502.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United Kingdom / Medical Research Council / / MC/ U132670597

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase

   

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[Title] Notch and Ikaros: not only converging players in T cell leukemia.

Notch3 overexpression has been observed in virtually 100% of T cell acute lymphoblastic leukemia (T-ALL).

A high percentage of infant B- and T-ALLs also display an increased expression of non DNA-binding Ikaros isoforms.

We recently suggested that pre-TCR is the missing link between Notch and Ikaros in T cell leukemogenesis.

Our studies demonstrate that the presence of pre-TCR is required to sustain a Notch3-induced altered expression of spliced Ikaros isoforms.

Moreover, we identified HuD, an RNA-binding protein able to regulate both mRNA stability and alternative splicing, as the potential pre-TCR-dependent mediator of Notch3 activity.

Our findings may help in clarifying the regulatory mechanism of Ikaros alternative splicing and suggest a crosstalk among Notch3, pre-TCR signalling and spliced Ikaros variants in T cell leukemogenesis, mediated by HuD.

[MeSH-major] Ikaros Transcription Factor / physiology. Leukemia, T-Cell / metabolism. Receptors, Notch / physiology

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(PMID = 18032925.001).

[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; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Notch; 148971-36-2 / Ikaros Transcription Factor

[Number-of-references] 66

   

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EGFP fluorescence revealed that ZIP3 was expressed in the inner cell mass of the blastocyst and later during embryonic development in many tissues.

In knockout mice stressed with a zinc-deficient diet during pregnancy or at weaning, a subtle increase in the sensitivity to abnormal morphogenesis of the embryo and to depletion of thymic pre-T cells, respectively, was noted.

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[Cites] Cell Mol Life Sci. 2002 Apr;59(4):627-47 [12022471.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13042-7 [9789037.001]

[Cites] J Biol Chem. 2002 Jul 19;277(29):26389-95 [11997387.001]

[Cites] J Nutr. 2002 Nov;132(11):3301-7 [12421843.001]

[Cites] J Nutr. 2003 Jan;133(1):45-50 [12514265.001]

[Cites] Nucleic Acids Res. 2003 Jan 15;31(2):532-50 [12527760.001]

[Cites] Biochim Biophys Acta. 2003 Apr 1;1611(1-2):16-30 [12659941.001]

[Cites] J Nutr. 2003 May;133(5):1403-8 [12730429.001]

[Cites] J Biol Chem. 2003 Aug 29;278(35):33474-81 [12801924.001]

[Cites] J Nutr. 2003 Nov;133(11):3378-85 [14608047.001]

[Cites] J Biol Chem. 2003 Dec 12;278(50):50142-50 [14525987.001]

[Cites] Cell Mol Life Sci. 2004 Jan;61(1):49-68 [14704853.001]

[Cites] J Biol Chem. 2004 Feb 6;279(6):4523-30 [14612438.001]

[Cites] Nature. 2004 May 20;429(6989):298-302 [15129296.001]

[Cites] J Biol Chem. 2004 Jun 4;279(23):24631-9 [15054103.001]

[Cites] Annu Rev Nutr. 2004;24:151-72 [15189117.001]

[Cites] Annu Rev Nutr. 2004;24:277-98 [15189122.001]

[Cites] Genesis. 2004 Oct;40(2):74-81 [15452870.001]

[Cites] Gastroenterology. 1977 Sep;73(3):587-92 [196972.001]

[Cites] Arch Fr Pediatr. 1978 Jan;35(1):63-73 [637663.001]

[Cites] Ann Dermatol Venereol. 1977 Nov;104(11):737-44 [612256.001]

[Cites] Acta Paediatr Scand. 1981 Mar;70(2):269-73 [7234413.001]

[Cites] J Nutr. 1999 Sep;129(9):1643-8 [10460198.001]

[Cites] J Biol Chem. 2004 Nov 19;279(47):49082-90 [15358787.001]

[Cites] J Biol Chem. 2004 Dec 3;279(49):51433-41 [15322118.001]

[Cites] J Biol Chem. 2005 Jan 7;280(1):787-95 [15509557.001]

[Cites] Am J Physiol Cell Physiol. 2005 May;288(5):C1042-7 [15634741.001]

[Cites] Biochim Biophys Acta. 2000 May 1;1465(1-2):190-8 [10748254.001]

[Cites] Epilepsy Res. 2000 Apr;39(2):153-69 [10759303.001]

[Cites] J Nutr. 2000 May;130(5S Suppl):1360S-6S [10801944.001]

[Cites] J Nutr. 2000 May;130(5S Suppl):1399S-406S [10801951.001]

[Cites] J Biol Chem. 2000 Nov 3;275(44):34803-9 [10952993.001]

[Cites] J Nutr. 2001 Jan;131(1):46-52 [11208937.001]

[Cites] Annu Rev Nutr. 2001;21:429-52 [11375444.001]

[Cites] Nutr Rev. 2002 Apr;60(4):121-4 [12002684.001]

[Cites] Pediatrics. 1982 Jun;69(6):773-7 [6918908.001]

[Cites] Cell. 1984 May;37(1):171-7 [6722869.001]

[Cites] Annu Rev Nutr. 1985;5:43-68 [3896272.001]

[Cites] Cell. 1987 Nov 6;51(3):503-12 [2822260.001]

[Cites] Biochemistry. 1990 Jun 19;29(24):5647-59 [2200508.001]

[Cites] J Lab Clin Med. 1990 Sep;116(3):275-6 [2401844.001]

[Cites] Prog Food Nutr Sci. 1990;14(2-3):193-258 [2293243.001]

[Cites] Br J Nutr. 1993 May;69(3):835-48 [8329358.001]

[Cites] Nucleic Acids Res. 1994 Nov 25;22(23):5016-23 [7800494.001]

[Cites] Science. 1996 Feb 23;271(5252):1081-5 [8599083.001]

[Cites] J Nutr. 1996 Apr;126(4):825-33 [8613884.001]

[Cites] Curr Opin Cell Biol. 1997 Aug;9(4):573-7 [9263657.001]

[Cites] Nat Genet. 1997 Nov;17(3):292-7 [9354792.001]

[Cites] Hum Mol Genet. 2002 Jul 15;11(15):1775-84 [12095919.001]

(PMID = 15964816.001).

[ISSN] 0270-7306

[Journal-full-title] Molecular and cellular biology

[ISO-abbreviation] Mol. Cell. Biol.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / DK50181

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

[Publication-country] United States

[Chemical-registry-number] 0 / Carrier Proteins; 0 / Cation Transport Proteins; 0 / Slc39a3 protein, mouse; 0 / zinc-binding protein; 147336-22-9 / Green Fluorescent Proteins; J41CSQ7QDS / Zinc

[Other-IDs] NLM/ PMC1156975

   

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Recent studies have highlighted the role of Notch signalling in the development of T cell acute lymphoblasic leukaemia (T-ALL).

The aims of this study were to determine the effect of Notch signalling on apoptosis in human T-ALL cell lines and to identify targets of Notch signalling that may mediate this effect.

Microarray analysis revealed that GIMAP5, a gene coding for an anti-apoptotic intracellular protein, is upregulated by Notch in T-ALL cell lines.

[MeSH-major] Apoptosis. GTP-Binding Proteins / biosynthesis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. Receptors, Notch / metabolism. Signal Transduction

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[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

(PMID = 20817506.001).

[ISSN] 1096-0961

[Journal-full-title] Blood cells, molecules & diseases

[ISO-abbreviation] Blood Cells Mol. Dis.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / GIMAP5 protein, human; 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / NOTCH3 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Receptors, Notch; EC 3.6.1.- / GTP-Binding Proteins

   

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BACKGROUND: Extranodal non-Hodgkin lymphoma (NHL) accounts for much of the increase in NHL incidence in the past three decades in the United States, but its descriptive epidemiology is scarce in the literature.

We grouped anatomic sites of extranodal NHLs according to the Surveillance, Epidemiology, and End Results (SEER) site recodes, and histology subtypes according to the nested classification of lymphoid neoplasms developed by the Pathology Working Group of the International Lymphoma Epidemiology Consortium.

RESULTS: Blacks and Asians/Pacific Islanders (APIs) experienced incidence rates about the same as or lower than whites' for B-cell extranodal NHL as a whole and most of its histologic subtypes.

The significant exceptions are: API men had a 40% higher rate of marginal zone lymphoma (MZL) than white men, and API women had a 12% higher rate of diffuse large B-cell lymphoma (DLBCL) than white women.

The rates of all T-cell extranodal NHLs combined and peripheral T-cell lymphoma (PTCL) among black women exceeded those of white women by 46% and 18%, respectively.

Blacks had higher rates of the two most common types of T-cell extranodal NHL and APIs had higher rate of the two common types of B-cell types than whites.

[MeSH-major] Lymphoma, Non-Hodgkin / epidemiology. Lymphoma, Non-Hodgkin / pathology

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(PMID = 19853554.001).

[ISSN] 1877-783X

[Journal-full-title] Cancer epidemiology

[ISO-abbreviation] Cancer Epidemiol

[Language] eng

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

[Publication-country] Netherlands