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1. Wang ZY, Chen QS: [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Apr;13(2):169-73
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  • [Title] [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial].
  • One of the important approaches for further prolonging remission duration and eradicating minimal residual disease in acute leukemia is immunotherapy.
  • Four kinds of immunotherapy for acute leukemia are under investigation:.
  • (1) monoclonal antibodies, among them, Mylotarg (cytotoxic antibiotic calicheamicin linked to CD33 Mab) is given for the treatment of refractory or relapsed acute myeloid leukemia and molecular relapse in acute promyelocytic leukemia with good results, Campath-1H (antiCD52 Mab) is administered in the treatment of prolymphocytic leukemia and Rituximab (anti-CD20 Mab) in B-PLL with high complete remission rates.
  • Other Mabs under preclinical and clinical trials include anti-IL-2 receptor Mab for the treatment of acute T lymphocytic leukemia, anti-220 kD Mab-6G7 for acute leukemias, recombinant immune toxin BL22 (anti-CD22) for hairy cell leukemia and Mabs labeled with radio-isotopes for different types of acute leukemias;.
  • (2) adoptive cellular immunotherapy using cytokine-induced killer cell, alloreactive NK cells, allogeneic or autologous leukemic-specific CD8(+) cytotoxic T lymphocytes, and other immune effector cells;.
  • (4) leukemia vaccines of several different formulations including antigen-specific, leukemia cell-based, leukemia antigen-pulsed dendritic cell (DC) and leukemia-derived DC vaccines, the latter two formulations are more attractive.
  • In conclusion, up to now, the most effective example of immunotherapy in acute leukemia is provided by the administration of Mabs, and the majority of other approaches in immunotherapy for acute leukemia although promising, need further studies.

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  • (PMID = 15854271.001).
  • [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] Editorial; English Abstract
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines
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2. 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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3. 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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4. 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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5. 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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6. 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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  • [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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7. Cristóbal I, Blanco FJ, Garcia-Orti L, Marcotegui N, Vicente C, Rifon J, Novo FJ, Bandres E, Calasanz MJ, Bernabeu C, Odero MD: SETBP1 overexpression is a novel leukemogenic mechanism that predicts adverse outcome in elderly patients with acute myeloid leukemia. Blood; 2010 Jan 21;115(3):615-25
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  • [Title] SETBP1 overexpression is a novel leukemogenic mechanism that predicts adverse outcome in elderly patients with acute myeloid leukemia.
  • Acute myeloid leukemias (AMLs) result from multiple genetic alterations in hematopoietic stem cells.
  • The prevalence of SETBP1 overexpression in AML at diagnosis (n = 192) was 27.6% and was associated with unfavorable cytogenetic prognostic group, monosomy 7, and EVI1 overexpression (P < .01).
  • [MeSH-major] Carrier Proteins / genetics. Cell Transformation, Neoplastic / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics

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  • (PMID = 19965692.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Nuclear Proteins; 0 / SETBP1 protein, human
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8. Sadananda Adiga MN, Chandy S, Ramachandra N, Appaji L, Aruna Kumari BS, Ramaswamy G, Savithri HS, Krishnamoorthy L: Methylenetetrahydrofolate reductase gene polymorphisms and risk of acute lymphoblastic leukemia in children. Indian J Cancer; 2010 Jan-Mar;47(1):40-5
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  • [Title] Methylenetetrahydrofolate reductase gene polymorphisms and risk of acute lymphoblastic leukemia in children.
  • Leukemias are malignancies arising from rapidly proliferating hematopoietic cells having great requirement of DNA synthesis.
  • This case-control study was undertaken to analyze the association of the MTHFR gene polymorphisms 677 C"T and 1298 A"C and the risk of acute lymphoblastic leukemia in children.
  • MATERIALS AND METHODS: Eighty-six patients aged below 15 years with a confirmed diagnosis of acute lymphoblastic leukemia (ALL) and 99 matched controls were taken for this study.
  • [MeSH-major] Genetic Predisposition to Disease. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20071789.001).
  • [ISSN] 1998-4774
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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9. 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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10. Yamashita Y, Yuan J, Suetake I, Suzuki H, Ishikawa Y, Choi YL, Ueno T, Soda M, Hamada T, Haruta H, Takada S, Miyazaki Y, Kiyoi H, Ito E, Naoe T, Tomonaga M, Toyota M, Tajima S, Iwama A, Mano H: Array-based genomic resequencing of human leukemia. Oncogene; 2010 Jun 24;29(25):3723-31
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  • [Title] Array-based genomic resequencing of human leukemia.
  • To identify oncogenes in leukemias, we performed large-scale resequencing of the leukemia genome using DNA sequence arrays that determine approximately 9 Mbp of sequence corresponding to the exons or exon-intron boundaries of 5648 protein-coding genes.
  • Hybridization of genomic DNA from CD34-positive blasts of acute myeloid leukemia (n=19) or myeloproliferative disorder (n=1) with the arrays identified 9148 nonsynonymous nucleotide changes.
  • Further screening for JAK3 mutations showed novel and known transforming changes in a total of 9 out of 286 cases of leukemia.
  • Our data have thus shown a unique profile of gene mutations in human leukemia.
  • [MeSH-major] Genomics / methods. Leukemia / genetics. Oligonucleotide Array Sequence Analysis / methods. Sequence Analysis, DNA / methods
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Transformation, Neoplastic. DNA (Cytosine-5-)-Methyltransferase / chemistry. DNA (Cytosine-5-)-Methyltransferase / genetics. Genome, Human / genetics. Humans. Janus Kinase 3 / genetics. Mice. Molecular Sequence Data. Mutation

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  • (PMID = 20400977.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A; EC 2.7.10.2 / Janus Kinase 3
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11. Frazer JK, Meeker ND, Rudner L, Bradley DF, Smith AC, Demarest B, Joshi D, Locke EE, Hutchinson SA, Tripp S, Perkins SL, Trede NS: Heritable T-cell malignancy models established in a zebrafish phenotypic screen. Leukemia; 2009 Oct;23(10):1825-35
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  • [Title] Heritable T-cell malignancy models established in a zebrafish phenotypic screen.
  • T-cell neoplasias are common in pediatric oncology, and include acute lymphoblastic leukemia (T-ALL) and lymphoblastic lymphoma (T-LBL).
  • These cancers have worse prognoses than their B-cell counterparts, and their treatments carry significant morbidity.
  • Although many pediatric malignancies have characteristic translocations, most T-lymphocyte-derived diseases lack cytogenetic hallmarks.
  • Although dysregulation of the NOTCH1 pathway occurs in a substantial fraction of cases, many other genetic lesions of T-cell malignancy have not yet been determined.
  • Using transgenic fish with T-lymphocyte-specific expression of enhanced green fluorescent protein (EGFP), we performed chemical mutagenesis, screened animals for GFP(+) tumors, and identified multiple lines with a heritable predisposition to T-cell malignancy.
  • T-cell receptor analyses confirmed their clonality.
  • Malignancies were transplantable and contained leukemia-initiating cells, like their human correlates.
  • In summary, we have identified multiple zebrafish mutants that recapitulate human T-cell neoplasia and show heritable transmission.

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  • (PMID = 19516274.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / K08 HD053350-03; United States / NCI NIH HHS / CA / P30-CA042014; United States / NICHD NIH HHS / HD / K08-HD53350; United States / NICHD NIH HHS / HD / R21 HD060310; United States / NICHD NIH HHS / HD / R21 HD060310-01; United States / NIDDK NIH HHS / DK / T32-DK007115; United States / NIDDK NIH HHS / DK / T32 DK007115; United States / NICHD NIH HHS / HD / K08 HD053350; United States / NIAID NIH HHS / AI / R21-AI079784; United States / NICHD NIH HHS / HD / K12 HD001410; United States / NICHD NIH HHS / HD / K12-HD001410; United States / NICHD NIH HHS / HD / K08 HD053350-02; United States / NCI NIH HHS / CA / P30 CA042014
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ NIHMS112911; NLM/ PMC2761994
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12. Medyouf H, Alcalde H, Berthier C, Guillemin MC, dos Santos NR, Janin A, Decaudin D, de Thé H, Ghysdael J: Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia. Nat Med; 2007 Jun;13(6):736-41
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  • [Title] Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia.
  • In the T-cell lineage, calcineurin activation is important for pre-T-cell receptor (TCR) signaling, TCR-mediated positive selection of thymocytes into mature T cells, and many aspects of the immune response.
  • We observed sustained calcineurin activation in human B- and T-cell lymphomas and in all mouse models of lymphoid malignancies analyzed.
  • In intracellular NOTCH1 (ICN1)- and TEL-JAK2-induced T-cell lymphoblastic leukemia, two mouse models relevant to human malignancies, in vivo inhibition of calcineurin activity by CsA or FK506 induced apoptosis of leukemic cells and rapid tumor clearance, and substantially prolonged mouse survival.
  • In contrast, ectopic expression of a constitutively activated mutant of calcineurin favored leukemia progression.
  • Moreover, CsA treatment induced apoptosis in human lymphoma and leukemia cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Calcineurin / metabolism. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / enzymology
  • [MeSH-minor] Animals. Calcineurin Inhibitors. Cell Line, Tumor. Cyclosporine / pharmacology. Disease Models, Animal. Enzyme Activation / drug effects. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Oncogene Proteins, Fusion / deficiency. Oncogene Proteins, Fusion / genetics. Receptor, Notch1 / physiology. Tacrolimus / pharmacology

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  • [CommentIn] Nat Med. 2007 Jun;13(6):669-71 [17554330.001]
  • (PMID = 17515895.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Calcineurin Inhibitors; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; 0 / TEL-JAK2 fusion protein, mouse; 83HN0GTJ6D / Cyclosporine; EC 3.1.3.16 / Calcineurin; WM0HAQ4WNM / Tacrolimus
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13. Rubnitz JE, Onciu M, Pounds S, Shurtleff S, Cao X, Raimondi SC, Behm FG, Campana D, Razzouk BI, Ribeiro RC, Downing JR, Pui CH: Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital. Blood; 2009 May 21;113(21):5083-9
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  • [Title] Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.
  • To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia.
  • Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL).
  • Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML.
  • We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.
  • We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients.

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  • (PMID = 19131545.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2686179
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14. Henrich S, Crossett B, Christopherson RI: Differentially expressed nuclear proteins in human CCRF-CEM, HL-60, MEC-1 and Raji cells correlate with cellular properties. Proteomics Clin Appl; 2007 Oct;1(10):1252-65
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  • The human cell lines CCRF-CEM (T-cell acute lymphocytic leukemia), HL-60 (acute myeloid leukemia), MEC-1 (B-cell chronic lymphocytic leukemia) and Raji (Burkitt's B-cell lymphoma) have been analysed for differences in their nuclear proteomes.
  • Using 2-D DIGE, 55 nuclear proteins have been identified that are differentially expressed (p<0.025) between the four cell lines, including proteins associated with transcription, proliferation, DNA repair and apoptosis.
  • Of these 55 proteins, 22 were over-expressed in just one cell line, and four were down-regulated in one cell line.
  • Proteins uniquely over-expressed between myeloid and lymphoid cell lines include those that may have use as markers for diagnosis, disease progression and B-cell maturation and differentiation.
  • Expression of various proliferation-associated nuclear proteins correlated with relative growth rates of the cell lines, giving these proteins potential diagnostic applications for distinction of chronic versus acute subtypes of haematological malignancies.
  • Identification of these differentially expressed nuclear proteins should facilitate elucidation of the molecular mechanisms underlying leukocyte differentiation and transformation to leukemias and lymphomas.
  • The nuclear expression profiles should enable classification of subtypes of leukemia, and identify potential nuclear protein targets for development of diagnostic and therapeutic strategies.

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  • [Copyright] Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21136623.001).
  • [ISSN] 1862-8346
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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15. 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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16. Rezvani K, Brenchley JM, Price DA, Kilical Y, Gostick E, Sewell AK, Li J, Mielke S, Douek DC, Barrett AJ: T-cell responses directed against multiple HLA-A*0201-restricted epitopes derived from Wilms' tumor 1 protein in patients with leukemia and healthy donors: identification, quantification, and characterization. Clin Cancer Res; 2005 Dec 15;11(24 Pt 1):8799-807
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  • [Title] T-cell responses directed against multiple HLA-A*0201-restricted epitopes derived from Wilms' tumor 1 protein in patients with leukemia and healthy donors: identification, quantification, and characterization.
  • PURPOSE: Antigens derived from the Wilms' tumor (WT1) protein, which is overexpressed in leukemias, are attractive targets for immunotherapy.
  • Four HLA-A*0201-restricted WT1-derived epitopes have been identified: WT37, WT126, WT187, and WT235.
  • EXPERIMENTAL DESIGN: To detect very low frequencies of WT1-specific CD8+ T cells, we used quantitative reverse transcription-PCR to measure IFN-gamma mRNA production by WT1 peptide-pulsed CD8+ T cells from 12 healthy donors, 8 patients with chronic myelogenous leukemia, 6 patients with acute myelogenous leukemia, and 8 patients with acute lymphoblastic leukemia.
  • RESULTS: Responses were detected in 5 of 8 chronic myelogenous leukemia patients, 4 of 6 patients with acute myelogenous leukemia, and 7 of 12 healthy donors.
  • No responses were detected in patients with acute lymphoblastic leukemia.
  • The magnitude and extent of these CD8+ T-cell responses was greater in patients with myeloid leukemias than in healthy donors.
  • Using fluorescent peptide-MHC class I tetramers incorporating mutations in the alpha3 domain (D227K/T228A) that abrogate binding to the CD8 coreceptor, we were able to confirm the presence of high-avidity T-cell clones within the antigen-specific repertoire.
  • CONCLUSION: The natural occurrence of high-avidity WT1-specific CD8+ T cells in the periphery could facilitate vaccination strategies to expand immune responses against myeloid leukemias.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. HLA-A Antigens / immunology. Immunodominant Epitopes / immunology. Leukemia / immunology. WT1 Proteins / immunology
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. HLA-A2 Antigen. Humans. Molecular Sequence Data. Peptides / immunology. Peptides / pharmacology

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  • (PMID = 16361568.001).
  • [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
  • [Grant] United Kingdom / Medical Research Council / / G108/441
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Immunodominant Epitopes; 0 / Peptides; 0 / WT1 Proteins
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17. Kazemi T, Asgarian-Omran H, Memarian A, Shabani M, Sharifian RA, Vossough P, Ansaripour B, Rabbani H, Shokri F: Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia. Cancer Immunol Immunother; 2009 Jun;58(6):989-96
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  • [Title] Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia.
  • Recent studies have demonstrated expression of Fc receptor-like (FCRL) molecules, a newly identified family with preferential B-cell lineage expression, in some chronic B-cell leukemias with possible implication for classification and/or targeted immunotherapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cell Surface / genetics. Receptors, Fc / genetics. Receptors, Immunologic / genetics

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  • (PMID = 18802695.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / FCRL2 protein, human; 0 / FCRL4 protein, human; 0 / FCRL5 protein, human; 0 / FCRLA protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Fc; 0 / Receptors, Immunologic
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18. Rainis L, Toki T, Pimanda JE, Rosenthal E, Machol K, Strehl S, Göttgens B, Ito E, Izraeli S: The proto-oncogene ERG in megakaryoblastic leukemias. Cancer Res; 2005 Sep 1;65(17):7596-602
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  • [Title] The proto-oncogene ERG in megakaryoblastic leukemias.
  • Acquired additions of chromosome 21 are a common finding in leukemias, suggesting a contributory role to leukemogenesis.
  • About 10% of patients with a germ line trisomy 21 (Down syndrome) are born with transient megakaryoblastic leukemia.
  • We show that ERG is expressed in hematopoietic stem cells, megakaryoblastic cell lines, and in primary leukemic cells from Down syndrome patients.
  • ERG expression is induced upon megakaryocytic differentiation of the erythroleukemia cell lines K562 and UT-7, and forced expression of ERG in K562 cells induces erythroid to megakaryoblastic phenotypic switch.
  • Furthermore, both ERG and ETS2 bind in vivo the hematopoietic enhancer of SCL/TAL1, a key regulator of hematopoietic stem cell and megakaryocytic development.
  • We propose that trisomy 21 facilitates the occurrence of megakaryoblastic leukemias through a shift toward the megakaryoblastic lineage caused by the excess expression of ERG, and possibly by other chromosome 21 genes, such as RUNX1 and ETS2, in hematopoietic progenitor cells, coupled with a differentiation arrest caused by the acquisition of mutations in GATA1.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Oncogene Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Base Sequence. Basic Helix-Loop-Helix Transcription Factors. Cell Lineage. Chromosomes, Human, Pair 21 / genetics. Erythroid-Specific DNA-Binding Factors. GATA1 Transcription Factor. HeLa Cells. Hematopoietic Stem Cells / metabolism. Humans. K562 Cells. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Erythroblastic, Acute / pathology. Molecular Sequence Data. Promoter Regions, Genetic. Proto-Oncogene Proteins / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16140924.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
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19. Wichmann C, Becker Y, Chen-Wichmann L, Vogel V, Vojtkova A, Herglotz J, Moore S, Koch J, Lausen J, Mäntele W, Gohlke H, Grez M: Dimer-tetramer transition controls RUNX1/ETO leukemogenic activity. Blood; 2010 Jul 29;116(4):603-13
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  • RUNX1/ETO, the fusion protein resulting from the chromosomal translocation t(8;21), is one of the most frequent translocation products in acute myeloid leukemia.
  • RUNX1/ETO dimers do not block myeloid differentiation, are unable to enhance the self-renewal capacity of hematopoietic progenitors, and fail to induce leukemia in a murine transplantation model.
  • Our data reveal the existence of an essential structural motif (hot spot) at the NHR2 dimer-tetramer interface, suitable for a molecular intervention in t(8;21) leukemias.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Leukemia / metabolism. Protein Multimerization / physiology. Proto-Oncogene Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Amino Acid Sequence. Amino Acid Substitution / physiology. Cell Differentiation / genetics. Cells, Cultured. Humans. K562 Cells. Models, Molecular. Molecular Dynamics Simulation. Mutant Proteins / metabolism. Mutant Proteins / physiology. Protein Interaction Domains and Motifs / genetics. Protein Interaction Domains and Motifs / physiology. Protein Interaction Mapping. U937 Cells

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  • (PMID = 20430957.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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20. Roecker AM, Allison JC, Kisor DF: Nelarabine: efficacy in the treatment of clinical malignancies. Future Oncol; 2006 Aug;2(4):441-8
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  • Nelarabine is indicated for the treatment of adult and pediatric patients with T-cell acute lymphoblastic leukemia or T-cell lymphoblastic lymphoma whose disease has not responded to, or has relapsed after treatment with, at least two chemotherapy regimens.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16922610.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arabinonucleosides; 60158CV180 / nelarabine
  • [Number-of-references] 22
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21. 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


22. Batinić D, Dubravcić K, Rajić L, Mikulić M, Labar B: [Biphenotypic and bilineal acute leukemias]. Acta Med Croatica; 2008 Oct;62(4):387-90
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  • [Title] [Biphenotypic and bilineal acute leukemias].
  • Human acute leukemias (AL) are classified as myeloid or lymphoid according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.
  • However, in the minority of cases leukemic cells express markers of more than one lineage, which has led to the introduction of a new subgroup of acute leukemias termed mixed or biphenotypic acute leukemias (BAL).
  • In an effort to distinguish between BAL and those AL with aberrant expression of markers of other lineage, the European Group for the Immunological Characterization of Acute Leukemias (EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for myeloid, B- and/or T-lymphoid lineage, respectively.
  • In addition to BAL in which a single cell population expresses both myeloid and lymphoid differentiation markers, this new group of leukemias also comprises cases that present with two separate blast populations (acute bilineal leukemia, aBLL).
  • In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare disease constituting 1%-2% of AL cases that contains B- or T-lymphoid along with myeloid blasts.
  • Unfortunately, optimal therapy is not known, although regimens designed for acute lymphoblastic leukemia may result in a better response rate.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19209464.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 30
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23. DeAngelo DJ: The treatment of adolescents and young adults with acute lymphoblastic leukemia. Hematology Am Soc Hematol Educ Program; 2005;:123-30
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  • [Title] The treatment of adolescents and young adults with acute lymphoblastic leukemia.
  • Intensive chemotherapy regimens for children with acute lymphoblastic leukemia (ALL) have greatly improved, and the majority of children with precursor B-cell ALL are able to achieve a complete remission (CR), with an induction rate approaching 98% and a 5-year estimated event-free survival rate (EFS) of approximately 80%.
  • In addition, new insights into the molecular pathogenesis of T cell ALL have led to new therapeutic strategies.

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  • (PMID = 16304369.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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24. Huang YF, Shangguan D, Liu H, Phillips JA, Zhang X, Chen Y, Tan W: Molecular assembly of an aptamer-drug conjugate for targeted drug delivery to tumor cells. Chembiochem; 2009 Mar 23;10(5):862-8
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  • In this study, we covalently link the antitumor agent doxorubicin (Dox) to the DNA aptamer sgc8c, which was selected by the cell-SELEX method.
  • In doing so, we expected that this sgc8c-Dox conjugate would specifically kill the target CCRF-CEM (T-cell acute lymphoblastic leukemia, T-cell ALL) cells, but with minimal toxicity towards nontarget cells.
  • Cell viability tests demonstrate that the sgc8c-Dox conjugates not only possess potency similar to unconjugated Dox, but also have the required molecular specificity that is lacking in most current targeted drug delivery strategies.
  • Furthermore, we found that nonspecific uptake of membrane-permeable Dox to nontarget cell lines could also be inhibited by linking the drug with the aptamer; thus, the conjugates are selective for cells that express higher amounts of target proteins.

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  • (PMID = 19253922.001).
  • [ISSN] 1439-7633
  • [Journal-full-title] Chembiochem : a European journal of chemical biology
  • [ISO-abbreviation] Chembiochem
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM079359; United States / NIGMS NIH HHS / GM / R01 GM079359-01; None / None / / R01 GM079359-01; United States / NIGMS NIH HHS / GM / R01 GM079359-02; United States / NIGMS NIH HHS / GM / R01 GM079359-03; None / None / / R01 GM079359-02; None / None / / R01 GM079359-01S1; United States / NIGMS NIH HHS / GM / R01 GM079359-01S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Aptamers, Nucleotide; 0 / Drug Carriers; 0 / Immunoconjugates; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ NIHMS149610; NLM/ PMC2992821
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25. 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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26. 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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27. Masuda S, Kumano K, Suzuki T, Tomita T, Iwatsubo T, Natsugari H, Tojo A, Shibutani M, Mitsumori K, Hanazono Y, Ogawa S, Kurokawa M, Chiba S: Dual antitumor mechanisms of Notch signaling inhibitor in a T-cell acute lymphoblastic leukemia xenograft model. Cancer Sci; 2009 Dec;100(12):2444-50
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  • [Title] Dual antitumor mechanisms of Notch signaling inhibitor in a T-cell acute lymphoblastic leukemia xenograft model.
  • Constitutive activation of Notch signaling is required for the proliferation of a subgroup of human T-cell acute lymphoblastic leukemias (T-ALL).
  • Treatment of established subcutaneous tumors with GSI resulted in partial or complete regression of tumors arising from four T-ALL cell lines that were also sensitive to GSI in vitro.
  • These findings indicate that the remarkable efficacy of GSI might be attributable to dual mechanisms, directly via apoptosis of DND-41 cells through the inhibition of cell-autonomous Notch signaling, and indirectly via disturbance of tumor angiogenesis through the inhibition of non-cell-autonomous Notch signaling.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Receptors, Notch / antagonists & inhibitors. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Mice. Mice, SCID. Xenograft Model Antitumor Assays

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  • (PMID = 19775286.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Notch; EC 3.4.- / Amyloid Precursor Protein Secretases
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28. Ehlers S, Herbst C, Zimmermann M, Scharn N, Germeshausen M, von Neuhoff N, Zwaan CM, Reinhardt K, Hollink IH, Klusmann JH, Lehrnbecher T, Roettgers S, Stary J, Dworzak M, Welte K, Creutzig U, Reinhardt D: Granulocyte colony-stimulating factor (G-CSF) treatment of childhood acute myeloid leukemias that overexpress the differentiation-defective G-CSF receptor isoform IV is associated with a higher incidence of relapse. J Clin Oncol; 2010 May 20;28(15):2591-7
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  • [Title] Granulocyte colony-stimulating factor (G-CSF) treatment of childhood acute myeloid leukemias that overexpress the differentiation-defective G-CSF receptor isoform IV is associated with a higher incidence of relapse.
  • PURPOSE: This prospective, multicenter Acute Myeloid Leukemia Berlin-Frankfurt-Muenster (AML-BFM) 98 study randomly tested the ability of granulocyte colony-stimulating factor (G-CSF) to reduce infectious complications and to improve outcomes in children and adolescents with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: Of 154 SR patients in the AML-BFM 98 cohort, 50 patients were tested for G-CSF receptor (G-CSFR) RNA isoform I and IV expression, G-CSFR cell surface expression, and acquired mutations in the G-CSFR gene.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Receptors, Granulocyte Colony-Stimulating Factor / biosynthesis


29. 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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30. Look AT: Investigator profile. An interview with A. Thomas Look, M.D. Interview by Vicki Glaser. Zebrafish; 2005;2(4):231-6
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  • Work in Dr. Look's laboratory focuses on the molecular pathogenesis of leukemia.
  • His group has been credited with the identification and functional analysis of several chimeric oncogenes activated by chromosomal translocations, including the E2A-HLF transcription factor, which was shown to act through an evolutionarily conserved genetic pathway to promote leukemia cell survival.
  • Their efforts in human T-cell acute lymphoblastic leukemia have revealed key multistep mutational pathways that drive the pathogenesis of this disease and demonstrated that NOTCH1 receptors are mutationally activated in a majority of these cases.
  • Look's laboratory developed the first transgenic model of leukemia in the zebrafish, opening the way for chemical and genome-wide genetic modifier screens in a vertebrate disease model.

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  • (PMID = 18248181.001).
  • [ISSN] 1557-8542
  • [Journal-full-title] Zebrafish
  • [ISO-abbreviation] Zebrafish
  • [Language] eng
  • [Publication-type] Interview
  • [Publication-country] United States
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31. Gutiérrez NC, López-Pérez R, Hernández JM, Isidro I, González B, Delgado M, Fermiñán E, García JL, Vázquez L, González M, San Miguel JF: Gene expression profile reveals deregulation of genes with relevant functions in the different subclasses of acute myeloid leukemia. Leukemia; 2005 Mar;19(3):402-9
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  • [Title] Gene expression profile reveals deregulation of genes with relevant functions in the different subclasses of acute myeloid leukemia.
  • Bone marrow samples from 43 adult patients with de novo diagnosed acute myeloid leukemia (AML)--10 acute promyelocytic leukemias (APL) with t(15;17), four AML with inv(16), seven monocytic leukemias and 22 nonmonocytic leukemias--were analyzed using high-density oligonucleotide microarrays.
  • Hierarchical clustering analysis segregated APL, AML with inv(16), monocytic leukemias and the remaining AML into separate groups.
  • Genes involved in cell adhesion represented the most altered functional category in monocytic leukemias.
  • All the eight leukemias that were either refractory to treatment or that relapsed afterwards were assigned to cluster B.
  • [MeSH-major] Gene Expression Profiling / methods. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cluster Analysis. Female. Humans. Leukemia, Monocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Male. Middle Aged. Phylogeny. Retrospective Studies


32. 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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33. 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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34. Meyer C, Schneider B, Reichel M, Angermueller S, Strehl S, Schnittger S, Schoch C, Jansen MW, van Dongen JJ, Pieters R, Haas OA, Dingermann T, Klingebiel T, Marschalek R: Diagnostic tool for the identification of MLL rearrangements including unknown partner genes. Proc Natl Acad Sci U S A; 2005 Jan 11;102(2):449-54
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  • Approximately 50 different chromosomal translocations of the human MLL gene are currently known and associated with high-risk acute leukemia.
  • The large number of different MLL translocation partner genes makes a precise diagnosis a demanding task.
  • This method was applied to biopsy material derived from 40 leukemia patients known to carry MLL abnormalities.
  • Furthermore, the determined patient-specific fusion sequences are useful for minimal residual disease monitoring of MLL associated acute leukemias.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] GTPase-Activating Proteins. Histone-Lysine N-Methyltransferase. Humans. Membrane Glycoproteins / genetics. Membrane Proteins / genetics. Myeloid-Lymphoid Leukemia Protein. Receptors, Interleukin-1 / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15626757.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / GTPase-Activating Proteins; 0 / MLL protein, human; 0 / Membrane Glycoproteins; 0 / Membrane Proteins; 0 / Receptors, Interleukin-1; 0 / SMAP1 protein, human; 0 / TIRAP protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC544299
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35. Hwang C, Jang S, Choi DK, Kim S, Lee JH, Lee Y, Kim CD, Lee JH: The role of nkx2.5 in keratinocyte differentiation. Ann Dermatol; 2009 Nov;21(4):376-81
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  • BACKGROUND: Nkx2.5 is a homeodomain-containing nuclear transcription protein that has been associated with acute T-lymphoblastic leukemia.
  • In addition, the expression of Nkx2.5 was significantly increased in psoriasis and squamous cell carcinoma, but was barely detected in atopic dermatitis and basal cell carcinoma.
  • CONCLUSION: These results suggest that Nkx2.5 may play a role in the change from proliferation to differentiation of keratinocytes and in the pathogenesis of skin disease with aberrant keratinocyte differentiation.

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  • (PMID = 20523827.001).
  • [ISSN] 2005-3894
  • [Journal-full-title] Annals of dermatology
  • [ISO-abbreviation] Ann Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2861273
  • [Keywords] NOTNLM ; Keratinocyte differentiation / Nkx2.5 / Transcription factor
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36. Chen W, Wang E, Lu Y, Gaal KK, Huang Q: Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review. Am J Clin Pathol; 2010 Jan;133(1):75-82
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  • [Title] Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review.
  • Therapy-related acute lymphoblastic leukemia (t-ALL) is a rare secondary leukemia following chemotherapy and/or radiotherapy for primary malignancies.
  • Chromosomal 11q23 abnormality, frequently detected in therapy-related acute myeloid leukemia, is the most common cytogenetic alteration in t-ALL.
  • However, t-ALL cases without 11q23 abnormality have been rarely described.
  • In the 48 cases, an 11q23 abnormality involving the MLL gene locus was the predominant chromosomal aberration (32 [67%]), followed by t(9;22) (6 [13%]) and a normal karyotype (4 [8%]).
  • Compared with t-ALL cases with an 11q23 abnormality, cases without an 11q23 abnormality had a relatively longer latency period (median, 36 vs 19 months) and a different primary malignancy spectrum.
  • The t(8;14)(q11.2;q32), a rare, nonrandom, balanced chromosomal translocation differing from the more common translocation involving c-MYC on chromosome 8q24, was seen in 1 adult t-ALL case, which may suggest another possible pathogenesis of this disease.
  • [MeSH-major] Chromosomes, Human, Pair 11. Combined Modality Therapy / adverse effects. Neoplasms / therapy. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 20023261.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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37. 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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38. Bacher U, Haferlach C, Schnittger S, Kohlmann A, Kern W, Haferlach T: Mutations of the TET2 and CBL genes: novel molecular markers in myeloid malignancies. Ann Hematol; 2010 Jul;89(7):643-52
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  • In acute myeloid leukemia (AML), clinical variability exists within distinct subgroups.
  • Recently, mutations of the tet oncogene family member 2 (TET2) and Casitas B-cell lymphoma (CBL) genes became the focus of interest.
  • Sequencing studies revealed heterogeneous mutations in 10-25% of patients with acute myeloid leukemia (AML), MDS, and MPNs, while the frequency might be higher in chronic myelomonocytic leukemia (CMML).
  • In rare cases of human AML (<2%), CBL mutants were identified, with a higher frequency in core binding factor leukemias.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromosomes, Human, Pair 4 / metabolism. DNA-Binding Proteins / metabolism. Leukemia, Myeloid, Acute / metabolism. Mutation. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-cbl / metabolism


39. 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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40. Fasseu M, Aplan PD, Chopin M, Boissel N, Bories JC, Soulier J, von Boehmer H, Sigaux F, Regnault A: p16INK4A tumor suppressor gene expression and CD3epsilon deficiency but not pre-TCR deficiency inhibit TAL1-linked T-lineage leukemogenesis. Blood; 2007 Oct 1;110(7):2610-9
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  • [Title] p16INK4A tumor suppressor gene expression and CD3epsilon deficiency but not pre-TCR deficiency inhibit TAL1-linked T-lineage leukemogenesis.
  • Inactivation of the CDKN2 genes that encode the p16(INK4A) and p14(ARF) proteins occurs in the majority of human T-cell acute lymphoblastic leukemias (T-ALLs).
  • In TAL1xLMO1 mice, leukemia develops in 100% of mice at 5 months.
  • We report here that expression of P16(INK4A) in developing TAL1xLMO1 thymocytes blocks leukemogenesis in the majority of the mice, and the leukemias that eventually develop show P16(INK4A) loss of expression.
  • Events related to the T-cell receptor beta selection process are thought to be important for leukemic transformation.

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  • (PMID = 17507663.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CCND3 protein, human; 0 / CD3E protein, human; 0 / Ccnd3 protein, mouse; 0 / Cyclin D3; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclins; 0 / LIM Domain Proteins; 0 / Lmo1 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell; 0 / Tal1 protein, mouse; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC1988920
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41. 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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42. Romana SP, Radford-Weiss I, Ben Abdelali R, Schluth C, Petit A, Dastugue N, Talmant P, Bilhou-Nabera C, Mugneret F, Lafage-Pochitaloff M, Mozziconacci MJ, Andrieu J, Lai JL, Terre C, Rack K, Cornillet-Lefebvre P, Luquet I, Nadal N, Nguyen-Khac F, Perot C, Van den Akker J, Fert-Ferrer S, Cabrol C, Charrin C, Tigaud I, Poirel H, Vekemans M, Bernard OA, Berger R, Groupe Francophone de Cytogénétique Hématologique: NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique. Leukemia; 2006 Apr;20(4):696-706
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique.
  • In order to gain additional clinico-hematological data and to identify new partners of NUP98, the Groupe Francophone de Cytogénétique Hématologique (GFCH) collected cases of hematological malignancies where a 11p15 rearrangement was detected.
  • Genes of the HOXA cluster and the nuclear-receptor set domain (NSD) genes were frequently fused to NUP98, mainly in de novo myeloid malignancies whereas the DDX10 and TOP1 genes were equally rearranged in de novo and in therapy-related myeloid proliferations.
  • Involvement of ADD3 and C6ORF80 genes were detected, respectively, in myeloid disorders and in T-cell acute lymphoblastic leukemia (T-ALL), whereas the RAP1GDS1 gene was fused to NUP98 in T-ALL.

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  • (PMID = 16467868.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Receptors, Cytoplasmic and Nuclear; 157907-48-7 / HoxA protein
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43. Belov L, Huang P, Chrisp JS, Mulligan SP, Christopherson RI: Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells. J Immunol Methods; 2005 Oct 20;305(1):10-9
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  • [Title] Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells.
  • We have developed a microarray (DotScan) that enables rapid immunophenotyping and classification of leukaemias and lymphomas by measuring the capture of cells by immobilized dots of 82 CD antibodies [Belov, L., de la Vega, O., dos Remedios, C.G., Mulligan, S.P., 2001.
  • Immunophenotyping of leukemia using a cluster of differentiation antibody microarray. Cancer Res.
  • Identification of repertoires of surface antigens on leukemias using an antibody microarray.
  • After blocking the remaining nitrocellulose surface, individual arrays were incubated with each of 7 cell types from a human leukaemia cell panel consisting of three cell lines, CCRF-CEM (a T-cell acute lymphocytic leukaemia), MEC-1 (derived from B-cell chronic lymphocytic leukaemia) and HL-60 (a promyelocytic leukaemia), and four leukaemias from patients: a T-cell prolymphocytic leukaemia, a B-cell chronic lymphocytic leukaemia, and two acute myeloid leukaemias.
  • Leukaemia cells were captured by those immobilized antibodies for which they expressed the corresponding surface molecule.
  • The data obtained show the unique expression profiles of the 7 cell types in the leukaemia cell panel obtained with the DotScan microarray, and the differential capture patterns for these 7 cell types screened against the 498 antibodies in the HLDA8 microarray constructed for this study.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antigens, CD / analysis. Leukemia / classification. Protein Array Analysis / methods
  • [MeSH-minor] Cell Line, Tumor. Collodion / chemistry. Flow Cytometry. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / immunology. Leukemia, Myeloid / classification. Leukemia, Myeloid / immunology. Leukemia, T-Cell / classification. Leukemia, T-Cell / immunology

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  • (PMID = 16125720.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 9004-70-0 / Collodion
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44. Adams H, Liebisch P, Schmid P, Dirnhofer S, Tzankov A: Diagnostic utility of the B-cell lineage markers CD20, CD79a, PAX5, and CD19 in paraffin-embedded tissues from lymphoid neoplasms. Appl Immunohistochem Mol Morphol; 2009 Mar;17(2):96-101
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  • [Title] Diagnostic utility of the B-cell lineage markers CD20, CD79a, PAX5, and CD19 in paraffin-embedded tissues from lymphoid neoplasms.
  • The specificity and sensitivity of CD19, CD20, CD79a, and PAX5 for detection of B-cell lineage lymphoma/leukemia derivation was determined on tissue microarrays containing 148 Hodgkin lymphomas, 358 B-cell and 16 T-cell lymphomas, 50 myelomas, and 69 acute leukemias.
  • CD19 had the weakest specificity, because it was expressed in 3 T-cell lymphomas, but its sensitivity was better than CD79a.
  • In Hodgkin lymphoma cases, the presence of B-cell markers in Hodgkin and Reed-Sternberg cells decreased in the following order: PAX5>CD20>CD79a>CD19.
  • In acute leukemia, CD20 turned to be the most specific, and PAX5 and CD19 the most sensitive markers for B-lineage derivation.
  • In conclusion, an optimal B-cell lineage panel for daily routine on paraffin-embedded tissues should consist of CD20 and CD79a, and eventually, PAX5 for mature lymphoid neoplasms and PAX5 and CD19, and eventually, CD20 in (acute) precursor cell leukemias, because they cover most of the sensitivity and specificity needed.

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  • (PMID = 18838917.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD79; 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
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45. Faber J, Krivtsov AV, Stubbs MC, Wright R, Davis TN, van den Heuvel-Eibrink M, Zwaan CM, Kung AL, Armstrong SA: HOXA9 is required for survival in human MLL-rearranged acute leukemias. Blood; 2009 Mar 12;113(11):2375-85
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  • [Title] HOXA9 is required for survival in human MLL-rearranged acute leukemias.
  • Leukemias that harbor translocations involving the mixed lineage leukemia gene (MLL) possess unique biologic characteristics and often have an unfavorable prognosis.
  • Gene expression analyses demonstrate a distinct profile for MLL-rearranged leukemias with consistent high-level expression of select Homeobox genes, including HOXA9.
  • Here, we investigated the effects of HOXA9 suppression in MLL-rearranged and MLL-germline leukemias using RNA interference.
  • Gene expression profiling after HOXA9 suppression demonstrated co-down-regulation of a program highly expressed in human MLL-AML and murine MLL-leukemia stem cells, including HOXA10, MEIS1, PBX3, and MEF2C.
  • We demonstrate that HOXA9 depletion in 17 human AML/ALL cell lines (7 MLL-rearranged, 10 MLL-germline) induces proliferation arrest and apoptosis specifically in MLL-rearranged cells (P = .007).
  • Moreover, mice transplanted with HOXA9-depleted t(4;11) SEMK2 cells revealed a significantly lower leukemia burden, thus identifying a role for HOXA9 in leukemia survival in vivo.
  • Our data indicate an important role for HOXA9 in human MLL-rearranged leukemias and suggest that targeting HOXA9 or downstream programs may be a novel therapeutic option.

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  • (PMID = 19056693.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / P01 CA66996
  • [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-Binding Proteins; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / RNA, Small Interfering; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC2656267
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46. 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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47. Cai Y, Xu Z, Xie J, Ham AJ, Koury MJ, Hiebert SW, Brandt SJ: Eto2/MTG16 and MTGR1 are heteromeric corepressors of the TAL1/SCL transcription factor in murine erythroid progenitors. Biochem Biophys Res Commun; 2009 Dec 11;390(2):295-301
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  • The TAL1 (or SCL) gene, originally discovered through its involvement by a chromosomal translocation in T-cell acute lymphoblastic leukemia, encodes a basic helix-loop-helix (bHLH) transcription factor essential for hematopoietic and vascular development.

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  • (PMID = 19799863.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL049118; United States / NHLBI NIH HHS / HL / HL049118-15; United States / NHLBI NIH HHS / HL / R01 HL49118; United States / NHLBI NIH HHS / HL / R01 HL049118-15; United States / NCI NIH HHS / CA / 5P30CA068485; United States / NCI NIH HHS / CA / P30 CA068485
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CBFA2T2 myeloid-transforming gene-related protein; 0 / Cbfa2t3 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Tal1 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ NIHMS151956; NLM/ PMC2774815
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48. Palomero T, McKenna K, O-Neil J, Galinsky I, Stone R, Suzukawa K, Stiakaki E, Kalmanti M, Fox EA, Caligiuri MA, Aster JC, Look AT, Ferrando AA: Activating mutations in NOTCH1 in acute myeloid leukemia and lineage switch leukemias. Leukemia; 2006 Nov;20(11):1963-6
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  • [Title] Activating mutations in NOTCH1 in acute myeloid leukemia and lineage switch leukemias.
  • Activating mutations in NOTCH1 are found in over 50% of human T-cell lymphoblastic leukemias (T-ALLs).
  • Here, we report the analysis for activating NOTCH1 mutations in a large number of acute myeloid leukemia (AML) primary samples and cell lines.
  • We found activating mutations in NOTCH1 in a single M0 primary AML sample, in three (ML1, ML2 and CTV-1) out of 23 AML cell lines and in the diagnostic (myeloid) and relapsed (T-lymphoid) clones in a patient with lineage switch leukemia.
  • Importantly, the ML1 and ML2 AML cell lines are derived from an AML relapse in a patient initially diagnosed with T-ALL.
  • The presence of NOTCH1 mutations in myeloid and T-lymphoid clones in lineage switch leukemias establishes the common clonal origin of the diagnostic and relapse blast populations and suggests a stem cell origin of NOTCH1 mutations during the molecular pathogenesis of these tumors.
  • [MeSH-major] Cell Lineage / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Receptor, Notch1 / genetics
  • [MeSH-minor] Acute Disease. Base Sequence. Cell Line, Tumor. Gene Deletion. Hematopoietic Stem Cells / pathology. Hematopoietic Stem Cells / physiology. Humans. Point Mutation. Recurrence. T-Lymphocytes / pathology

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  • (PMID = 17008890.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109901; United States / NCI NIH HHS / CA / CA68484
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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49. Chiarini F, Grimaldi C, Ricci F, Tazzari PL, Evangelisti C, Ognibene A, Battistelli M, Falcieri E, Melchionda F, Pession A, Pagliaro P, McCubrey JA, Martelli AM: Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia. Cancer Res; 2010 Oct 15;70(20):8097-107
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  • [Title] Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia.
  • Recent findings have highlighted that constitutively active phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is a common feature of T-cell acute lymphoblastic leukemia (T-ALL), where it upregulates cell proliferation, survival, and drug resistance.
  • Here, we have analyzed the therapeutic potential of the novel dual PI3K/mTOR inhibitor NVP-BEZ235, an orally bioavailable imidazoquinoline derivative, which has entered clinical trials for solid tumors, on both T-ALL cell lines and patient samples.
  • NVP-BEZ235 was cytotoxic to a panel of T-ALL cell lines as determined by MTT assays.
  • NVP-BEZ235 treatment resulted in cell cycle arrest and apoptosis.
  • Remarkably, NVP-BEZ235 targeted the side population of both T-ALL cell lines and patient lymphoblasts, which might correspond to leukemia-initiating cells, and synergized with chemotherapeutic agents (cyclophosphamide, cytarabine, dexamethasone) currently used for treating T-ALL patients.
  • Taken together, our findings indicate that longitudinal inhibition at two nodes of the PI3K/Akt/mTOR network with NVP-BEZ235, either alone or in combination with chemotherapeutic drugs, may be an efficient treatment of those T-ALLs that have aberrant upregulation of this signaling pathway for their proliferation and survival.
  • [MeSH-major] Imidazoles / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Quinolines / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Autophagy / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Coculture Techniques. Flow Cytometry. Humans. Jurkat Cells / drug effects. Mice. Stromal Cells / drug effects


50. Greene WK, Sontani Y, Sharp MA, Dunn DS, Kees UR, Bellgard MI: A promoter with bidirectional activity is located between TLX1/HOX11 and a divergently transcribed novel human gene. Gene; 2007 Apr 15;391(1-2):223-32
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  • The chromosomal region 10q24 is involved in reciprocal translocations with one of the T-cell receptor loci in a significant proportion of human T-cell acute lymphoblastic leukemias.
  • Our finding that TDI is transcriptionally co-activated in leukemic cells that aberrantly express TLX1, additionally suggests that it may have the potential to act as a co-operating oncogene in leukemogenesis.
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. K562 Cells. Luciferases / genetics. Luciferases / metabolism. Molecular Sequence Data. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA. Sequence Homology, Nucleic Acid. Transfection. beta-Galactosidase / genetics. beta-Galactosidase / metabolism

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  • (PMID = 17303350.001).
  • [ISSN] 0378-1119
  • [Journal-full-title] Gene
  • [ISO-abbreviation] Gene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 143275-75-6 / TLX1 protein, human; EC 1.13.12.- / Luciferases; EC 3.2.1.23 / beta-Galactosidase
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51. Reckard JM, Chung MH, Varma MK, Zagorski SM: Management of intraabdominal hypertension by percutaneous catheter drainage. J Vasc Interv Radiol; 2005 Jul;16(7):1019-21
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  • The authors report a case of an 18-year-old man with T-cell acute lymphocytic leukemia who developed hemorrhagic pancreatitis after chemotherapy.
  • [MeSH-minor] Acute Disease. Adolescent. Hemorrhage / complications. Humans. Leukemia-Lymphoma, Adult T-Cell / complications. Male. Pancreatitis / complications. Ultrasonics. Ultrasonography

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  • (PMID = 16002511.001).
  • [ISSN] 1051-0443
  • [Journal-full-title] Journal of vascular and interventional radiology : JVIR
  • [ISO-abbreviation] J Vasc Interv Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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52. Wrzesień-Kuś A, Robak T, Wierzbowska A, Lech-Marańda E, Pluta A, Wawrzyniak E, Krawczyńska A, Kuliczkowski K, Mazur G, Kiebiński M, Dmoszyńska A, Wach M, Hellmann A, Baran W, Hołowiecki J, Kyrcz-Krzemień S, Grosicki S, Polish Adult Leukemia Group: A multicenter, open, noncomparative, phase II study of the combination of cladribine (2-chlorodeoxyadenosine), cytarabine, granulocyte colony-stimulating factor and mitoxantrone as induction therapy in refractory acute myeloid leukemia: a report of the Polish Adult Leukemia Group. Ann Hematol; 2005 Sep;84(9):557-64
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  • [Title] A multicenter, open, noncomparative, phase II study of the combination of cladribine (2-chlorodeoxyadenosine), cytarabine, granulocyte colony-stimulating factor and mitoxantrone as induction therapy in refractory acute myeloid leukemia: a report of the Polish Adult Leukemia Group.
  • Purine nucleoside analogues, cladribine (2-chlorodeoxyadenosine, 2-CdA) and fludarabine (FAMP) are active agents in acute myeloid leukemias (AMLs).
  • Disease-free survival (1 year) was 68.6%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Cladribine / administration & dosage. Cytarabine / administration & dosage. Drug Therapy, Combination. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Hematologic Diseases / chemically induced. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Remission Induction / methods. Salvage Therapy / methods. Survival Analysis

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  • (PMID = 15856358.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] Germany
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 47M74X9YT5 / Cladribine; BZ114NVM5P / Mitoxantrone; CLAG protocol
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53. Chang PY, Draheim K, Kelliher MA, Miyamoto S: NFKB1 is a direct target of the TAL1 oncoprotein in human T leukemia cells. Cancer Res; 2006 Jun 15;66(12):6008-13
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  • [Title] NFKB1 is a direct target of the TAL1 oncoprotein in human T leukemia cells.
  • We recently showed that a subset of human T acute lymphoblastic leukemia (T-ALL) cell lines expresses low basal levels of p50, a nuclear factor-kappaB (NF-kappaB)/Rel family member, resulting in their capacity to activate the atypical p65:cRel complex rather than the classic p50:p65 dimer.
  • When TAL1 expression is reduced in CEM T leukemia cells, basal NFKB1 expression is increased, and the levels of p65:cRel complex and transcription of its target gene, such as intercellular adhesion molecule-1 (ICAM-1), are reduced in response to etoposide treatment.
  • Moreover, a significant negative correlation between NFKB1 and TAL1 or LMO1 was found in primary human TAL1/LMO1 double-positive T-ALL samples previously described by Ferrando et al. Thus, TAL1 modulates NFKB1 expression and an NF-kappaB-dependent transcriptional program in a subset of human T-cell leukemia cells.

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  • (PMID = 16778171.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / R01-CA077474; United States / NCI NIH HHS / CA / R01-CA081065
  • [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 / NF-kappa B p50 Subunit; 0 / NFKB1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factor RelA; 135471-20-4 / TAL1 protein, human; 6PLQ3CP4P3 / Etoposide
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54. De Keersmaecker K, Rocnik JL, Bernad R, Lee BH, Leeman D, Gielen O, Verachtert H, Folens C, Munck S, Marynen P, Fornerod M, Gilliland DG, Cools J: Kinase activation and transformation by NUP214-ABL1 is dependent on the context of the nuclear pore. Mol Cell; 2008 Jul 11;31(1):134-42
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  • We show that NUP214-ABL1 displays attenuated transforming capacity as compared to BCR-ABL1 and that NUP214-ABL1 preferentially transforms T cells, which is in agreement with its unique occurrence in T cell acute lymphoblastic leukemia.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Nuclear Pore / enzymology. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Animals. Cell Line. Enzyme Activation. Humans. Mice. Nuclear Pore Complex Proteins / metabolism

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  • (PMID = 18614052.001).
  • [ISSN] 1097-4164
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA8484
  • [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 / NUP214-ABL1 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases
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55. Taki T, Taniwaki M: Chromosomal translocations in cancer and their relevance for therapy. Curr Opin Oncol; 2006 Jan;18(1):62-8
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  • Observation of high frequencies of mutations in NOTCH1, NPM and JAK2 in T-cell acute lymphoblastic leukemia, acute myeloid leukemia with normal karyotype and myeloproliferative disorders (polycythemia vera, essential thrombocythemia and idiopathic myelofibrosis) have provided important suggestions for a better understanding of chromosomal translocations.

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  • (PMID = 16357566.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 46
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56. Beesley AH, Firth MJ, Ford J, Weller RE, Freitas JR, Perera KU, Kees UR: Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism. Br J Cancer; 2009 Jun 16;100(12):1926-36
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  • [Title] Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism.
  • Glucocorticoids (GCs) are among the most important drugs for acute lymphoblastic leukaemia (ALL), yet despite their clinical importance, the exact mechanisms involved in GC cytotoxicity and the development of resistance remain uncertain.
  • We examined the baseline profile of a panel of T-ALL cell lines to determine factors that contribute to GC resistance without prior drug selection.
  • The data also provide the first evidence that altered expression of wild-type MLL may contribute to GC-resistant phenotypes.
  • [MeSH-major] Cell Proliferation / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Methylprednisolone / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Signal Transduction / drug effects


57. Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M: Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma. Int J Hematol; 2007 Apr;85(3):212-8
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  • [Title] Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
  • We analyzed NOTCH1 gene mutation in 53 adults with mature T-cell leukemia/lymphoma: 21 patients with adult T-cell leukemia (ATL), 25 with T-cell non-Hodgkin's lymphoma (T-NHL), and 7 with T-cell prolymphocytic leukemia.
  • We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an ATL patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-cell lymphoma-unspecified (PTCL-u).
  • These findings suggest that nonsense mutation in the PEST domain in the ATL case was associated with NOTCH1 signaling through a pathway different from that for T-cell acute lymphoblastic leukemia (T-ALL).
  • Although NOTCH1 mutation occurs infrequently in mature T-cell leukemia/lymphoma, NOTCH1 may be involved in leukemogenesis associated with various forms of T-cell leukemia/lymphoma rather than only with T-ALL.
  • [MeSH-major] Codon, Nonsense. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Receptor, Notch1 / genetics

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  • (PMID = 17483057.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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58. Valmary S, Danjoux M, Delsol G, Brousset P: [Diagnostic value of anti-terminal deoxynucleotidyl transferase antibody (TdT) in hematologic pathology]. Ann Pathol; 2005 Feb;25(1):25-32
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  • [Transliterated title] Intérêt diagnostique de l'anticorps anti-terminal désoxynucleotidyl transférase (TdT) en pathologie hématologique.
  • AIMS: The diagnosis of primitive hematologic malignancies depends on a panel of monoclonal antibodies which is growing over time.
  • The distinction between immature (lymphoblastic lymphoma/acute lymphoblastic leukaemia) and mature lymphoma is sometimes difficult.
  • In this study, we evaluated anti-TdT antibody in the diagnosis and classification of these proliferations.
  • MATERIALS AND METHODS: 13 lesions were examined by immunohistochemistry: 4 B and T lymphoblastic lymphomas, 2 Burkitt's lymphomas, 5 B and T acute lymphoblastic leukemias and 2 acute monoblastic leukemias.
  • TdT is not expressed by mature B or T cell lymphomas such as Burkitt's lymphomas.
  • Significant numbers of cases of acute myeloblastic leukemias are TdT positive but could be easily distinguished from lymphoblastic proliferations.
  • CONCLUSION: Anti-TdT antibody represents a useful marker for differentiating lymphoma/acute lymphoblastic leukemia from other lymphomas.
  • This marker, available in routine diagnosis should be systematically included in the panel of antibodies used for immunophenotyping hematologic malignancies.
  • [MeSH-major] Antibodies. DNA Nucleotidylexotransferase / analysis. DNA Nucleotidylexotransferase / immunology. Hematologic Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Burkitt Lymphoma / diagnosis. Child. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Immunophenotyping. Leukemia, Monocytic, Acute / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, B-Cell / diagnosis. Lymphoma, T-Cell / diagnosis. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 15981929.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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59. Dohda T, Maljukova A, Liu L, Heyman M, Grandér D, Brodin D, Sangfelt O, Lendahl U: Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines. Exp Cell Res; 2007 Aug 15;313(14):3141-52
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  • [Title] Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines.
  • In T-cell acute lymphoblastic leukemia (T-ALL) NOTCH 1 receptors are frequently mutated.
  • This leads to aberrantly high Notch signaling, but how this translates into deregulated cell cycle control and the transformed cell type is poorly understood.
  • Notch activity, measured immediately downstream of the NOTCH 1 receptor, is high, but expression of the canonical downstream Notch response genes HES 1 and HEY 2 is low both in primary cells from T-ALL patients and in T-ALL cell lines.
  • We show that in T-ALL cell lines, recruitment of NOTCH 1 intracellular domain (ICD) to the SKP2 promoter was accompanied by high SKP2 and low p27Kip1 protein levels.
  • T-ALL cells show a rapid G1-S cell cycle transition, while blocked Notch signaling resulted in G0/G1 cell cycle arrest, also observed by transfection of p27Kip1 or, to a smaller extent, a dominant negative SKP2 allele.
  • Collectively, our data suggest that the aberrantly high Notch signaling in T-ALL maintains SKP2 at a high level and reduces p27Kip1, leading to more rapid cell cycle progression.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. S-Phase Kinase-Associated Proteins / metabolism. Signal Transduction / physiology. T-Lymphocytes / metabolism
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Cycle / physiology. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Child. Cyclin-Dependent Kinase Inhibitor p27. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. Repressor Proteins / genetics. Repressor Proteins / metabolism

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  • (PMID = 17560996.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / HEY1 protein, human; 0 / HEY2 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Repressor Proteins; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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60. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
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  • [Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with AML.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • The first patient (case 1) relapsed after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.
  • Since CALM-AF10- positive leukemias have been shown to have poor prognosis with conventional therapy, molecular tests for CALM-AF10 rearrangement would be necessary to detect minimal residual disease during follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic

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  • (PMID = 20445327.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
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61. Rao SS, O'Neil J, Liberator CD, Hardwick JS, Dai X, Zhang T, Tyminski E, Yuan J, Kohl NE, Richon VM, Van der Ploeg LH, Carroll PM, Draetta GF, Look AT, Strack PR, Winter CG: Inhibition of NOTCH signaling by gamma secretase inhibitor engages the RB pathway and elicits cell cycle exit in T-cell acute lymphoblastic leukemia cells. Cancer Res; 2009 Apr 1;69(7):3060-8
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  • [Title] Inhibition of NOTCH signaling by gamma secretase inhibitor engages the RB pathway and elicits cell cycle exit in T-cell acute lymphoblastic leukemia cells.
  • NOTCH signaling is deregulated in the majority of T-cell acute lymphoblastic leukemias (T-ALL) as a result of activating mutations in NOTCH1.
  • We have investigated the mechanisms of GSI sensitivity across a panel of T-ALL cell lines, yielding an approach for patient stratification based on pathway activity and also providing a rational combination strategy for enhanced response to GSI.
  • Furthermore, inhibition of the NOTCH pathway activity signature correlates with the induction of the cyclin-dependent kinase inhibitors CDKN2D (p19(INK4d)) and CDKN1B (p27(Kip1)), leading to derepression of RB and subsequent exit from the cell cycle.
  • Consistent with this evidence of cell cycle exit, short-term exposure of GSI resulted in sustained molecular and phenotypic effects after withdrawal of the compound.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Cyclic S-Oxides / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protease Inhibitors / pharmacology. Receptor, Notch1 / antagonists & inhibitors. Retinoblastoma Protein / metabolism. Thiadiazoles / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cyclin-Dependent Kinase 4 / antagonists & inhibitors. Cyclin-Dependent Kinase Inhibitor p19 / biosynthesis. Cyclin-Dependent Kinase Inhibitor p27. G1 Phase / drug effects. G1 Phase / genetics. Gene Expression Profiling. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Phosphorylation. S Phase / drug effects. S Phase / genetics. Signal Transduction / drug effects. Transcription, Genetic. Transfection

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  • (PMID = 19318552.001).
  • [ISSN] 1538-7445
  • [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 / CDKN1B protein, human; 0 / CDKN2D protein, human; 0 / Cyclic S-Oxides; 0 / Cyclin-Dependent Kinase Inhibitor p19; 0 / Intracellular Signaling Peptides and Proteins; 0 / MRK 003; 0 / NOTCH1 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Retinoblastoma Protein; 0 / Thiadiazoles; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 3.4.- / Amyloid Precursor Protein Secretases
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62. Ning BT, Tang YM, Chen YH, Shen HQ, Qian BQ: Comparison between CD19 and CD20 expression patterns on acute leukemic cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):943-7
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  • [Title] Comparison between CD19 and CD20 expression patterns on acute leukemic cells.
  • In order to provide the evidences for CD19 as a better antibody targeting molecule for B lineage acute leukemias than CD20 through the multi-parameter flow-cytometry analysis of leukemia cells, the samples from 321 patients with acute leukemia (AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.
  • The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with B lineage acute lymphoblastic leukemia (B lineage ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with B lineage/Myeloid (B/My) acute mixed lineage leukemia (AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).
  • Both of the two antigens were negative in 29 patients with acute T lymphoblastic leukemia and 7 patients with T/My AMLL.
  • The positive rates of CD19 and CD20 in 152 patients with acute myeloid leukemia (AML) were 7.2% and 2.0%, respectively.
  • The specificity of CD19 and CD20 in B lymphocytic lineage was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).
  • It is concluded that CD19 continuously and steadily express on almost all subtypes of B lineage leukemic cells with homogeneous pattern while only a small number of leukemias express CD20.
  • These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-lineage acute leukemia.

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  • (PMID = 16403255.001).
  • [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] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20
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63. Spokoini R, Kfir-Erenfeld S, Yefenof E, Sionov RV: Glycogen synthase kinase-3 plays a central role in mediating glucocorticoid-induced apoptosis. Mol Endocrinol; 2010 Jun;24(6):1136-50
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  • It is still unclear how glucocorticoids (GCs) induce apoptosis of thymocytes and T lymphoma cells.
  • Emergence of GC-resistant lymphoma cells is a major obstacle in GC therapy, emphasizing the need for novel strategies that maintain the sensitivity of lymphoma cells to the proapoptotic effects of GC.
  • Chemical inhibition of GSK3 by SB216763, BIO-Acetoxime, or LiCl and GSK3 inhibition using a dominant-negative mutant of GSK3 impede this cell death process, indicating that GSK3 is involved in transmitting the apoptotic signal.
  • GC resistance in lymphoma cells can be relieved by inhibiting the phosphatidylinositol-3 kinase-Akt survival pathway, which inactivates GSK3.
  • Notch1, a transcription factor frequently activated in T acute lymphoblastic leukemia cells, confers GC resistance through activation of Akt.
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / metabolism. Bcl-2-Like Protein 11. Cell Line. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Enzyme Activation / drug effects. Glycogen Synthase Kinase 3 beta. Humans. Ligands. Membrane Proteins / metabolism. Mice. Models, Biological. Protein Binding / drug effects. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptors, Glucocorticoid / metabolism. Receptors, Notch / metabolism

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  • (PMID = 20371704.001).
  • [ISSN] 1944-9917
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Bcl2l11 protein, mouse; 0 / Glucocorticoids; 0 / Ligands; 0 / Membrane Proteins; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Glucocorticoid; 0 / Receptors, Notch; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.1 / GSK3B protein, human; EC 2.7.11.1 / Glycogen Synthase Kinase 3 beta; EC 2.7.11.1 / Gsk3b protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 2.7.11.26 / glycogen synthase kinase 3 alpha
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64. Nowak AK, Lake RA, Robinson BW: Combined chemoimmunotherapy of solid tumours: improving vaccines? Adv Drug Deliv Rev; 2006 Oct 1;58(8):975-90
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  • It is now clear that the way a chemotherapeutic drug kills a tumour cell determines how that dying cell interacts with the immune system and whether the interaction leads to an immune response.
  • Furthermore, lymphodepletion triggers homeostatic T cell reconstitution, creating new populations of pre-T cells that need education in the thymic environment.

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  • (PMID = 17005292.001).
  • [ISSN] 0169-409X
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cancer Vaccines
  • [Number-of-references] 105
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65. Dourado M, Sarmento AB, Pereira SV, Alves V, Silva T, Pinto AM, Rosa MS: CD26/DPPIV expression and 8-azaguanine response in T-acute lymphoblastic leukaemia cell lines in culture. Pathophysiology; 2007 May;14(1):3-10
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  • [Title] CD26/DPPIV expression and 8-azaguanine response in T-acute lymphoblastic leukaemia cell lines in culture.
  • Dipeptidyl peptidase IV, a cell membrane surface protease also known as CD26 (CD26/DPPIV), is known to play multiple functions in human organism, where it is largely expressed, for instance, in the development of human cancer and metastasis as well as in chemotherapy response.
  • The objective of this work was to study the CD26 membrane expression and DPPIV activity in T-acute leukaemia cell lines (CEM and MOLT3) in culture, in order to observe the modification of its expression under the 8-azaguanine treatment.
  • Cell line samples were incubated, some without different azaguanine concentration and others with, ranging from 10 to 100muM.
  • Cell surface CD26 expression has been identified by flow cytometry and DPPIV activity, in cultured medium, was fluorimetrically measured.
  • Results we have observed showed that 8-azaguanine induced a decrease in cell viability in a dose, time and cell type dependent manner with MOLT3 cells being the most sensitive to 8-azaguanine citotoxic effects (24h IC50: +/-10muM) when compared with CEM cells (24h IC50: +/-100muM).
  • In the same experimental conditions, MOLT3 cell treated with 8-azaguanine shows an increase in CD26 expression (MIF) compared with that of CEM cell submitted to the same conditions (65.4+/-1.3 versus 18.7+/-1.7).

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  • (PMID = 17055708.001).
  • [ISSN] 0928-4680
  • [Journal-full-title] Pathophysiology : the official journal of the International Society for Pathophysiology
  • [ISO-abbreviation] Pathophysiology
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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66. Santamaría-Quesada C, Vargas M, Venegas P, Calvo M, Obando C, Valverde B, Cartín W, Carrillo JM, Jimenez R, González M: Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica. J Pediatr Hematol Oncol; 2009 Feb;31(2):131-5
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  • [Title] Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica.
  • In Central America, nearly 70% of pediatric cancer is related to hemato-oncologic disorders, especially acute lymphoblastic leukemia (ALL).
  • Preliminary studies have described a high incidence of childhood leukemia in these countries; however, no molecular analyses of these malignancies have yet been carried out.
  • We studied diagnostic samples from 84 patients from the National Children's Hospital in San Jose, Costa Rica (65 precursor B-ALL, 5 T-cell ALL, and 14 acute myeloblastic leukemia).
  • The observed rate of leukemia was 52.2 cases per million children per year.
  • Twelve out of 65 (18.4%) precursor B-ALL tested positive for TEL-AML1 and 3 cases for BCR-ABL (4.6%).
  • None of the T-cell ALL cases were positive for either SIL-TAL1 or HOX11L2.
  • Within 14 acute myeloblastic leukemia patients, we confirmed 2 cases with FLT3-internal tandem duplication+, 1 patient with AML1-ETO, and only 1 case carrying a PML-RARalpha rearrangement.
  • The present study confirms the relatively high incidence of pediatric leukemia in Costa Rica and constitutes the first report regarding the incidence of the main molecular alterations of childhood leukemia in our region.
  • [MeSH-major] Leukemia / epidemiology. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Child. Costa Rica / epidemiology. Cytogenetic Analysis. Gene Rearrangement. Humans. Mutation. Oncogene Proteins, Fusion / analysis

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  • (PMID = 19194200.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
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67. Malcovati L: Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia. Haematologica; 2006 Mar;91(3):290A
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  • [Title] Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Genes, Homeobox / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Recombination, Genetic / genetics

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  • [CommentOn] Haematologica. 2006 Mar;91(3):317-21 [16531254.001]
  • (PMID = 16531247.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] Italy
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68. De la Iglesia Iñigo S, López-Jorge CE, Gómez-Casares MT, Lemes Castellano A, Martín Cabrera P, López Brito J, Suárez Cabrera A, Molero Labarta T: Induction of apoptosis in leukemic cell lines treated with captopril, trandolapril and losartan: a new role in the treatment of leukaemia for these agents. Leuk Res; 2009 Jun;33(6):810-6
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  • [Title] Induction of apoptosis in leukemic cell lines treated with captopril, trandolapril and losartan: a new role in the treatment of leukaemia for these agents.
  • We investigated the effect of ACE inhibitors (ACEI) captopril (>1mM) and trandolapril (>0.05 mM) and losartan (0.2 mM) on K562 cell line and K562 transfected with c-myc, bcl-x and bcl-2 (KmycB, Kbclx and Kbcl2 respectively).
  • ACEI and losartan inhibited cell growth, decreased c-myc expression and increased apoptosis.
  • This work offers a new possible line of treatment for some acute myeloid leukemias and a new area of clinical research.
  • [MeSH-major] Angiotensin-Converting Enzyme Inhibitors / pharmacology. Apoptosis / drug effects. Captopril / pharmacology. Indoles / pharmacology. Leukemia, Erythroblastic, Acute / pathology. Losartan / pharmacology
  • [MeSH-minor] Blotting, Northern. Blotting, Western. Cell Proliferation. Genes, myc. Humans. K562 Cells. Polymerase Chain Reaction

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  • (PMID = 19010543.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Indoles; 1T0N3G9CRC / trandolapril; 9G64RSX1XD / Captopril; JMS50MPO89 / Losartan
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69. Borriello A, Locasciulli A, Bianco AM, Criscuolo M, Conti V, Grammatico P, Cappellacci S, Zatterale A, Morgese F, Cucciolla V, Delia D, Della Ragione F, Savoia A: A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2007 Jan;21(1):72-8
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  • [Title] A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia.
  • Fanconi anemia (FA) is an autosomal recessive disease characterized by pancitopenia, congenital malformations, predisposition to cancers and chromosomal instability.
  • We report the clinical and molecular features of a patient initially identified as a potential FA case only because of chemotherapy toxicity during the treatment of a T-lineage acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fanconi Anemia Complementation Group D2 Protein / genetics. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation
  • [MeSH-minor] Amino Acid Substitution. Antigens, CD. Antigens, CD13. Antigens, Differentiation, Myelomonocytic. Child. Chromosomal Instability. Disease Progression. Fanconi Anemia / genetics. Humans. Infection / etiology. Infection / genetics. Male. Pancytopenia / chemically induced. Pancytopenia / genetics. Remission Induction. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 17096012.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Italy / Telethon / / TGM06S01
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FANCD2 protein, human; 0 / Fanconi Anemia Complementation Group D2 Protein; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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70. Nishimura S, Takahashi S, Kamikatahira H, Kuroki Y, Jaalouk DE, O'Brien S, Koivunen E, Arap W, Pasqualini R, Nakayama H, Kuniyasu A: Combinatorial targeting of the macropinocytotic pathway in leukemia and lymphoma cells. J Biol Chem; 2008 Apr 25;283(17):11752-62
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  • [Title] Combinatorial targeting of the macropinocytotic pathway in leukemia and lymphoma cells.
  • Ligand-directed delivery of agents to leukemia and lymphoma cells has the potential to yield new mechanistic disease insights and targeted therapies.
  • From the screening of acute T-lymphoblastic leukemia Molt-4 cells with a random phage-display peptide library, we isolated a phage displaying the sequence CAYHRLRRC.
  • This peptide contains a lymph node-homing motif (Cys-Ala-Tyr) and a cell-penetrating motif (Arg-Leu-Arg-Arg).
  • Binding of this ligand-directed phage to a large panel of leukemia/lymphoma cells and to patient-derived samples was much higher than to non-leukemia control cells.
  • Flow cytometry with fluorescein-labeled peptide and endocytosis blocking with specific inhibitors revealed that CAYHRLRRC is indeed taken up through macropinocytosis in Molt-4 and K562 human leukemia cells.
  • Unexpectedly, the cell surface receptor for the CAYHRLRRC peptide is not a heparan sulfate proteoglycan as it would be predicted for other cell-penetrating peptides.
  • Confirming this interpretation, a CAYHRLRRC-directed peptidomimetic-induced cell death in all the leukemia and lymphoma cells was evaluated, whereas a control transactivator of transcription protein (tat)-directed proapoptotic peptidomimetic was non-selective.
  • In summary, the targeting peptide CAYHRLRRC is selectively internalized through macropinocytosis in leukemia and lymphoma cells and has potential as a drug lead for ligand-directed anti-leukemia therapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Gene Expression Regulation, Leukemic. Leukemia / metabolism. Lymphoma / metabolism
  • [MeSH-minor] Catalysis. Cell Line, Tumor. Cell Survival. Chemistry, Pharmaceutical / methods. Drug Design. Humans. K562 Cells. Ligands. Peptide Library. Peptides / chemistry. Pinocytosis

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  • (PMID = 18292083.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Peptide Library; 0 / Peptides
  • [Other-IDs] NLM/ PMC3762554
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71. Xue SL, Wu DP, Sun AN, Tang XW: CAG regimen enables relapsed or refractory T-cell acute lymphocytic leukemia patients to achieve complete remission: a report of six cases. Am J Hematol; 2008 Feb;83(2):167-70
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  • [Title] CAG regimen enables relapsed or refractory T-cell acute lymphocytic leukemia patients to achieve complete remission: a report of six cases.
  • Patients with either relapsed or refractory T-cell acute lymphocytic leukemia (T-ALL) are candidates for allogeneic hematopoietic stem cell transplantation (allo-HSCT).
  • The CAG regimen (cytosine arabinoside 10 mg/m(2) subcutaneously every 12 hr, day 1-14; aclarubicin 5-7 mg/m(2) intravenously daily, day 1-8; and concurrent use of G-CSF 200 microg/m(2)/day subcutaneously) was devised originally for the treatment of relapsed acute myelogenous leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy

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  • (PMID = 17874449.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin; CAG protocol
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72. Wada T, Kikuchi J, Nishimura N, Shimizu R, Kitamura T, Furukawa Y: Expression levels of histone deacetylases determine the cell fate of hematopoietic progenitors. J Biol Chem; 2009 Oct 30;284(44):30673-83
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  • [Title] Expression levels of histone deacetylases determine the cell fate of hematopoietic progenitors.
  • In contrast, acute myeloid leukemias showed HDAC overexpression and histone hypoacetylation.
  • Small interfering RNA-mediated knockdown of HDAC1 enhanced myeloid differentiation in immature hematopoietic cell lines and perturbed erythroid differentiation in progenitor cells.
  • These findings suggest that HDAC is not merely an auxiliary factor of genetic elements but plays a direct role in the cell fate decision of hematopoietic progenitors.
  • [MeSH-minor] Bone Marrow Cells / cytology. CCAAT-Binding Factor / physiology. Cell Differentiation. Cell Line, Tumor. Cells, Cultured. GATA1 Transcription Factor / physiology. Histone Deacetylases / analysis. Histone Deacetylases / genetics. Histone Deacetylases / physiology. Humans. Leukemia, Myeloid. Myeloid Cells. Transcription, Genetic

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  • (PMID = 19736310.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Binding Factor; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC2781621
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73. Cox CV, Martin HM, Kearns PR, Virgo P, Evely RS, Blair A: Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia. Blood; 2007 Jan 15;109(2):674-82
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  • [Title] Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.
  • A significant proportion of children with T-cell acute lymphoblastic leukemia (T-ALL) continue to fail therapy.
  • Consequently, characterization of the cells that proliferate to maintain the disease should provide valuable information on the most relevant therapeutic targets.
  • The majority of cells capable of long-term proliferation in vitro were derived from the CD34+/CD4- and CD34+/CD7- subfractions.
  • The immunophenotype and genotype of the original leukemia cells were preserved with serial passage in the NOD/SCID mice.
  • These data demonstrate the long-term repopulating ability of the CD34+/CD4- and CD34+/CD7- subfractions in T-ALL and suggest that a cell with a more primitive phenotype was the target for leukemic transformation in these cases.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Stem Cells / immunology. Stem Cells / pathology
  • [MeSH-minor] Adolescent. Animals. Cell Culture Techniques. Cell Proliferation. Cell Separation. Cells, Cultured. Child. Child, Preschool. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Genotype. Humans. Immunophenotyping. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. Xenograft Model Antitumor Assays


74. Te Boekhorst PA, Lamers CH, Schipperus MR, Hintzen RQ, van der Holt B, Cornelissen JJ, Löwenberg B, Gratama JW: T-lymphocyte reconstitution following rigorously T-cell-depleted versus unmodified autologous stem cell transplants. Bone Marrow Transplant; 2006 Apr;37(8):763-72
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  • [Title] T-lymphocyte reconstitution following rigorously T-cell-depleted versus unmodified autologous stem cell transplants.
  • We compared the kinetics of T-cell recovery after extensive ex vivo and in vivo T-cell depleted autologous stem cell transplantation (SCT) for multiple sclerosis (MS; n=8) with unmodified SCT for hematological malignancies (HM; n=39).
  • Unexpectedly, the kinetics of T-cell recovery between 3 and 12 months post transplant was similar in T-depleted and unmodified SCT.
  • Before SCT, the HM patients showed lymphopenia of all T-cell subsets, upregulated HLA-DR and CD95 expression and increased cytokine responses.
  • We suggest that the similar kinetics of T-cell recovery in the two patient groups may be explained by the susceptibility to apoptosis of the activated CD4(+) T-cells in the autografts of the HM patients.
  • This susceptibility to apoptosis would interfere with a swift and sustained CD4(+) T-cell regeneration post SCT.
  • [MeSH-major] Multiple Sclerosis / blood. Multiple Sclerosis / therapy. Stem Cell Transplantation / methods. T-Lymphocytes / metabolism. Transplantation, Autologous / methods

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  • (PMID = 16518423.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Antigens, CD3; 0 / Antigens, CD4; 0 / Antigens, CD95; 0 / Cytokines; 0 / Interleukin-2; 126880-86-2 / L-Selectin; 82115-62-6 / Interferon-gamma; EC 3.1.3.48 / Antigens, CD45
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75. Bertrand Y: [Recommendations of the French Society for the Control of Cancers and Leukemias in Children for the treatment of tumor lysis syndrome: results of a pediatric survey]. Arch Pediatr; 2005 Oct;12 Spec No 1:13-5
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  • [Title] [Recommendations of the French Society for the Control of Cancers and Leukemias in Children for the treatment of tumor lysis syndrome: results of a pediatric survey].
  • [Transliterated title] Recommandations de la société française de lutte contre les cancers et les leucémies de l'enfant (SFCE) pour le traitement du syndrome de lyse tumorale (SLT): résultats d'un observatoire pédiatrique.
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Leukemia, Myeloid, Acute / drug therapy. Lymphoma, B-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Recombinant Proteins. Risk Factors

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  • (PMID = 17076005.001).
  • [ISSN] 0929-693X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antimetabolites; 0 / Antineoplastic Agents; 0 / Recombinant Proteins; EC 1.7.3.3 / Urate Oxidase; EC 1.7.3.3. / rasburicase
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76. Mustjoki S, Ekblom M, Arstila TP, Dybedal I, Epling-Burnette PK, Guilhot F, Hjorth-Hansen H, Höglund M, Kovanen P, Laurinolli T, Liesveld J, Paquette R, Pinilla-Ibarz J, Rauhala A, Shah N, Simonsson B, Sinisalo M, Steegmann JL, Stenke L, Porkka K: Clonal expansion of T/NK-cells during tyrosine kinase inhibitor dasatinib therapy. Leukemia; 2009 Aug;23(8):1398-405
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  • Fifteen patients had a cytotoxic T-cell and seven patients had an NK-cell phenotype.
  • All T-cell expansions were clonal.
  • Responses to dasatinib were good and included complete, unexpectedly long-lasting remissions in patients with advanced leukemia.
  • In a phase II clinical study on 46 Philadelphia chromosome-positive acute lymphoblastic leukemia, patients with lymphocytosis had superior survival compared with patients without lymphocytosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Killer Cells, Natural / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lymphocytosis / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. T-Lymphocyte Subsets / drug effects. T-Lymphocytes, Cytotoxic / drug effects. Thiazoles / pharmacology

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  • [CommentIn] Acta Haematol. 2016;136(4):219-228 [27656875.001]
  • (PMID = 19295545.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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77. Magić Z, Novković T, Cikota B, Tasić-Radić O, Tarabar O, Stamatović D: Genetic alterations in B-cell non-Hodgkin's lymphoma. Vojnosanit Pregl; 2005 Feb;62(2):87-96
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  • [Title] Genetic alterations in B-cell non-Hodgkin's lymphoma.
  • BACKGROUND: Although the patients with diagnosed B-NHL are classified into the same disease stage on the basis of clinical, histopathological, and immunological parameters, they respond significantly different to the applied treatment.
  • This points out the possibility that within the same group of lymphoma there are different diseases at molecular level.
  • For that reason many studies deal with the detection of gene alterations in lymphomas to provide a better framework for diagnosis and treatment of these hematological malignancies.
  • There were 34 cases of B-cell non-Hodgkin's lymphoma (B-NHL), 5 cases of T-cell non-Hodgkin's lymphoma (T-NHL) and 6 cases of chronic lymphadenitis (CL).
  • The mononuclear cell fraction of the peripheral blood of 12 patients with B-NHL was analyzed for the presence of monoclonality at the time of diagnosis and in 3 to 6 months time intervals after an autologous bone marrow transplantation (BMT).
  • All the patients (12) with B-NHL had dominant clone of B-lymphocyte in the peripheral blood at the time of diagnosis while only in 2 of 12 patients MRD was detected 3 or 6 months after BMT.
  • This technique is also very effecient for tracking minimal residual disease in lymphomas and leukemias and for monitoring clonal evolution in acute and chronic lymphoblastic leukemias and lymphomas.
  • [MeSH-major] Lymphoma, B-Cell / genetics
  • [MeSH-minor] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Genetic Markers. Humans. Point Mutation. Proto-Oncogenes / genetics. Translocation, Genetic

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  • (PMID = 15787160.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Yugoslavia
  • [Chemical-registry-number] 0 / Genetic Markers
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78. Dail M, Li Q, McDaniel A, Wong J, Akagi K, Huang B, Kang HC, Kogan SC, Shokat K, Wolff L, Braun BS, Shannon K: Mutant Ikzf1, KrasG12D, and Notch1 cooperate in T lineage leukemogenesis and modulate responses to targeted agents. Proc Natl Acad Sci U S A; 2010 Mar 16;107(11):5106-11
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  • Mice that accurately model the genetic diversity found in human cancer are valuable tools for interrogating disease mechanisms and investigating novel therapeutic strategies.
  • We performed insertional mutagenesis with the MOL4070LTR retrovirus in Mx1-Cre, Kras(G12D) mice and generated a large cohort of T lineage acute lymphoblastic leukemias (T-ALLs).
  • We tested tumor-derived cell lines to identify biomarkers of therapeutic response to targeted inhibitors.
  • Whereas all T-ALLs tested were sensitive to a dual-specificity phosphoinosityl 3-kinase/mammalian target of rapamycin inhibitor, biochemical evidence of Notch1 activation correlated with sensitivity to gamma-secretase inhibition.
  • In addition, Kras(G12D) T-ALLs were more responsive to a MAP/ERK kinase inhibitor in vitro and in vivo.

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  • (PMID = 20194733.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / R37 CA72614; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R37 CA072614; United States / NCI NIH HHS / CA / U01 CA84221; United States / NCI NIH HHS / CA / T32 CA128583; United States / NCI NIH HHS / CA / K08 CA119105
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Mutant Proteins; 0 / Notch1 protein, mouse; 0 / PD 0325901; 0 / Receptor, Notch1; 0 / Zfpn1a1 protein, mouse; 148971-36-2 / Ikaros Transcription Factor; 9N3CBB0BIQ / Diphenylamine; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2841878
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79. Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP: Cooperative genetic defects in TLX3 rearranged pediatric T-ALL. Leukemia; 2008 Apr;22(4):762-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

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  • (PMID = 18185524.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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80. Szczepański T, Harrison CJ, van Dongen JJ: Genetic aberrations in paediatric acute leukaemias and implications for management of patients. Lancet Oncol; 2010 Sep;11(9):880-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic aberrations in paediatric acute leukaemias and implications for management of patients.
  • The process of malignant transformation in paediatric acute leukaemias is complex, requiring at least two deleterious events resulting in DNA damage.
  • In this review we summarise the most common genetic aberrations for the three main subtypes of paediatric acute leukaemia: B-cell-precursor acute lymphoblastic leukaemia, T-cell acute lymphoblastic leukaemia and acute myeloid leukaemia.
  • Some genetic aberrations represent sensitive targets for molecular detection of minimal residual disease.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Chromosome Aberrations. Leukemia / genetics

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20435517.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 76
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81. Buie LW, Epstein SS, Lindley CM: Nelarabine: a novel purine antimetabolite antineoplastic agent. Clin Ther; 2007 Sep;29(9):1887-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Nelarabine was approved by the US Food and Drug Administration (FDA) in October 2005 for the treatment of T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) that has not responded to or has relapsed after treatment with at least 2 chemotherapy regimens.
  • Nelarabine has activity in T-cell malignancies, as evaluated in 2 Phase I and 5 Phase II studies.
  • In PGAA 2001, patients with T-ALL in first relapse (n = 33) had an objective response rate of 55% (16 with a complete response [CR] and 2 with a partial response [PR]), and those with T-ALL in second relapse (n = 30) had an objective response rate of 27% (7 CR and 1 PR).
  • Among patients with central nervous system-positive T-ALL or T-cell non-Hodgkins lymphoma (T-NHL) (n = 21), 33% had an objective response (5 CR and 2 PR); among patients with T-ALL or T-NHL with extramedullary relapse (n = 22), 14% had a PR.
  • CALGB 19801 included 39 adult patients with T-cell malignancies, of whom 7 (18%) had a CR and an additional 2 (5%) had a CR without full hematologic recovery.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Arabinonucleosides / therapeutic use. Hematologic Neoplasms / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Purine Nucleosides / therapeutic use

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  • (PMID = 18035189.001).
  • [ISSN] 0149-2918
  • [Journal-full-title] Clinical therapeutics
  • [ISO-abbreviation] Clin Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Arabinonucleosides; 0 / Purine Nucleosides; 60158CV180 / nelarabine
  • [Number-of-references] 29
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82. Nishida S, Hosen N, Shirakata T, Kanato K, Yanagihara M, Nakatsuka S, Hoshida Y, Nakazawa T, Harada Y, Tatsumi N, Tsuboi A, Kawakami M, Oka Y, Oji Y, Aozasa K, Kawase I, Sugiyama H: AML1-ETO rapidly induces acute myeloblastic leukemia in cooperation with the Wilms tumor gene, WT1. Blood; 2006 Apr 15;107(8):3303-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML1-ETO rapidly induces acute myeloblastic leukemia in cooperation with the Wilms tumor gene, WT1.
  • AML1-ETO, a chimeric gene frequently detected in acute myelogenous leukemia (AML), inhibits the differentiation of myeloid progenitors by suppressing genes associated with myeloid differentiation and increases the replating ability of clonogenic myeloid progenitors.
  • The Wilms tumor gene (WT1), which has been identified as the gene responsible for Wilms tumor, is expressed at high levels in almost all human leukemias.
  • AML1-ETO-transduced bone marrow (BM) cells from WT1-Tg mice exhibited inhibition of myeloid differentiation at more immature stages and higher in vitro colony-forming ability compared with AML1-ETO-transduced BM cells from wild-type mice.
  • [MeSH-major] Cell Differentiation / genetics. Cell Transformation, Neoplastic / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid Progenitor Cells / metabolism. Oncogene Proteins, Fusion / genetics. WT1 Proteins / genetics

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  • (PMID = 16380455.001).
  • [ISSN] 0006-4971
  • [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
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / WT1 Proteins
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83. Seror E, Coquerel B, Gautheret-Dejean A, Ballerini P, Landman-Parker J, Leverger G, Schneider P, Vannier JP: Quantitation of Human herpes virus 6 genome in children with acute lymphoblastic leukemia. J Med Virol; 2008 Apr;80(4):689-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitation of Human herpes virus 6 genome in children with acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia is the main type of leukemia in children.
  • The potential role of HHV-6 in the pathogenesis of pediatric acute lymphoblastic leukemia was investigated.
  • HHV-6 genome copy number was measured by quantitative real-time PCR (RQ-PCR) in bone marrow or peripheral blood samples obtained from 36 children (median age = 4 years) with B acute lymphoblastic leukemia (n = 31) and T acute lymphoblastic leukemia (n = 5) at diagnosis and during complete remission.
  • A total of 24.7% of samples were positive for HHV-6 genome: 13.9% were leukemia samples and 34.1% were complete remission samples.
  • Viral load was low with values lower at diagnosis (median viral copy number = 22.9) than at complete remission (median copy number = 60.1).
  • These results argue against a role of HHV6 infection in the development of pediatric acute lymphoblastic leukemia.
  • [MeSH-major] DNA, Viral / analysis. Herpesvirus 6, Human / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / virology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / virology. Roseolovirus Infections / complications. Roseolovirus Infections / virology

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  • (PMID = 18297709.001).
  • [ISSN] 0146-6615
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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84. Pozner A, Lotem J, Xiao C, Goldenberg D, Brenner O, Negreanu V, Levanon D, Groner Y: Developmentally regulated promoter-switch transcriptionally controls Runx1 function during embryonic hematopoiesis. BMC Dev Biol; 2007;7:84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Runx1 transcription factor is a key regulator of early hematopoiesis and a frequent target of chromosomal translocations in acute leukemias.
  • Early thymus development and thymopoiesis were also abrogated as reflected by thymic hypocellularity and loss of corticomedullary demarcation.
  • Differentiation of CD4/CD8 thymocytes was impaired and their apoptosis was enhanced due to altered expression of T-cell receptors.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Developmental. Hematopoiesis, Extramedullary / genetics. Promoter Regions, Genetic. Thymus Gland / embryology
  • [MeSH-minor] Alleles. Animals. Apoptosis. Cell Differentiation. Colony-Forming Units Assay. DNA Primers. Embryo, Mammalian. Embryonic Stem Cells / cytology. Flow Cytometry. Genes, Lethal. Hematopoietic Stem Cells / cytology. In Situ Hybridization. Mice. Mice, Knockout. Phenotype. Reverse Transcriptase Polymerase Chain Reaction