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1. Shvidel L, Sigler E, Vorst E, Feldberg E, Voskoboinic N, Shtalrid M, Berrebi A: A novel cytogenetic aberration found in stem cell leukemia/lymphoma syndrome. Leukemia; 2008 Mar;22(3):644-6
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  • [Title] A novel cytogenetic aberration found in stem cell leukemia/lymphoma syndrome.
  • [MeSH-major] Chromosomes, Human, Pair 12 / ultrastructure. Chromosomes, Human, Pair 8 / ultrastructure. Hematopoietic Stem Cells / pathology. Leukemia, Myelomonocytic, Acute / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Primary Myelofibrosis / genetics. Translocation, Genetic
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Disease Progression. Fatal Outcome. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Syndrome

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  • (PMID = 17928887.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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2. Tschan MP, Reddy VA, Ress A, Arvidsson G, Fey MF, Torbett BE: PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity. Oncogene; 2008 May 29;27(24):3489-93
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  • The transcription factor PU.1 is essential for terminal myeloid differentiation, B- and T-cell development, erythropoiesis and hematopoietic stem cell maintenance.
  • PU.1 functions as oncogene in Friend virus-induced erythroleukemia and as tumor suppressor in acute myeloid leukemias.
  • Moreover, Friend virus-induced erythroleukemia requires maintenance of PU.1 expression and the disruption of p53 function greatly accelerates disease progression.
  • It has been hypothesized that p53-mediated expression of the p21(Cip1) cell cycle inhibitor during differentiation of pre-erythroleukemia cells promotes selection against p53 function.
  • We demonstrate that PU.1 reduces the transcriptional activity of the p53 tumor suppressor family and thus inhibits activation of genes important for cell cycle regulation and apoptosis.
  • Lastly, knocking down endogenous PU.1 in p53 wild-type REH B-cell precursor leukemia cells leads to increased expression of the p53 target p21(Cip1).
  • [MeSH-minor] Apoptosis. Blotting, Western. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Humans. Immunoprecipitation. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein Isoforms. RNA, Small Interfering / pharmacology. Transcriptional Activation. Tumor Cells, Cultured. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism

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  • (PMID = 18193090.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI49165; United States / NIDDK NIH HHS / DK / DK49886
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / proto-oncogene protein Spi-1; 0 / tumor suppressor protein p73
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3. Akhoondi S, Sun D, von der Lehr N, Apostolidou S, Klotz K, Maljukova A, Cepeda D, Fiegl H, Dafou D, Marth C, Mueller-Holzner E, Corcoran M, Dagnell M, Nejad SZ, Nayer BN, Zali MR, Hansson J, Egyhazi S, Petersson F, Sangfelt P, Nordgren H, Grander D, Reed SI, Widschwendter M, Sangfelt O, Spruck C: FBXW7/hCDC4 is a general tumor suppressor in human cancer. Cancer Res; 2007 Oct 1;67(19):9006-12
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  • The highest mutation frequencies were found in tumors of the bile duct (cholangiocarcinomas, 35%), blood (T-cell acute lymphocytic leukemia, 31%), endometrium (9%), colon (9%), and stomach (6%).
  • Furthermore, we show that Fbxw7Arg465 hotspot mutant can abrogate wild-type Fbxw7 function through a dominant negative mechanism.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Genes, Tumor Suppressor. Neoplasms / genetics. Ubiquitin-Protein Ligases / genetics

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  • [ErratumIn] Cancer Res. 2008 Feb 15;68(4):1245. Dofou, Dimitra [corrected to Dafou, Dimitra]
  • (PMID = 17909001.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Protein Isoforms; 6R795CQT4H / 5-Methylcytosine; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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4. Fu JF, Liang DC, Shih LY: Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL. Am J Clin Pathol; 2007 Jan;127(1):24-30
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  • [Title] Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL.
  • t(11;19)(q23;p13.3); is one of the common chromosomal translocations in acute leukemias involving MLL rearrangements.
  • In a study of acute leukemias, 148 patients were identified to have MLL rearrangements by Southern blot analysis.
  • Of 15 patients with MLL/ENL, 7 had precursor B-cell acute lymphoblastic leukemia, 4 had T-cell acute lymphoblastic leukemia, and 4 had acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Oncogene Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 17145626.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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5. Thompson BJ, Buonamici S, Sulis ML, Palomero T, Vilimas T, Basso G, Ferrando A, Aifantis I: The SCFFBW7 ubiquitin ligase complex as a tumor suppressor in T cell leukemia. J Exp Med; 2007 Aug 6;204(8):1825-35
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  • [Title] The SCFFBW7 ubiquitin ligase complex as a tumor suppressor in T cell leukemia.
  • Recent studies have shown that activating mutations of NOTCH1 are responsible for the majority of T cell acute lymphoblastic leukemia (T-ALL) cases.
  • Furthermore, we identify inactivating FBW7 mutations in a large fraction of human T-ALL lines and primary leukemias.
  • Our data suggest that FBW7 is a novel tumor suppressor in T cell leukemia, and implicate the loss of FBW7 function as a potential mechanism of drug resistance in T-ALL.

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  • (PMID = 17646408.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120196-02; United States / NCI NIH HHS / CA / R01 CA105129; United States / NCI NIH HHS / CA / CA120196; United States / NCI NIH HHS / CA / R01 CA120196-02; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01CA105129
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Stem Cell Factor; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2118676
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6. Tanaka M, Kano Y, Akutsu M, Tsunoda S, Izumi T, Yazawa Y, Miyawaki S, Mano H, Furukawa Y: The cytotoxic effects of gemtuzumab ozogamicin (mylotarg) in combination with conventional antileukemic agents by isobologram analysis in vitro. Anticancer Res; 2009 Nov;29(11):4589-96
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  • BACKGROUND: The CD33 antigen is expressed on leukemia cells in most patients with acute myeloid leukemia (AML) and acute promyelocytic leukemia (APL), and in 20% of patients with acute lymphoblastic leukemia (ALL), while it is absent from pluripotent hematopoietic stem cells and nonhematopoietic cells.
  • Gemtuzumab ozogamicin (GO) is an immunoconjugate of an anti-CD33 antibody linked to calicheamicin, which is a potent cytotoxic agent that causes double-strand DNA breaks, resulting in cell death.
  • GO was developed against CD33 antigen-positive leukemias.
  • MATERIALS AND METHODS: The cytotoxic effects of GO in combination with antileukemic agents were studied against human CD33 antigen-positive leukemia HL-60, U937, TCC-S and NALM20 cells.
  • The leukemia cells were exposed simultaneously to GO and to the other agents for 4 days.
  • Cell growth inhibition was determined using a MTT reduction assay.
  • [MeSH-major] Aminoglycosides / pharmacology. Antibodies, Monoclonal / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Immunotoxins / pharmacology. Leukemia / drug therapy
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Antibodies, Monoclonal, Humanized. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Cell Line, Tumor. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dose-Response Relationship, Drug. Doxorubicin / administration & dosage. Drug Synergism. Etoposide / administration & dosage. HL-60 Cells. Humans. Idarubicin / administration & dosage. Methotrexate / administration & dosage. Mitoxantrone / administration & dosage. Sialic Acid Binding Ig-like Lectin 3. U937 Cells. Vincristine / administration & dosage

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  • (PMID = 20032408.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; BZ114NVM5P / Mitoxantrone; E7WED276I5 / 6-Mercaptopurine; YL5FZ2Y5U1 / Methotrexate; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
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7. Zeng Y, Ni X, Meng WT, Wen Q, Jia YQ: [Inhibitive effect of artesunate on human lymphoblastic leukemia/lymphoma cells]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2009 Nov;40(6):1038-43
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  • [Title] [Inhibitive effect of artesunate on human lymphoblastic leukemia/lymphoma cells].
  • OBJECTIVE: To test the effect of Artesunate (ART) on the proliferation of Raji cells, Jurkat cells and acute lymphoblastic leukemia (ALL) primary cells; to determine the synergistic antiproliferation effect between ART and Vincristine (VCR) or Cytarabine(Ara-C) on Raji and Jurkat cells; and to explore the mechanism of ART induced apoptosis of tumor cells in vitro.
  • CONCLUSION: ART alone or combined with chemotherapy drugs could inhibit the proliferation of B/T lymphocytic tumor cell lines as well ALL primary cells in vitro, probably through the mechanism of apoptosis, which suggest that ART is likely to be a potential drug in the treatment of leukemia/lymphoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Artemisinins / pharmacology. Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Blood-Brain Barrier / drug effects. Cell Line, Tumor. Cytarabine / pharmacology. Drug Synergism. Humans. Jurkat Cells

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  • (PMID = 20067115.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Artemisinins; 04079A1RDZ / Cytarabine; 60W3249T9M / artesunate
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8. Kode J, Dudhal N, Banavali S, Chiplunkar S: T-cell receptor gamma and delta junctional gene rearrangements as diagnostic and prognostic biomarker for T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2006 Apr;47(4):769-70
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  • [Title] T-cell receptor gamma and delta junctional gene rearrangements as diagnostic and prognostic biomarker for T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Biomarkers, Tumor. Gene Rearrangement. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, gamma-delta / metabolism

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  • (PMID = 16886283.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Antigen, T-Cell, gamma-delta
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9. Cossu F: Genetics of SCID. Ital J Pediatr; 2010;36:76
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  • Human SCID (Severe Combined Immunodeficiency) is a prenatal disorder of T lymphocyte development, that depends on the expression of numerous genes.
  • The knowledge of the genetic basis of SCID is essential for diagnosis (e.g., clinical phenotype, lymphocyte profile) and treatment (e.g., use and type of pre-hematopoietic stem cell transplant conditioning).Over the last years novel genetic defects causing SCID have been discovered, and the molecular and immunological mechanisms of SCID have been better characterized.
  • Distinct forms of SCID show both common and peculiar (e.g., absence or presence of nonimmunological features) aspects, and they are currently classified into six groups according to prevalent pathophysiological mechanisms: impaired cytokine-mediated signaling; pre-T cell receptor defects; increased lymphocyte apoptosis; defects in thymus embryogenesis; impaired calcium flux; other mechanisms.This review is the updated, extended and largely modified translation of the article "Cossu F: Le basi genetiche delle SCID", originally published in Italian language in the journal "Prospettive in Pediatria" 2009, 156:228-238.
  • [MeSH-minor] Genetic Therapy. Genotype. Hematopoietic Stem Cell Transplantation. Humans. Infant, Newborn. Neonatal Screening. T-Lymphocytes / pathology

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  • (PMID = 21078154.001).
  • [ISSN] 1824-7288
  • [Journal-full-title] Italian journal of pediatrics
  • [ISO-abbreviation] Ital J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2999594
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10. Garbe AI, Krueger A, Gounari F, Zúñiga-Pflücker JC, von Boehmer H: Differential synergy of Notch and T cell receptor signaling determines alphabeta versus gammadelta lineage fate. J Exp Med; 2006 Jun 12;203(6):1579-90
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  • [Title] Differential synergy of Notch and T cell receptor signaling determines alphabeta versus gammadelta lineage fate.
  • Thymic precursors expressing the pre-T cell receptor (TCR), the gammadeltaTCR, or the alphabetaTCR can all enter the CD4+ 8+ alphabeta lineage, albeit with different efficacy.
  • In particular, in alphabeta lineage commitment, the pre-TCR synergizes more efficiently with Notch signals than the other two TCRs, whereas gammadeltaTCR-expressing cells can survive and expand in the absence of Notch signals, even though Notch signaling enhances their proliferation.
  • These observations suggest a new model of alphabeta versus gammadelta lineage choice in which lineage fate is determined by the extent of synergy between TCR and Notch signaling and in which the evolutionarily recent advent of the cell-autonomously signaling pre-TCR increased the efficacy of alphabeta T cell generation.

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  • (PMID = 16754723.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA10990; United States / NIAID NIH HHS / AI / R01 AI47281; United States / NIAID NIH HHS / AI / R01 AI047281; United States / NIAID NIH HHS / AI / R01 AI45846
  • [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 / Homeodomain Proteins; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / Receptors, Notch; 128559-51-3 / RAG-1 protein
  • [Other-IDs] NLM/ PMC2118312
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11. Sigalas P, Tourvas AD, Moulakakis A, Pangalis G, Kontopidou F: Nelarabine induced complete remission in an adult with refractory T-lineage acute lymphoblastic leukemia: A case report and review of the literature. Leuk Res; 2009 Jul;33(7):e61-3
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  • [Title] Nelarabine induced complete remission in an adult with refractory T-lineage acute lymphoblastic leukemia: A case report and review of the literature.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Salvage Therapy

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  • (PMID = 19157550.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 60158CV180 / nelarabine
  • [Number-of-references] 23
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12. Derré L, Bruyninx M, Baumgaertner P, Ferber M, Schmid D, Leimgruber A, Zoete V, Romero P, Michielin O, Speiser DE, Rufer N: Distinct sets of alphabeta TCRs confer similar recognition of tumor antigen NY-ESO-1157-165 by interacting with its central Met/Trp residues. Proc Natl Acad Sci U S A; 2008 Sep 30;105(39):15010-5
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  • Here, we studied T cell receptor (TCR) primary structure and function of 605 HLA-A*0201/NY-ESO-1(157-165)-specific CD8 T cell clones derived from five melanoma patients.
  • All remaining T cell clones belong to two additional sets expressing BV1 or BV13 TCRs, associated with alpha-chains with highly diverse VJ usage, CDR3 amino acid sequence, and length.
  • Yet, all T cell clonotypes recognize tumor antigen with similar functional avidity.
  • Two residues, Met-160 and Trp-161, located in the middle region of the NY-ESO-1(157-165) peptide, are critical for recognition by most of the T cell clonotypes.
  • [MeSH-major] Neoplasm Proteins / immunology. Peptide Fragments / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology

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  • (PMID = 18809922.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / peptide NY-ESO-1 157-165; 2ZD004190S / Threonine; AE28F7PNPL / Methionine
  • [Other-IDs] NLM/ PMC2567484
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13. Martínez-Delgado B, Cuadros M, Honrado E, Ruiz de la Parte A, Roncador G, Alves J, Castrillo JM, Rivas C, Benítez J: Differential expression of NF-kappaB pathway genes among peripheral T-cell lymphomas. Leukemia; 2005 Dec;19(12):2254-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of NF-kappaB pathway genes among peripheral T-cell lymphomas.
  • Nuclear factor kappa B (NF-kappaB) is one important pathway in T-cell proliferation and survival.
  • In a previously reported microarray study, we found NF-kappaB pathway genes differentially expressed between peripheral (PTCL) and lymphoblastic lymphomas.
  • This distinction was found among all T-cell lymphoma categories analyzed (PTCL unspecified, angioimmunoblastic, cutaneous and natural killer/T lymphomas) with the exception of anaplastic lymphomas (ALCL), which were characterized by reduced NF-kappaB expression in anaplastic cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, T-Cell, Peripheral / genetics. NF-kappa B / genetics

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  • (PMID = 16270046.001).
  • [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 / NF-kappa B
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14. Mullighan CG: Mutations of NOTCH1, FBXW7, and prognosis in T-lineage acute lymphoblastic leukemia. Haematologica; 2009 Oct;94(10):1338-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutations of NOTCH1, FBXW7, and prognosis in T-lineage acute lymphoblastic leukemia.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. T-Lymphocytes / pathology. Ubiquitin-Protein Ligases / genetics
  • [MeSH-minor] Cell Lineage / physiology. Humans. Mutation / genetics. Prognosis

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  • [CommentOn] Haematologica. 2009 Oct;94(10):1383-90 [19794083.001]
  • (PMID = 19794079.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2754947
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15. Thörn I, Botling J, Hermansson M, Lönnerholm G, Sundström C, Rosenquist R, Barbany G: Monitoring minimal residual disease with flow cytometry, antigen-receptor gene rearrangements and fusion transcript quantification in Philadelphia-positive childhood acute lymphoblastic leukemia. Leuk Res; 2009 Aug;33(8):1047-54
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  • [Title] Monitoring minimal residual disease with flow cytometry, antigen-receptor gene rearrangements and fusion transcript quantification in Philadelphia-positive childhood acute lymphoblastic leukemia.
  • In this study, we followed minimal residual disease (MRD) in eight children with Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL) using (i) flow cytometry (FCM), (ii) real-time quantitative PCR of IG/TCR gene rearrangements and (iii) RT-PCR detecting fusion gene transcripts.
  • [MeSH-major] Flow Cytometry / methods. Gene Expression Regulation, Leukemic. Gene Rearrangement, T-Lymphocyte. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-abl / biosynthesis. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19157547.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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16. Dessars B, Heimann P, Swillens S, El Housni H: Limitations and practical procedure in BclII-Ig heavy chain gene rearrangement real-time quantitative polymerase chain reaction. J Mol Diagn; 2006 Feb;8(1):133-6
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  • Follicular lymphoma is characterized by the t(14;18)(q32;q21) translocation, which juxtaposes Ig heavy chain gene (IgH) sequences with the BclII gene.
  • Several publications have highlighted the importance of molecular follow-up in follicular lymphoma, demonstrating that the detection of cells bearing the BclII-IgH rearrangement by real-time quantitative polymerase chain reaction (RQ-PCR) can anticipate a clinical relapse.
  • While we were designing the assay using Taqman technology, Moppett et al (Moppett J, van der Velden VHJ, Wijkhuijs AJM, Hancock J, van Dongen JJM, Goulden N: Inhibition affecting RQ-PCR-based assessment of minimal residual disease in acute lymphoblastic leukemia: reversal by addition of bovine serum albumin.
  • Leukemia 2003, 17:268-270) reported PCR inhibition problems in around 15% of blood and bone marrow samples, affecting the DNA quantification and thus the assessment of minimal residual disease.
  • In our studies, we observed the same phenomenon in a single follicular lymphoma case and extended our study to other available cases.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Follicular / complications. Polymerase Chain Reaction / methods. Proto-Oncogene Proteins c-bcl-2 / genetics

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  • (PMID = 16436645.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Organic Chemicals; 0 / Proto-Oncogene Proteins c-bcl-2; 163795-75-3 / SYBR Green I
  • [Other-IDs] NLM/ PMC1867576
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17. de Graaf AO, van Krieken JH, Tönnissen E, Wissink W, van de Locht L, Overes I, Dolstra H, de Witte T, van der Reijden BA, Jansen JH: Expression of C-IAP1, C-IAP2 and SURVIVIN discriminates different types of lymphoid malignancies. Br J Haematol; 2005 Sep;130(6):852-9
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  • (De-)regulation of apoptosis plays an important role in normal and malignant lymphopoiesis.
  • Apoptosis-regulating genes of the BCL-2 family and the recently identified inhibitors of apoptosis (IAP) family have been implicated in different types of non-Hodgkin lymphoma (NHL).
  • In total, 137 samples from B- and T-cell acute lymphoblastic leukaemia (ALL), B-cell chronic lymphocytic leukaemia (CLL), six different NHL types and three control tissue types were analysed.
  • CLL samples, as well as B-ALL and follicular lymphoma samples showed high similarity in the expression of these apoptosis-regulating genes and could be distinguished from each other and other diseases and controls.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Lymphoid / diagnosis. Lymphoma, Non-Hodgkin / diagnosis. Neoplasm Proteins / metabolism
  • [MeSH-minor] Apoptosis. Diagnosis, Differential. Discriminant Analysis. Humans. Inhibitor of Apoptosis Proteins. Microtubule-Associated Proteins / metabolism. Polymerase Chain Reaction / methods. Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Ubiquitin-Protein Ligases

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  • (PMID = 16156855.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC2 protein, human; 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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18. Zuo YX, Zhang LP, Lu AD, Wang B, Liu GL: [Clinical characteristics of children with B cell type acute lymphoblastic leukemia carrying different fusion gene]. Zhongguo Dang Dai Er Ke Za Zhi; 2010 Mar;12(3):172-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical characteristics of children with B cell type acute lymphoblastic leukemia carrying different fusion gene].
  • OBJECTIVE: To investigate whether there were differences in the clinical characteristics, cytogenetic characteristics, immunophenotype and prognosis in children with B cell type acute lymphoblastic leukemia (B-ALL) carrying different fusion genes.
  • Data including clinical characteristics, morphology, immunophenotype and cytogenetic characteristics were collected, and the disease-free survival (DFS) was evaluated.
  • Up to now,17 children who survived were disease-free.
  • Twelve children showed pre-B-ALL immunophenotype.
  • In the 11 children with BCR/ABL+B-ALL, 10 children showed common B type immunophenotype.
  • Their morphologic diagnosis was FAB-L1.
  • Both showed the Pro-B-ALL immunophenotype.
  • One child discontinued treatment at the early stage of chemotherapy, and the other child survived disease-free until now.
  • [MeSH-major] Gene Fusion. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Female. Homeodomain Proteins / genetics. Humans. Immunophenotyping. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 20350423.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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19. Gez S, Crossett B, Christopherson RI: Differentially expressed cytosolic proteins in human leukemia and lymphoma cell lines correlate with lineages and functions. Biochim Biophys Acta; 2007 Sep;1774(9):1173-83
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  • [Title] Differentially expressed cytosolic proteins in human leukemia and lymphoma cell lines correlate with lineages and functions.
  • Identification of cytosolic proteins differentially expressed between types of leukemia and lymphoma may provide a molecular basis for classification and understanding their cellular properties.
  • Two-dimensional fluorescence difference gel electrophoresis (DIGE) and mass spectrometry have been used to identify proteins that are differentially expressed in cytosolic extracts from four human leukemia and lymphoma cell lines: HL-60 (acute promyelocytic leukemia), MEC1 (B-cell chronic lymphocytic leukemia), CCRF-CEM (T-cell acute lymphoblastic leukemia) and Raji (B-cell Burkitt's lymphoma).
  • A total of 247 differentially expressed proteins were identified between the four cell lines.
  • Analysis of the data by principal component analysis identified 22 protein spots (17 different protein species) differentially expressed at more than a 95% variance level between these cell lines.
  • Several of these proteins were differentially expressed in only one cell line: HL-60 (myeloperoxidase, phosphoprotein 32 family member A, ras related protein Rab-11B, protein disulfide-isomerase, ran-specific GTPase-activating protein, nucleophosmin and S-100 calcium binding protein A4), and Raji (ezrin).
  • Several of these proteins were differentially expressed in two cell lines: Raji and MEC1 (C-1-tetrahydrofolate synthase, elongation factor 2, alpha- and beta-tubulin, transgelin-2 and stathmin).
  • The differentially expressed proteins identified in these four cell lines correlate with cellular properties and provide insights into the molecular basis of these malignancies.
  • [MeSH-major] Cytosol / metabolism. Leukemia / metabolism. Lymphoma / metabolism. Neoplasm Proteins / biosynthesis
  • [MeSH-minor] Cell Line, Tumor. Cell Lineage. Cytoskeletal Proteins / biosynthesis. Electrophoresis, Gel, Two-Dimensional. Gene Expression Profiling. HL-60 Cells. Humans. Phosphopyruvate Hydratase / biosynthesis. Ubiquitin-Conjugating Enzymes / biosynthesis

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  • (PMID = 17698427.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Neoplasm Proteins; 0 / ezrin; EC 4.2.1.11 / Phosphopyruvate Hydratase; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
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20. Arellano ML, Langston A, Winton E, Flowers CR, Waller EK: Treatment of relapsed acute leukemia after allogeneic transplantation: a single center experience. Biol Blood Marrow Transplant; 2007 Jan;13(1):116-23
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  • [Title] Treatment of relapsed acute leukemia after allogeneic transplantation: a single center experience.
  • Relapsed acute leukemia after allogeneic transplantation has a poor prognosis and most reports have focused on the role of second transplantations in relapsed patients.
  • We report our single-institution experience on the management of relapsed acute leukemia after allogeneic transplantation.
  • We aimed to describe the outcome of relapsed acute leukemia after allogeneic transplantation at our institution and investigate whether maneuvers intended to augment donor T cell allogeneic reactivity were associated with durable graft-versus-leukemia effects.
  • We analyzed 310 patients with acute leukemia who received allogeneic hematopoietic progenitor cell transplants from HLA-matched donors between 1982 and 2005 (229 with acute myelogenous leukemia, 81 with acute lymphoblastic leukemia).
  • One hundred of 310 patients (32%) with acute leukemia relapsed after transplantation, including 28 of 81 patients (35%) with acute lymphoblastic leukemia and 72 of 229 (31%) with acute myelogenous leukemia at a median of 136 days after transplantation.
  • The outlook for patients with post-transplant relapse of acute leukemia is extremely poor; currently, no single therapy consistently results in durable remissions.
  • [MeSH-major] Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Hematopoietic Stem Cell Transplantation. Interferon-alpha / therapeutic use. Leukemia, Myeloid, Acute / therapy. Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 17222760.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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21. Kohlmann A, Schoch C, Dugas M, Schnittger S, Hiddemann W, Kern W, Haferlach T: New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes. Leukemia; 2005 Jun;19(6):953-64
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  • [Title] New insights into MLL gene rearranged acute leukemias using gene expression profiling: shared pathways, lineage commitment, and partner genes.
  • Rearrangements of the MLL gene occur in both acute lymphoblastic and acute myeloid leukemias (ALL, AML).
  • This study addressed the global gene expression pattern of these two leukemia subtypes with respect to common deregulated pathways and lineage-associated differences.
  • We analyzed 73 t(11q23)/MLL leukemias in comparison to 290 other acute leukemias and demonstrate that 11q23 leukemias combined are characterized by a common specific gene expression signature.
  • Additionally, in unsupervised and supervised data analysis algorithms, ALL and AML cases with t(11q23) segregate according to the lineage they are derived from, that is, myeloid or lymphoid, respectively.
  • Through the use of novel biological network analyses, essential regulators of early B cell development, PAX5 and EBF, were shown to be associated with a clear B-lineage commitment in lymphoblastic t(11q23)/MLL leukemias.
  • Taken together, the identified molecular expression pattern of MLL fusion gene samples and biological networks revealed new insights into the aberrant transcriptional program in 11q23/MLL leukemias.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Cell Lineage / genetics. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Multigene Family. Myeloid-Lymphoid Leukemia Protein. Oligonucleotide Array Sequence Analysis. Transcription, Genetic. Translocation, Genetic

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  • (PMID = 15815718.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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22. Manabe A, Ohara A, Hasegawa D, Koh K, Saito T, Kiyokawa N, Kikuchi A, Takahashi H, Ikuta K, Hayashi Y, Hanada R, Tsuchida M, Tokyo Children's Cancer Study Group: Significance of the complete clearance of peripheral blasts after 7 days of prednisolone treatment in children with acute lymphoblastic leukemia: the Tokyo Children's Cancer Study Group Study L99-15. Haematologica; 2008 Aug;93(8):1155-60
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  • [Title] Significance of the complete clearance of peripheral blasts after 7 days of prednisolone treatment in children with acute lymphoblastic leukemia: the Tokyo Children's Cancer Study Group Study L99-15.
  • BACKGROUND: Treatment response has become one of the most important prognostic factors in childhood acute lymphoblastic leukemia.
  • We evaluated the significance of the complete clearance of peripheral leukemic blasts on survival in children with acute lymphoblastic leukemia.
  • DESIGN AND METHODS: Seven hundred and fifty-four children diagnosed with acute lymphoblastic leukemia, consecutively enrolled from 1999 to 2003 in the TCCSG L99-15 study, were eligible for analysis.
  • The event-free survival for Day8NoBlasts patients with B-lineage acute lymphoblastic leukemia and T-cell acute lymphoblastic leukemia was 89.8+/-2.1% (n=226) and 95.7+/-4.3% (n=23), respectively.
  • In a multivariate analysis, age at diagnosis, the initial white blood cell count, immunophenotype, and gender did not remain as independent risk factors for treatment failure, whereas Day8NoBlasts and marked hyperdiploidy (more than 50 chromosomes) became statistically significant.
  • CONCLUSIONS: Children with Day8NoBlasts constituted one third of all the cases with childhood acute lymphoblastic leukemia with an excellent outcome, and should be candidates for curative management with less intensive treatment.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Blast Crisis / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Prednisolone / therapeutic use

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  • [CommentIn] Haematologica. 2008 Aug;93(8):1124-8 [18669975.001]
  • (PMID = 18519521.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9PHQ9Y1OLM / Prednisolone
  • [Investigator] Isoyama K; Kinoshita A; Kamijo T; Kumagai MA; Yabe H; Morimoto T; Maeda M; Sugita K; Noguchi Y; Kaneko T; Sugita K; Sotomatsu M; Kajiwara M; Okimoto Y; Ohta S; Saito M; Fukushima T
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23. Smith MA: Update on developmental therapeutics for acute lymphoblastic leukemia. Curr Hematol Malig Rep; 2009 Jul;4(3):175-82
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  • [Title] Update on developmental therapeutics for acute lymphoblastic leukemia.
  • This is an exciting time in drug development for acute lymphoblastic leukemia (ALL).
  • Another important trend in ALL drug development is the increasing understanding at the molecular level of the genomic changes that occur in B-precursor and T-cell ALL.
  • Molecularly targeted agents of interest discussed in this review include novel antibody-based drugs targeted against leukemia surface antigens, proteasome inhibitors, mTOR inhibitors, JAK inhibitors, Aurora A kinase inhibitors, and inhibitors of Bcl-2 family proteins.
  • [MeSH-major] Drug Discovery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 20425431.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aniline Compounds; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Nucleosides; 0 / Sulfonamides; XKJ5VVK2WD / navitoclax
  • [Number-of-references] 79
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24. De Keersmaecker K, Lahortiga I, Mentens N, Folens C, Van Neste L, Bekaert S, Vandenberghe P, Odero MD, Marynen P, Cools J: In vitro validation of gamma-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-cell acute lymphoblastic leukemia. Haematologica; 2008 Apr;93(4):533-42
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  • [Title] In vitro validation of gamma-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Activating NOTCH1 mutations are common in T-cell acute lymphoblastic leukemia.
  • Inhibition of NOTCH1 signaling with gamma-secretase inhibitors causes cell cycle block, but only after treatment for several days.
  • We further documented the effects of gamma-secretase inhibitor treatment on T-cell acute lymphoblastic leukemia cell lines and tested whether combining gamma-secretase inhibitors with other anti-cancer drugs offers a therapeutic advantage.
  • DESIGN AND METHODS: The effect of gamma-secretase inhibitor treatment and combinations of gamma-secretase inhibitors with chemotherapy or glucocorticoids was assessed on T-cell acute lymphoblastic leukemia cell lines.
  • We sequenced NOTCH1 in T-cell acute lymphoblastic leukemia cases with ABL1 fusions and tested combinations of gamma-secretase inhibitors and the ABL1 inhibitor imatinib in a T-cell acute lymphoblastic leukemia cell line.
  • RESULTS: gamma-secretase inhibitor treatment for 5-7 days reversibly inhibited cell proliferation, caused cell cycle block in sensitive T-cell acute lymphoblastic leukemia cell lines, and caused differentiation of some T-cell acute lymphoblastic leukemia cell lines.
  • The cytotoxic effects of the chemotherapeutic agent vincristine were not significantly enhanced by addition of gamma-secretase inhibitors to T-cell acute lymphoblastic leukemia cell lines, but gamma-secretase inhibitor treatment sensitized cells to the effect of dexamethasone.
  • NOTCH1 mutations were identified in all T-cell acute lymphoblastic leukemia patients with ABL1 fusions and in a T-cell acute lymphoblastic leukemia cell line expressing NUP214-ABL1.
  • In this cell line, the anti-proliferative effect of imatinib was increased by pre-treatment with gamma-secretase inhibitors.
  • CONCLUSIONS: Short-term treatment of T-cell acute lymphoblastic leukemia cell lines with gamma-secretase inhibitors had limited effects on cell proliferation and survival.
  • Combinations of gamma-secretase inhibitors with other drugs may be required to obtain efficient therapeutic effects in T-cell acute lymphoblastic leukemia, and not all combinations may be useful.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Benzodiazepinones / pharmacology. Carbamates / pharmacology. Dipeptides / pharmacology. Enzyme Inhibitors / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Neoplasm Proteins / antagonists & inhibitors. Receptor, Notch1 / antagonists & inhibitors
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. DNA, Neoplasm / genetics. Daunorubicin / administration & dosage. Daunorubicin / pharmacology. Dexamethasone / administration & dosage. Dexamethasone / pharmacology. Drug Screening Assays, Antitumor. Drug Synergism. Humans. Imatinib Mesylate. In Vitro Techniques. Mutation. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / genetics. Piperazines / administration & dosage. Piperazines / pharmacology. Pyrimidines / administration & dosage. Pyrimidines / pharmacology. Sequence Analysis, DNA. Vincristine / administration & dosage. Vincristine / pharmacology

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  • [CommentIn] Haematologica. 2008 Apr;93(4):493-7 [18379008.001]
  • (PMID = 18322257.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzodiazepinones; 0 / Carbamates; 0 / DNA, Neoplasm; 0 / Dipeptides; 0 / Enzyme Inhibitors; 0 / L 685458; 0 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8A1O1M485B / Imatinib Mesylate; EC 3.4.- / Amyloid Precursor Protein Secretases; ZS7284E0ZP / Daunorubicin
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25. De Keersmaecker K, Marynen P, Cools J: Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia. Haematologica; 2005 Aug;90(8):1116-27
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  • [Title] Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia.
  • Over the past 20 years, a large number of genes involved in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL) has been identified by molecular characterization of recurrent chromosomal aberrations and more subtle genetic defects.
  • When reviewing the current list of oncogenes and tumor suppressor genes, it becomes clear that these can be grouped into four classes of mutations, which are involved in: (i) cell cycle deregulation;.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 16079112.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 129
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26. Kaya Z, Gursel T, Bakkaloglu SA, Kocak U, Atasever T, Oktar SO: Evaluation of renal function in Turkish children receiving BFM-95 therapy for acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2007 Jun;24(4):257-67
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  • [Title] Evaluation of renal function in Turkish children receiving BFM-95 therapy for acute lymphoblastic leukemia.
  • This study examined renal function in 42 children with acute lymphoblastic leukemia (ALL) treated according to BFM-95 protocol.
  • There was only mild tubular abnormality in 5.8% of patients (n = 17) in group 3, who were examined at a single time point a mean of 56.1 +/- 12.5 months after completion chemotherapy.
  • These data show that consolidation therapy with HDMTX is frequently associated with acute renal toxicity in children with ALL but does not leave clinically significant late sequelae.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Kidney Diseases / chemically induced. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17613868.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; ALL-BFM-95 protocol
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27. Willemze R, Rodrigues CA, Labopin M, Sanz G, Michel G, Socié G, Rio B, Sirvent A, Renaud M, Madero L, Mohty M, Ferra C, Garnier F, Loiseau P, Garcia J, Lecchi L, Kögler G, Beguin Y, Navarrete C, Devos T, Ionescu I, Boudjedir K, Herr AL, Gluckman E, Rocha V, Eurocord-Netcord and Acute Leukaemia Working Party of the EBMT: KIR-ligand incompatibility in the graft-versus-host direction improves outcomes after umbilical cord blood transplantation for acute leukemia. Leukemia; 2009 Mar;23(3):492-500
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  • [Title] KIR-ligand incompatibility in the graft-versus-host direction improves outcomes after umbilical cord blood transplantation for acute leukemia.
  • Donor killer cell immunoglobulin-like receptor (KIR)-ligand incompatibility is associated with decreased relapse incidence (RI) and improved leukemia-free survival (LFS) after haploidentical and HLA-mismatched unrelated hematopoietic stem cell transplantation.
  • We assessed outcomes of 218 patients with acute myeloid leukemia (AML n=94) or acute lymphoblastic leukemia (n=124) in complete remission (CR) who had received a single-unit unrelated cord blood transplant (UCBT) from a KIR-ligand-compatible or -incompatible donor.
  • UCBT for acute leukemia in CR from KIR-ligand-incompatible donors is associated with decreased RI and improved LFS and OS.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Graft vs Leukemia Effect / immunology. HLA Antigens / immunology. Histocompatibility. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Female. Herpesvirus 4, Human / physiology. Humans. Incidence. Infant. Killer Cells, Natural / immunology. Male. Middle Aged. Receptors, KIR / immunology. Remission Induction. Retrospective Studies. Transplantation, Homologous / immunology. Treatment Outcome. Virus Activation. Young Adult


28. Iversen PO, Sørensen DR, Tronstad KJ, Gudbrandsen OA, Rustan AC, Berge RK, Drevon CA: A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia. Clin Cancer Res; 2006 Jun 1;12(11 Pt 1):3525-31
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  • [Title] A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia.
  • PURPOSE: Polyunsaturated fatty acids (PUFA) and the sulfur-substituted fatty acid tetradecylthioacetic acid (TTA) inhibit proliferation and induce apoptosis in lymphoma and leukemic cell lines, but it is unknown if they can modify leukemogenesis in the intact organism.
  • EXPERIMENTAL DESIGN: We now examined the effects of PUFA and TTA in rats transplanted with either acute promyelocytic leukemia or acute T-cell leukemia.
  • RESULTS: Whereas TTA prolonged survival (P < 0.05) in both types of rat leukemia, n-3 PUFA had no significant effect compared with controls.
  • CONCLUSIONS: Dietary intake of TTA, but not of n-3 PUFA, in rats with acute leukemia, prolonged their survival.
  • TTA intake was also associated with reduced leukemic cell burden as well as diminished extramedullar dissemination.
  • TTA represents a modified fatty acid that exerts unique effects on malignant hematopoietic cells, and the present study indicates that TTA may have a therapeutic potential in patients with acute leukemias.
  • [MeSH-major] Fatty Acids, Unsaturated / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Sulfides / administration & dosage
  • [MeSH-minor] Animals. Apoptosis / drug effects. Diet. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Humans. Leukemic Infiltration / diagnosis. Matrix Metalloproteinases / drug effects. Neoplasm Metastasis. Rats. Structure-Activity Relationship. Survival Rate. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • (PMID = 16740779.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated; 0 / Sulfides; 2921-20-2 / 1-(carboxymethylthio)tetradecane; EC 3.4.24.- / Matrix Metalloproteinases
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29. Sinclair P, Harrison CJ, Jarosová M, Foroni L: Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36). Haematologica; 2005 May;90(5):602-11
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  • [Title] Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).
  • BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia.
  • In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • [MeSH-major] Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15921375.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion
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30. Cecchinato V, Chiaramonte R, Nizzardo M, Cristofaro B, Basile A, Sherbet GV, Comi P: Resveratrol-induced apoptosis in human T-cell acute lymphoblastic leukaemia MOLT-4 cells. Biochem Pharmacol; 2007 Dec 3;74(11):1568-74
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  • [Title] Resveratrol-induced apoptosis in human T-cell acute lymphoblastic leukaemia MOLT-4 cells.
  • Resveratrol acts both by suppressing cell proliferation and inducing apoptosis in a variety of cancer cell lines.
  • In this study, we show that RES induces apoptosis in MOLT-4 acute lymphoblastic leukaemia cells by modulating three different pathways that regulate cells survival and cell death.
  • It induces an increase in the levels of the pro-apoptotic proteins p53, its effector p21waf and Bax.
  • [MeSH-minor] Anticarcinogenic Agents / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Glycogen Synthase Kinase 3 / genetics. Glycogen Synthase Kinase 3 / metabolism. Humans. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. Lithium Chloride / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptors, Notch / genetics. Receptors, Notch / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sesquiterpenes. Signal Transduction / drug effects. Terpenes / pharmacology. Time Factors. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17868649.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Receptors, Notch; 0 / Sesquiterpenes; 0 / Stilbenes; 0 / Terpenes; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 37297-20-4 / phytoalexins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; G4962QA067 / Lithium Chloride; Q369O8926L / resveratrol
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31. Soulier J, Clappier E, Cayuela JM, Regnault A, García-Peydró M, Dombret H, Baruchel A, Toribio ML, Sigaux F: HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL). Blood; 2005 Jul 1;106(1):274-86
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  • [Title] HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL).
  • Using a combination of molecular cytogenetic and large-scale expression analysis in human T-cell acute lymphoblastic leukemias (T-ALLs), we identified and characterized a new recurrent chromosomal translocation, targeting the major homeobox gene cluster HOXA and the TCRB locus.
  • Real-time quantitative polymerase chain reaction (RQ-PCR) analysis showed that the expression of the whole HOXA gene cluster was dramatically dysregulated in the HOXA-rearranged cases, and also in MLL and CALM-AF10-related T-ALL cases, strongly suggesting that HOXA genes are oncogenic in these leukemias.
  • Inclusion of HOXA-translocated cases in a general molecular portrait of 92 T-ALLs based on large-scale expression analysis shows that this rearrangement defines a new homogeneous subgroup, which shares common biologic networks with the TLX1- and TLX3-related cases.
  • Because T-ALLs derive from T-cell progenitors, expression profiles of the distinct T-ALL subgroups were analyzed with respect to those of normal human thymic subpopulations.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Differentiation / genetics. Child. Child, Preschool. Female. Gene Expression Profiling. Humans. Infant. Male. Middle Aged. Multigene Family. T-Lymphocytes / cytology. T-Lymphocytes / physiology

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  • (PMID = 15774621.001).
  • [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 / Homeodomain Proteins; 157907-48-7 / HoxA protein
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32. Cudillo L, Tendas A, Picardi A, Dentamaro T, Del Principe MI, Amadori S, de Fabritiis P: Successful treatment of disseminated fusariosis with high dose liposomal amphotericin-B in a patient with acute lymphoblastic leukemia. Ann Hematol; 2006 Feb;85(2):136-8
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  • [Title] Successful treatment of disseminated fusariosis with high dose liposomal amphotericin-B in a patient with acute lymphoblastic leukemia.
  • [MeSH-major] Amphotericin B / therapeutic use. Fusarium / metabolism. Mycoses / complications. Mycoses / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16220312.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / liposomal amphotericin B; 7XU7A7DROE / Amphotericin B
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33. Schrøder H, Kjeldahl M, Boesen AM, Nielsen OJ, Schmidt K, Johnsen HE, Gregersen H, Heyman M, Gustafsson G: Acute lymphoblastic leukemia in adolescents between 10 and 19 years of age in Denmark--secondary publication. Dan Med Bull; 2006 Feb;53(1):76-9
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  • [Title] Acute lymphoblastic leukemia in adolescents between 10 and 19 years of age in Denmark--secondary publication.
  • INTRODUCTION: Data seem to indicate that young adults with acute lymphoblastic leukemia (ALL) have a better survival when treated with pediatric protocols compared with adult ALL protocols.
  • RESULTS: There were no difference with respect to the distribution of T-ALL, CNS-leukemia, total white blood count and high risk chromosomal abnormalities between the two groups.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Daunorubicin / administration & dosage. Doxorubicin / administration & dosage. Female. Humans. Male. Methotrexate / administration & dosage. Neoplasm Recurrence, Local. Prednisone / administration & dosage. Prognosis. Retrospective Studies. Stem Cell Transplantation. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 16761337.001).
  • [ISSN] 1603-9629
  • [Journal-full-title] Danish medical bulletin
  • [ISO-abbreviation] Dan Med Bull
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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34. Yan WH, Lin A, Chen BG, Luo WD, Dai MZ, Chen XJ, Xu HH, Li BL: Unfavourable clinical implications for HLA-G expression in acute myeloid leukaemia. J Cell Mol Med; 2008 Jun;12(3):889-98
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  • [Title] Unfavourable clinical implications for HLA-G expression in acute myeloid leukaemia.
  • In the current study, HLA-G expression was analysed in different types of patients: de novo acute myeloid leukaemia (AML, n = 54), B cell acute lymphoblastic leukaemia (B-ALL, n= 13), chronic myeloid leukaemia (CML, n= 9) and myelodysplastic syndrome (MDS, n= 11).
  • In AML, HLA-G-positive patients had a significant higher bone marrow leukaemic blast cell percentage when compared with that of HLA-G-negative patients (P < 0.01).
  • Total T-cell percentage was dramatically decreased in HLA-G-positive patients (P < 0.05).
  • Ex vivo cytotoxicity analysis revealed that HLA-G expression in AML leukaemic cells could directly inhibit NK cell cytolysis (P < 0.01).
  • [MeSH-major] HLA Antigens / immunology. Histocompatibility Antigens Class I / immunology. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 18494931.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Fluorescent Dyes; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I; EC 1.1.1.27 / L-Lactate Dehydrogenase; I223NX31W9 / Fluorescein-5-isothiocyanate
  • [Other-IDs] NLM/ PMC4401132
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35. Weinberg OK, Arber DA: Mixed-phenotype acute leukemia: historical overview and a new definition. Leukemia; 2010 Nov;24(11):1844-51
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  • [Title] Mixed-phenotype acute leukemia: historical overview and a new definition.
  • Acute leukemia with a mixed phenotype is a rare disease and comprises 2-5% of all acute leukemias.
  • These disorders have been known historically by a variety of names, such as mixed lineage leukemia, bilineal leukemia and biphenotypic leukemia, and the criteria for diagnosis have often been arbitrary.
  • The scoring criteria proposed by the European Group for the Immunological Characterization of Leukemias represented a major attempt to define this disorder.
  • In 2008, the World Health Organization classification of hematopoietic and lymphoid tumors proposed a simpler diagnostic algorithm, which relies on fewer and more lineage-specific markers to define mixed-phenotype acute leukemia (MPAL).
  • Several studies have suggested that patients with acute leukemia of mixed phenotype have a worse clinical outcome when compared with matched controls with acute myeloid leukemia or acute lymphoblastic leukemia.
  • Further studies are needed to confirm the significance of MPAL as currently defined, to determine a standardized treatment approach and to better understand the biological and clinical aspects of this disease.
  • [MeSH-major] Leukemia / genetics
  • [MeSH-minor] Acute Disease. Antigens, CD / analysis. Biomarkers, Tumor / analysis. Blast Crisis / pathology. Gene Rearrangement. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / genetics. Leukemia, T-Cell / classification. Leukemia, T-Cell / genetics. Phenotype

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  • (PMID = 20844566.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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36. Perbellini O, Scupoli MT: Adult T-cell acute lymphoblastic leukemia: prognostic impact of myeloid-associated antigens. Expert Rev Hematol; 2009 Feb;2(1):27-9
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  • [Title] Adult T-cell acute lymphoblastic leukemia: prognostic impact of myeloid-associated antigens.
  • Despite the recent improvement in the treatment of the disease, the prognosis of adult T-cell acute lymphoblastic leukemia (T-ALL) remains poor.

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  • [CommentOn] Acta Haematol. 2008;120(1):5-10 [18635939.001]
  • (PMID = 21082991.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
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37. Yamaji K, Okamoto T, Yokota S, Watanabe A, Horikoshi Y, Asami K, Kikuta A, Hyakuna N, Saikawa Y, Ueyama J, Watanabe T, Okada M, Taga T, Kanegane H, Kogawa K, Chin M, Iwai A, Matsushita T, Shimomura Y, Hori T, Tsurusawa M, Japanese Childhood Cancer Leukemia Study Group: Minimal residual disease-based augmented therapy in childhood acute lymphoblastic leukemia: a report from the Japanese Childhood Cancer and Leukemia Study Group. Pediatr Blood Cancer; 2010 Dec 15;55(7):1287-95
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  • [Title] Minimal residual disease-based augmented therapy in childhood acute lymphoblastic leukemia: a report from the Japanese Childhood Cancer and Leukemia Study Group.
  • BACKGROUND: The majority of minimal residual disease (MRD)-positive patients with acute lymphoblastic leukemia (ALL) have poor outcomes.
  • PROCEDURE: Between 2000 and 2004, 305 eligible patients with precursor B or T-cell ALL were enrolled in the ALL2000 study.
  • The ALL941-based therapy protocol utilized PCR MRD assays using Immunoglobulin and T-cell receptor gene rearrangements.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Neoplasm, Residual. Prognosis. Risk Factors. Survival Rate. Treatment Outcome


38. van Anders SM, Hamilton LD, Schmidt N, Watson NV: Associations between testosterone secretion and sexual activity in women. Horm Behav; 2007 Apr;51(4):477-82
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  • On three separate nights, they provided pre-activity, post-activity, and next-morning saliva samples and completed brief questionnaires at the last two timepoints.
  • Women's T was higher pre-intercourse than pre-control activity.
  • Women's T was also higher post-intercourse than post-control activity, though the percent change in T from pre- to post-activity was highest for cuddling, then intercourse, then exercise.

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  • (PMID = 17320881.001).
  • [ISSN] 0018-506X
  • [Journal-full-title] Hormones and behavior
  • [ISO-abbreviation] Horm Behav
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone
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39. Kameda T, Shide K, Shimoda HK, Hidaka T, Kubuki Y, Katayose K, Taniguchi Y, Sekine M, Kamiunntenn A, Maeda K, Nagata K, Matsunaga T, Shimoda K: Absence of gain-of-function JAK1 and JAK3 mutations in adult T cell leukemia/lymphoma. Int J Hematol; 2010 Sep;92(2):320-5
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  • [Title] Absence of gain-of-function JAK1 and JAK3 mutations in adult T cell leukemia/lymphoma.
  • Somatic JAK1 mutations are found in 18% of adult precursor T acute lymphoblastic leukemias and somatic JAK3 mutations are found in 3.3% of cutaneous T cell lymphomas.
  • Adult T cell leukemia/lymphoma (ATLL) is a type of T cell neoplasm, and activation of JAK/STAT pathways is sometimes observed in them.
  • [MeSH-major] Janus Kinase 1 / genetics. Janus Kinase 3 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adult. Cell Differentiation. Cell Proliferation. DNA Mutational Analysis. Humans. Japan. Polymorphism, Single Nucleotide

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  • (PMID = 20697856.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3
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40. Thörn I, Forestier E, Thuresson B, Wasslavik C, Malec M, Li A, Lindström-Eriksson E, Botling J, Barbany G, Jacobsson S, Olofsson T, Porwit A, Sundström C, Rosenquist R: Applicability of IG/TCR gene rearrangements as targets for minimal residual disease assessment in a population-based cohort of Swedish childhood acute lymphoblastic leukaemia diagnosed 2002-2006. Eur J Haematol; 2010 Feb 1;84(2):117-27
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  • [Title] Applicability of IG/TCR gene rearrangements as targets for minimal residual disease assessment in a population-based cohort of Swedish childhood acute lymphoblastic leukaemia diagnosed 2002-2006.
  • Minimal residual disease (MRD) detection during the early treatment phase has become an important stratification parameter in many childhood acute lymphoblastic leukaemia (ALL) treatment protocols.
  • From 334 childhood ALL cases diagnosed during 2002-2006, we analysed 279 diagnostic samples (84%) by screening for rearranged immunoglobulin (IG) and T-cell receptor (TCR) genes.
  • Overall, clonal IG/TCR rearrangements were detected in 97% (236/244) of B-cell precursor ALL (BCP ALL) and 94% (33/35) of T-ALL.
  • [MeSH-major] Gene Rearrangement, B-Lymphocyte. Gene Rearrangement, T-Lymphocyte. Monitoring, Physiologic / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19895569.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
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41. Vaskova M, Mejstrikova E, Kalina T, Martinkova P, Omelka M, Trka J, Stary J, Hrusak O: Transfer of genomics information to flow cytometry: expression of CD27 and CD44 discriminates subtypes of acute lymphoblastic leukemia. Leukemia; 2005 May;19(5):876-8
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  • [Title] Transfer of genomics information to flow cytometry: expression of CD27 and CD44 discriminates subtypes of acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, CD27 / biosynthesis. Antigens, CD44 / biosynthesis. Flow Cytometry / methods. Gene Expression Profiling. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 15759032.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Antigens, CD44
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42. Chim CS, Wong KY, Qi Y, Loong F, Lam WL, Wong LG, Jin DY, Costello JF, Liang R: Epigenetic inactivation of the miR-34a in hematological malignancies. Carcinogenesis; 2010 Apr;31(4):745-50
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  • We studied the role of miR-34a methylation in a panel of hematological malignancies including acute leukemia [acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL)], chronic leukemia [chronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML)], multiple myeloma (MM) and non-Hodgkin's lymphoma (NHL).
  • The methylation status of miR-34a promoter was studied in 12 cell lines and 188 diagnostic samples by methylation-specific polymerase chain reaction. miR-34a promoter was unmethylated in normal controls but methylated in 75% lymphoma and 37% myeloma cell lines.
  • Hypomethylating treatment led to re-expression of pri-miR-34a transcript in lymphoma cells with homozygous miR-34a methylation.
  • In primary samples at diagnosis, miR-34a methylation was detected in 4% CLL, 5.5% MM samples and 18.8% of NHL at diagnosis but none of ALL, AML and CML (P = 0.011).
  • Amongst lymphoid malignancies, miR-34a was preferentially methylated in NHL (P = 0.018), in particular natural killer (NK)/T-cell lymphoma.
  • In conclusion, amongst hematological malignancies, miR-34a methylation is preferentially hypermethylated in NHL, in particular NK/T-cell lymphoma, in a tumor-specific manner, therefore the role of miR-34a in lymphomagenesis warrants further study.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Female. Genes, p53. Humans. Loss of Heterozygosity. Male. Middle Aged. Polymerase Chain Reaction. Promoter Regions, Genetic

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  • [ErratumIn] Carcinogenesis. 2014 Nov;35(11):2631
  • (PMID = 20118199.001).
  • [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 / MIRN34 microRNA, human; 0 / MicroRNAs
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43. Gorello P, La Starza R, Varasano E, Chiaretti S, Elia L, Pierini V, Barba G, Brandimarte L, Crescenzi B, Vitale A, Messina M, Grammatico S, Mancini M, Matteucci C, Bardi A, Guarini A, Martelli MF, Foà R, Mecucci C: Combined interphase fluorescence in situ hybridization elucidates the genetic heterogeneity of T-cell acute lymphoblastic leukemia in adults. Haematologica; 2010 Jan;95(1):79-86
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  • [Title] Combined interphase fluorescence in situ hybridization elucidates the genetic heterogeneity of T-cell acute lymphoblastic leukemia in adults.
  • BACKGROUND: Molecular lesions in T-cell acute lymphoblastic leukemias affect regulators of cell cycle, proliferation, differentiation, survival and apoptosis in multi-step pathogenic pathways.
  • Full genetic characterization is needed to identify events concurring in the development of these leukemias.
  • DESIGN AND METHODS: We designed a combined interphase fluorescence in situ hybridization strategy to study 25 oncogenes/tumor suppressor genes in T-cell acute lymphoblastic leukemias and applied it in 23 adult patients for whom immunophenotyping, karyotyping, molecular studies, and gene expression profiling data were available.
  • The results were confirmed and integrated with those of multiplex-polymerase chain reaction analysis and gene expression profiling in another 129 adults with T-cell acute lymphoblastic leukemias.
  • It found abnormalities known to be associated with T-cell acute lymphoblastic leukemias, i.e.
  • Multiplex-polymerase chain reaction analysis and gene expression profiling of 129 further cases found five additional cases of TAF_I-NUP214-positive T-cell acute lymphoblastic leukemia.
  • CONCLUSIONS: Our combined interphase fluorescence in situ hybridization strategy greatly improved the detection of genetic abnormalities in adult T-cell acute lymphoblastic leukemias.
  • The estimated incidence of TAF_I-NUP214, a new recurrent fusion in adult T-cell acute lymphoblastic leukemias, was 4.6% (7/152).
  • [MeSH-major] Comparative Genomic Hybridization. Genetic Heterogeneity. In Situ Hybridization, Fluorescence. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • (PMID = 20065082.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2805748
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44. Zhang WW, Habeebu S, Sheehan AM, Naeem R, Hernandez VS, Dreyer ZE, López-Terrada D: Molecular monitoring of 8p11 myeloproliferative syndrome in an infant. J Pediatr Hematol Oncol; 2009 Nov;31(11):879-83
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  • The 8p11 myeloproliferative syndrome is a rare hematologic malignancy derived from a pluripotent hematopoietic stem cell associated with rearrangements involving the fibroblast growth factor receptor 1 (FGFR1) gene located on chromosome 8p11.
  • Typical pathologic findings include myeloid hyperplasia, lymphadenopathy, precursor T-lymphoblastic lymphoma, and eosinophilia.
  • The disease is usually associated with an aggressive course and progression to acute myeloid leukemia is frequent.
  • We report here the first case of 8p11 myeloproliferative syndrome in an infant and demonstrate the value of molecular testing in the diagnosis and minimal disease monitoring of this rare disease.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 8 / genetics. DNA-Binding Proteins / genetics. Myeloproliferative Disorders / genetics. Oncogene Proteins, Fusion / genetics. Receptor, Fibroblast Growth Factor, Type 1 / genetics. Transcription Factors / genetics. Translocation, Genetic

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  • (PMID = 19829149.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 0 / ZMYM2 protein, human; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
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45. Ausserlechner MJ, Obexer P, Geley S, Kofler R: G1 arrest by p16INK4A uncouples growth from cell cycle progression in leukemia cells with deregulated cyclin E and c-Myc expression. Leukemia; 2005 Jun;19(6):1051-7
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  • [Title] G1 arrest by p16INK4A uncouples growth from cell cycle progression in leukemia cells with deregulated cyclin E and c-Myc expression.
  • The cell cycle inhibitor p16(INK4A) is frequently inactivated in acute lymphoblastic T-cell leukemia (T-ALL).
  • CCRF-CEM cells with tetracycline-regulated p16(INK4A) expression underwent stable G1-phase cell cycle arrest for 72 h followed by massive apoptosis. p16(INK4A) expression caused pRB hypophosphorylation and repression of certain E2F target genes.
  • Thus, p16(INK4A), although unable to repress the expression of deregulated cyclin E and c-Myc, functionally inactivated these potential oncogenes. p16(INK4A)-arrested cells showed morphologic changes, induction of T-cell-specific surface markers and repression of telomerase activity, suggesting differentiation.
  • Taken together, p16(INK4A) reconstitution in p16(INK4A)-deficient T-ALL cells induced cell cycle arrest in the presence of cyclin E and c-Myc expression, uncoupled growth from cell cycle progression and caused a sequential process of growth, differentiation and apoptosis.
  • [MeSH-major] Cyclin E / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Genes, myc / physiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology
  • [MeSH-minor] Apoptosis / physiology. Biomarkers, Tumor. Cell Differentiation / physiology. Cell Division / physiology. Child. G1 Phase / physiology. Gene Expression Regulation, Leukemic. Humans. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Phosphorylation. Retinoblastoma-Like Protein p107. T-Lymphocytes / pathology. T-Lymphocytes / physiology. Telomerase / metabolism. Transcriptional Activation / physiology

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  • (PMID = 15800668.001).
  • [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 / Biomarkers, Tumor; 0 / Cyclin E; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / RBL1 protein, human; 0 / Retinoblastoma-Like Protein p107; EC 2.7.7.49 / Telomerase
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46. Glouchkova L, Ackermann B, Zibert A, Meisel R, Siepermann M, Janka-Schaub GE, Goebel U, Troeger A, Dilloo D: The CD70/CD27 pathway is critical for stimulation of an effective cytotoxic T cell response against B cell precursor acute lymphoblastic leukemia. J Immunol; 2009 Jan 1;182(1):718-25
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  • [Title] The CD70/CD27 pathway is critical for stimulation of an effective cytotoxic T cell response against B cell precursor acute lymphoblastic leukemia.
  • However, in B cell precursor acute lymphoblastic leukemia, the most common childhood malignancy, the role of CD70 in stimulation of antileukemic T cell responses has so far not been delineated.
  • Herein we demonstrate that in B cell precursor acute lymphoblastic leukemia expression of CD70 is low but can be induced upon blast activation via CD40.
  • Both CD70 and CD80/CD86 up-regulated on CD40-stimulated blasts contribute to primary stimulation of T cell proliferation and cytokine production in an additive manner.
  • These two signals also cooperate in the prevention of T cell anergy.
  • In contrast to blockade of CD70 during the effector phase, inhibition of CD70-mediated costimulation during generation of antileukemic T cells prevents effector cell proliferation and reduces their cytotoxic capacity.
  • Modulation of the CD70/CD27 pathway may thus represent a novel therapeutic approach for augmenting magnitude and quality of the antileukemic response in B cell precursor acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, CD27 / physiology. Antigens, CD70 / physiology. Lymphocyte Activation / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Signal Transduction / immunology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] B-Lymphocyte Subsets / immunology. B-Lymphocyte Subsets / pathology. Cell Differentiation / immunology. Cell Proliferation. Coculture Techniques. Cytotoxicity Tests, Immunologic. Humans. Lymphocyte Culture Test, Mixed. Stem Cells / immunology. Stem Cells / pathology. Tumor Cells, Cultured. Up-Regulation / immunology

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  • (PMID = 19109206.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Antigens, CD70; 0 / CD70 protein, human
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47. Reinfjell T, Lofstad GE, Veenstra M, Vikan A, Diseth TH: Health-related quality of life and intellectual functioning in children in remission from acute lymphoblastic leukaemia. Acta Paediatr; 2007 Sep;96(9):1280-5
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  • [Title] Health-related quality of life and intellectual functioning in children in remission from acute lymphoblastic leukaemia.
  • AIM: To evaluate the health-related quality of life (HRQOL) and intellectual functioning of children in remission from acute lymphoblastic leukaemia (ALL).
  • [MeSH-major] Cognition / physiology. Health Status. Precursor Cell Lymphoblastic Leukemia-Lymphoma / psychology. Quality of Life / psychology

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  • [CommentIn] Acta Paediatr. 2007 Sep;96(9):1265-8 [17718778.001]
  • (PMID = 17590194.001).
  • [ISSN] 0803-5253
  • [Journal-full-title] Acta paediatrica (Oslo, Norway : 1992)
  • [ISO-abbreviation] Acta Paediatr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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48. Hu L, Shi J, Wang L: Down-regulation of beta-catenin nuclear localization by aspirin correlates with growth inhibition of Jurkat cell line. J Huazhong Univ Sci Technolog Med Sci; 2006;26(6):731-4
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  • [Title] Down-regulation of beta-catenin nuclear localization by aspirin correlates with growth inhibition of Jurkat cell line.
  • In this study, we examined the effects of aspirin on the growth rates, subcellular distribution of beta-catenin protein, the expression of beta-catenin/TCF signaling pathway target gene cyclin D1 mRNA, and cell cycle of Jurkat cell line (Human T-acute lymphoblastic leukemia).
  • Our results showed that the treatment with aspirin inhibited the growth of Jurkat cell line.
  • Aspirin induced G0/G1 cell cycle arrest in Jurkat cells.
  • The effects of aspirin include down-regulation of beta-catenin nuclear localization and G0/G1 cell cycle arrest, which might serve as a means of growth inhibition in aspirin-treated human Jurkat cell line.
  • [MeSH-minor] Cell Cycle. Cell Cycle Checkpoints. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Down-Regulation / drug effects. Humans. Jurkat Cells

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  • [Cites] Oncogene. 2001 Feb 1;20(5):645-53 [11313997.001]
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  • (PMID = 17357503.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / CTNNB1 protein, human; 0 / beta Catenin; 136601-57-5 / Cyclin D1; R16CO5Y76E / Aspirin
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49. Saussoy P, Vaerman JL, Druez V, Deneys V, Straetmans N, Cornu G, Ferrant A, Latinne D: Expression of lineage markers using real-time quantitative polymerase chain reaction (RT-qPCR) in normal and in leukemia bone marrow. Clin Chem Lab Med; 2009;47(4):419-26
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  • [Title] Expression of lineage markers using real-time quantitative polymerase chain reaction (RT-qPCR) in normal and in leukemia bone marrow.
  • BACKGROUND: The study of lineage markers by real-time quantitative polymerase chain reaction (RT-qPCR) at diagnosis enables differentiation between acute myeloblastic leukemia, B- or T-lineage acute lymphoblastic leukemia, without cell sorting.
  • Our objective was to assess the relationship between protein expression and the amount of lineage marker mRNA in acute leukemia samples and to determine whether four lineage markers could be used to differentiate between normal and acute leukemia bone marrow (BM) without cell sorting.
  • METHODS: Quantification of the mRNA of CD19, CD79a, CD3e, and myeloperoxidase was performed by RT-qPCR on 130 acute leukemia BM samples at diagnosis and on 20 BM samples from healthy donors, without cell sorting.
  • Immunophenotyping of leukemia samples was performed after manual gating around the blastic population.
  • The mRNA expression levels of these four lineage markers allowed the distinction between normal samples and 100% of acute leukemia samples.
  • CONCLUSIONS: With 92% congruence for protein expression and amount of mRNA in acute leukemias, these four lineage markers, essential for diagnosis and subclassification of acute leukemias by flow cytometry, also represent excellent candidate genes when using RT-qPCR technology as a diagnostic tool for molecular cancer class prediction.

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  • (PMID = 19327122.001).
  • [ISSN] 1434-6621
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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50. Hager-Theodorides AL, Dessens JT, Outram SV, Crompton T: The transcription factor Gli3 regulates differentiation of fetal CD4- CD8- double-negative thymocytes. Blood; 2005 Aug 15;106(4):1296-304
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  • Analysis of null mutants showed that Gli3 is involved at the transitions from DN1 to CD44+ CD25+ DN (DN2) cell and from DN to CD4+ CD8+ double-positive (DP) cell.
  • Gli3 is required for differentiation from DN to DP thymocyte, after pre-T-cell receptor (TCR) signaling but is not necessary for pre-TCR-induced proliferation or survival.
  • The effect of Gli3 was dose dependent, suggesting its direct involvement in the transcriptional regulation of genes controlling T-cell differentiation during fetal development.
  • [MeSH-major] Antigens, CD / analysis. Cell Differentiation. DNA-Binding Proteins / physiology. Nerve Tissue Proteins / physiology. T-Lymphocytes / cytology. Thymus Gland / cytology. Transcription Factors / physiology
  • [MeSH-minor] Animals. Antigens, CD4. Antigens, CD8. Cell Lineage. Embryo, Mammalian / cytology. Embryo, Mammalian / immunology. Gene Expression Regulation, Developmental. Kruppel-Like Transcription Factors. Mice. Mice, Inbred C57BL. Mice, Mutant Strains


51. Möricke A, Reiter A, Zimmermann M, Gadner H, Stanulla M, Dördelmann M, Löning L, Beier R, Ludwig WD, Ratei R, Harbott J, Boos J, Mann G, Niggli F, Feldges A, Henze G, Welte K, Beck JD, Klingebiel T, Niemeyer C, Zintl F, Bode U, Urban C, Wehinger H, Niethammer D, Riehm H, Schrappe M, German-Austrian-Swiss ALL-BFM Study Group: Risk-adjusted therapy of acute lymphoblastic leukemia can decrease treatment burden and improve survival: treatment results of 2169 unselected pediatric and adolescent patients enrolled in the trial ALL-BFM 95. Blood; 2008 May 1;111(9):4477-89
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  • [Title] Risk-adjusted therapy of acute lymphoblastic leukemia can decrease treatment burden and improve survival: treatment results of 2169 unselected pediatric and adolescent patients enrolled in the trial ALL-BFM 95.
  • The trial ALL-BFM 95 for treatment of childhood acute lymphoblastic leukemia was designed to reduce acute and long-term toxicity in selected patient groups with favorable prognosis and to improve outcome in poor-risk groups by treatment intensification.
  • These aims were pursued through a stratification strategy using white blood cell count, age, immunophenotype, treatment response, and unfavorable genetic aberrations providing an excellent discrimination of risk groups.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [ErratumIn] Blood. 2009 Apr 30;113(18):4478. Dosage error in article text
  • (PMID = 18285545.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine
  • [Investigator] Beck J; Bode U; Boos J; Feldges A; Gadner H; Havers W; Henze G; Kornhuber B; Kühl J; Lampert F; Maass E; Mittler U; Niemeyer C; Niethammer D; Niggli F; Reiter A; Riehm H; Ritter J; Schrappe M; Urban C; Wehinger H; Welte K; Zintl F; Mertens R; Imbach R; Signer E; Heidemann P; Rager K; Imbach P; Wündisch GF; Henze G; Gaedicke G; Dörffel W; Bode U; Eberl W; Mau G; Jacobi H; Hofmann K; Thaben JD; Möbius D; Andler W; Niekrens C; Breu H; Scharfe V; Zickler P; Weinmann G; Beck JD; Havers W; Kremens B; Müller G; Kornhuber B; Niemeyer C; Reiter A; Lampert F; Lakomek M; Urban C; Gerein V; Exadaktylos P; Burdach S; Riehm H; Welte K; Selle B; Tautz Ch; Graf N; Dengg K; Zintl F; Gutwein FJ; Nessler G; Dupuis W; Wehinger H; Rodehüser M; Kaulfersch W; Rister M; Berthold F; Schneppenheim R; Suttorp M; Sternschulte W; Garcia RM; Domula M; Mutz I; Moser R; Schmitt K; Ebetsberger G; Stöllinger O; Nobile Buetti L; Bucsky P; Dominick HC; Caflisch U; Mittler U; Sauer O; Christiansen H; Tillmann W; Müller-Weihrich S; Bender-Götze C; Jürgens H; Ritter J; Jobke A; Schwarzer U; Schofer O; Eggers G; Treuner J; Geib R; Jones N; Dickerhoff R; Neubert D; Göbel FJ; Ploier R; Feldges A; Greiner J; Rauh W; Niethammer D; Klingebiel T; Debatin KM; Kleihauer E; Franke D; Gadner H; Peters Ch; Mann G; Otte J; Kühl J; Krohn HP; Niggli F
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52. Smith MT, McHale CM, Wiemels JL, Zhang L, Wiencke JK, Zheng S, Gunn L, Skibola CF, Ma X, Buffler PA: Molecular biomarkers for the study of childhood leukemia. Toxicol Appl Pharmacol; 2005 Aug 07;206(2):237-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular biomarkers for the study of childhood leukemia.
  • Various specific chromosome rearrangements, including t(8;21), t(15;17), and inv(16), are found in acute myeloid leukemia (AML) and in childhood acute lymphocytic leukemia (ALL), t(12;21) and t(1;19) are common.
  • These findings show that most childhood leukemias begin before birth and that maternal and perinatal exposures such as chemical and infectious agents are likely to be critical.
  • Indeed, we have reported that exposure to indoor pesticides during pregnancy and the first year of life raises leukemia risk, but that later exposures do not.
  • We have also examined aberrant gene methylation in different cytogenetic subgroups and have found striking differences between them, suggesting that epigenetic events are also important in the development of some forms of childhood leukemia.
  • Further, at least two studies now show that the inactivating NAD(P)H:quinone acceptor oxidoreductase (NQO1) C609T polymorphism is positively associated with leukemias arising in the first 1-2 years of life and polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene have been associated with adult and childhood ALL.
  • Thus, low folate intake and compounds that are detoxified by NQO1 may be important in elevating leukemia risk in children.
  • Finally, we are exploring the use of proteomics to subclassify leukemia, because cytogenetic analysis is costly and time-consuming.
  • Several proteins have been identified that may serve as useful biomarkers for rapidly identifying different forms of childhood leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15967214.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES0098137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 935E97BOY8 / Folic Acid; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  • [Number-of-references] 55
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53. Nagel S, Venturini L, Meyer C, Kaufmann M, Scherr M, Drexler HG, MacLeod RA: Multiple mechanisms induce ectopic expression of LYL1 in subsets of T-ALL cell lines. Leuk Res; 2010 Apr;34(4):521-8
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  • [Title] Multiple mechanisms induce ectopic expression of LYL1 in subsets of T-ALL cell lines.
  • Basic helix-loop-helix (bHLH) transcription factors are essential for lymphocytic differentiation.
  • Here, we have analyzed the complete bHLH family in T-cell acute lymphoblastic leukemia cell lines by expression profiling.
  • Additionally, one LYL1-expressing cell line exhibited amplification of TRMT1.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Gene Expression Regulation, Leukemic. Neoplasm Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Cell Line, Tumor. Cluster Analysis. Gene Amplification. Gene Expression Profiling. HeLa Cells. Humans. Jurkat Cells. Oligonucleotide Array Sequence Analysis. Sequence Deletion / physiology. Signal Transduction / genetics. Transfection. Up-Regulation / genetics

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19608273.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / LYL1 protein, human; 0 / Neoplasm Proteins
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54. Rosenman MB, Vik T, Hui SL, Breitfeld PP: Hospital resource utilization in childhood cancer. J Pediatr Hematol Oncol; 2005 Jun;27(6):295-300
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  • All hospital encounters for these patients starting from the time of diagnosis to 3 years from diagnosis were identified using hospital administrative data.
  • The patients were categorized into four diagnostic groups: lymphoid malignancies (acute lymphoblastic leukemia and lymphoma), myeloid leukemias (acute myeloid leukemia and chronic myeloid leukemia), central nervous system tumors, and solid tumors.
  • Predictive models for total resource consumption (total hospital charges) and intensive care use were derived.
  • One hundred sixty-five of the 195 were admitted to Riley Hospital for Children at least once during the 3-year period following diagnosis.
  • Among these 165, mean age at diagnosis was 6.9 years (minimum newborn, maximum 18.7 years).
  • The distribution of 165 diagnoses was as follows: 65 (39%) with lymphoid malignancy, 13 (8%) with myeloid leukemia, 36 (22%) with central nervous system tumors, and 51 (31%) with solid tumors.
  • Sixty-two patients (38%) used the pediatric intensive care unit (PICU) at least once; 22 patients (13%) underwent stem cell transplantation.
  • Half of these charges were incurred in the first 4.5 months after diagnosis.
  • Half of all hospital charges accrued to only 12.7% of patients; these patients were more likely to have a diagnosis of myeloid leukemia, to have undergone stem cell transplantation, and to have used the PICU.
  • There were three independent predictors of hospital charges (log transformed): stem cell transplantation, PICU utilization, and death within 3 years of diagnosis.
  • PICU utilization was predicted by tumor type (myeloid leukemia and central nervous system tumors were positive predictors of PICU utilization; lymphoid malignancy and solid tumors were negative predictors), stem cell transplantation, and death within 3 years of diagnosis.

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  • (PMID = 15956880.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NLM NIH HHS / LM / 1T15 LM 07117
  • [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
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55. Huang X, Chen S, Shen Q, Yang L, Li B, Zhong L, Geng S, Du X, Li Y: Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia. J Hematol Oncol; 2010;3(1):44
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  • [Title] Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia.
  • BACKGROUND: In a human T-cell acute lymphoblastic leukemia (T-ALL) cell line (Molt-4), siRNA-mediated suppression of BCL11B expression was shown to inhibit proliferation and induce apoptosis, functions which may be related to genes involved in apoptosis (such as TNFSF10 and BCL2L1) and TGF-β pathways (such as SPP1and CREBBP).
  • [MeSH-major] CREB-Binding Protein / biosynthesis. Gene Expression Regulation, Neoplastic / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Repressor Proteins / biosynthesis. Tumor Suppressor Proteins / biosynthesis. bcl-X Protein / biosynthesis

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  • (PMID = 21080944.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL11B protein, human; 0 / BCL2L1 protein, human; 0 / CREBBP protein, human; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; 0 / bcl-X Protein; EC 2.3.1.48 / CREB-Binding Protein
  • [Other-IDs] NLM/ PMC2992472
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56. Ohnuki K, Watanabe Y, Takahashi Y, Kobayashi S, Watanabe S, Ogawa S, Kotani M, Kozono H, Tanabe K, Abe R: Antigen-specific CD4+ effector T cells: analysis of factors regulating clonal expansion and cytokine production: clonal expansion and cytokine production by CD4+ effector T cells. Biochem Biophys Res Commun; 2009 Mar 20;380(4):742-7
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  • In order to fully understand T cell-mediated immunity, the mechanisms that regulate clonal expansion and cytokine production by CD4(+) antigen-specific effector T cells in response to a wide range of antigenic stimulation needs clarification.
  • For this purpose, panels of antigen-specific CD4(+) T cell clones with different thresholds for antigen-induced proliferation were generated by repeated stimulation with high- or low-dose antigen.
  • There was no significant difference in antigen-dependent cytokine production by TG40 cells transfected with TCR obtained from either high- or low-dose-responding T cell clones, suggesting that the affinity of TCRs for their ligands is not primary determinant of T cell antigen reactivity.
  • The proliferative responses of all T cell clones to both peptide stimulation and to TCRbeta crosslinking revealed parallel dose-response curves.
  • Finally, the antigen responses of high- and low-peptide-responding T cell clones reveal that clonal expansion and cytokine production of effector T cells occur independently of antigen concentration.
  • [MeSH-minor] Animals. Cell Adhesion Molecules / metabolism. Clone Cells. Flow Cytometry. Mice. Mice, Inbred BALB C. Ovalbumin / immunology. Peptide Fragments / immunology. Receptors, Antigen, T-Cell / metabolism

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  • (PMID = 19338745.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / OVA 323-339; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell; 9006-59-1 / Ovalbumin
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57. Terme JM, Wencker M, Favre-Bonvin A, Bex F, Gazzolo L, Duc Dodon M, Jalinot P: Cross talk between expression of the human T-cell leukemia virus type 1 Tax transactivator and the oncogenic bHLH transcription factor TAL1. J Virol; 2008 Aug;82(16):7913-22
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  • [Title] Cross talk between expression of the human T-cell leukemia virus type 1 Tax transactivator and the oncogenic bHLH transcription factor TAL1.
  • The human T-cell leukemia virus type 1 (HTLV-1) Tax transactivator is known to induce or repress various cellular genes, several of them encoding transcription factors.
  • As Tax is known to deregulate various basic bHLH factors, we looked more specifically at its effect on TAL1 (T-cell acute lymphoblastic leukemia 1), also known as SCL (stem cell leukemia).
  • Indeed, TAL1 is deregulated in a high percentage of T-cell acute lymphoblastic leukemia cells, and its oncogenic properties are well-established.
  • These data show the existence of a positive feedback loop between Tax and TAL1 expression and support the notion that this proto-oncogene participates in generation of adult T-cell leukemia/lymphoma by increasing the amount of the Tax oncoprotein but also possibly by its own transforming activities.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Leukemia-Lymphoma, Adult T-Cell / virology. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Binding Sites. Cell Line. Feedback, Physiological. HeLa Cells. Humans. Models, Biological. NF-kappa B / metabolism. Promoter Regions, Genetic. Thymus Gland / cytology

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  • (PMID = 18495761.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 0 / tax protein, Human T-lymphotrophic virus 1; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC2519563
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58. Fu L, Kogoshi H, Nara N, Tohda S: NOTCH1 mutations are rare in acute myeloid leukemia. Leuk Lymphoma; 2006 Nov;47(11):2400-3
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  • [Title] NOTCH1 mutations are rare in acute myeloid leukemia.
  • Mutations in the NOTCH1 gene were investigated in 12 primary acute myeloid leukemia (AML) cell samples and eight AML cell lines.
  • This mutation was different from those previously reported for T-cell acute lymphoblastic leukemia, in which more than half the cases had the mutations.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Receptor, Notch1 / genetics

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  • [CommentIn] Leuk Lymphoma. 2006 Nov;47(11):2280-1 [17107898.001]
  • (PMID = 17107915.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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59. Van Vlierberghe P, van Grotel M, Tchinda J, Lee C, Beverloo HB, van der Spek PJ, Stubbs A, Cools J, Nagata K, Fornerod M, Buijs-Gladdines J, Horstmann M, van Wering ER, Soulier J, Pieters R, Meijerink JP: The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia. Blood; 2008 May 1;111(9):4668-80
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  • [Title] The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner that possibly delineate specific T-ALL subgroups.
  • This deletion results in a conserved SET-NUP214 fusion product, which was also identified in the T-ALL cell line LOUCY.
  • We conclude that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest.

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  • (PMID = 18299449.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA11560
  • [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 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / Homeodomain Proteins; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / SET protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ PMC2343598
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60. Adam de Beaumais T, Dervieux T, Fakhoury M, Medard Y, Azougagh S, Zhang D, Yakouben K, Jacqz-Aigrain E: The impact of high-dose methotrexate on intracellular 6-mercaptopurine disposition during interval therapy of childhood acute lymphoblastic leukemia. Cancer Chemother Pharmacol; 2010 Sep;66(4):653-8
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  • [Title] The impact of high-dose methotrexate on intracellular 6-mercaptopurine disposition during interval therapy of childhood acute lymphoblastic leukemia.
  • PURPOSE: Low-dose methotrexate (MTX) therapy is the cornerstone treatment of acute lymphoblastic leukemia (ALL) and may enhance the activation of 6-mercaptopurine (6-MP) to 6-thioguanine nucleotides (6-TGN).
  • However, a return to pre-infusion of 6-TGN levels was observed by the time of the following HDMTX course 14 days later (P < 0.001).
  • RBC MTX polyglutamates accumulation followed Michaelis-Menten kinetics but was not associated with the change in pre-infusion 6-TGN levels which remained stable during the interval period.
  • [MeSH-major] 6-Mercaptopurine / pharmacokinetics. Antimetabolites, Antineoplastic / adverse effects. Antimetabolites, Antineoplastic / pharmacokinetics. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • Hazardous Substances Data Bank. THIOGUANINE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
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  • (PMID = 20033410.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; E7WED276I5 / 6-Mercaptopurine; FTK8U1GZNX / Thioguanine; YL5FZ2Y5U1 / Methotrexate
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61. Okabe S, Tauchi T, Ohyashiki K: Establishment of a new Philadelphia chromosome-positive acute lymphoblastic leukemia cell line (SK-9) with T315I mutation. Exp Hematol; 2010 Sep;38(9):765-72
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  • [Title] Establishment of a new Philadelphia chromosome-positive acute lymphoblastic leukemia cell line (SK-9) with T315I mutation.
  • Although strategies to overcome resistance-mediated T315I mutation may improve the survival of BCR-ABL-positive leukemia patients, there is little information on cell-based studies.
  • MATERIALS AND METHODS: We established a new human BCR-ABL-positive acute lymphoblastic leukemia (ALL) cell line, SK-9 with the T315I mutation, from the peripheral blood of a 36-year-old female patient.
  • The common B-cell phenotype is a feature of the SK-9 cell line.
  • We examined the drug sensitivity of imatinib, dasatinib, and nilotinib using a cell proliferation assay and an immunoblot assay.
  • Cell proliferation did not decrease after imatinib, dasatinib, or nilotinib treatment as compared to the BCR-ABL-positive chronic myeloid leukemia cell line K562.
  • CONCLUSION: This cell line may provide a useful model for in vitro and in vivo cellular and molecular studies of BCR-ABL-positive ALL with T315I mutation.
  • [MeSH-major] Cell Line, Tumor / enzymology. Fusion Proteins, bcr-abl / metabolism. Mutation, Missense. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology
  • [MeSH-minor] Amino Acid Substitution. Animals. Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Disease Models, Animal. Female. Humans. Lymph Nodes / enzymology. Lymph Nodes / pathology. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous


62. Hosking FJ, Papaemmanuil E, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Taylor M, Tomlinson IP, Greaves M, Houlston RS: Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk. Blood; 2010 Jun 3;115(22):4472-7
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  • [Title] Genome-wide homozygosity signatures and childhood acute lymphoblastic leukemia risk.
  • To examine whether homozygosity is associated with an increased risk of developing childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL), we analyzed 824 ALL cases and 2398 controls genotyped for 292 200 tagging SNPs.

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  • (PMID = 20231427.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / / 10417; United Kingdom / Cancer Research UK / / C1298/A8362
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Erythropoietin
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63. Taylor GM, Richards S, Wade R, Hussain A, Simpson J, Hill F, Mitchell C, Eden T, UKCCS and CCLG Investigators: Relationship between HLA-DP supertype and survival in childhood acute lymphoblastic leukaemia: evidence for selective loss of immunological control of residual disease? Br J Haematol; 2009 Apr;145(1):87-95
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  • [Title] Relationship between HLA-DP supertype and survival in childhood acute lymphoblastic leukaemia: evidence for selective loss of immunological control of residual disease?
  • We recently reported that two of six HLA-DP supertypes (DP1-4, 6, 8) were associated with susceptibility (DP2) and resistance (DP1) to childhood acute lymphoblastic leukaemia (ALL).
  • This may involve abrogation of DP1/3-restricted T-cell control of residual disease due to selective effects of chemotherapy.
  • [MeSH-major] Biomarkers, Tumor / genetics. HLA-DP Antigens / genetics. Neoplasm, Residual / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Adolescent. Chi-Square Distribution. Child. Child, Preschool. Disease-Free Survival. Female. Genetic Predisposition to Disease. Genotype. HLA-DP beta-Chains. Humans. Immunosuppressive Agents / therapeutic use. Infant. Kaplan-Meier Estimate. Male. Methotrexate / therapeutic use. Prognosis. Randomized Controlled Trials as Topic. Statistics, Nonparametric. Treatment Outcome

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  • [CommentIn] Br J Haematol. 2011 Apr;153(1):131-3 [21275963.001]
  • (PMID = 19183185.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HLA-DP Antigens; 0 / HLA-DP beta-Chains; 0 / HLA-DPw1 antigen; 0 / HLA-DPw2 antigen; 0 / HLA-DPw3 antigen; 0 / HLA-DPw4 antigen; 0 / Immunosuppressive Agents; YL5FZ2Y5U1 / Methotrexate
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64. Dzhagalov I, Dunkle A, He YW: The anti-apoptotic Bcl-2 family member Mcl-1 promotes T lymphocyte survival at multiple stages. J Immunol; 2008 Jul 1;181(1):521-8
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  • Genetic studies have demonstrated that the Bcl-2 family member Mcl-1 is an important anti-apoptotic protein in the development of multiple cell types including T lymphocytes.
  • In this study, we examined the expression pattern of Mcl-1 in different populations of T cells at the single-cell level and found that Mcl-1 protein is constitutively expressed in all T cell populations and up-regulated upon TCR stimulation.
  • We then investigated the role of Mcl-1 in the survival of these different populations by conditionally deleting Mcl-1 at various T cell stages.

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  • (PMID = 18566418.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI074754; United States / NIAID NIH HHS / AI / AI054658-05; United States / NCI NIH HHS / CA / R01 CA092123; United States / NCI NIH HHS / CA / CA092123-05; United States / NIAID NIH HHS / AI / R01 AI054658-05; United States / NIAID NIH HHS / AI / AI54683; United States / NCI NIH HHS / CA / R01 CA092123-05; United States / NCI NIH HHS / CA / CA92123; United States / NIAID NIH HHS / AI / R01 AI054658
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein
  • [Other-IDs] NLM/ NIHMS66462; NLM/ PMC2561902
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65. Verbeek WH, Van De Water JM, Al-Toma A, Oudejans JJ, Mulder CJ, Coupé VM: Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population-based registry in The Netherlands. Scand J Gastroenterol; 2008;43(11):1322-8
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  • [Title] Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population-based registry in The Netherlands.
  • OBJECTIVE: Enteropathy-associated T-cell lymphomas (EATLs) are T-cell non-Hodgkin lymphomas of the small bowel, which are specifically associated with coeliac disease (CD).
  • We included all T-cell lymphomas detected between January 2000 and December 2006 that initially presented in the small bowel.
  • Finally, the distribution of characteristics such as the localization, the Marsh classification and method of diagnosis are described.
  • Most EATLs were localized in the proximal small intestine and the diagnosis was made by surgical resection in the majority of cases.
  • CONCLUSIONS: EATL is a rare disease with an incidence of 0.10 per 100,000 inhabitants per year, occurring in older age, with a peak incidence in the 7th decade.
  • [MeSH-major] Celiac Disease / epidemiology. Lymphoma, T-Cell / epidemiology

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  • (PMID = 18618372.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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66. Clofarabine: new drug. Children with acute lymphoblastic leukaemia: a last resort. Prescrire Int; 2007 Dec;16(92):238-9
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  • [Title] Clofarabine: new drug. Children with acute lymphoblastic leukaemia: a last resort.
  • (1) Standard treatments fail in about 20% of children with acute lymphoblastic leukaemia.
  • About half these latter patients were able to undergo potentially curative haematopoietic stem-cell transplantation. (4) Preliminary results from another non comparative trial suggest similar efficacy. (5) Short-term adverse effects are frequent and often serious, and include gastrointestinal disorders, infections, tumour lysis syndrome, and cardiac, renal and hepatobiliary disorders.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Arabinonucleosides / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18092403.001).
  • [ISSN] 1167-7422
  • [Journal-full-title] Prescrire international
  • [ISO-abbreviation] Prescrire Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides
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67. Ishizawa J, Fujita H, Iguchi M, Tachibana T, Taguchi J, Ishigatsubo Y: Quantification of circulating varicella-zoster virus DNA for follow-up in a case of visceral varicella-zoster infection ameliorated with intravenous acyclovir. Int J Hematol; 2007 Apr;85(3):242-5
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  • We describe a patient with acute lymphocytic leukemia (ALL) who developed visceral varicella-zoster virus (VZV) infection following cord blood stem cell transplantation (CBSCT) and was successfully treated with intravenous acyclovir (ACV).
  • A diagnosis of visceral varicella-zoster disease was made, and early intravenous ACV therapy successfully alleviated the epigastric pain and skin lesions within 2 weeks.
  • [MeSH-minor] Adult. Cord Blood Stem Cell Transplantation / adverse effects. DNA, Viral / blood. DNA, Viral / drug effects. Female. Humans. Injections, Intravenous. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 17483062.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / DNA, Viral; X4HES1O11F / Acyclovir
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68. Babusíková O, Zelezníková T, Mlcáková A, Kusenda J, Stevulová L: The knowledge on the 3rd type hematogones could contribute to more precise detection of small numbers of precursor B-acute lymphoblastic leukemia. Neoplasma; 2005;52(6):502-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The knowledge on the 3rd type hematogones could contribute to more precise detection of small numbers of precursor B-acute lymphoblastic leukemia.
  • Bone marrow hematogones (benign B-lymphocyte precursors) may cause diagnostic problems due to their morphologic and immunophenotypic similarities with neoplastic lymphoblasts.
  • Bone marrow hematogones were separately assessed as hematogones 1 population of early stage and hematogones 2 of mid-stage precursor B-cells, respectively.
  • In some (about 30%) of hematogones a third type hematogones could be assessed in bone marrow samples.
  • This small B-cell subpopulation was defined by CD10-positivity, coexpressing more mature markers CD19,CD20,CD22 and CD45bright.
  • Quantitative immunophenotyping of this study completed the percent antigen expression data in two main hematogone subtypes and lymphocytes in 16 bone marrow specimens and precursor B-ALL lymphoblasts in some samples.
  • Increased information on benign B-lymphocyte precursors, especially that of existence of the 3rd type hematogones could provide a basis for better discrimination of B-leukemia cells even in a very small amounts.
  • [MeSH-major] Antigens, CD / analysis. B-Lymphocytes / immunology. Bone Marrow / immunology. Bone Marrow Cells / cytology. Burkitt Lymphoma / diagnosis. Immunophenotyping

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  • (PMID = 16284697.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD
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69. Dufourg MN, Landman-Parker J, Auclerc MF, Schmitt C, Perel Y, Michel G, Levy P, Couillault G, Gandemer V, Tabone MD, Demeocq F, Vannier JP, Leblanc T, Leverger G, Baruchel A: Age and high-dose methotrexate are associated to clinical acute encephalopathy in FRALLE 93 trial for acute lymphoblastic leukemia in children. Leukemia; 2007 Feb;21(2):238-47
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  • [Title] Age and high-dose methotrexate are associated to clinical acute encephalopathy in FRALLE 93 trial for acute lymphoblastic leukemia in children.
  • The objective of the study was to assess acute neurotoxicity associated with triple intrathecal therapy (TIT)+/-high-dose methotrexate (HD MTX) in children with acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Brain Diseases, Metabolic / chemically induced. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17170721.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Neurotoxins; YL5FZ2Y5U1 / Methotrexate
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70. Or R, Hadar E, Bitan M, Resnick IB, Aker M, Ackerstein A, Samuel S, Tsirigotis P, Gesundheit B, Slavin S, Shapira MY: Safety and efficacy of donor lymphocyte infusions following mismatched stem cell transplantation. Biol Blood Marrow Transplant; 2006 Dec;12(12):1295-301
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  • [Title] Safety and efficacy of donor lymphocyte infusions following mismatched stem cell transplantation.
  • The use of a mismatched allograft necessitates T cell depletion for prevention of uncontrolled graft-versus-host disease (GVHD), thus impairing a graft-versus-leukemia effect.
  • Data on donor lymphocyte infusion (DLI) after mismatched stem cell transplantation are lacking.
  • Death was frequent and usually related to the basic disease rather than to DLI complications.
  • Future developments using cell therapy with selective or targeted anticancer activity are warranted, with special attention to prophylactic treatment of T cell depleted mismatched allografts recipients.
  • [MeSH-major] Graft Enhancement, Immunologic. Leukemia, Myeloid / surgery. Lymphocyte Transfusion. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child, Preschool. Feasibility Studies. Female. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Graft vs Leukemia Effect. HLA Antigens / immunology. Histocompatibility. Humans. Kaplan-Meier Estimate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukocyte Reduction Procedures. Lymphoma / surgery. Male. Middle Aged. Myelodysplastic Syndromes / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Remission Induction. Survival Analysis. Tissue Donors. Transplantation Conditioning. Tumor Burden

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  • (PMID = 17162211.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
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71. Yu Q, Sharma A, Sen JM: TCF1 and beta-catenin regulate T cell development and function. Immunol Res; 2010 Jul;47(1-3):45-55
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  • [Title] TCF1 and beta-catenin regulate T cell development and function.
  • T cell factor-1 (TCF1) critically regulates T cell development.
  • We have genetically manipulated the beta-catenin gene and generated mutant mice that have shown an essential role for beta-catenin and TCF1 during pre-T cell receptor (TCR) and TCR-dependent stages of T cell development.
  • [MeSH-major] Cell Differentiation. Gene Expression Regulation. T Cell Transcription Factor 1 / metabolism. T-Lymphocytes / cytology. T-Lymphocytes / immunology. beta Catenin / metabolism
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Humans. Mice. Receptors, Antigen, T-Cell / genetics. Receptors, Antigen, T-Cell / metabolism. Signal Transduction

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  • (PMID = 20082155.001).
  • [ISSN] 1559-0755
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AG000768-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; 0 / T Cell Transcription Factor 1; 0 / beta Catenin
  • [Other-IDs] NLM/ NIHMS172600; NLM/ PMC2891409
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72. Chen P, Chen YZ, Wu Y, Huang HF, Li NN: [Identification of the isoform in type II receptor of transforming growth factor-beta in patients with acute leukemia and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):221-4
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  • [Title] [Identification of the isoform in type II receptor of transforming growth factor-beta in patients with acute leukemia and its clinical significance].
  • Recent research indicates that TGF-beta and type II receptor (TbetaR-II) play an important role in the pathogenesis of tumor.
  • To identify the mutation of TbetaR-II in patients with acute leukemia, the bone marrow samples from 6 patients with acute leukemia and 11 normal individuals as control were detected by long-range RT-PCR.
  • The results showed that there was existance of the isoform of TbetaR-II in 2 cases out of 6 patients with acute leukemia.
  • In conclusion, there was the isoform of TbetaR-II in partial patients with acute leukemia, and the isoform may be related with prognosis.

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  • (PMID = 16638184.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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73. Nishi H, Tomida C, Gotoh M, Yamagata K, Akiyama H, Shimokama T: Chronic renal failure with severe mesangiolysis in a hematopoietic stem cell transplant recipient. Ren Fail; 2006;28(6):519-22
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  • [Title] Chronic renal failure with severe mesangiolysis in a hematopoietic stem cell transplant recipient.
  • Chronic progressive renal failure is a well-recognized complication in hematopoietic stem cell transplantation (HSCT) recipients.
  • This study describes a 38-year-old female patient with acute lymphoblastic leukemia treated with HSCT who developed chronic renal dysfunction after transplantation.
  • [MeSH-major] Glomerular Mesangium / pathology. Hematopoietic Stem Cell Transplantation / adverse effects. Kidney Failure, Chronic / pathology
  • [MeSH-minor] Adult. Female. Humans. Peritoneal Dialysis. Postoperative Complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation Conditioning / adverse effects. Treatment Outcome

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  • (PMID = 16928623.001).
  • [ISSN] 0886-022X
  • [Journal-full-title] Renal failure
  • [ISO-abbreviation] Ren Fail
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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74. Zeng HL, Han XA, Gu C, Zhu HY, Huang XS, Gu JQ, Zhong Q, Liu GJ, Ming WJ, Cai XN: [Reactive oxygen species and mitochondrial membrane potential changes in leukemia cells during 6-gingerol induced apoptosis]. Zhong Yao Cai; 2010 Apr;33(4):584-7
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  • [Title] [Reactive oxygen species and mitochondrial membrane potential changes in leukemia cells during 6-gingerol induced apoptosis].
  • OBJECTIVE: To observe the effects of 6-gingerol on reactive oxygen species (ROS) and mitochondrial membrane potential(deltapsim) of chronic myeloid leukemia K562 cells and human acute T lymphoblastic leukemia MOLT4 cells, to investigate the role of mitochondrial pathway in the signal transduction of leukemia cell.
  • CONCLUSIONS: 6-gingerol can significantly increase ROS levels of K562 cells and MOLT4 cells, decrease deltapsim of K562 cells,induce apoptosis of leukemia cells by mitochondrial pathway.
  • [MeSH-major] Apoptosis / drug effects. Catechols / pharmacology. Fatty Alcohols / pharmacology. Ginger / chemistry. Leukemia, Lymphoid / pathology. Membrane Potential, Mitochondrial / drug effects. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Antioxidants / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. Humans. K562 Cells

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  • (PMID = 20845790.001).
  • [ISSN] 1001-4454
  • [Journal-full-title] Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials
  • [ISO-abbreviation] Zhong Yao Cai
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Antioxidants; 0 / Catechols; 0 / Fatty Alcohols; 0 / Reactive Oxygen Species; 925QK2Z900 / gingerol
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75. Hagemeijer A, Graux C: ABL1 rearrangements in T-cell acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Apr;49(4):299-308
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  • [Title] ABL1 rearrangements in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is the result of multiple oncogenic insults of thymocytes.
  • [MeSH-major] Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-abl / genetics

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  • (PMID = 20073070.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  • [Number-of-references] 60
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76. Jundt F, Schwarzer R, Dörken B: Notch signaling in leukemias and lymphomas. Curr Mol Med; 2008 Feb;8(1):51-9
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  • [Title] Notch signaling in leukemias and lymphomas.
  • Aberrant Notch activation is linked to cancer since 1991 when mammalian Notch1 was first identified as part of the translocation t(7;9) in a subset of human T-cell acute lymphoblastic leukemias (T-ALL).
  • Depending on tumor type Notch interferes with differentiation, proliferation, survival, cell-cycle progression, angiogenesis, and possibly self-renewal.
  • In hematopoietic neoplasms, recent findings indicate an important role of Notch for T-ALL induction and progression and the pathogenesis of human T- and B-cell-derived lymphomas.
  • This review will focus on the most recent findings on Notch signaling in leukemias and lymphomas and its potential role in the maintenance of malignant stem cells.
  • [MeSH-major] Leukemia / metabolism. Lymphoma / metabolism. Receptors, Notch / metabolism. Signal Transduction / physiology

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  • (PMID = 18289013.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Notch
  • [Number-of-references] 128
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77. Brewer JL, Ericson SG: An improved methodology to detect human T cell receptor beta variable family gene expression patterns. J Immunol Methods; 2005 Jul;302(1-2):54-67
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  • [Title] An improved methodology to detect human T cell receptor beta variable family gene expression patterns.
  • Comprehensive gene expression analysis of the T cell receptor repertoire of an individual can be very useful in evaluating the immune response in a variety of conditions.
  • Antibody-based analysis methods can detect approximately 60% of the human T cell receptor beta variable (TCRBV) proteins, while gene expression analysis, primarily through employment of the polymerase chain reaction (PCR), has had somewhat greater success in the detection of additional TCRBV families.
  • We describe here a real-time reverse transcription polymerase chain reaction-based method, which allows efficient automation and integration of amplification, detection, and analysis with sequence-specific detection of all T cell receptor beta variable gene families, subfamilies, and alleles.
  • [MeSH-major] Gene Expression Profiling / methods. Multigene Family. Receptors, Antigen, T-Cell, alpha-beta / biosynthesis. Receptors, Antigen, T-Cell, alpha-beta / genetics
  • [MeSH-minor] DNA Primers. Fluorometry / methods. Genetic Variation. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Humans. Polymerase Chain Reaction / methods. RNA, Messenger / biosynthesis

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  • (PMID = 16038929.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5 P20 RR16440-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, Antigen, T-Cell, alpha-beta
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78. Braun FK, Fecker LF, Schwarz C, Walden P, Assaf C, Dürkop H, Sterry W, Eberle J: Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells. J Invest Dermatol; 2007 Oct;127(10):2425-37
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  • [Title] Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells.
  • Control of apoptosis via death ligands plays a basic role for lymphocyte homeostasis and lymphoma development.
  • In this study, cutaneous T-cell lymphoma (CTCL) cell lines revealed pronounced resistance to death ligands as compared to cell lines of T-cell acute lymphoblastic leukemia (T-ALL).
  • The proapoptotic activity of tumor necrosis factor (TNF)-alpha was blocked, sensitivity to TNF-related apoptosis-inducing ligand was significantly reduced, and 1/4 CTCL cell lines was resistant to CD95 activation.
  • No indication for a responsibility of typical downstream regulators of apoptosis was obtained, but loss of CD95 was found in 1/4, loss of TNF-R1 in 3/4, loss of caspase-10 in 2/4, loss of Bid in 1/4, and overexpression of cellular flice inhibitory protein was found in 4/4 CTCL cell lines.
  • [MeSH-major] Apoptosis / physiology. Lymphoma, T-Cell, Cutaneous / pathology. Receptors, Death Domain / antagonists & inhibitors. Signal Transduction / physiology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD95 / physiology. BH3 Interacting Domain Death Agonist Protein / physiology. CASP8 and FADD-Like Apoptosis Regulating Protein / physiology. Caspase 10 / physiology. Cell Line, Tumor. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Male. Middle Aged. TNF-Related Apoptosis-Inducing Ligand / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand / physiology. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 17495957.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Receptors, Death Domain; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspase 10
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79. Wissink EH, Verbrugge I, Vink SR, Schader MB, Schaefer U, Walczak H, Borst J, Verheij M: TRAIL enhances efficacy of radiotherapy in a p53 mutant, Bcl-2 overexpressing lymphoid malignancy. Radiother Oncol; 2006 Aug;80(2):214-22
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  • MATERIALS AND METHODS: The p53 mutant human T acute lymphoblastic leukemia line Jurkat transduced with the Bcl-2 gene was used as model system in vitro and in a subcutaneous transplant setting in immunodeficient mice.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / radiotherapy. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 16916556.001).
  • [ISSN] 0167-8140
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 04Y7590D77 / Isoleucine
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80. Panetta JC, Sparreboom A, Pui CH, Relling MV, Evans WE: Modeling mechanisms of in vivo variability in methotrexate accumulation and folate pathway inhibition in acute lymphoblastic leukemia cells. PLoS Comput Biol; 2010 Dec 02;6(12):e1001019
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  • [Title] Modeling mechanisms of in vivo variability in methotrexate accumulation and folate pathway inhibition in acute lymphoblastic leukemia cells.
  • Methotrexate (MTX) is widely used for the treatment of childhood acute lymphoblastic leukemia (ALL).
  • We studied 194 of 356 patients enrolled on St. Jude Total XV protocol for newly diagnosed ALL with the goal of characterizing the intracellular pharmacokinetics of MTXPG in leukemia cells; relating these pharmacokinetics to ALL lineage, ploidy and molecular subtype; and using a folate pathway model to simulate optimal treatment strategies.
  • Serial MTX concentrations were measured in plasma and intracellular MTXPG concentrations were measured in circulating leukemia cells.
  • In addition, a folate pathway model was adapted to simulate the effects of treatment strategies on the inhibition of de novo purine synthesis (DNPS).
  • This study has provided new insights into the intracellular disposition of MTX in leukemia cells and how it affects treatment efficacy.

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  • (PMID = 21152005.001).
  • [ISSN] 1553-7358
  • [Journal-full-title] PLoS computational biology
  • [ISO-abbreviation] PLoS Comput. Biol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01CA078224; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / R37CA36401; United States / NCI NIH HHS / CA / P30CA021765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / GM 61393
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 25513-46-6 / Polyglutamic Acid; 82334-40-5 / methotrexate polyglutamate; 935E97BOY8 / Folic Acid; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC2996318
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81. Soszynska K, Mucha B, Debski R, Skonieczka K, Duszenko E, Koltan A, Wysocki M, Haus O: The application of conventional cytogenetics, FISH, and RT-PCR to detect genetic changes in 70 children with ALL. Ann Hematol; 2008 Dec;87(12):991-1002
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  • We investigated bone marrow cells of 70 acute lymphoblastic leukemia children by conventional cytogenetics (CC), fluorescence in situ hybridization (FISH), and reverse transcription polymerase chain reaction (RT-PCR) methods.
  • CC and RT-PCR for fusion genes BCR/ABL, MLL/AF4, E2A/PBX1, TEL/AML1 were performed at diagnosis in each patient.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Genes, abl / genetics. Homeodomain Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18633615.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 146150-85-8 / E2A-Pbx1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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82. Geurts JJ, Blezer EL, Vrenken H, van der Toorn A, Castelijns JA, Polman CH, Pouwels PJ, Bö L, Barkhof F: Does high-field MR imaging improve cortical lesion detection in multiple sclerosis? J Neurol; 2008 Feb;255(2):183-91
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  • [Title] Does high-field MR imaging improve cortical lesion detection in multiple sclerosis?
  • OBJECTIVE: Cortical lesions in multiple sclerosis (MS) are notoriously difficult to visualize with standard MR imaging (MRI) techniques.
  • However, the use of higher field-strengths with intrinsically higher signal-to-noise, which can partly be used to increase spatial resolution, may improve cortical lesion detection.
  • Therefore, in this post mortem study, the sensitivity of high field-strength MRI (4.7 T) for cortical lesions was investigated, and compared to that of standard field-strength (1.5 T).
  • Proteolipid protein (PLP)-stained tissue sections (10 microm) of the same brain slices were matched to the corresponding MR images, and cortical lesions were scored on all three MR sequences (blinded to histology) and in tissue sections (blinded to MRI).
  • Sensitivity of the sequences for four cortical lesion types was calculated.
  • RESULTS: Sensitivity for purely intracortical lesions (histological lesion types II, III, and IV; n = 128) was below 10 % for both 1.5 T and 4.7 T MRI, while mixed gray matter-white matter (type I) lesions (n = 5) were detected in four out of five cases.
  • CONCLUSIONS: MRI sensitivity for post mortem detection of cortical lesions is low, even when a higher field-strength was used.
  • It varies, however, for different subtypes of cortical lesions.

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  • (PMID = 18231704.001).
  • [ISSN] 0340-5354
  • [Journal-full-title] Journal of neurology
  • [ISO-abbreviation] J. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fixatives; 1HG84L3525 / Formaldehyde
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83. Sasson SC, Smith S, Seddiki N, Zaunders JJ, Bryant A, Koelsch KK, Weatherall C, Munier ML, McGinley C, Yeung J, Mulligan SP, Moore J, Cooper DA, Milliken S, Kelleher AD: IL-7 receptor is expressed on adult pre-B-cell acute lymphoblastic leukemia and other B-cell derived neoplasms and correlates with expression of proliferation and survival markers. Cytokine; 2010 Apr;50(1):58-68
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  • [Title] IL-7 receptor is expressed on adult pre-B-cell acute lymphoblastic leukemia and other B-cell derived neoplasms and correlates with expression of proliferation and survival markers.
  • The interleukin (IL)-7 receptor (IL-7R) is expressed on human pre-B but not mature B-cells.
  • We hypothesised that aberrant expression of IL-7R contributes to B-cell oncogenesis.
  • BMMC) from patients with B-cell derived neoplasms, chronic human immunodeficiency virus type-1 (HIV-1) infection alone, or healthy volunteers.
  • CD127 expression was elevated in pre-B-cell acute lymphoblastic leukemia (pre-B-ALL) and in some cases of Non-Hodgkin's Lymphoma (B-NHL).
  • Plasma IL-7 levels were higher in pre-B-ALL, B-cell chronic lymphocytic leukemia (B-CLL) and HIV-1 associated B-NHL (HIV-B-NHL) compared with control groups.
  • CD127+ pre-B-ALL cells had higher expression of Ki-67, Bcl-2 and CD132 than CD127- counterparts.
  • Unlike T-lineage cells, CD127+ pre-B-ALL cells did not down-regulate CD127 in response to exogenous IL-7.
  • Patients with B-cell derived neoplasms had elevated circulating IL-10 and decreased BAFF.
  • These findings support a role for the IL-7/IL-7R system in B-cell oncogenesis.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptors, Interleukin-7 / immunology
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Cell Membrane / metabolism. Cell Proliferation. Cryopreservation. Cytokines / blood. Female. Flow Cytometry. Humans. Interleukin Receptor Common gamma Subunit / metabolism. Ki-67 Antigen / metabolism. Male. Middle Aged. Phenotype. Prospective Studies. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retrospective Studies. Survival Analysis. T-Lymphocytes / pathology

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  • [Copyright] 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20060740.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / IL2RG protein, human; 0 / Interleukin Receptor Common gamma Subunit; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Interleukin-7
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84. Sharma VM, Calvo JA, Draheim KM, Cunningham LA, Hermance N, Beverly L, Krishnamoorthy V, Bhasin M, Capobianco AJ, Kelliher MA: Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc. Mol Cell Biol; 2006 Nov;26(21):8022-31
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  • [Title] Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc.
  • Recent work with mouse models and human leukemic samples has shown that gain-of-function mutation(s) in Notch1 is a common genetic event in T-cell acute lymphoblastic leukemia (T-ALL).
  • To identify Notch1 target genes in leukemia, we developed mouse T-cell leukemic lines that express intracellular Notch1 in a doxycycline-dependent manner.
  • Using gene expression profiling and chromatin immunoprecipitation, we identified c-myc as a novel, direct, and critical Notch1 target gene in T-cell leukemia. c-myc mRNA levels are increased in primary mouse T-cell tumors that harbor Notch1 mutations, and Notch1 inhibition decreases c-myc mRNA levels and inhibits leukemic cell growth.
  • Consistent with these findings, retroviral insertional mutagenesis screening of our T-cell leukemia mouse model revealed common insertions in either notch1 or c-myc genes.

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  • (PMID = 16954387.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA-096889
  • [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 / Enzyme Inhibitors; 0 / Myc protein, mouse; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC1636748
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85. Nishiwaki S, Inamoto Y, Sakamaki H, Kurokawa M, Iida H, Ogawa H, Fukuda T, Ozawa Y, Kobayashi N, Kasai M, Mori T, Iwato K, Yoshida T, Onizuka M, Kawa K, Morishima Y, Suzuki R, Atsuta Y, Miyamura K: Allogeneic stem cell transplantation for adult Philadelphia chromosome-negative acute lymphocytic leukemia: comparable survival rates but different risk factors between related and unrelated transplantation in first complete remission. Blood; 2010 Nov 18;116(20):4368-75
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  • [Title] Allogeneic stem cell transplantation for adult Philadelphia chromosome-negative acute lymphocytic leukemia: comparable survival rates but different risk factors between related and unrelated transplantation in first complete remission.
  • To identify factors to improve the outcomes of related and unrelated allogeneic stem cell transplantations (allo-SCT) for Philadelphia chromosome-negative acute lymphocytic leukemia (Ph(-) ALL) in the first complete remission (CR1), we retrospectively analyzed 1139 Ph(-) ALL patients using the registry data, particularly the details of 641 patients transplanted in CR1.
  • Among patients transplanted in CR1, relapse rates were significantly higher in related allo-SCT compared with unrelated allo-SCT, and multivariate analysis demonstrated that less than 6 months from diagnosis to allo-SCT alone was associated with relapse.
  • On the other hand, nonrelapse mortality (NRM) was significantly higher in unrelated allo-SCT compared with related allo-SCT, and multivariate analysis demonstrated that 10 months or longer from diagnosis to allo-SCT, human leukocyte antigen mismatch, and abnormal karyotype were associated with NRM.
  • [MeSH-major] Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation

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  • (PMID = 20664060.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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86. Aref S, Mabed M, El-Sherbiny M, Selim T, Metwaly A: Cyclin D1 expression in acute leukemia. Hematology; 2006 Feb;11(1):31-4
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  • [Title] Cyclin D1 expression in acute leukemia.
  • BACKGROUND: Disorders of the cell cycle regulatory machinery play a key role in the pathogenesis of cancer.
  • Over expression of cyclin D1 protein has been reported in several solid tumors and certain lymphoid malignancies, but little is known about the involvement of cyclin D1 in acute leukemia.
  • PATIENTS AND METHODS: In this study, we analyzed the expression of cyclin D1 at protein level in, 40 newly diagnosed patients with acute myeloid leukemia (AML), 10 patients with acute lymphoblastic leukemia (ALL), and 11 normal controls using flow cytometry.
  • The ALL cases with cyclin D1 over expression were significantly correlated to blast cell counts in the peripheral blood and bone marrow (BM) but not with hemoglobin level, WBC, and platelets count.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Cyclin D1 / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood

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  • (PMID = 16522546.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 136601-57-5 / Cyclin D1
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87. Park HH, Kim M, Lee BH, Lim J, Kim Y, Lee EJ, Min WS, Kang CS, Kim WI, Shim SI, Han K: Intracellular IL-4, IL-10, and IFN-gamma levels of leukemic cells and bone marrow T cells in acute leukemia. Ann Clin Lab Sci; 2006;36(1):7-15
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  • [Title] Intracellular IL-4, IL-10, and IFN-gamma levels of leukemic cells and bone marrow T cells in acute leukemia.
  • The quantitative levels of intracellular cytokines IL-4, IL-10, and IFN-gamma (ie, the number of bound PE-conjugated antibody molecules/cell) of leukemic cells and bone marrow T cells (bmT cells) of acute leukemia patients were analyzed by flow cytometry.
  • The leukemic cell IL-4 level was highest in the monocytic AML group (1735 +/- 1056) and lowest in the dysplastic AML group (960 +/- 545).
  • The IFN-gamma level was highest in the acute promyelocytic leukemia (APL) group (495 +/- 159), and lowest in the ALL group (252 +/- 119).
  • The IL-10 level was not significantly different among the diagnosis groups.
  • The leukemic cell cytokine levels were lowest and bmT cell cytokine levels were highest in the dysplastic AML group.
  • The cytokine levels of bmT cells at the time of CR became normal and were not different among the diagnosis groups.
  • In summary, leukemic cell and bmT cell cytoplasmic expression profiles of IL-4, IL-10, and IFN-gamma are characteristic for each diagnostic group of acute leukemia patients and the profiles of bmT cells are normal at the time of CR.
  • [MeSH-major] Bone Marrow Cells / metabolism. Interferon-gamma / blood. Interleukin-10 / blood. Interleukin-4 / blood. Leukemia / metabolism. T-Lymphocytes / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Remission Induction

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  • (PMID = 16501231.001).
  • [ISSN] 0091-7370
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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88. Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA: WT1 mutations in T-ALL. Blood; 2009 Jul 30;114(5):1038-45
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  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.
  • [MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

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  • (PMID = 19494353.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE15931
  • [Grant] United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2721784
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89. Kaćanski N, Konstantinidis N, Kolarović J, Slavković B, Vujić D: [Biphenotypic acute leukaemia: case reports of two paediatric patients]. Med Pregl; 2010 Nov-Dec;63(11-12):867-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Biphenotypic acute leukaemia: case reports of two paediatric patients].
  • INTRODUCTION: Biphenotypic acute leukaemia is an uncommon type of leukaemia whose blasts co-express myeloid and B-or T-lymphoid antigens.
  • CASE REPORT: We describe two cases of paediatric patients with biphenotypic acute leukaemia.
  • She was treated with combined acute myeloid leukaemia/acute lymphoblastic leukaemia induction therapy followed by autologous stem cell transplantation.
  • The patient died due to the complications of stem cell transplantation procedure.
  • She received acute myeloid leukaemia induction therapy.
  • DISCUSSION: Immunophenotype is essential to establish the diagnosis of biphenotypic acute leukaemia according to the scoring system adopted by the European Group of Immunological Classification of Leukaemia.
  • There is no agreement about uniformity in treatment for the patients with this type of leukaemia.
  • Biphenotypic acute leukaemia is a high risk leukaemia which requires a more intensive treatment.
  • CONCLUSION: Therapy for every patient with biphenotypic acute leukaemia should depend on their immunophenotype and gene rearrangement profiles.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy

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  • (PMID = 21553470.001).
  • [ISSN] 0025-8105
  • [Journal-full-title] Medicinski pregled
  • [ISO-abbreviation] Med. Pregl.
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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90. Fais F, Tenca C, Cimino G, Coletti V, Zanardi S, Bagnara D, Saverino D, Zarcone D, De Rossi G, Ciccone E, Grossi CE: CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis. Leukemia; 2005 Apr;19(4):551-6
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  • [Title] CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis.
  • Acute lymphoblastic leukemia (ALL) is the most frequent malignancy of childhood.
  • We investigated CD1d expression in 80 pediatric B-cell precursor (BCP) ALL cases defined according to immunophenotype, cytogenetic features and age at onset.
  • CD1d+ ALLs were significantly associated with infant leukemia, pro-B phenotype and mixed-lineage leukemia (MLL)/AF4 gene rearrangement.
  • Analysis of bone marrow (BM) cells derived from normal donors revealed that CD19+/CD1d+ cells were mostly mature B lymphocytes.
  • [MeSH-major] Antigens, CD1 / metabolism. Hematopoietic Stem Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Antigens, CD1d. B-Lymphocytes / cytology. Biomarkers, Tumor / metabolism. Cell Communication. Cell Line. Child. Galactosylceramides / metabolism. Humans. Infant. Killer Cells, Natural / cytology. Killer Cells, Natural / metabolism. Predictive Value of Tests. Prognosis. Survival Rate

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  • (PMID = 15744356.001).
  • [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 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Biomarkers, Tumor; 0 / CD1D protein, human; 0 / Galactosylceramides; 0 / alpha-galactosylceramide
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91. Souroullas GP, Salmon JM, Sablitzky F, Curtis DJ, Goodell MA: Adult hematopoietic stem and progenitor cells require either Lyl1 or Scl for survival. Cell Stem Cell; 2009 Feb 6;4(2):180-6
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  • Scl and Lyl1 encode two related basic-helix-loop-helix transcription factors implicated in T cell acute lymphoblastic leukemia.
  • Previous studies showed that Scl is essential for embryonic and adult erythropoiesis, while Lyl1 is important for B cell development.

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  • (PMID = 19200805.001).
  • [ISSN] 1875-9777
  • [Journal-full-title] Cell stem cell
  • [ISO-abbreviation] Cell Stem Cell
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL096360; United States / NHLBI NIH HHS / HL / HL 08100; United States / NIDDK NIH HHS / DK / DK058192-09; United States / NIDDK NIH HHS / DK / R01 DK058192-09; United States / NIBIB NIH HHS / EB / R01 EB005173; United States / NIBIB NIH HHS / EB / EB 005173; United States / NIBIB NIH HHS / EB / R01 EB005173-04; United States / NIDDK NIH HHS / DK / R01 DK058192; United States / NHLBI NIH HHS / HL / U54 HL081007-04; United States / NIBIB NIH HHS / EB / EB005173-04; United States / NIDDK NIH HHS / DK / DK 58192; United States / NHLBI NIH HHS / HL / HL081007-04
  • [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 / Lyl1 protein, mouse; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse
  • [Other-IDs] NLM/ NIHMS100258; NLM/ PMC2672304
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92. Iwamoto S, Mihara K, Downing JR, Pui CH, Campana D: Mesenchymal cells regulate the response of acute lymphoblastic leukemia cells to asparaginase. J Clin Invest; 2007 Apr;117(4):1049-57
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  • [Title] Mesenchymal cells regulate the response of acute lymphoblastic leukemia cells to asparaginase.
  • Because of their low asparagine synthetase (ASNS) expression and asparagine biosynthesis, acute lymphoblastic leukemia (ALL) cells are exquisitely sensitive to asparagine depletion.
  • However, ASNS expression levels in bone marrow-derived mesenchymal cells (MSCs), which form the microenvironment where leukemic cells grow, were on average 20 times higher than those in ALL cells.
  • Asparagine secretion by MSCs was directly related to their ASNS expression levels, suggesting a mechanism - increased concentrations of asparagine in the leukemic cell microenvironment - for the protective effects we observed.