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1. Yamagami T, Porada CD, Pardini RS, Zanjani ED, Almeida-Porada G: Docosahexaenoic acid induces dose dependent cell death in an early undifferentiated subtype of acute myeloid leukemia cell line. Cancer Biol Ther; 2009 Feb;8(4):331-7
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  • [Title] Docosahexaenoic acid induces dose dependent cell death in an early undifferentiated subtype of acute myeloid leukemia cell line.
  • Acute myeloid leukemia (AML) is the most frequently diagnosed adulthood leukemia, yet current therapies offer a cure rate of less than 30%.
  • This may be due in part to the fact that the leukemia-initiating cells in AML reside within the rare and highly primitive CD34(+)CD38(-) hematopoietic stem/progenitor cell (HSC) population that are often resistant to chemotherapy.
  • In the present studies, we investigated DHA's effect on the primitive and undifferentiated AML cell line KG1a, to explore the potential of this fatty acid to serve as adjuvant therapy for AML.
  • Treatment of KG1a cells with DHA for 96 hours did not lead to maturation or cell cycle modification when compared to an untreated KG1a control (n = 4).
  • Since we also show that DHA does not have a detrimental effect on normal hematopoiesis our results suggest that DHA could potentially serve as an well-tolerated adjuvant in the treatment of AML patients.

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  • [CommentIn] Cancer Biol Ther. 2009 Feb;8(4):338-9 [19197147.001]
  • (PMID = 19197149.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL070566; United States / NHLBI NIH HHS / HL / HL70566; United States / NHLBI NIH HHS / HL / R01 HL073737; United States / NHLBI NIH HHS / HL / HL052955-14A1; United States / NHLBI NIH HHS / HL / R01 HL052955; United States / NHLBI NIH HHS / HL / R01 HL052955-14A1; United States / NHLBI NIH HHS / HL / HL73737
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / bcl-2-Associated X Protein; 25167-62-8 / Docosahexaenoic Acids; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS122907; NLM/ PMC3954154
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2. Webert KE, Cook RJ, Couban S, Carruthers J, Lee KA, Blajchman MA, Lipton JH, Brandwein JM, Heddle NM: A multicenter pilot-randomized controlled trial of the feasibility of an augmented red blood cell transfusion strategy for patients treated with induction chemotherapy for acute leukemia or stem cell transplantation. Transfusion; 2008 Jan;48(1):81-91
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  • [Title] A multicenter pilot-randomized controlled trial of the feasibility of an augmented red blood cell transfusion strategy for patients treated with induction chemotherapy for acute leukemia or stem cell transplantation.
  • Patients with acute leukemia receiving induction chemotherapy or those undergoing stem cell transplantation were assigned to one of two treatment groups: standard transfusion strategy (transfusion of 2 units of red blood cells [RBCs] when their Hb level was less than 80 g/L) or an augmented transfusion strategy (transfusion of 2 units of RBCs when their Hb level was less than 120 g/L).
  • The proportions of patients experiencing clinically significant bleeding and the time to first bleed were not significantly different between the control and experimental groups.
  • The proportion of patient-days with platelet (PLT) transfusions was not different between the experimental and control groups.
  • The mean number of donor exposures (PLT and RBC transfusions) was not different between experimental and control groups.
  • [MeSH-major] Erythrocyte Transfusion / methods. Hemorrhage / etiology. Leukemia / complications. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Antineoplastic Agents / therapeutic use. Feasibility Studies. Female. Hematopoietic Stem Cell Transplantation. Hemoglobins / analysis. Humans. Male. Middle Aged. Pilot Projects

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  • (PMID = 17894791.001).
  • [ISSN] 0041-1132
  • [Journal-full-title] Transfusion
  • [ISO-abbreviation] Transfusion
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hemoglobins
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3. Escobar MA, Hoelz DJ, Sandoval JA, Hickey RJ, Grosfeld JL, Malkas LH: Profiling of nuclear extract proteins from human neuroblastoma cell lines: the search for fingerprints. J Pediatr Surg; 2005 Feb;40(2):349-58
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  • [Title] Profiling of nuclear extract proteins from human neuroblastoma cell lines: the search for fingerprints.
  • PURPOSE: Neuroblastoma (NB) commonly presents with advanced disease at diagnosis and is associated with poor survival.
  • METHODS: Three different human NB cell lines SK-N-AS, SK-N-DZ, and SK-N-FI were subjected to series of biochemical fractionation steps to extract nuclear proteins.
  • RESULTS: Multiple proteins were identified in these human NB cell lines including SET (a ubiquitous nuclear protein), stathmin (a cytosolic signal transduction protein), and grp94 (a heat shock protein).
  • SET is a putative oncogene associated with the chromosomal translocation (6;9) leading to acute undifferentiated leukemia.
  • The first protein has not been previously associated with NB.
  • CONCLUSIONS: The identification of these 3 previously unrecognized cancer-related potential biomarkers in human NB cell lines may prove useful in developing diagnostic tests.
  • [MeSH-minor] Cell Line, Tumor. Chromatography, Liquid. Chromosomal Proteins, Non-Histone / analysis. DNA Fingerprinting. Electrophoresis, Gel, Two-Dimensional. Gene Expression Profiling. HSP70 Heat-Shock Proteins / analysis. Histone Chaperones. Humans. Mass Spectrometry / methods. Membrane Proteins / analysis. Proteomics / methods. Stathmin / analysis. Transcription Factors / analysis

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  • (PMID = 15750928.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA57350; United States / NCI NIH HHS / CA / CA83199
  • [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 / Biomarkers, Tumor; 0 / Chromosomal Proteins, Non-Histone; 0 / HSP70 Heat-Shock Proteins; 0 / Histone Chaperones; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / SET protein, human; 0 / Stathmin; 0 / Transcription Factors; 0 / glucose-regulated proteins
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4. Hu X, Li X, Valverde K, Fu X, Noguchi C, Qiu Y, Huang S: LSD1-mediated epigenetic modification is required for TAL1 function and hematopoiesis. Proc Natl Acad Sci U S A; 2009 Jun 23;106(25):10141-6
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  • However, perturbation of its activity often leads to T cell leukemia.
  • Here, we show that TAL1 is associated with histone demethylase complexes containing lysine-specific demethylase 1 (LSD1), RE1 silencing transcription factor corepressor (CoREST), histone deacetylase 1 (HDAC1), and histone deacetylase 2 in erythroleukemia and T cell leukemia cells.
  • Consistent with the rapid changes of TAL1-corepressor complex during differentiation, TAL1 recruits LSD1 to the silenced p4.2 promoter in undifferentiated, but not in differentiated, murine erythroleukemia (MEL) cells.

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  • (PMID = 19497860.001).
  • [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 / NHLBI NIH HHS / HL / HL091929; United States / Intramural NIH HHS / / ; United States / NHLBI NIH HHS / HL / R01 HL091929; United States / NHLBI NIH HHS / HL / R01 HL090589; United States / NHLBI NIH HHS / HL / HL090589
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 135471-20-4 / TAL1 protein, human; EC 1.14.11.- / Histone Demethylases; EC 1.5.- / KDM1A protein, human; EC 1.5.- / Oxidoreductases, N-Demethylating
  • [Other-IDs] NLM/ PMC2700898
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5. Anisimov SV, Morizane A, Correia AS: Risks and mechanisms of oncological disease following stem cell transplantation. Stem Cell Rev; 2010 Sep;6(3):411-24
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  • [Title] Risks and mechanisms of oncological disease following stem cell transplantation.
  • Unique biological properties of stem cells make them a precious source of cell material for treatment of a number of pathological conditions.
  • Among issues inhibiting transition of stem cell technologies to the clinics, the risk of oncological complications of stem cell-based therapies is the most critical.
  • A massive amount of clinical and experimental data demonstrates that both hematological (including acute and chronic myeloid leukemia) and non-hematological (including teratoma and non-teratoma tumors) malignancies could arise from donor stem cells of different types.
  • A wide spectrum of mechanisms could underlie the development of oncological disease in recipients, including: i) blast transformation of proliferating donor stem cells under persistent action of certain factors in the recipient, thus causing de novo malignancies;.
  • ii) contamination of donor cell material with malignant cells;.
  • iii) transmission of particular viral subtypes with donor stem cells, combined with immunosuppression therapy effects;.
  • iv) uncontrollable proliferation of residual undifferentiated stem cells of various plasticity; and v) karyotypic instability in stem cells following prolonged culturing/expansion in vitro.
  • Potential preventive strategies are diverse and include i) high-throughput cell sorting-based strategies;.
  • ii) introduction of suicide genes into the donor stem cell genome;.
  • [MeSH-major] Neoplasms / etiology. Stem Cell Transplantation / adverse effects

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  • (PMID = 20300888.001).
  • [ISSN] 1558-6804
  • [Journal-full-title] Stem cell reviews
  • [ISO-abbreviation] Stem Cell Rev
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
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6. Smith AM, Sanchez MJ, Follows GA, Kinston S, Donaldson IJ, Green AR, Göttgens B: A novel mode of enhancer evolution: the Tal1 stem cell enhancer recruited a MIR element to specifically boost its activity. Genome Res; 2008 Sep;18(9):1422-32
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  • [Title] A novel mode of enhancer evolution: the Tal1 stem cell enhancer recruited a MIR element to specifically boost its activity.
  • The stem cell leukemia TAL1 (also known as SCL) transcription factor is essential for the normal development of blood stem cells and we have previously shown that the Tal1 +19 enhancer directs expression to hematopoietic stem cells, hematopoietic progenitors, and to endothelium.
  • Here we demonstrate that an adjacent region 1 kb upstream (+18 element) is in an open chromatin configuration and carries active histone marks but does not function as an enhancer in transgenic mice.
  • Instead, it boosts activity of the +19 enhancer both in stable transfection assays and during differentiation of embryonic stem (ES) cells carrying single-copy reporter constructs targeted to the Hprt locus.

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  • (PMID = 18687876.001).
  • [ISSN] 1088-9051
  • [Journal-full-title] Genome research
  • [ISO-abbreviation] Genome Res.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [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 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC2527711
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7. Kahng J, Shin SY, Han K: [Proportions of cells expressing CD38-/CD34+, CD38+/CD34+, CD19+/CD34+, or CD13,33+/CD34+ in the regenerating bone marrows during complete remission of acute leukemia or after bone marrow transplantation]. Korean J Lab Med; 2007 Dec;27(6):406-13
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  • [Title] [Proportions of cells expressing CD38-/CD34+, CD38+/CD34+, CD19+/CD34+, or CD13,33+/CD34+ in the regenerating bone marrows during complete remission of acute leukemia or after bone marrow transplantation].
  • BACKGROUND: The hemopoietic stem cells increase in number during the regeneration after chemotherapy or bone marrow transplantation (BMT).
  • Although the proportion of hemopoietic stem cells and their differentiation have been studied by immunophenotyping using the flow cytometry, no substantial research efforts have been directed toward the regenerating marrow.
  • We attempted to discover the proportions of undifferentiated stem cells, committed stem cells, B cell precursors, and myeloid precursors in the regenerating bone marrows during complete remission (CR) and after engraftment of BMT.
  • METHODS: Bone marrow samples from 82 patients with acute leukemia in CR and from 25 patients after BMT engraftment, along with 22 control samples, were used to find the numbers of CD38-/CD34+, CD38+/CD34+, CD19+/CD34+, and CD13,33+/CD34+ cells in the large lymphocyte gate by flow cytometry.
  • We cross-analyzed our results in terms of groups: CR, BMT, and initial diagnosis groups.
  • RESULTS: The proportions of CD38-/CD34+, CD38+/CD34+, CD19+/CD34+, and CD13,33+/CD34+ cells are more highly distributed in acute B-lymphoblastic leukemia than the normal group and also in the CR than the BMT group.
  • [MeSH-major] Antigens, CD19 / metabolism. Antigens, CD34 / metabolism. Antigens, CD38 / metabolism. Bone Marrow Transplantation. Leukemia / metabolism
  • [MeSH-minor] Acute Disease. Bone Marrow / physiology. Flow Cytometry. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / therapeutic use. Hematopoietic Stem Cells / immunology. Hematopoietic Stem Cells / metabolism. Humans. Immunophenotyping. Regeneration. Remission Induction

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  • (PMID = 18160830.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD34; 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.2.2.5 / Antigens, CD38
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8. Atallah E, Cortes J: Optimal initial therapy for patients with newly diagnosed chronic myeloid leukemia in chronic phase. Curr Opin Hematol; 2007 Mar;14(2):138-44
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  • [Title] Optimal initial therapy for patients with newly diagnosed chronic myeloid leukemia in chronic phase.
  • PURPOSE OF REVIEW: Imatinib mesylate, a tyrosine kinase inhibitor, has revolutionized the therapy of newly diagnosed patients with chronic myeloid leukemia.
  • Prior to imatinib, treatment algorithms for chronic myeloid leukemia patients recommended stem cell transplantation for patients less than 50 years old who had a donor and could undergo stem cell transplantation.
  • Other than stem cell transplantation, interferon was the only drug that could induce cytogenetic remissions in minority of patients.
  • The use of imatinib before stem cell transplant did not have an effect on mortality or morbidity posttransplant.
  • SUMMARY: Currently, imatinib is considered first line therapy in all patients with early chronic phase chronic myeloid leukemia with stem cell transplant reserved for patients who have disease resistant to imatinib therapy.
  • Our aim is to review current recommendations for initial therapy of patients with early chronic phasechronic myeloid leukemia, current areas of controversy and future directions.
  • [MeSH-major] Leukemia, Myeloid, Chronic-Phase / therapy
  • [MeSH-minor] Benzamides. Disease Management. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17255791.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 53
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9. Tan S, Wang G, Peng M, Zhang X, Shen G, Jiang J, Chen F: Detection of myeloperoxidase activity in primary leukemic cells by an enhanced chemiluminescent assay for differentiation between acute lymphoblastic and non-lymphoblastic leukemia. Clin Chim Acta; 2009 May;403(1-2):216-8
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  • [Title] Detection of myeloperoxidase activity in primary leukemic cells by an enhanced chemiluminescent assay for differentiation between acute lymphoblastic and non-lymphoblastic leukemia.
  • BACKGROUND: Myeloperoxidase (MPO) plays a crucial role in the differentiation of acute lymphoblastic leukemia (ALL) and acute non-lymphoblastic leukemia (ANLL).
  • In this report, we proposed the application of the enhanced chemiluminescent (ECL) technique to the determination of MPO activity in blasts of acute leukemia (AL).
  • METHODS: Bone-marrow samples were obtained from 23 patients with AL (ALL, 5 cases; ANLL, 13 cases; AUL, 1 cases; mixed-lineage AL, 4 cases).
  • In addition, this technique was able to demonstrate MPO activity in 4 mixed-lineage AL cases which did not stain for MPO in cytochemistry preparations.
  • [MeSH-major] Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Luminescent Measurements / methods. Peroxidase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Diagnosis, Differential. Female. HL-60 Cells. Humans. Infant. Male. Middle Aged


10. Wöhrer S, Rabitsch W, Shehata M, Kondo R, Esterbauer H, Streubel B, Sillaber C, Raderer M, Jaeger U, Zielinski C, Valent P: Mesenchymal stem cells in patients with chronic myelogenous leukaemia or bi-phenotypic Ph+ acute leukaemia are not related to the leukaemic clone. Anticancer Res; 2007 Nov-Dec;27(6B):3837-41
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  • [Title] Mesenchymal stem cells in patients with chronic myelogenous leukaemia or bi-phenotypic Ph+ acute leukaemia are not related to the leukaemic clone.
  • BACKGROUND: Human mesenchymal stem cells (MSCs) are thought to be multipotent cells which primarily reside in the bone marrow.
  • Besides their well-known ability to replicate as undifferentiated cells and to differentiate into diverse lineages of mesenchymal tissues, they were recently suggested to also give rise to haematopoietic and leukaemic/cancer stem cells.
  • In this study, the relationship between MSCs and leukemic stem cells in patients with either chronic myelogenous leukaemia (CML) or the more primitive variant, Ph+ bi-phenotypic leukaemia was investigated.
  • PATIENTS AND METHODS: Cultured MSCs from 5 patients with CML and 3 patients with bi-phenotypic Ph+ leukaemia, all of them positive for BCP-ABL, were analysed with conventional cytogenetics, fluorescence in situ hybridisation (FISH) and polymerase chain reaction (PCR) for the presence of t(9;22) and BCR-ABL.
  • CONCLUSION: MSCs in patients with CML or Ph+ bi-phenotypic leukaemia are not related to the malignant cell clone.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Mesenchymal Stromal Cells / pathology
  • [MeSH-minor] Cell Growth Processes / physiology. Chromosome Aberrations. Fusion Proteins, bcr-abl / genetics. Humans. In Situ Hybridization, Fluorescence. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18225540.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / abl-bcr fusion protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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11. Panagopoulos I, Kerndrup G, Carlsen N, Strömbeck B, Isaksson M, Johansson B: Fusion of NUP98 and the SET binding protein 1 (SETBP1) gene in a paediatric acute T cell lymphoblastic leukaemia with t(11;18)(p15;q12). Br J Haematol; 2007 Jan;136(2):294-6
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  • [Title] Fusion of NUP98 and the SET binding protein 1 (SETBP1) gene in a paediatric acute T cell lymphoblastic leukaemia with t(11;18)(p15;q12).
  • Three NUP98 chimaeras have previously been reported in T cell acute lymphoblastic leukaemia (T-ALL): NUP98/ADD3, NUP98/CCDC28A, and NUP98/RAP1GDS1.
  • Nested polymerase chain reaction did not amplify the reciprocal SETBP1/NUP98, suggesting that NUP98/SETBP1 transcript is pathogenetically important.
  • SETBP1 has previously not been implicated in leukaemias; however, it encodes a protein that specifically interacts with SET, fused to NUP214 in a case of acute undifferentiated leukaemia.
  • [MeSH-major] Carrier Proteins / genetics. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 18. Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 17233820.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / SETBP1 protein, human; 0 / nuclear pore complex protein 98
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12. Eiter LC, Hall NW, Day CS, Saluta G, Kucera GL, Bierbach U: Gold(I) analogues of a platinum-acridine antitumor agent are only moderately cytotoxic but show potent activity against Mycobacterium tuberculosis. J Med Chem; 2009 Nov 12;52(21):6519-22
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  • Cationic gold(I) complexes containing 1-[2-(acridin-9-ylamino)ethyl]-1,3-dimethylthiourea (1), [AuL(1)](n+) (where L is Cl(-), Br(-), SCN(-), PEt(3), PPh(3), or 1), derived from a class of analogous platinum(II) antitumor agents, have been synthesized.
  • Unlike platinum, gold does not form permanent adducts with DNA, and its complexes are 2 orders of magnitude less cytotoxic in non-small-cell lung cancer cells than the most active platinum-based agent.

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  • (PMID = 19803526.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101880-06; United States / NCI NIH HHS / CA / R01 CA101880; United States / NCI NIH HHS / CA / CA101880; United States / NCI NIH HHS / CA / R01 CA101880-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-(2-(acridin-9-ylamino)ethyl)-1,3-dimethylthiourea; 0 / Acridines; 0 / Antineoplastic Agents; 0 / Antitubercular Agents; 0 / Chelating Agents; 0 / Coordination Complexes; 0 / DNA Adducts; 0 / DNA, Bacterial; 0 / Ligands; 0 / Organogold Compounds; 49DFR088MY / Platinum; 7440-57-5 / Gold; 8W8T17847W / Urea; GYV9AM2QAG / Thiourea
  • [Other-IDs] NLM/ NIHMS150910; NLM/ PMC3176588
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13. Attar EC, De Angelo DJ, Supko JG, D'Amato F, Zahrieh D, Sirulnik A, Wadleigh M, Ballen KK, McAfee S, Miller KB, Levine J, Galinsky I, Trehu EG, Schenkein D, Neuberg D, Stone RM, Amrein PC: Phase I and pharmacokinetic study of bortezomib in combination with idarubicin and cytarabine in patients with acute myelogenous leukemia. Clin Cancer Res; 2008 Mar 1;14(5):1446-54
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  • [Title] Phase I and pharmacokinetic study of bortezomib in combination with idarubicin and cytarabine in patients with acute myelogenous leukemia.
  • PURPOSE: Proteasome inhibition results in cytotoxicity to the leukemia stem cell in vitro.
  • We conducted this phase I study to determine if the proteasome inhibitor bortezomib could be safely added to induction chemotherapy in patients with acute myelogenous leukemia (AML).
  • Pharmacokinetic studies revealed that the total body clearance of bortezomib decreased significantly (P < 0.01, N = 26) between the first (mean +/- SD, 41.9 +/- 17.1 L/h/m(2)) and third (18.4 +/- 7.0 L/h/m(2)) doses.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Leukemia, Myeloid, Acute / metabolism

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  • (PMID = 18316568.001).
  • [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 States / NCI NIH HHS / CA / P01 CA066996
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Boronic Acids; 0 / Pyrazines; 04079A1RDZ / Cytarabine; 69G8BD63PP / Bortezomib; ZRP63D75JW / Idarubicin
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14. Benitez D, Tkatchouk E, Gonzalez AZ, Goddard WA 3rd, Toste FD: On the impact of steric and electronic properties of ligands on gold(I)-catalyzed cycloaddition reactions. Org Lett; 2009 Nov 5;11(21):4798-801
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  • Both steric and electronic properties of the AuL(+) catalyst affect the electronic structure of the intermediate gold-stabilized carbene and its subsequent reactivity.

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  • (PMID = 19780543.001).
  • [ISSN] 1523-7052
  • [Journal-full-title] Organic letters
  • [ISO-abbreviation] Org. Lett.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM073932-04S1; United States / NIGMS NIH HHS / GM / R01 GM073932; United States / NIGMS NIH HHS / GM / R01 GM073932-04S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkadienes; 0 / Organogold Compounds; 4AV0LZ8QKB / propadiene; 7440-57-5 / Gold
  • [Other-IDs] NLM/ NIHMS149287; NLM/ PMC2783583
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15. Ran D, Taubert I, Schubert M, Eckstein V, Bellos F, Ho AD: Leukemia stem cell candidates in acute myeloid leukemia predict refractoriness to conventional chemotherapy and adverse clinical outcome. J Stem Cells Regen Med; 2010;6(2):135-6
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  • [Title] Leukemia stem cell candidates in acute myeloid leukemia predict refractoriness to conventional chemotherapy and adverse clinical outcome.

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  • (PMID = 24693144.001).
  • [ISSN] 0973-7154
  • [Journal-full-title] Journal of stem cells & regenerative medicine
  • [ISO-abbreviation] J Stem Cells Regen Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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16. Hochman E, Kinston S, Harmelin A, Göttgens B, Izraeli S: The SCL 3' enhancer responds to Hedgehog signaling during hemangioblast specification. Exp Hematol; 2006 Dec;34(12):1643-50
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  • Stem cell leukemia (SCL), a basic helix-loop-helix (bHLH) transcription factor, is essential for the specification and function of the hemangioblast.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Enhancer Elements, Genetic / genetics. Hedgehog Proteins / physiology. Hematopoiesis / physiology. Hematopoietic Stem Cells / metabolism. Proto-Oncogene Proteins / genetics. Signal Transduction / physiology
  • [MeSH-minor] Animals. Binding Sites. Cells, Cultured. Embryonic Stem Cells / metabolism. Humans. Kruppel-Like Transcription Factors / metabolism. Mice. Mice, Transgenic. Zinc Finger Protein GLI1

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  • (PMID = 17157160.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0800784
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Gli protein, mouse; 0 / Hedgehog Proteins; 0 / Kruppel-Like Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 0 / Zinc Finger Protein GLI1
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17. Ichijo T, Chrousos GP, Kino T: Activated glucocorticoid receptor interacts with the INHAT component Set/TAF-Ibeta and releases it from a glucocorticoid-responsive gene promoter, relieving repression: implications for the pathogenesis of glucocorticoid resistance in acute undifferentiated leukemia with Set-Can translocation. Mol Cell Endocrinol; 2008 Feb 13;283(1-2):19-31
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  • [Title] Activated glucocorticoid receptor interacts with the INHAT component Set/TAF-Ibeta and releases it from a glucocorticoid-responsive gene promoter, relieving repression: implications for the pathogenesis of glucocorticoid resistance in acute undifferentiated leukemia with Set-Can translocation.
  • Set/template-activating factor (TAF)-Ibeta, part of the Set-Can oncogene product found in acute undifferentiated leukemia, is a component of the inhibitor of acetyltransferases (INHAT) complex.
  • Set-Can fusion protein, on the other hand, did not interact with GR, was constitutively co-precipitated with GREs and suppressed GRIP1-induced enhancement of GR transcriptional activity and histone acetylation.
  • Thus, Set/TAF-Ibeta acts as a ligand-activated GR-responsive transcriptional repressor, while Set-Can does not retain physiologic responsiveness to ligand-bound GR, possibly contributing to the poor responsiveness of Set-Can-harboring leukemic cells to glucocorticoids.
  • [MeSH-major] Chromosomal Proteins, Non-Histone / metabolism. Glucocorticoids / pharmacology. Leukemia / pathology. Oncogene Proteins, Fusion / metabolism. Promoter Regions, Genetic / genetics. Receptors, Glucocorticoid / metabolism. Transcription Factors / metabolism. Translocation, Genetic

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  • (PMID = 18096310.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD008732-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Glucocorticoids; 0 / Histone Chaperones; 0 / Ligands; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Phosphoproteins; 0 / Receptors, Glucocorticoid; 0 / Repressor Proteins; 0 / SET protein, human; 0 / SET-CAN fusion protein, human; 0 / Transcription Factors; EC 2.3.1.48 / Histone Acetyltransferases
  • [Other-IDs] NLM/ NIHMS42142; NLM/ PMC2350211
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18. Chauhan S, Telhan A, Agarwal V, Varma N: Acute undifferentiated leukaemia in adult presenting as arthritis. Singapore Med J; 2006 Nov;47(11):1004-5
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  • [Title] Acute undifferentiated leukaemia in adult presenting as arthritis.
  • [MeSH-major] Arthritis / etiology. Leukemia / complications. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Diagnosis, Differential. Humans. Male

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  • (PMID = 17075674.001).
  • [ISSN] 0037-5675
  • [Journal-full-title] Singapore medical journal
  • [ISO-abbreviation] Singapore Med J
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Singapore
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19. Unger C, Kärner E, Treschow A, Stellan B, Felldin U, Concha H, Wendel M, Hovatta O, Aints A, Ahrlund-Richter L, Dilber MS: Lentiviral-mediated HoxB4 expression in human embryonic stem cells initiates early hematopoiesis in a dose-dependent manner but does not promote myeloid differentiation. Stem Cells; 2008 Oct;26(10):2455-66
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  • [Title] Lentiviral-mediated HoxB4 expression in human embryonic stem cells initiates early hematopoiesis in a dose-dependent manner but does not promote myeloid differentiation.
  • The variation of HoxB4 expression levels might be a key regulatory mechanism in the differentiation of human embryonic stem cell (hESC)-derived hematopoietic stem cells (HSCs).
  • High levels of HoxB4 expression correlated to an improved yield of cells expressing CD34, CD38, the stem cell leukemia gene, and vascular epithelium-cadherin.
  • However, no improvement in myeloid cell maturation was observed, as determined by colony formation assays.
  • In contrast, hESCs with low HoxB4 levels did not show any elevated hematopoietic development.
  • These data suggest that HoxB4-induced effects on hESC-derived HSCs are concentration-dependent during in vitro development and reduce proliferation of other cell types in vitro and in vivo.
  • [MeSH-major] Cell Differentiation. Embryonic Stem Cells / cytology. Embryonic Stem Cells / metabolism. Hematopoiesis / genetics. Homeodomain Proteins / genetics. Lentivirus / genetics. Myeloid Cells / cytology. Transcription Factors / genetics
  • [MeSH-minor] Animals. Biomarkers / metabolism. Cell Proliferation. Colony-Forming Units Assay. Gene Expression Regulation, Developmental. Genetic Vectors / genetics. Green Fluorescent Proteins / metabolism. HeLa Cells. Humans. Male. Mice. Mice, SCID. Octamer Transcription Factor-3 / metabolism. Teratoma / pathology. Transduction, Genetic

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  • (PMID = 18617691.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / Transcription Factors; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins
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20. Kong KY, Williamson EA, Rogers JH, Tran T, Hromas R, Dahl R: Expression of Scl in mesoderm rescues hematopoiesis in the absence of Oct-4. Blood; 2009 Jul 2;114(1):60-3
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  • In embryonic stem cells, Oct-4 concentration is critical in determining the development of endoderm, mesoderm, and trophectoderm.
  • However, hematopoiesis can be rescued in the absence of Oct-4 after mesoderm specification if the essential hematopoietic transcription factor stem cell leukemia is expressed.

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  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102283; United States / NHLBI NIH HHS / HL / R01 HL075783; United States / NCI NIH HHS / CA / CA102283; United States / NHLBI NIH HHS / HL / HL075783
  • [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 / Octamer Transcription Factor-3; 0 / Pou5f1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Recombinant Proteins; 0 / Tal1 protein, mouse
  • [Other-IDs] NLM/ PMC2710954
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21. Crespo O, Gimeno MC, Laguna A, Larraz C, Villacampa MD: Highly luminescent gold(I)-silver(I) and gold(I)-copper(I) chalcogenide clusters. Chemistry; 2007;13(1):235-46
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  • The reactions of [AuClL] with Ag(2)O, where L represents the heterofunctional ligands PPh(2)py and PPh(2)CH(2)CH(2)py, give the trigoldoxonium complexes [O(AuL)(3)]BF(4).
  • Treatment of these compounds with thio- or selenourea affords the triply bridging sulfide or selenide derivatives [E(AuL)(3)]BF(4) (E=S, Se).

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  • (PMID = 17009375.001).
  • [ISSN] 0947-6539
  • [Journal-full-title] Chemistry (Weinheim an der Bergstrasse, Germany)
  • [ISO-abbreviation] Chemistry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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22. Patterson LJ, Gering M, Patient R: Scl is required for dorsal aorta as well as blood formation in zebrafish embryos. Blood; 2005 May 01;105(9):3502-11
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  • The transcription factor, Scl/Tal1 (stem cell leukemia protein), is essential for hematopoiesis but thought to be required only for remodeling of endothelium in mouse embryos.
  • We conclude that scl is especially critical for the development of arteries where adult hematopoietic stem cells emerge, implicating scl in the formation of hemogenic endothelium.
  • [MeSH-minor] Animals. Basic Helix-Loop-Helix Transcription Factors. Blood Circulation / genetics. Embryo, Nonmammalian. Endothelium, Vascular / cytology. Endothelium, Vascular / embryology. Endothelium, Vascular / growth & development. Gene Expression Regulation, Developmental. Hematopoietic Stem Cells / cytology. Mice. Neovascularization, Physiologic. Zebrafish

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  • (PMID = 15644413.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137981013
  • [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 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish
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23. Zhang Y, Payne KJ, Zhu Y, Price MA, Parrish YK, Zielinska E, Barsky LW, Crooks GM: SCL expression at critical points in human hematopoietic lineage commitment. Stem Cells; 2005 Jun-Jul;23(6):852-60
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  • The stem cell leukemia (SCL or tal-1) gene was initially identified as a translocation partner in a leukemia that possessed both lymphoid and myeloid differentiation potential.
  • Mice that lacked SCL expression showed a complete block in hematopoiesis; thus, SCL was associated with hematopoietic stem cell (HSC) function.
  • Using recently defined surface immunophenotypes, we fluorescence-activated cell-sorted (FACS) highly purified populations of primary human hematopoietic progenitors for reverse transcription-polymerase chain reaction (RT-PCR) analysis of SCL expression.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / physiology. Hematopoietic Stem Cells / metabolism. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins / physiology. Transcription Factors / biosynthesis. Transcription Factors / physiology
  • [MeSH-minor] Animals. Antigens, CD34 / biosynthesis. Basic Helix-Loop-Helix Transcription Factors. Bone Marrow Cells / cytology. Cell Differentiation. Cell Line. Cell Lineage. Cell Separation. Cells, Cultured. Down-Regulation. Flow Cytometry. Humans. Immunophenotyping. Mice. Models, Biological. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / cytology. Thymus Gland / metabolism. Time Factors

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  • (PMID = 15917481.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK066163; United States / NCI NIH HHS / CA / P01CA59318; United States / NHLBI NIH HHS / HL / P50HL54850; United States / NHLBI NIH HHS / HL / R01HL77912
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
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24. Gill JA, Lowe L, Nguyen J, Liu PP, Blake T, Venkatesh B, Aplan PD: Enforced expression of Simian virus 40 large T-antigen leads to testicular germ cell tumors in zebrafish. Zebrafish; 2010 Dec;7(4):333-41
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  • [Title] Enforced expression of Simian virus 40 large T-antigen leads to testicular germ cell tumors in zebrafish.
  • Testicular germ cell tumors (TGCTs) are the most common malignancy in young men.
  • In addition, enforced expression of the zebrafish stem cell leukemia (scl) gene in the zebrafish testes also generated TGCTs in transgenic fish.
  • [MeSH-major] Antigens, Viral, Tumor / genetics. Disease Models, Animal. Neoplasms, Germ Cell and Embryonal / pathology. Testicular Neoplasms / pathology. Zebrafish

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  • (PMID = 21158563.001).
  • [ISSN] 1557-8542
  • [Journal-full-title] Zebrafish
  • [ISO-abbreviation] Zebrafish
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 SC010378-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor
  • [Other-IDs] NLM/ NIHMS248829; NLM/ PMC3057562
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25. Sahin F, Sercan Z, Ertan Y, Ocakci S, Ay E, Vural F, Yuksel E, Tombuloglu M, Saydam G: Rapid transformation of atypical myeloproliferative disorder with consistent t(8;13) to B-cell acute lymphoblastic leukemia: a case report. Hematology; 2007 Dec;12(6):489-92
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  • [Title] Rapid transformation of atypical myeloproliferative disorder with consistent t(8;13) to B-cell acute lymphoblastic leukemia: a case report.
  • 8p11 myeloproliferative syndrome (EMS; also known as the stem cell leukemia syndrome-SCLL) is a rare atypical myeloproliferative disorder associated with chromosomal abnormalities involving the 8p11 chromosomal band.
  • Disease phenotype associated with this translocation has some typical features such as poor prognosis, and transformation to mainly acute leukemia and non-Hodgkin lymphoma; commonly with a T-cell phenotype in which obtaining and maintenance of remission is difficult by conventional chemotherapy.
  • We hereby present a case diagnosed as atypical chronic myeloproliferative disease with consistent t(8;13)(p12;q12) and transformed rapidly to pre-B-cell acute lymphoblastic leukemia which is a rare clinical presentation.
  • [MeSH-major] Burkitt Lymphoma / etiology. Cell Transformation, Neoplastic. Myeloproliferative Disorders / pathology. Translocation, Genetic

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  • (PMID = 17852454.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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26. Zhang WJ, Park C, Arentson E, Choi K: Modulation of hematopoietic and endothelial cell differentiation from mouse embryonic stem cells by different culture conditions. Blood; 2005 Jan 1;105(1):111-4
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  • [Title] Modulation of hematopoietic and endothelial cell differentiation from mouse embryonic stem cells by different culture conditions.
  • Embryonic stem (ES) cells can differentiate into many different somatic cells in culture.
  • To better correlate hematopoietic and endothelial cell differentiation of ES cells in currently available protocols, we compared fetal liver kinase-1 (Flk-1)-, stem cell leukemia (Scl)-, and vascular endothelial-cadherin (VE-cadherin)-expressing cells generated in embryoid bodies (EBs) and on OP9 cells.
  • Cell sorting and replating studies showed that Scl+ cells, not Flk-1+ or VE-cadherin+ cells, were enriched for primitive and definitive hematopoietic progenitors.
  • Our studies indicate that optimal hematopoietic and endothelial cell differentiation occur in EBs and on OP9 cells, respectively.
  • [MeSH-major] Cell Culture Techniques / methods. Cell Differentiation. Embryo, Mammalian / cytology. Endothelial Cells / cytology. Hematopoiesis. Hematopoietic Stem Cells / cytology

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  • (PMID = 15231577.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL55337; United States / NHLBI NIH HHS / HL / R01 HL63736
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers; 0 / Cadherins; 0 / Culture Media; 0 / cadherin 5
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27. Jin JO, Park HY, Kim JW, Park JI, Hong YS, Min do S, Kwak JY: Phosphatidic acid induces the differentiation of human acute promyelocytic leukemic cells into dendritic cell-like. J Cell Biochem; 2007 Jan 1;100(1):191-203
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  • [Title] Phosphatidic acid induces the differentiation of human acute promyelocytic leukemic cells into dendritic cell-like.
  • We investigated whether phosphatidic acid (PA) can differentiate the promyelocytic leukemia (PML)-retinoic acid receptor alpha (RAR alpha)-expressing acute promyelocytic leukemic cell line, NB4, to dendritic cell (DC)-like cells.
  • Increased functional capacities were also found in PA-differentiated and TNF-alpha-activated NB4 cells with respect to changes in T-cell proliferation, cytokine production, endocytic activity, and cytolytic capacity against undifferentiated NB4 cells.
  • These results suggest that PA induces differentiation of NB4 cells into DC-like cells and that the upregulation of antigen presenting cell markers is mediated by the activation of ERK and the downregulation of PML-RAR alpha levels.
  • [MeSH-major] Cell Differentiation / physiology. Dendritic Cells / pathology. Leukemia, Promyelocytic, Acute / pathology. Phosphatidic Acids / physiology

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  • [Copyright] 2006 Wiley-Liss, Inc.
  • (PMID = 16924673.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Biomarkers; 0 / Cytokines; 0 / Flavonoids; 0 / Oncogene Proteins, Fusion; 0 / Phosphatidic Acids; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 102731-57-7 / dioctanoylphosphatidic acid; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.4.4 / Phospholipase D
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28. Gluzman DF, Nadgornaya VA, Sklyarenko LM, Ivanovskaya TS, Poludnenko LY, Ukrainskaya NI: Immunocytochemical markers in acute leukaemias diagnosis. Exp Oncol; 2010 Sep;32(3):195-9
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  • [Title] Immunocytochemical markers in acute leukaemias diagnosis.
  • The study included 1742 patients with acute myeloblastic leukaemias (AML) and acute lymphoblastic leukaemias (ALL), Kyiv city residents and patients from 20 regions of Ukraine.
  • Bone marrow and blood smears were sent at diagnosis to Reference Center.
  • Different types of AML were defined by the expression of the cell surface and cytoplasmic antigens.
  • Immunocytochemical study was required especially in diagnosing of AML with minimal differentiation, acute megakaryoblastic leukaemia, acute erythroid leukaemia and acute leukaemias of ambiguous lineage.
  • Acute lymphoblastic leukaemias was broadly classified into B-lineage and T-lineage ALL.
  • Immunocytochemical examination was required to diagnose AL of ambiguous lineage with no clear evidence of lineage differentiation (acute undifferentiated leukaemia) or those with blasts that express markers of more than one lineage (mixed phenotype acute leukaemias).
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / immunology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocyte Subsets / immunology. Lymphocyte Subsets / pathology

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  • (PMID = 21403617.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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29. Rossi S, Canal F, Licci S, Zanatta L, Laurino L, Gottardi M, Gherlinzoni F, Dei Tos AP: Cytogenetic evidence of metastatic myxoid liposarcoma and therapy-related myelodysplastic syndrome in a bone marrow biopsy. Hum Pathol; 2009 Jul;40(7):1040-4
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  • Microscopic examination of the bone marrow biopsy revealed dysplastic features, with abnormal localization of immature precursors and micromegakaryocytes, and islands of undifferentiated oval small/medium-size cells, suggestive of acute myeloid leukemia arising in the setting of a myelodysplastic syndrome.
  • Immunohistochemistry was not discriminant.
  • Cytogenetic analyses of bone marrow aspirate disclosed the presence of 2 different rearrangements, subsequently confirmed by fluorescent in situ hybridization and was crucial in making the correct diagnosis.
  • [MeSH-minor] Adult. Anemia, Refractory / pathology. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Marrow Cells / pathology. Chromosomes, Human, Pair 11. Combined Modality Therapy / adverse effects. Female. Humans. Leukemia, Myeloid, Acute / pathology. Soft Tissue Neoplasms / pathology. Thigh / pathology


30. van Dalen EC, Raphaël MF, Caron HN, Kremer LC: Treatment including anthracyclines versus treatment not including anthracyclines for childhood cancer. Cochrane Database Syst Rev; 2009;(1):CD006647
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  • [Title] Treatment including anthracyclines versus treatment not including anthracyclines for childhood cancer.
  • OBJECTIVES: To compare antitumour efficacy of treatment including or not including anthracyclines in children with childhood cancer.
  • MAIN RESULTS: We identified RCTs for 5 types of tumour: acute lymphoblastic leukaemia (ALL) (n=3; 912 children), Wilms' tumour (n=1; 316 children), rhabdomyosarcoma/undifferentiated sarcoma (n=1; 413 children), Ewing's sarcoma (n=1; 94 children), and non-Hodgkin lymphoma (n=1; 284 children).
  • For both rhabdomyosarcoma/undifferentiated sarcoma and non-Hodgkin lymphoma no difference in antitumour efficacy between the treatment groups was identified.
  • No significant difference between both treatment groups was identified, but in all individual studies there was a suggestion of a lower rate of clinical cardiotoxicity in patients who did not receive anthracyclines.
  • However, it should be noted that "no evidence of effect", as identified in this review, is not the same as "evidence of no effect".
  • For Wilms' tumour, rhabdomyosarcoma/undifferentiated sarcoma, Ewing's sarcoma, and non-Hodgkin lymphoma only 1 RCT was available and therefore, no definitive conclusions can be made about the antitumour efficacy of treatment with or without anthracyclines in these tumours.
  • [MeSH-minor] Bone Neoplasms / drug therapy. Child. Heart Diseases / chemically induced. Humans. Kidney Neoplasms / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Randomized Controlled Trials as Topic. Sarcoma / drug therapy. Wilms Tumor / drug therapy

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  • [UpdateIn] Cochrane Database Syst Rev. 2011;(1):CD006647 [21249679.001]
  • (PMID = 19160293.001).
  • [ISSN] 1469-493X
  • [Journal-full-title] The Cochrane database of systematic reviews
  • [ISO-abbreviation] Cochrane Database Syst Rev
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic
  • [Number-of-references] 172
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31. Terme JM, Wencker M, Favre-Bonvin A, Bex F, Gazzolo L, Duc Dodon M, Jalinot P: Cross talk between expression of the human T-cell leukemia virus type 1 Tax transactivator and the oncogenic bHLH transcription factor TAL1. J Virol; 2008 Aug;82(16):7913-22
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  • [Title] Cross talk between expression of the human T-cell leukemia virus type 1 Tax transactivator and the oncogenic bHLH transcription factor TAL1.
  • The human T-cell leukemia virus type 1 (HTLV-1) Tax transactivator is known to induce or repress various cellular genes, several of them encoding transcription factors.
  • As Tax is known to deregulate various basic bHLH factors, we looked more specifically at its effect on TAL1 (T-cell acute lymphoblastic leukemia 1), also known as SCL (stem cell leukemia).
  • Indeed, TAL1 is deregulated in a high percentage of T-cell acute lymphoblastic leukemia cells, and its oncogenic properties are well-established.
  • These data show the existence of a positive feedback loop between Tax and TAL1 expression and support the notion that this proto-oncogene participates in generation of adult T-cell leukemia/lymphoma by increasing the amount of the Tax oncoprotein but also possibly by its own transforming activities.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Leukemia-Lymphoma, Adult T-Cell / virology. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Binding Sites. Cell Line. Feedback, Physiological. HeLa Cells. Humans. Models, Biological. NF-kappa B / metabolism. Promoter Regions, Genetic. Thymus Gland / cytology

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  • (PMID = 18495761.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 0 / tax protein, Human T-lymphotrophic virus 1; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC2519563
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32. Xu Y, Leung CG, Lee DC, Kennedy BK, Crispino JD: MTB, the murine homolog of condensin II subunit CAP-G2, represses transcription and promotes erythroid cell differentiation. Leukemia; 2006 Jul;20(7):1261-9
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  • [Title] MTB, the murine homolog of condensin II subunit CAP-G2, represses transcription and promotes erythroid cell differentiation.
  • In this report, we show that MTB (more than blood), which was initially isolated in a yeast two-hybrid screen for proteins that interact with the basic helix-loop-helix (bHLH) protein stem cell leukemia (SCL), and later identified as the murine homolog of the condensin II subunit CAP-G2, participates in erythroid cell development.
  • Consistent with the model that MTB may function together with SCL/E12 heterodimer during erythroid cell development, MTB is highly expressed in the erythroid lineage and is upregulated upon erythroid differentiation.
  • Moreover, overexpression of MTB promotes the terminal differentiation of the murine erythroleukemia erythroid cell line.

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  • (PMID = 16673016.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK061464-05; United States / NIDDK NIH HHS / DK / R01 DK061464; United States / NIDDK NIH HHS / DK / R01 DK-61464; United States / NIDDK NIH HHS / DK / R01 DK061464-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Luzp5 protein, mouse; 0 / Multiprotein Complexes; 0 / Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / TCF Transcription Factors; 0 / Tal1 protein, mouse; 0 / Tcf7l1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; 0 / condensin complexes; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.6.1.- / Adenosine Triphosphatases
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33. Park AH, Muntz HR, Smith ME, Afify Z, Pysher T, Pavia A: Pediatric invasive fungal rhinosinusitis in immunocompromised children with cancer. Otolaryngol Head Neck Surg; 2005 Sep;133(3):411-6
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  • METHODS: Retrospective chart review of 9 patients who developed invasive FS compared to 8 patients who did not develop invasive FS during the study period.
  • Nine patients were diagnosed with 10 episodes of FS; 1 patient developed FS with different organisms on 2 separate occasions separated by 6 months; 8 patients were not diagnosed with FS.
  • Eight patients had acute myelogenous leukemia (AML); 6 patients had acute lymphoblastic leukemia (ALL); 1 patient had Burkitt's lymphoma, 1 patient had undifferentiated leukemia; and 1 patient had biphenotypic acute leukemia.
  • All patients in the non-FS group normalized their ANCs; 2 of the 9 patients in the FS group did not normalize their ANC.

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  • (PMID = 16143192.001).
  • [ISSN] 0194-5998
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Buzzai M, Licht JD: New molecular concepts and targets in acute myeloid leukemia. Curr Opin Hematol; 2008 Mar;15(2):82-7
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  • [Title] New molecular concepts and targets in acute myeloid leukemia.
  • PURPOSE OF REVIEW: Most patients with acute myeloid leukemia treated with chemotherapy relapse.
  • It is increasingly recognized that the cause of chemoresistance and relapse resides within the leukemia stem cell population.
  • Successful eradication of leukemia stem cells would require a comprehensive profile of both the acquired molecular lesions and intrinsic features of leukemia stem cells.
  • This review describes recent work identifying molecular markers that may lead to development of novel therapeutics, ultimately aiming to eradicate leukemia stem cells in acute myeloid leukemia.
  • RECENT FINDINGS: In recent years, novel specific cell surface antigens have allowed identification of leukemia stem cells and permitted their distinction from normal hematopoietic stem cells.
  • Novel concepts of leukemia stem cells and niche interaction have elucidated the mechanisms that control leukemia stem cell survival and chemoresistance.
  • Recent detection of genetic aberrations affecting regulators of HOX gene expression and chromatin modifying enzymes, such as CDX2 and hDOT1L, respectively, elucidates new key players in stem cell self-renewal and leukemic transformation.
  • SUMMARY: The discovery of novel markers and survival pathways for leukemia stem cells has increased our potential to specifically target and eliminate the leukemic stem cell compartment, which is likely to improve clinical outcomes in acute myeloid leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Hematopoietic Stem Cells / drug effects. Leukemia, Myeloid, Acute

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  • (PMID = 18300752.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA59936
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoconjugates; 0 / NCR2 protein, human; 0 / Natural Cytotoxicity Triggering Receptor 2; 0 / Receptors, Immunologic; 0 / Receptors, Interleukin-3
  • [Number-of-references] 51
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35. Ren M, Li X, Cowell JK: Genetic fingerprinting of the development and progression of T-cell lymphoma in a murine model of atypical myeloproliferative disorder initiated by the ZNF198-fibroblast growth factor receptor-1 chimeric tyrosine kinase. Blood; 2009 Aug 20;114(8):1576-84
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  • [Title] Genetic fingerprinting of the development and progression of T-cell lymphoma in a murine model of atypical myeloproliferative disorder initiated by the ZNF198-fibroblast growth factor receptor-1 chimeric tyrosine kinase.
  • A mouse model of human ZNF198-fibroblast growth factor receptor-1 (FGFR1) stem cell leukemia lymphoma has been developed to investigate mechanisms of oncogenesis and progression.
  • Using array-based comparative genomic hybridization, we followed disease progression after serial transplantation of ZNF198-FGFR1-transformed stem cells that give rise to a distinct myeloproliferative disorder and T-lymphoblastic leukemia.
  • A consistent, frequently homozygous, chr14:53880459-55011545 deletion, containing the T-cell receptor alpha and delta genes, was identified in the bone marrow, spleen, and lymph nodes in all cases.
  • The absence of cell-surface T-cell receptor alpha in tumor cells precludes CD3 recruitment, resulting in loss of a functional T-cell receptor complex, supporting the idea that prevention of maturation of CD4(+)/CD8(+) double-positive immature T cells is important in ZNF198-FGFR1 disease development.
  • Up-regulation of the B-cell line 2, interleukin 7 receptor alpha and interleuking 2 receptor alpha prosurvival genes in these undifferentiated tumor precursor cells suggests one mechanism that allows them to escape apoptosis in the thymus.
  • Thus, we have defined an important event in the process of ZNF198-FGFR1-induced T-cell leukemia.

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  • (PMID = 19506298.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076167; United States / NCI NIH HHS / CA / CA076167
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / Zmym2 protein, mouse; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
  • [Other-IDs] NLM/ PMC2731638
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36. Abrams SL, Steelman LS, Shelton JG, Chappell W, Bäsecke J, Stivala F, Donia M, Nicoletti F, Libra M, Martelli AM, McCubrey JA: Enhancing therapeutic efficacy by targeting non-oncogene addicted cells with combinations of signal transduction inhibitors and chemotherapy. Cell Cycle; 2010 May;9(9):1839-46
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  • The effects of inhibition of the Raf/MEK/ERK and PI3K/Akt/mTOR signaling pathways and chemotherapeutic drugs on cell cycle progression and drug sensitivity were examined in cytokine-dependent FL5.12 hematopoietic cells.
  • We examined their effects, as these cells resemble normal hematopoietic precursor cells as they do not exhibit "oncogene-addicted" growth, while they do display "cytokine-addicted" proliferation as cytokine removal resulted in apoptosis in greater than 80% of the cells within 48 hrs.
  • When cytokine-dependent FL5.12 cells were cultured in the presence of IL-3, which stimulated multiple proliferation and anti-apoptotic cascades, MEK, PI3K and mTOR inhibitors transiently suppressed but did not totally inhibit cell cycle progression or induce apoptosis while chemotherapeutic drugs such as doxorubicin and paclitaxel were more effective in inducing cell cycle arrest and apoptosis.
  • Doxorubicin was more effective in inducing cell death than paclitaxel.
  • Cytokine-dependent cells which proliferate in vitro and are not "oncogene-addicted" may represent a pre-malignant stage, more refractory to treatment with targeted therapy.
  • It is important to develop methods to inhibit the growth of such cytokine-dependent cells as they may resemble the leukemia stem cell and other cancer initiating cells.

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  • (PMID = 20436269.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA098195; United States / NCI NIH HHS / CA / R01CA098195
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Butadienes; 0 / Chromones; 0 / Interleukin-3; 0 / Intracellular Signaling Peptides and Proteins; 0 / Morpholines; 0 / Nitriles; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; P88XT4IS4D / Paclitaxel; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC3781183
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37. Rasaiyaah J, Yong K, Katz DR, Kellam P, Chain BM: Dendritic cells and myeloid leukaemias: plasticity and commitment in cell differentiation. Br J Haematol; 2007 Aug;138(3):281-90
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  • [Title] Dendritic cells and myeloid leukaemias: plasticity and commitment in cell differentiation.
  • This review examines the relationship between the acute and chronic myeloid leukaemias and cells with DC properties.
  • DCs are non-dividing terminally differentiated cells, and ex vivo leukaemic cells or cell lines show little similarity to DCs.
  • However, many leukaemias differentiate further in response to defined stimuli, and retain a degree of lineage plasticity.
  • Recent data suggest that the most 'dendritic-like' cells can be derived from more undifferentiated myeloid leukaemias, such as the myelomonocytic Mutz-3 cell line.
  • [MeSH-major] Dendritic Cells / pathology. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Cell Differentiation. Cell Line, Tumor. Cell Lineage. Chronic Disease. Humans. Immunity, Innate. Immunotherapy, Adoptive

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  • (PMID = 17614817.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 66
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38. Elmaagacli AH, Koldehoff M, Zakrzewski JL, Steckel NK, Ottinger H, Beelen DW: Growth factor-independent 1B gene (GFI1B) is overexpressed in erythropoietic and megakaryocytic malignancies and increases their proliferation rate. Br J Haematol; 2007 Jan;136(2):212-9
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  • We evaluated the GFI1B expression in erythroleukaemia and megakaryocytic leukaemia, as well as in patients with other subtypes of acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL), chronic myeloid leukaemia (CML), myelodysplastic syndrome (MDS), severe aplastic anaemia (SAA), myelofibrosis with myeloid metaplasia (MMM) and in healthy volunteers.
  • GFI1B expression was increased at least threefold in patients with erythroleukaemia (P < 0.01 compared with controls) and megakaryocytic leukaemia (P < 0.05) as well as in their corresponding leukaemic cell lines HEL, K562, CMK and M-07e.
  • Patients with undifferentiated or monocytic AML, ALL, MMM, MDS and CML had no significantly altered GFI1B expression, whereas GFI1B expression was decreased 10-fold in patients with SAA (P < 0.0001 compared with controls).
  • Silencing GFI1B by transfection with small interfering RNA (siRNA) markedly reduced the proliferation rate in the leukaemic cell lines HEL, K562 and NB4 (P < 0.01).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia / metabolism. Proto-Oncogene Proteins / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Anemia, Aplastic / metabolism. Antigens, CD34 / immunology. Apoptosis. Case-Control Studies. Cell Cycle. Cell Line, Tumor. Gene Expression. Genes, myc. Humans. Immunophenotyping. Leukemia, Erythroblastic, Acute / metabolism. Leukemia, Megakaryoblastic, Acute / metabolism. RNA Interference. RNA, Messenger / analysis. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Transfection / methods. rho GTP-Binding Proteins / genetics

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  • (PMID = 17156408.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / GFI1B protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Repressor Proteins; EC 3.6.5.2 / rho GTP-Binding Proteins
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39. Ferry JA: Burkitt's lymphoma: clinicopathologic features and differential diagnosis. Oncologist; 2006 Apr;11(4):375-83
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  • [Title] Burkitt's lymphoma: clinicopathologic features and differential diagnosis.
  • Since its initial designation as Burkitt's lymphoma, this type of lymphoma and lymphomas closely resembling it have received a variety of names in different classifications of lymphomas and leukemias: undifferentiated lymphoma, Burkitt's and non-Burkitt's type in the modified Rappaport Classification, malignant lymphoma, small non-cleaved cell, Burkitt's type in the Working Formulation, Burkitt's lymphoma and high-grade B-cell lymphoma, Burkitt-like in the REAL Classification, and acute lymphoblastic leukemia, L3 type in the FAB Classification.
  • The differential diagnosis of Burkitt's lymphoma is broad, and precise diagnosis based on histologic, immunophenotypic, and genetic features remains the critical first step in planning appropriate therapy.
  • [MeSH-minor] Diagnosis, Differential. Humans. Neoplasm Staging


40. Abrahamsson AE, Geron I, Gotlib J, Dao KH, Barroga CF, Newton IG, Giles FJ, Durocher J, Creusot RS, Karimi M, Jones C, Zehnder JL, Keating A, Negrin RS, Weissman IL, Jamieson CH: Glycogen synthase kinase 3beta missplicing contributes to leukemia stem cell generation. Proc Natl Acad Sci U S A; 2009 Mar 10;106(10):3925-9
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  • [Title] Glycogen synthase kinase 3beta missplicing contributes to leukemia stem cell generation.
  • Recent evidence suggests that a rare population of self-renewing cancer stem cells (CSC) is responsible for cancer progression and therapeutic resistance.
  • Chronic myeloid leukemia (CML) represents an important paradigm for understanding the genetic and epigenetic events involved in CSC production.
  • CML progresses from a chronic phase (CP) in hematopoietic stem cells (HSC) that harbor the BCR-ABL translocation, to blast crisis (BC), characterized by aberrant activation of beta-catenin within granulocyte-macrophage progenitors (GMP).
  • Here we show that BC CML myeloid progenitors, in particular GMP, serially transplant leukemia in immunocompromised mice and thus are enriched for leukemia stem cells (LSC).
  • Notably, cDNA sequencing of Wnt/beta-catenin pathway regulatory genes, including adenomatous polyposis coli, GSK3beta, axin 1, beta-catenin, lymphoid enhancer factor-1, cyclin D1, and c-myc, revealed a novel in-frame splice deletion of the GSK3beta kinase domain in the GMP of BC samples that was not detectable by sequencing in blasts or normal progenitors.

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  • (PMID = 19237556.001).
  • [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 / 2P01CA49605; United States / NCI NIH HHS / CA / R01 CA086017; United States / NCI NIH HHS / CA / CA86017; United States / NHLBI NIH HHS / HL / K23 HL004409; United States / NHLBI NIH HHS / HL / K23 HL04409; United States / NCI NIH HHS / CA / P01 CA049605; United States / NCI NIH HHS / CA / R01 CA086065; United States / NCI NIH HHS / CA / CA086065
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ PMC2646624
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41. Vaiselbuh SR, Edelman M, Lipton JM, Liu JM: Ectopic human mesenchymal stem cell-coated scaffolds in NOD/SCID mice: an in vivo model of the leukemia niche. Tissue Eng Part C Methods; 2010 Dec;16(6):1523-31
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  • [Title] Ectopic human mesenchymal stem cell-coated scaffolds in NOD/SCID mice: an in vivo model of the leukemia niche.
  • Human mesenchymal stem cells form the supportive structure in which the functional cells of a differentiated tissue reside.
  • We describe the creation of ectopic niches within polyurethane scaffolds coated with human mesenchymal stem cells.
  • When implanted subcutaneously in NOD/SCID mice, these niches supported engraftment of primary human acute myeloid leukemia cells.
  • The chemokine stromal-derived factor-1 (SDF-1 or CXCL12) and its receptor CXCR4 are critical for homing and migration of acute myeloid leukemia.
  • We believe that these scaffold niches provide a new and powerful tool to study the leukemia stem cell microenvironment and may be useful for identification of novel drug targets.
  • [MeSH-major] Choristoma / pathology. Leukemia / pathology. Mesenchymal Stromal Cells / cytology. Stem Cell Niche / pathology. Tissue Scaffolds
  • [MeSH-minor] Animals. Cells, Cultured. Coated Materials, Biocompatible / chemistry. Coated Materials, Biocompatible / pharmacology. Disease Models, Animal. Humans. Mesenchymal Stem Cell Transplantation. Mice. Mice, Inbred NOD. Mice, SCID. Neoplastic Stem Cells / cytology. Neoplastic Stem Cells / pathology. Transplantation, Heterologous. Tumor Microenvironment / physiology

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  • (PMID = 20586611.001).
  • [ISSN] 1937-3392
  • [Journal-full-title] Tissue engineering. Part C, Methods
  • [ISO-abbreviation] Tissue Eng Part C Methods
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coated Materials, Biocompatible
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42. Schlaeger TM, Mikkola HK, Gekas C, Helgadottir HB, Orkin SH: Tie2Cre-mediated gene ablation defines the stem-cell leukemia gene (SCL/tal1)-dependent window during hematopoietic stem-cell development. Blood; 2005 May 15;105(10):3871-4
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  • [Title] Tie2Cre-mediated gene ablation defines the stem-cell leukemia gene (SCL/tal1)-dependent window during hematopoietic stem-cell development.
  • The stem-cell leukemia gene (SCL/tal1) is essential for the formation of all blood lineages.
  • SCL is first expressed in mesodermal cells that give rise to embryonic blood cells, and continues to be expressed in fetal and adult hematopoietic stem cells (HSCs).
  • However, SCL is not required for the maintenance of established long-term repopulating (LTR) HSCs in the adult.
  • The time point at which HSC development becomes SCL independent has not been defined.
  • [MeSH-major] Cell Differentiation. DNA-Binding Proteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Integrases / metabolism. Proto-Oncogene Proteins / metabolism. Receptor, TIE-2 / metabolism. Transcription Factors / metabolism. Viral Proteins / metabolism


43. McCubrey JA, Steelman LS, Abrams SL, Bertrand FE, Ludwig DE, Bäsecke J, Libra M, Stivala F, Milella M, Tafuri A, Lunghi P, Bonati A, Martelli AM: Targeting survival cascades induced by activation of Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways for effective leukemia therapy. Leukemia; 2008 Apr;22(4):708-22
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  • [Title] Targeting survival cascades induced by activation of Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways for effective leukemia therapy.
  • The Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways are frequently activated in leukemia and other hematopoietic disorders by upstream mutations in cytokine receptors, aberrant chromosomal translocations as well as other genetic mechanisms.
  • Effective targeting of these pathways may result in suppression of cell growth and death of leukemic cells.
  • Furthermore it may be possible to combine various chemotherapeutic and antibody-based therapies with low molecular weight, cell membrane-permeable inhibitors which target the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to ultimately suppress the survival pathways, induce apoptosis and inhibit leukemic growth.
  • In this review, we summarize how suppression of these pathways may inhibit key survival networks important in leukemogenesis and leukemia therapy as well as the treatment of other hematopoietic disorders.
  • Targeting of these and additional cascades may also improve the therapy of chronic myelogenous leukemia, which are resistant to BCR-ABL inhibitors.
  • Furthermore, we discuss how targeting of the leukemia microenvironment and the leukemia stem cell are emerging fields and challenges in targeted therapies.
  • [MeSH-major] Apoptosis / drug effects. Drug Delivery Systems. Leukemia / drug therapy. Signal Transduction / drug effects


44. Beil M, Fleischer F, Paschke S, Schmidt V: Statistical analysis of the three-dimensional structure of centromeric heterochromatin in interphase nuclei. J Microsc; 2005 Jan;217(Pt 1):60-8
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  • In a previous study, we analysed the three-dimensional (3D) distribution patterns of centromere clusters (chromocentres) by confocal scanning laser microscopy and found that differentiation of the promyelocytic leukaemia cell line NB4 along the neutrophil lineage is associated with a progressive clustering of centromeres.
  • The pair correlation function revealed a higher frequency of chromocentre distances between 350 nm and 800 nm in undifferentiated NB4 cells as compared with differentiated cells.
  • In view of the observed decrease in the number of detectable chromocentres during differentiation, we hypothesize that these zones with a diameter of 350-800 nm in undifferentiated NB4 cells contract into zones with a diameter below 350 nm in differentiated cells.
  • [MeSH-major] Cell Differentiation / physiology. Centromere / ultrastructure. Data Interpretation, Statistical. Heterochromatin / ultrastructure. Image Processing, Computer-Assisted
  • [MeSH-minor] Cell Line, Tumor. Cell Nucleus / ultrastructure. Humans. Interphase / physiology. Leukemia, Promyelocytic, Acute / pathology. Microscopy, Confocal

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  • (PMID = 15655063.001).
  • [ISSN] 0022-2720
  • [Journal-full-title] Journal of microscopy
  • [ISO-abbreviation] J Microsc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Heterochromatin
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45. Zhang LZ, Ding X, Li XY, Cen JN, Chen ZX: [In vitro effects of anti-CD44 monoclonal antibody on the adhesion and migration of chronic myeloid leukemia stem cells]. Zhonghua Xue Ye Xue Za Zhi; 2010 Jun;31(6):398-402
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  • [Title] [In vitro effects of anti-CD44 monoclonal antibody on the adhesion and migration of chronic myeloid leukemia stem cells].
  • OBJECTIVE: To explore the effects of anti-CD44 monoclonal antibody-IM7 on the in vitro adhesion and migration of chronic myeloid leukemia stem cell (CML-LSC) and its mechanism.
  • METHODS: CD34(+)CD38(-)CD123(+) leukemic stem cells (LSC) from 20 newly-diagnosed chronic myeloid leukemia (CML) patients BM cells and CD34(+)CD38(-) hematopoietic stem cells (HSC) from 20 full-term newborn cord blood cells were isolated with EasySep(TM) magnet beads.
  • (1) After incubated with IM7, the LSC and HSC CD44 expression rates were (86.60 ± 2.10)% vs. (25.40 ± 1.70)% (P < 0.05), respectively. (2) The adhesive ability of the LSC to endothelial cells was decreased markedly after incubated with IM7, the OD value (A(570)) changing from pre-incubation of (0.62 ± 0.11) to post-incubation of (0.34 ± 0.07), while there was little change of A(570) in the HSC group. (3) The migration ability of the LSC group was inhibited evidently after incubated with IM7, the inhibition rate being 46% ∼ 63%, while little change of that in HSC group was detected. (4) The adhesive ability of the LSC group to marrow stromal cells was decreased markedly after incubated with IM7, while little change was found in that of HSC group.
  • [MeSH-major] Hematopoietic Stem Cells. Leukemia, Myelogenous, Chronic, BCR-ABL Positive


46. Ren X, Gomez GA, Zhang B, Lin S: Scl isoforms act downstream of etsrp to specify angioblasts and definitive hematopoietic stem cells. Blood; 2010 Jul 1;115(26):5338-46
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  • [Title] Scl isoforms act downstream of etsrp to specify angioblasts and definitive hematopoietic stem cells.
  • Recent lineage studies suggest that hematopoietic stem cells (HSCs) may be derived from endothelial cells.
  • We report here that zebrafish ets1-related protein (etsrp), which is essential for vascular endothelial development, also plays a critical role in the initiation of definitive hematopoiesis by controlling the expression of 2 stem cell leukemia (scl) isoforms (scl-alpha and scl-beta) in angioblasts.
  • Furthermore, both scl isoforms partially rescue runx1 but not ephrinb2a expression in embryos deficient in Vegf signaling.

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  • (PMID = 20185582.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK054508-13; United States / NHLBI NIH HHS / HL / F31 HL091713; United States / NIDDK NIH HHS / DK / R01 DK054508; United States / NIDDK NIH HHS / DK / Z01 DK054508; United States / NHLBI NIH HHS / HL / 5F31HL091713-02
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Etsrp protein, zebrafish; 0 / Protein Isoforms; 0 / Proto-Oncogene Protein c-fli-1; 0 / Proto-Oncogene Proteins; 0 / Zebrafish Proteins; 0 / runx1 protein, zebrafish; 0 / tal1 protein, zebrafish
  • [Other-IDs] NLM/ PMC2902133
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47. Dick JE: Complexity of the human acute myeloid leukemia stem cell compartment: implications for therapy. Biol Blood Marrow Transplant; 2005 Feb;11(2 Suppl 2):9-11
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  • [Title] Complexity of the human acute myeloid leukemia stem cell compartment: implications for therapy.
  • [MeSH-major] Leukemia, Myeloid / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Acute Disease. Cell Growth Processes. Humans

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  • (PMID = 15682167.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 19
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48. Schuringa JJ, Schepers H: Ex vivo assays to study self-renewal and long-term expansion of genetically modified primary human acute myeloid leukemia stem cells. Methods Mol Biol; 2009;538:287-300
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  • [Title] Ex vivo assays to study self-renewal and long-term expansion of genetically modified primary human acute myeloid leukemia stem cells.
  • With the emergence of the concept of the leukemia stem cell, assays to study them remain pivotal in understanding (leukemic) stem cell biology.
  • Although the in vivo NOD-SCID xenotransplantation model is still the favored model of choice in most cases, this system has some limitations as well, such as its cost-effectiveness, duration, and the lack of engraftability of cells from subsets of acute myeloid leukemia (AML) patients.
  • Here, we have described an ex vivo bone marrow stromal coculture system in which CD34(+) cells, but not CD34(-) cells, from the bone marrow or peripheral blood of AML patients can give rise to long-term cultures (LTC) that can be maintained for over 20 weeks.
  • Self-renewal within these L-CAs can be determined by sequential passaging of these L-CAs onto new MS5 stromal layers, which results in the generation of second, third, and fourth L-CAs that are able to sustain long-term expansion and generate high numbers of immature undifferentiated suspension cells.
  • Together, these tools should allow a further molecular elucidation of derailed signal transduction in AML stem cells.
  • [MeSH-major] Biological Assay / methods. Cell Culture Techniques / methods. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology. Transduction, Genetic / methods
  • [MeSH-minor] Animals. Antigens, CD34 / metabolism. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Line, Tumor. Cells, Cultured. Coculture Techniques. Humans. Lentivirus / genetics. Mice. Neoplasm Proteins. Stromal Cells / metabolism. Stromal Cells / pathology

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  • (PMID = 19277587.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Neoplasm Proteins
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49. Bockamp E, Antunes C, Maringer M, Heck R, Presser K, Beilke S, Ohngemach S, Alt R, Cross M, Sprengel R, Hartwig U, Kaina B, Schmitt S, Eshkind L: Tetracycline-controlled transgenic targeting from the SCL locus directs conditional expression to erythrocytes, megakaryocytes, granulocytes, and c-kit-expressing lineage-negative hematopoietic cells. Blood; 2006 Sep 1;108(5):1533-41
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  • The stem cell leukemia gene SCL, also known as TAL-1, encodes a basic helix-loop-helix transcription factor expressed in erythroid, myeloid, megakaryocytic, and hematopoietic stem cells.
  • Analysis of this mouse using different tetracycline-dependent reporter strains demonstrated that switchable transgene expression was restricted to erythrocytes, megakaryocytes, granulocytes, and, importantly, to the c-kit-expressing and lineage-negative cell fraction of the bone marrow.

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  • (PMID = 16675709.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA Primers; 0 / Proto-Oncogene Proteins; 0 / Recombinant Proteins; 0 / Tal1 protein, mouse; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; F8VB5M810T / Tetracycline
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50. Qadir M, Barcos M, Stewart CC, Sait SN, Ford LA, Baer MR: Routine immunophenotyping in acute leukemia: Role in lineage assignment and reassignment. Cytometry B Clin Cytom; 2006 Sep 15;70(5):329-34
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  • [Title] Routine immunophenotyping in acute leukemia: Role in lineage assignment and reassignment.
  • Diagnostic evaluation of acute leukemia at Roswell Park Cancer Institute has routinely included immunophenotyping by multiparameter flow cytometry.
  • In a retrospective analysis of 646 cases, morphology and cytochemistry established lineage in 612, but not in 34 (5%), of which 26, 5, and 3 were myeloid, undifferentiated, and lymphoid, respectively, based on immunophenotyping.
  • The data support routine inclusion of at least limited immunophenotyping in the diagnostic evaluation of acute leukemia.
  • [MeSH-major] Cell Lineage. Immunophenotyping. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • [Copyright] Copyright 2006 International Society for Analytical Cytology.
  • (PMID = 16739218.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056
  • [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 / Antigens, CD; 0 / Biomarkers, Tumor
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51. Wong P, Iwasaki M, Somervaille TC, So CW, Cleary ML: Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential. Genes Dev; 2007 Nov 1;21(21):2762-74
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  • [Title] Meis1 is an essential and rate-limiting regulator of MLL leukemia stem cell potential.
  • Oncogenic mutations of the MLL histone methyltransferase confer an unusual ability to transform non-self-renewing myeloid progenitors into leukemia stem cells (LSCs) by mechanisms that remain poorly defined.
  • Misregulation of Hox genes is likely to be critical for LSC induction and maintenance but alone it does not recapitulate the phenotype and biology of MLL leukemias, which are clinically heterogeneous--presumably reflecting differences in LSC biology and/or frequency.
  • TALE (three-amino-acid loop extension) class homeodomain proteins of the Pbx and Meis families are also misexpressed in this context, and we thus employed knockout, knockdown, and dominant-negative genetic techniques to investigate the requirements and contributions of these factors in MLL oncoprotein-induced acute myeloid leukemia.

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  • (PMID = 17942707.001).
  • [ISSN] 0890-9369
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / R37 CA042971; United States / NCI NIH HHS / CA / CA42971; United States / NCI NIH HHS / CA / CA55029
  • [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 / Neoplasm Proteins; 0 / Pbx2 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Tgif protein, mouse; 0 / myeloid ecotropic viral integration site 1 protein; 146150-81-4 / proto-oncogene protein Pbx3; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2045130
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52. Wong GC, Tan BH: Use of antibiotics in a haematology ward--an audit. Ann Acad Med Singapore; 2008 Jan;37(1):21-6
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  • Patients with acute myeloid leukaemia (AML) or acute lymphocytic leukaemia (ALL) who had febrile neutropenia after chemotherapy were reviewed.
  • Thirty-two had AML, 7 had ALL and 1 had undifferentiated leukaemia.
  • CONCLUSIONS: Given the complex nature of the cases, compliance was reasonable, as there were valid reasons in all cases where the guidelines were not adhered to.
  • [MeSH-minor] Adolescent. Adult. Aged. Drug Resistance, Microbial. Drug-Related Side Effects and Adverse Reactions. Female. Hospitals. Humans. Leukemia, Myeloid / drug therapy. Male. Medical Audit. Middle Aged. Neutropenia / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Retrospective Studies. Singapore

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  • (PMID = 18265893.001).
  • [ISSN] 0304-4602
  • [Journal-full-title] Annals of the Academy of Medicine, Singapore
  • [ISO-abbreviation] Ann. Acad. Med. Singap.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents
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53. Ribeiro-Silva A, Mendes CF, Costa IS, de Moura HB, Tiezzi DG, Andrade JM: Metastases to the breast from extramammary malignancies: a clinicopathologic study of 12 cases. Pol J Pathol; 2006;57(3):161-5
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  • Histological diagnoses of the primary tumor were as follows: non-Hodgkin diffuse large B-cell lymphoma (3 patients), acute mycloid leukemia (3 patients), serous papillary adenocarcinoma, well-differentiated adenocarcinoma, squamous cell carcinoma, undifferentiated neoplasm, mesothelioma, and melanoma.
  • The interval between diagnosis of primary cancer and the appearance of breast metastasis ranged from 0 to 108 months (mean: 17, median: 1).
  • In conclusion, metastasis can mimic either benign disease or primary malignancy and is often an unexpected diagnosis in a patient presenting with a breast mass.
  • Thus, an accurate diagnosis is important to avoid unnecessary mutilating surgery.

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  • (PMID = 17219743.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
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54. Chan WI, Huntly BJ: Leukemia stem cells in acute myeloid leukemia. Semin Oncol; 2008 Aug;35(4):326-35
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  • [Title] Leukemia stem cells in acute myeloid leukemia.
  • At the apex of these hierarchies sit so-called cancer stem cells or cancer-initiating cells, which are wholly responsible for the continued growth and propagation of the tumor.
  • The first such cancer stem cells were described in acute myeloid leukemia (AML).
  • Following treatment, the majority of tumors, including leukemias, initially respond.
  • A likely explanation for this is that leukemia stem cells are relatively insensitive to current therapies and that tumor bulk reduction reflects the death of leukemic blasts that lack tumor initiation potential.
  • This review will focus on what is known of the molecular and cellular biology of the leukemia stem cell and the leukemia stem cell niche in AML and then will identify molecular pathways critical for leukemia stem cells.
  • Finally, we will identify current and prospective therapeutic targets to facilitate eradication of leukemia stem cells.
  • It is hoped that, in defining the biology of cancer stem cells and how they differ from their adult tissue stem cell counterpart, we should identify therapeutic targets to improve treatment outcomes in leukemia and other malignant diseases.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Apoptosis. Cell Differentiation. Cell Lineage. Drug Delivery Systems. Humans. Signal Transduction

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  • (PMID = 18692683.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G116/187
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 64
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55. Curti A, Pandolfi S, Aluigi M, Isidori A, Alessandrini I, Chiodoni C, Testoni N, Colombo MP, Baccarani M, Lemoli RM: Interleukin-12 production by leukemia-derived dendritic cells counteracts the inhibitory effect of leukemic microenvironment on T cells. Exp Hematol; 2005 Dec;33(12):1521-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-12 production by leukemia-derived dendritic cells counteracts the inhibitory effect of leukemic microenvironment on T cells.
  • OBJECTIVE: Acute myeloid leukemia (AML) cells are poorly immunogenic and inhibit T-cell function.
  • AML-derived dendritic cells (AML-DCs) have better antigen-presentation capacity than undifferentiated leukemic blasts, but may not be fully competent to stimulate T cells previously inhibited by leukemic cells.
  • RESULTS: Mature AML-DCs stimulated naive and, to a lesser extent, leukemic cell (LC)-cultured T cells more efficiently than their immature counterparts and their activity was mediated by IL-12.
  • AML-DCs generated from CD14(-) AML samples (which represent 80% of total AML patients) were defective in IL-12 production and T-cell activation.
  • IL-12 gene-nucleofected AML-DCs derived from CD14(-) cells produced significant amounts of IL-12, maintained leukemia-specific karyotype, DC-like phenotype, and function.
  • CONCLUSION: IL-12 produced by AML-DCs plays a critical role in counteracting the inhibitory activity of LCs on T-cell function.
  • IL-12 gene can be successfully expressed into AML-DCs defective in endogenous IL-12 production by using a novel nonviral method that does not modify their phenotypical, cytogenetic, and functional features.
  • Genetically modified AML-DCs restore a near normal T-cell function.
  • [MeSH-major] Dendritic Cells / pathology. Interleukin-12 / genetics. Interleukin-12 / pharmacology. Leukemia, Myeloid / immunology. Lymphocyte Activation / immunology. T-Lymphocytes / drug effects

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  • (PMID = 16338495.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines; 0 / IL12A protein, human; 0 / Interleukin-12 Subunit p35; 0 / Interleukin-12 Subunit p40; 0 / Protein Subunits; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma
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56. Dass A, Stevenson A, Dubay GR, Tracy JB, Murray RW: Nanoparticle MALDI-TOF mass spectrometry without fragmentation: Au25(SCH2CH2Ph)18 and mixed monolayer Au25(SCH2CH2Ph)(18-x)(L)(x). J Am Chem Soc; 2008 May 7;130(18):5940-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • At increased laser pulse intensity, the first fragmentation step(s) for the Au25(SCH 2CH2Ph)18 nanoparticle results in losses of AuL units and, in particular, loss of Au4(SCH2CH2Ph)4.

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  • (PMID = 18393500.001).
  • [ISSN] 1520-5126
  • [Journal-full-title] Journal of the American Chemical Society
  • [ISO-abbreviation] J. Am. Chem. Soc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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57. Batlle M, Vall-Llovera F, Bechini J, Camps I, Marcos P, Vives S, Oriol A, Ribera JM: [Neutropenic enterocolitis in adult patients with acute leukemia or stem cell transplant recipients: study of 7 cases]. Med Clin (Barc); 2007 Nov 10;129(17):660-3
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  • [Title] [Neutropenic enterocolitis in adult patients with acute leukemia or stem cell transplant recipients: study of 7 cases].
  • [Transliterated title] Enterocolitis neutropénica en adultos con leucemia aguda o receptores de un trasplante de progenitores hematopoyéticos: estudio de 7 casos.
  • BACKGROUND AND OBJECTIVE: Neutropenic enterocolitis (NE) is a complication arising in neutropenic patients with acute leukemia or solid tumours while treated with intensive chemotherapy.
  • The optimal therapeutic procedures have not been well established.
  • Acute myeloblastic leukemia was the most frequent diagnosis (5 cases).
  • Two other patients had received an stem cell transplantation.
  • CONCLUSIONS: NE is a severe complication of patients with hematologic malignancies submitted to intensive chemotherapy or receiving stem cell transplantation.
  • [MeSH-major] Enterocolitis, Neutropenic / etiology. Leukemia, Myeloid, Acute / complications. Stem Cell Transplantation / adverse effects

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  • (PMID = 18005634.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents
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58. Park DM, Zhuang Z, Chen L, Szerlip N, Maric I, Li J, Sohn T, Kim SH, Lubensky IA, Vortmeyer AO, Rodgers GP, Oldfield EH, Lonser RR: von Hippel-Lindau disease-associated hemangioblastomas are derived from embryologic multipotent cells. PLoS Med; 2007 Feb;4(2):e60
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  • BACKGROUND: To determine the origin of the neoplastic cell in central nervous system (CNS) hemangioblastomas in von Hippel-Lindau disease (VHL) and its role in tumor formation and distribution, we characterized and differentiated neoplastic cells from hemangioblastomas removed from VHL patients.
  • Consistent with an embryologically derived hemangioblast, the neoplastic cells demonstrated coexpression of the mesodermal markers brachyury, Flk-1 (vascular endothelial growth factor-2), and stem cell leukemia (Scl).
  • The neoplastic cells also expressed hematopoietic stem cell antigens and receptors including CD133, CD34, c-kit, Scl, erythropoietin, and erythropoietin receptor.
  • CONCLUSIONS: The neoplastic cell of origin for CNS hemangioblastomas in VHL patients is the mesoderm-derived, embryologically arrested hemangioblast.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Hemangioblastoma / pathology. Multipotent Stem Cells / pathology. von Hippel-Lindau Disease / complications
  • [MeSH-minor] Adolescent. Adult. Antigens, CD13 / genetics. Blotting, Western. Cell Degranulation. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. RNA, Neoplasm / genetics. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured


59. Jamieson CH: Chronic myeloid leukemia stem cells. Hematology Am Soc Hematol Educ Program; 2008;:436-42
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  • [Title] Chronic myeloid leukemia stem cells.
  • Chronic myeloid leukemia (CML) is typified by robust marrow and extramedullary myeloid cell production.
  • However, regardless of greatly reduced mortality rates with BCR-ABL targeted therapy, most patients harbor quiescent CML stem cells that may be a reservoir for disease progression to blast crisis.
  • While the hematopoietic stem cell (HSC) origin of CML was first suggested over 30 years ago, only recently have the HSC and progenitor cell-specific effects of the molecular mutations that drive CML been investigated.
  • This has provided the impetus for investigating the genetic and epigenetic events governing HSC and progenitor cell resistance to therapy and their role in disease progression.
  • Accumulating evidence suggests that the acquired BCR-ABL mutation initiates chronic phase CML and results in aberrant stem cell differentiation and survival.
  • This eventually leads to the production of an expanded progenitor population that aberrantly acquires self-renewal capacity resulting in leukemia stem cell (LSC) generation and blast crisis transformation.


60. Wu KF, Ma XT, Zheng GG, Song YH: [Leukemia stem cells and their microenvironment--editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Dec;15(6):1139-41
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  • [Title] [Leukemia stem cells and their microenvironment--editorial].
  • As pioneer of tumor stem cell research, leukemia stem cell research has not only important theoretical significance, but also clinical application potential.
  • The survival and development of stem cells are directly impacted by their microenvironment.
  • The research on leukemia stem cells and their microenvironment are now becoming a hot topic.
  • The author presumes that stem cells are a population with heterogenecity and hierarchy; any single cell from the population is difficult to form a clone; the interaction between the leukemia stem cell and its microenvironment can be described by the concept of leukemia stem cell niche.
  • In this article, the leukemia cell population with heterogenecity and hierarchy as well as leukemia stem cell niche were summarized and discussed.

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  • (PMID = 18088452.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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61. Chao MP, Seita J, Weissman IL: Establishment of a normal hematopoietic and leukemia stem cell hierarchy. Cold Spring Harb Symp Quant Biol; 2008;73:439-49
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  • [Title] Establishment of a normal hematopoietic and leukemia stem cell hierarchy.
  • Many types of adult tissues, especially for high turnover tissues such as the blood and intestinal system, stand on a hierarchical tissue-specific stem cell system.
  • Tissue-specific stem cells concurrently have self-renewal capacity and potential to give rise to all types of mature cells in their tissue.
  • The differentiation process of the tissue-specific stem cell is successive restriction of these capacities.
  • The first progeny of tissue-specific stem cells are multipotent progenitors (MPPs) that lose long-term self-renewal capacity yet have full lineage potential.
  • In this chapter, we review our findings and other key experiments that have led to the establishment of the current cellular stem and progenitor hierarchy in the blood-forming systems of mice and humans for both normal and leukemic hematopoiesis.
  • We also review select signaling pathways intrinsic to normal hematopoietic and leukemic stem cell populations as well our recent findings elucidating the possible origin of the leukemia stem cell.
  • [MeSH-major] Hematopoiesis / physiology. Hematopoietic Stem Cells / cytology. Leukemia, Myeloid / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adult. Adult Stem Cells / cytology. Animals. Apoptosis. Cell Differentiation. Cell Movement. Cell Proliferation. Humans. Mice. Models, Biological. Multipotent Stem Cells / cytology. Species Specificity

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  • (PMID = 19022770.001).
  • [ISSN] 1943-4456
  • [Journal-full-title] Cold Spring Harbor symposia on quantitative biology
  • [ISO-abbreviation] Cold Spring Harb. Symp. Quant. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA86017
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 104
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62. Desouki MM, Post GR, Cherry D, Lazarchick J: PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms. Clin Med Res; 2010 Jul;8(2):84-8
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  • [Title] PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms.
  • OBJECTIVE: Undifferentiated tumors and hematolymphoid neoplasms can be diagnostically challenging due to potential overlap of morphologic features and variant antigen expression.
  • PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy.
  • The lack of PAX-5 expression in most CD30-positive non-hematopoietic malignancies (embryonal carcinoma and seminoma) and T-cell lymphomas, such as anaplastic large cell lymphoma (ALCL), suggests that the absence of PAX-5 may be used to confirm non-B-cell lineage.
  • RESULTS: Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5).
  • PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8).
  • Non-neoplastic bone marrow sections showed scattered nuclear staining in small B-cell lymphocytes/hematogones.
  • CONCLUSION: Overall, our results demonstrate that including PAX-5 in a panel with other immunomarkers helps establish B-cell lineage and increases diagnostic yield.
  • [MeSH-major] B-Cell-Specific Activator Protein / analysis. Biomarkers, Tumor / analysis. Lymphoma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Hodgkin Disease / diagnosis. Humans. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

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  • (PMID = 20660931.001).
  • [ISSN] 1554-6179
  • [Journal-full-title] Clinical medicine & research
  • [ISO-abbreviation] Clin Med Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ PMC2910102
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63. Ferrà C, Castellví J: [Cervical adenopathy in a patient with acute leukemia and stem cell transplantation]. Med Clin (Barc); 2005 Sep 3;125(7):270-7
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  • [Title] [Cervical adenopathy in a patient with acute leukemia and stem cell transplantation].
  • [Transliterated title] Adenopatías laterocervicales en un paciente con leucemia aguda y trasplante de progenitores hematopoyéticos.
  • [MeSH-major] Epstein-Barr Virus Infections / diagnosis. Hepatitis, Viral, Human / diagnosis. Hepatitis, Viral, Human / etiology. Herpes Simplex / diagnosis. Leukemia, Myeloid / therapy. Lymphoproliferative Disorders / diagnosis. Lymphoproliferative Disorders / etiology. Stem Cell Transplantation / adverse effects
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diagnosis, Differential. Herpesvirus 1, Human / isolation & purification. Herpesvirus 3, Human / isolation & purification. Herpesvirus 4, Human / isolation & purification. Humans. Lymphatic Metastasis / diagnosis. Male. Neck. Necrosis. Remission Induction

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  • (PMID = 16137489.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; Clinical Conference; Journal Article
  • [Publication-country] Spain
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64. Au WY, Wong KY, Leung RY, Tong AC: Isolated gingival relapse of acute lymphoblastic leukemia after transplantation. J Oral Pathol Med; 2008 Apr;37(4):249-51
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  • [Title] Isolated gingival relapse of acute lymphoblastic leukemia after transplantation.
  • A patient with a history of precursor B-cell leukemia presented with an isolated ulcerating gum lesion 8 years after allogeneic stem cell transplantation with severe graft versus host disease.
  • A biopsy revealed an undifferentiated malignant hemic lesion.
  • [MeSH-major] Gingival Neoplasms / pathology. Graft vs Leukemia Effect. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adult. Bone Marrow Neoplasms / surgery. Fatal Outcome. Female. Graft vs Host Disease / etiology. Hematopoiesis, Extramedullary. Humans. Recurrence. Stem Cell Transplantation / adverse effects

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  • (PMID = 18321346.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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65. Oh SH, Park TS, Cho SY, Kim MJ, Huh J, Kim B, Song SA, Lee JY, Jun KR, Shin JH, Kim HR, Lee JN: Acute myeloid leukemia associated with t(10;17)(p13-15;q12-21) and phagocytic activity by leukemic blasts: a clinical study and review of the literature. Cancer Genet Cytogenet; 2010 Oct 1;202(1):43-6
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  • [Title] Acute myeloid leukemia associated with t(10;17)(p13-15;q12-21) and phagocytic activity by leukemic blasts: a clinical study and review of the literature.
  • Translocation (10;17)(p13-15;q12-21) in acute leukemia is rarely reported in the literature.
  • Here, we present both a novel t(10;17) case study and a review of relevant literature on t(10;17) in acute leukemia (10 cases).
  • In summary, we came to the following preliminary conclusions: t(10;17) is associated with poorly differentiated acute leukemia subtype [90%; eight cases of acute myeloid leukemia (AML M0, M1) and one case of acute undifferentiated leukemia], phagocytic activity by blasts occurs (30%), and the survival time was short in three of the seven t(10;17) cases for whom follow-up data were available (median, 8 months).
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 17. Leukemia / drug therapy. Leukemia / genetics. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20804920.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 1.11.1.7 / Peroxidase; ZS7284E0ZP / Daunorubicin
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66. Delabesse E, Ogilvy S, Chapman MA, Piltz SG, Gottgens B, Green AR: Transcriptional regulation of the SCL locus: identification of an enhancer that targets the primitive erythroid lineage in vivo. Mol Cell Biol; 2005 Jun;25(12):5215-25
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  • The stem cell leukemia (SCL) gene, also known as TAL-1, encodes a basic helix-loop-helix protein that is essential for the formation of all hematopoietic lineages, including primitive erythropoiesis.
  • However, it is not known whether these SCL enhancers also regulate neighboring genes within the SCL locus, and the erythroid expression of SCL remains unexplained.
  • Here, we have quantitated transcripts from SCL and neighboring genes in multiple hematopoietic cell types.
  • A systematic survey of histone H3 and H4 acetylation throughout the SCL locus in different hematopoietic cell types identified several peaks of histone acetylation between SIL and MAP17, all of which corresponded to previously characterized SCL enhancers or to the MAP17 promoter.
  • Downstream of MAP17 (and 40 kb downstream of SCL exon 1a), an additional peak of acetylation was identified in hematopoietic cells and was found to correlate with expression of SCL but not other neighboring genes.
  • This +40 region is conserved in human-dog-mouse-rat sequence comparisons, functions as an erythroid cell-restricted enhancer in vitro, and directs beta-galactosidase expression to primitive, but not definitive, erythroblasts in transgenic mice.

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  • (PMID = 15923636.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [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 / Histones; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / PDZK1IP1 protein, human; 0 / Pdzk1ip1 protein, mouse; 0 / Pdzk1ip1 protein, rat; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC1140604
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67. Saito S, Nouno K, Shimizu R, Yamamoto M, Nagata K: Impairment of erythroid and megakaryocytic differentiation by a leukemia-associated and t(9;9)-derived fusion gene product, SET/TAF-Ibeta-CAN/Nup214. J Cell Physiol; 2008 Feb;214(2):322-33
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  • [Title] Impairment of erythroid and megakaryocytic differentiation by a leukemia-associated and t(9;9)-derived fusion gene product, SET/TAF-Ibeta-CAN/Nup214.
  • SET-CAN associated with the t(9;9) in acute undifferentiated leukemia encodes almost the entire sequence of SET and the C-terminal two-third portion of CAN, including the FG repeat region.
  • Characterization of the bone marrow cells of transgenic mice indicated impairment in hematopoietic differentiation of erythroid, megakaryocytic, and B cell lineages by SET-CAN.
  • Our results demonstrate that SET-CAN blocks the hematopoietic differentiation program--one of the characteristics of acute myeloid leukemia.
  • [MeSH-major] Erythroid Precursor Cells / physiology. Hematopoiesis / physiology. Leukemia / physiopathology. Megakaryocytes / physiology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Animals. Cell Differentiation. Chromosomal Proteins, Non-Histone / genetics. Chromosomes, Human, Pair 9. DNA, Complementary. Histone Chaperones. Humans. Mice. Mice, Transgenic. Nuclear Pore Complex Proteins / genetics. Promoter Regions, Genetic. RNA, Messenger / metabolism. Transcription Factors / genetics. Translocation, Genetic

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17620317.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA, Complementary; 0 / Histone Chaperones; 0 / Nuclear Pore Complex Proteins; 0 / Nup214 protein, mouse; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / SET protein, human; 0 / SET-CAN fusion protein, human; 0 / Transcription Factors
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68. Jäger R, Gisslinger H, Passamonti F, Rumi E, Berg T, Gisslinger B, Pietra D, Harutyunyan A, Klampfl T, Olcaydu D, Cazzola M, Kralovics R: Deletions of the transcription factor Ikaros in myeloproliferative neoplasms. Leukemia; 2010 Jul;24(7):1290-8
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  • Transformation to acute leukemia is a major complication of myeloproliferative neoplasms (MPNs), however, the genetic changes leading to transformation remain largely unknown.
  • We screened nine patients with post-MPN leukemia for chromosomal aberrations using microarray karyotyping.
  • We further examined the frequency of IKZF1 deletions in a total of 29 post-MPN leukemia and 526 MPN patients without transformation and observed a strong association of IKZF1 deletions with post-MPN leukemia in two independent cohorts.
  • IKZF1 deletions were observed in both undifferentiated and differentiated myeloid cell types, indicating that IKZF1 loss does not cause differentiation arrest but rather renders progenitors susceptible to transformation, most likely through chromosomal instability.
  • [MeSH-minor] Animals. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cells, Cultured. Gene Dosage. Gene Expression Profiling. Humans. Janus Kinase 2 / genetics. Loss of Heterozygosity. Mice. Mice, Inbred C57BL. Mutation / genetics. Oligonucleotide Array Sequence Analysis. Phosphorylation. Polymerase Chain Reaction. RNA, Messenger / genetics. Receptors, Thrombopoietin / genetics. STAT5 Transcription Factor / genetics. Stem Cells / metabolism


69. Staal-Viliare A, Latger-Cannard V, Didion J, Grégoire MJ, Lecompte T, Jonveaux P, Rio Y: CD203c /CD117-, an useful phenotype profile for acute basophilic leukaemia diagnosis in cases of undifferentiated blasts. Leuk Lymphoma; 2007 Feb;48(2):439-41
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  • [Title] CD203c /CD117-, an useful phenotype profile for acute basophilic leukaemia diagnosis in cases of undifferentiated blasts.
  • [MeSH-major] Blast Crisis / diagnosis. Leukemia, Basophilic, Acute / diagnosis. Phosphoric Diester Hydrolases / blood. Proto-Oncogene Proteins c-kit / blood. Pyrophosphatases / blood
  • [MeSH-minor] Aged. Diagnosis, Differential. Humans. Immunophenotyping. Male. Phenotype

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  • (PMID = 17325915.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ENPP3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.6.1.- / Pyrophosphatases
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70. Wall DA, Carter SL, Kernan NA, Kapoor N, Kamani NR, Brochstein JA, Frangoul H, Goyal RK, Horan JT, Pietryga D, Wagner JE, Kurtzberg J, COBLT Steering Committee: Busulfan/melphalan/antithymocyte globulin followed by unrelated donor cord blood transplantation for treatment of infant leukemia and leukemia in young children: the Cord Blood Transplantation study (COBLT) experience. Biol Blood Marrow Transplant; 2005 Aug;11(8):637-46
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  • [Title] Busulfan/melphalan/antithymocyte globulin followed by unrelated donor cord blood transplantation for treatment of infant leukemia and leukemia in young children: the Cord Blood Transplantation study (COBLT) experience.
  • A non-total body irradiation-containing preparative regimen was studied in young children (<4 years old) undergoing unrelated donor cord blood transplantation as part of the Cord Blood Transplantation trial for the treatment of acute lymphoblastic leukemia (n = 14), acute myeloid leukemia (n = 13), undifferentiated leukemia (n = 1), juvenile myelomonocytic leukemia (n = 2), and myelodysplastic syndromes (n = 2).
  • CINC estimates of grade III/IV acute GVHD at day 100 and chronic GVHD at 1 year were 0.25 (95% CI, 0.09-0.41) and 0.26 (95% CI, 0.09-0.44), respectively.
  • A preparative regimen containing a busulfan/melphalan/antithymocyte globulin preparative regimen is well tolerated in the setting of unrelated donor cord blood transplantation for childhood leukemia and can serve as a platform preparative regimen for intensifying host immunosuppression and antileukemic therapy to allow for improved engraftment and improved relapse-free survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cord Blood Stem Cell Transplantation. Leukemia / mortality. Leukemia / therapy

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  • (PMID = 16041314.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HB / N01-HB 67135; United States / NHLBI NIH HHS / HB / N01-HB 67139; United States / NHLBI NIH HHS / HB / N01-HB-67132; United States / NHLBI NIH HHS / HB / N01-HB-67138
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents, Alkylating; 0 / Immunosuppressive Agents; G1LN9045DK / Busulfan; Q41OR9510P / Melphalan
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71. van Gosliga D, Schepers H, Rizo A, van der Kolk D, Vellenga E, Schuringa JJ: Establishing long-term cultures with self-renewing acute myeloid leukemia stem/progenitor cells. Exp Hematol; 2007 Oct;35(10):1538-49
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  • [Title] Establishing long-term cultures with self-renewing acute myeloid leukemia stem/progenitor cells.
  • OBJECTIVE: With the emergence of the concept of the leukemia stem cell, assays to study them remain pivotal in understanding (leukemic) stem cell biology.
  • METHODS: We have cultured acute myeloid leukemia CD34(+) cells on bone marrow stroma.
  • RESULTS: A strong expansion was observed in about 75% of the acute myeloid leukemia cases (n = 30) and long-term cultures could be maintained for up to 24 weeks on MS5 bone marrow stromal cells.
  • Self-renewal within these L-CAs was determined by sequential passaging of these L-CAs onto new MS5 stromal layers, which resulted in the generation of second, third, and fourth L-CAs, which were able to sustain long-term expansion and generated high numbers of immature undifferentiated suspension cells.
  • CONCLUSION: We present a novel long-term leukemic stem/progenitor assay in which new drugs can be tested and in which genes can be overexpressed or downmodulated using a lentiviral approach in order to obtain more insight into the process of leukemic transformation and self-renewal.
  • [MeSH-major] Bone Marrow Cells / pathology. Cell Line, Tumor / pathology. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology. Tumor Stem Cell Assay

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  • (PMID = 17889721.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
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72. Fukukawa C, Shima H, Tanuma N, Okada T, Kato N, Adachi Y, Kikuchi K: The oncoprotein I-2PP2A/SET negatively regulates the MEK/ERK pathway and cell proliferation. Int J Oncol; 2005 Mar;26(3):751-6
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  • [Title] The oncoprotein I-2PP2A/SET negatively regulates the MEK/ERK pathway and cell proliferation.
  • I-2PP2A/SET, the translocation breakpoint-encoded protein expressed in acute undifferentiated leukemia, was identified as an inhibitor of protein phosphatase 2A (PP2A).
  • Induction of exogenous I-2PP2A/SET at a ratio of 1:1 to the endogenous protein resulted in suppression of cell proliferation.
  • In contrast, siRNA-mediated depletion of I-2PP2A/SET resulted in enhanced cell proliferation.
  • To examine the mode of action by which I-2PP2A/SET suppresses cell proliferation, we determined the effect of over-expressed I-2PP2A/SET on ERK activation.
  • I-2PP2A/SET suppressed activation of ERK following EGF stimulation but did not affect activation levels of stress kinases, JNK and p38.
  • These data suggest that I-2PP2A/SET negatively regulates cell growth by inhibiting the G1/S transition and inhibiting the MEK/ERK pathway stimulated by external stimuli.
  • [MeSH-major] Cell Proliferation. Chromosomal Proteins, Non-Histone / genetics. Chromosomal Proteins, Non-Histone / pharmacology. Extracellular Signal-Regulated MAP Kinases / pharmacology. MAP Kinase Kinase Kinases / pharmacology. Phosphoprotein Phosphatases / genetics. Phosphoprotein Phosphatases / pharmacology. Transcription Factors / genetics. Transcription Factors / pharmacology
  • [MeSH-minor] Cell Cycle. Gene Expression Profiling. HeLa Cells. Histone Chaperones. Humans. Protein Phosphatase 2

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  • (PMID = 15703833.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / SET protein, human; 0 / Transcription Factors; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2
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73. Chen S, Avakian H, Burkert VD, Eugenio P, Adams G, Amarian M, Ambrozewicz P, Anghinolfi M, Asryan G, Bagdasaryan H, Baillie N, Ball JP, Baltzell NA, Barrow S, Batourine V, Battaglieri M, Beard K, Bedlinskiy I, Bektasoglu M, Bellis M, Benmouna N, Berman BL, Biselli AS, Bonner BE, Bouchigny S, Boiarinov S, Bosted P, Bradford R, Branford D, Briscoe WJ, Brooks WK, Bültmann S, Butuceanu C, Calarco JR, Careccia SL, Carman DS, Carnahan B, Cazes A, Cole PL, Collins P, Coltharp P, Cords D, Corvisiero P, Crabb D, Crannell H, Crede V, Cummings JP, DeMasi R, DeVita R, De Sanctis E, Degtyarenko PV, Denizli H, Dennis L, Deur A, Dharmawardane KV, Dhuga KS, Djalali C, Dodge GE, Donnelly J, Doughty D, Dugger M, Dytman S, Dzyubak OP, Egiyan H, Egiyan KS, El Fassi L, Elouadrhiri L, Fatemi R, Fedotov G, Feldman G, Feuerbach RJ, Forest TA, Funsten H, Garçon M, Gavalian G, Gilfoyle GP, Giovanetti KL, Girod FX, Goetz JT, Golovatch E, Gonenc A, Gothe RW, Griffioen KA, Guidal M, Guillo M, Guler N, Guo L, Gyurjyan V, Hadjidakis C, Hafidi K, Hakobyan H, Hakobyan RS, Hardie J, Heddle D, Hersman FW, Hicks K, Hleiqawi I, Holtrop M, Huertas M, Hyde-Wright CE, Ilieva Y, Ireland DG, Ishkhanov BS, Isupov EL, Ito MM, Jenkins D, Jo HS, Joo K, Juengst HG, Keith C, Kellie JD, Khandaker M, Kim KY, Kim K, Kim W, Klein A, Klein FJ, Klusman M, Kossov M, Kramer LH, Kubarovsky V, Kuhn J, Kuhn SE, Kuleshov SV, Lachniet J, Laget JM, Langheinrich J, Lawrence D, Li J, Lima AC, Livingston K, Lu H, Lukashin K, MacCormick M, Markov N, McAleer S, McKinnon B, McNabb JW, Mecking BA, Mestayer MD, Meyer CA, Mibe T, Mikhailov K, Minehart R, Mirazita M, Miskimen R, Mokeev V, Morand L, Morrow SA, Moteabbed M, Mueller J, Mutchler GS, Nadel-Turonski P, Napolitano J, Nasseripour R, Natasha N, Niccolai S, Niculescu G, Niculescu I, Niczyporuk BB, Niroula MR, Niyazov RA, Nozar M, O'Rielly GV, Osipenko M, Ostrovidov AI, Park K, Pasyuk E, Paterson C, Philips SA, Pierce J, Pivnyuk N, Pocanic D, Pogorelko O, Polli E, Popa I, Pozdniakov S, Preedom BM, Price JW, Prok Y, Protopopescu D, Qin LM, Raue BA, Riccardi G, Ricco G, Ripani M, Ritchie BG, Ronchetti F, Rosner G, Rossi P, Rowntree D, Rubin PD, Sabatié F, Salgado C, Santoro JP, Sapunenko V, Schumacher RA, Serov VS, Sharabian YG, Shaw J, Shvedunov NV, Skabelin AV, Smith ES, Smith LC, Sober DI, Stavinsky A, Stepanyan SS, Stepanyan S, Stokes BE, Stoler P, Strakovsky II, Strauch S, Suleiman R, Taiuti M, Tedeschi DJ, Thoma U, Tkabladze A, Tkachenko S, Todor L, Tur C, Ungaro M, Vanderhaeghen M, Vineyard MF, Vlassov AV, Watts DP, Weinstein LB, Weygand DP, Williams M, Wolin E, Wood MH, Yegneswaran A, Yun J, Zana L, Zhang J, Zhao B, Zhao Z, CLAS Collaboration: Measurement of deeply virtual compton scattering with a polarized-proton target. Phys Rev Lett; 2006 Aug 18;97(7):072002
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  • The longitudinal target-spin asymmetry AUL for the exclusive electroproduction of high-energy photons was measured for the first time in ep-->e;'pgamma.

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  • (PMID = 17026221.001).
  • [ISSN] 0031-9007
  • [Journal-full-title] Physical review letters
  • [ISO-abbreviation] Phys. Rev. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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74. Fields-Zinna CA, Sampson JS, Crowe MC, Tracy JB, Parker JF, deNey AM, Muddiman DC, Murray RW: Tandem mass spectrometry of thiolate-protected Au nanoparticles Na(x)Au25(SC2H4Ph)(18-y)(S(C2H4O)5CH3)(y). J Am Chem Soc; 2009 Sep 30;131(38):13844-51
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  • Prominent among the fragments is [Na(2)AuL(2)](1+), one precursor of which is identified as another nanoparticle fragment in the higher m/z region.
  • The detailed dissociation/rearrangement mechanisms of these species are not established, but they are observed in other mass spectrometry experiments, including those under non-CID conditions, namely, electrospray ionization mass spectrometry (ESI-MS) with both time-of-flight (TOF) and FT-ICR analyzers.

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  • (PMID = 19736992.001).
  • [ISSN] 1520-5126
  • [Journal-full-title] Journal of the American Chemical Society
  • [ISO-abbreviation] J. Am. Chem. Soc.
  • [Language] eng
  • [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 / Sulfhydryl Compounds; 7440-57-5 / Gold
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75. Funayama K, Murai F, Shimane M, Nomura H, Asano S: Adhesion-induced drug resistance in leukemia stem cells. Pharmacology; 2010;86(2):79-84
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  • [Title] Adhesion-induced drug resistance in leukemia stem cells.
  • The co-culture of TF-1 leukemia cells and MS-5 stromal cells produces a cobblestone area which partially mimics the leukemia stem cell niche.
  • The adhering leukemia cells are shown to become less sensitive to cytarabine, etoposide and daunorubicin.
  • These changes are associated with an increased proportion of the G0/G1 phase, increased upregulation of cyclin-dependent kinase inhibitors, and increased levels of Bcl-2, but not with any change in the expression of BAX or drug transporters such as ABCG2 and MDR1, compared to monocultured leukemic cells.
  • These findings suggest that adhesion alone can lead to drug resistance in leukemic stem cells by various mechanisms.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Leukemia / physiopathology. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / physiology. Stem Cell Niche / physiopathology. Stromal Cells / physiology
  • [MeSH-minor] Bone Marrow Cells / physiology. Cell Adhesion. Cell Cycle. Cell Line, Tumor. Coculture Techniques. Cyclin-Dependent Kinase Inhibitor Proteins / genetics. Cyclin-Dependent Kinase Inhibitor Proteins / metabolism. Cytarabine / pharmacology. Daunorubicin / pharmacokinetics. Daunorubicin / pharmacology. Etoposide / pharmacology. Humans. Lysosomes / metabolism. Osmolar Concentration. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Up-Regulation. Vacuolar Proton-Translocating ATPases / genetics. Vacuolar Proton-Translocating ATPases / metabolism

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • [ErratumIn] Pharmacology. 2010;86(4):202
  • (PMID = 20689339.001).
  • [ISSN] 1423-0313
  • [Journal-full-title] Pharmacology
  • [ISO-abbreviation] Pharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin-Dependent Kinase Inhibitor Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; EC 3.6.1.- / Vacuolar Proton-Translocating ATPases; ZS7284E0ZP / Daunorubicin
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76. Juarez MA, Su F, Chun S, Kiel MJ, Lyons SE: Distinct roles for SCL in erythroid specification and maturation in zebrafish. J Biol Chem; 2005 Dec 16;280(50):41636-44
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  • The stem cell leukemia (SCL) transcription factor is essential for vertebrate hematopoiesis.
  • Although all hematopoietic functions were rescued by wild-type Scl mRNA, an Scl DNA binding mutant rescued primitive and definitive hematopoiesis but did not rescue primitive erythroid maturation.
  • [MeSH-minor] Alternative Splicing. Animals. Cell Differentiation. Cell Lineage. DNA / chemistry. DNA-Binding Proteins. Electrophoresis, Agar Gel. Erythroid-Specific DNA-Binding Factors / metabolism. Hematopoiesis. In Situ Hybridization. Models, Genetic. Mutation. Phenotype. Protein Structure, Tertiary. RNA / chemistry. RNA, Antisense / chemistry. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells. Transcription Factors. Zebrafish

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  • ZFIN. ZFIN .
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  • (PMID = 16210319.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K22-CA095024-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / Proto-Oncogene Proteins; 0 / RNA, Antisense; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish; 63231-63-0 / RNA; 9007-49-2 / DNA
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77. Jelínek F, Sobotková E, Vonka V: Characteristics of two mouse bcr-abl-transformed cell lines. II. Pathological lesions induced in mice. Folia Biol (Praha); 2005;51(4):93-102
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  • [Title] Characteristics of two mouse bcr-abl-transformed cell lines. II. Pathological lesions induced in mice.
  • We classified the disease induced by both of the cell lines as acute myeloid undifferentiated leukaemia (AML MO).
  • [MeSH-major] Cell Line, Transformed. Cell Transformation, Neoplastic / genetics. Genes, abl. Leukemia, Myeloid / pathology. Neoplasms, Experimental / pathology
  • [MeSH-minor] Acute Disease. Animals. Disease Progression. Endothelial Cells / pathology. Female. Immunohistochemistry. Leukemic Infiltration. Lung / pathology. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Spine / pathology. Spleen / immunology. Spleen / pathology

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  • (PMID = 16180544.001).
  • [ISSN] 0015-5500
  • [Journal-full-title] Folia biologica
  • [ISO-abbreviation] Folia Biol. (Praha)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
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78. Gujral S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Jain H, Pais A, Amre Kadam PS, Banavali SD, Arora B, Kumar P, Hari Menon VG, Kurkure PA, Parikh PM, Mahadik S, Chogule AB, Shinde SC, Nair CN: Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India. Cytometry B Clin Cytom; 2009 May;76(3):199-205
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  • [Title] Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India.
  • BACKGROUND: To analyze the spectrum of various types and subtypes of acute leukemia.
  • METHODS: Two thousand five hundred and eleven consecutive new referral cases of acute leukemia (AL) were evaluated based on WHO classification.
  • RESULTS: It included 1,471 cases (58%) of acute lymphoblastic leukemia (ALL), 964 cases (38%) of acute myeloid leukemia (AML), 45 cases (1.8%) of chronic myelogenous leukemia in blast crisis (CMLBC), 37 cases (1.5%) of biphenotypic acute leukemia (BAL), 1 case of Triphenotypic AL, and 2 cases of acute undifferentiated leukemia (AUL).
  • Common subtypes of ALL were B-cell ALL (76%), which comprised of intermediate stage/CALLA positive (73%), early precursor/proBALL (3%).
  • T-cell ALL constituted 24% (351 cases) of ALL.
  • CONCLUSION: B-cell ALL was the commonest subtype in children and AML in adults.
  • A minimal primary panel of nine antibodies consisting of three myeloid markers (CD13, CD33, and CD117), B-cell lymphoid marker (CD19), T-cell marker (CD7), with CD45, CD10, CD34, and HLADR could assign lineage to 92% of AL.
  • [MeSH-major] Immunophenotyping. Leukemia / immunology. Leukemia / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Histocytochemistry. Humans. In Situ Hybridization. India. Infant. Infant, Newborn. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • [Copyright] (c) 2008 Clinical Cytometry Society.
  • (PMID = 18803279.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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79. Staal-Viliare A, Latger-Cannard V, Rault JP, Didion J, Grégoire MJ, Bologna S, Witz B, Jonveaux P, Lecompte T, Rio Y: [A case of de novo acute basophilic leukaemia: diagnostic criteria and review of the literature]. Ann Biol Clin (Paris); 2006 Jul-Aug;64(4):361-5
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  • [Title] [A case of de novo acute basophilic leukaemia: diagnostic criteria and review of the literature].
  • We report a case of a de novo acute basophilic leukaemia, revealed by an infectious pneumopathy in a 73 year old man.
  • The blood and bone marrow smears showed a mixture of undifferentiated blast cells and basophiloblasts (high nucleo-cytoplasmic ratio, coarse basophilic cytoplasmic granules), along with basophilic precursors and basophilic polymorphonuclears.
  • This clinical prompted allows us to review the literature on acute basophilic leukaemia and to state on the different diagnostic criteria of this rare disorder.
  • [MeSH-major] Leukemia, Basophilic, Acute / blood. Leukemia, Basophilic, Acute / diagnosis

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  • (PMID = 16829481.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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80. Jamieson CH, Barroga CF, Vainchenker WP: Miscreant myeloproliferative disorder stem cells. Leukemia; 2008 Nov;22(11):2011-9
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  • [Title] Miscreant myeloproliferative disorder stem cells.
  • Myeloproliferative disorders (MPDs), typified by robust marrow and extramedullary hematopoiesis, have a propensity to progress to acute leukemia.
  • Although the hematopoietic stem cell (HSC) origin of MPDs was suggested over 30 years ago, only recently the HSC-specific effects of MPD molecular mutations have been investigated.
  • The pivotal role of BCR-ABL in chronic myeloid leukemia (CML) development provided the rationale for targeted therapy, which greatly reduced mortality rates.
  • Although JAK2 activation appears to be central to BCR-ABL-negative MPD pathogenesis, its effects may be cell type and context specific.
  • Recent evidence suggests that acquired mutations misdirect differentiation and survival of the MPD-initiating stem cell resulting in the production of aberrant self-renewing progenitors that subvert the microenvironment leading to leukemia stem cell generation and leukemic transformation.
  • Thus, combined therapies targeting aberrant molecular pathways may be required to redirect miscreant MPD stem cells.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Myeloid Progenitor Cells / pathology. Myeloproliferative Disorders / etiology. Myeloproliferative Disorders / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Cell Differentiation. Humans

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  • (PMID = 18923436.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 30
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81. Wojiski S, Guibal FC, Kindler T, Lee BH, Jesneck JL, Fabian A, Tenen DG, Gilliland DG: PML-RARalpha initiates leukemia by conferring properties of self-renewal to committed promyelocytic progenitors. Leukemia; 2009 Aug;23(8):1462-71
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  • [Title] PML-RARalpha initiates leukemia by conferring properties of self-renewal to committed promyelocytic progenitors.
  • Acute promyelocytic leukemia (APL) is characterized by hyperproliferation of promyelocytes, progenitors that are committed to terminal differentiation into granulocytes, making it an ideal disease in which to study the transforming potential of less primitive cell types.
  • We utilized a murine model of APL in which the PML-RARalpha oncogene is expressed from the endogenous cathepsin G promoter to test the hypothesis that leukemia stem cell (LSC) activity resides within the differentiated promyelocyte compartment.
  • Progression to acute leukemia was associated with an expansion of the promyelocyte compartment at the expense of other stem, progenitor and terminally differentiated populations.
  • Leukemic promyelocytes exhibited properties of self-renewal, and were capable of engendering leukemia in secondary recipient mice.
  • These findings are consistent with the hypothesis that cancer stem cells may arise from committed progenitors that lack stem cell properties, provided that the initiating mutation in cancer progression activates programs that confer properties of self-renewal.

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  • (PMID = 19322209.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA66996; United States / NCI NIH HHS / CA / P01 CA066996-130011; United States / NIDDK NIH HHS / DK / DK50654; United States / NCI NIH HHS / CA / CA066996-130011; United States / NCI NIH HHS / CA / P01 CA066996; United States / NIDDK NIH HHS / DK / DK050654-060004; United States / NCI NIH HHS / CA / P01 CA066996-120009; United States / Howard Hughes Medical Institute / / ; United States / NIDDK NIH HHS / DK / P01 DK050654; United States / NIDDK NIH HHS / DK / P01 DK050654-060004; United States / NCI NIH HHS / CA / CA066996-120009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; EC 3.4.- / Cathepsins; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.20 / CTSG protein, human; EC 3.4.21.20 / Cathepsin G; EC 3.4.21.20 / Ctsg protein, mouse
  • [Other-IDs] NLM/ NIHMS222020; NLM/ PMC2914549
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82. Cheng Y, Zhang Z, Slape C, Aplan PD: Cre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4- CD8- to CD4+ CD8+ transition. Neoplasia; 2007 Apr;9(4):315-21
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  • [Title] Cre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4- CD8- to CD4+ CD8+ transition.
  • In the most common form of stem cell leukemia (SCL) gene rearrangement, an interstitial deletion of 82 kb brings SCL under the control of regulatory elements that normally govern expression of the ubiquitously expressed SCL interrupting locus (SIL) gene, which is located directly upstream of SCL.
  • To investigate the effect of this fusion in a mouse model, a bacterial artificial chromosome (BAC) clone containing both human SIL and SCL genes was isolated, and loxP sites were inserted into intron 1 of both the SIL and SCL genes, corresponding to the sites at which recombination occurs in human T-cell acute lymphocytic leukemia patients.
  • These results demonstrate that conditional activation of SCL under control of SIL regulatory elements can impair normal T-cell development.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. CD4-Positive T-Lymphocytes / enzymology. CD8-Positive T-Lymphocytes / enzymology. Cell Differentiation / genetics. Extracellular Matrix Proteins / physiology. Gene Rearrangement, T-Lymphocyte / genetics. Integrases / genetics. Intracellular Signaling Peptides and Proteins / genetics. Protein-Lysine 6-Oxidase / physiology. Proto-Oncogene Proteins / genetics

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  • (PMID = 17460775.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 SC010379-06
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Extracellular Matrix Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins; 0 / STIL protein, human; 135471-20-4 / TAL1 protein, human; 149137-54-2 / Lox protein, mouse; EC 1.4.3.13 / Protein-Lysine 6-Oxidase; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
  • [Other-IDs] NLM/ PMC1854848
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83. Terme JM, Lhermitte L, Asnafi V, Jalinot P: TGF-beta induces degradation of TAL1/SCL by the ubiquitin-proteasome pathway through AKT-mediated phosphorylation. Blood; 2009 Jun 25;113(26):6695-8
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  • T-cell acute lymphoblastic leukemia 1 (TAL1), also known as stem cell leukemia (SCL), plays important roles in differentiation of hematopoietic and endothelial cells and is deregulated in a high percentage of T-cell acute lymphoblastic leukemia (T-ALL).

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  • (PMID = 19406989.001).
  • [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 / Androstadienes; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Leupeptins; 0 / Neoplasm Proteins; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transforming Growth Factor beta1; 0 / Ubiquitin; 1114-81-4 / Phosphothreonine; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 135471-20-4 / TAL1 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / STUB1 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases; XVA4O219QW / wortmannin
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84. Krivtsov AV, Wang Y, Feng Z, Armstrong SA: Gene expression profiling of leukemia stem cells. Methods Mol Biol; 2009;538:231-46
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  • [Title] Gene expression profiling of leukemia stem cells.
  • Characterization of gene expression programs and pathways important for normal and cancer stem cells has become an active area of investigation.
  • Microarray analysis of various cell populations provides an opportunity to assess genomewide expression programs to define cellular identity and to potentially identify pathways activated in various stem cells.
  • Here we describe methods to isolate a leukemia stem cell population, amplify RNA, and perform microarray analyses.
  • [MeSH-major] Flow Cytometry / methods. Gene Expression Profiling. Granulocyte-Macrophage Progenitor Cells / metabolism. Leukemia, Myeloid, Acute / genetics. Neoplastic Stem Cells / metabolism. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Animals. Leukemia, Experimental / genetics. Leukemia, Experimental / metabolism. Leukemia, Experimental / pathology. Mice. Mice, Inbred C57BL. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 19277590.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / P01 CA066996-15
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS369625; NLM/ PMC3339407
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85. Fraga MF, Berdasco M, Ballestar E, Ropero S, Lopez-Nieva P, Lopez-Serra L, Martín-Subero JI, Calasanz MJ, Lopez de Silanes I, Setien F, Casado S, Fernandez AF, Siebert R, Stifani S, Esteller M: Epigenetic inactivation of the Groucho homologue gene TLE1 in hematologic malignancies. Cancer Res; 2008 Jun 1;68(11):4116-22
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  • An undifferentiated status and the epigenetic inactivation of tumor-suppressor genes are hallmarks of transformed cells.
  • The Groucho homologue Transducin-like Enhancer of Split 1 (TLE1) is a multitasked transcriptional corepressor that acts through the acute myelogenous leukemia 1, Wnt, and Notch signaling pathways.
  • We have found that TLE1 undergoes promoter CpG island hypermethylation-associated inactivation in hematologic malignancies, such as diffuse large B-cell lymphoma and AML.
  • TLE1 reintroduction in hypermethylated leukemia/lymphoma cells causes growth inhibition in colony assays and nude mice, whereas TLE1-short hairpin RNA depletion in unmethylated cells enhances tumor growth.
  • [MeSH-minor] Animals. Base Sequence. Cell Line, Tumor. CpG Islands. DNA Methylation. DNA Primers. Humans. Mice. Mice, Nude. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18519670.001).
  • [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 / DNA Primers; 0 / Repressor Proteins; 0 / TLE1 protein, human
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86. Miller DR: A tribute to Sidney Farber-- the father of modern chemotherapy. Br J Haematol; 2006 Jul;134(1):20-6
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  • He recognised that folic acid stimulated leukaemic cell growth and enhanced disease progression.
  • His landmark study, published in 1948, demonstrated that a number of folic acid antagonists, including 4-aminopteroyl-glutamic acid (aminopterin) produced temporary remissions in children with acute undifferentiated leukaemia.
  • [MeSH-minor] History, 20th Century. Humans. Leukemia / drug therapy. United States

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  • (PMID = 16803563.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Biography; Historical Article; Journal Article
  • [Publication-country] England
  • [Personal-name-as-subject] Farber S
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87. Ueda T, Ito Y, Maeda M, Fukunaga Y: Massive periosteal reaction a presenting feature of acute megakaryocytic leukemia. Pediatr Int; 2007 Dec;49(6):1015-7
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  • [Title] Massive periosteal reaction a presenting feature of acute megakaryocytic leukemia.
  • Acute megakaryoblastic leukemia (AML M7) is a biologically heterogeneous form of acute myeloid leukemia accounting for 14.6% of cases.
  • In many instances in the past, AML M7 has been classified as undifferentiated leukemia, myelodysplasia, myelofibrosis or some other disease because of its complex clinical presentation or the difficulty of obtaining and interpreting bone marrow samples.
  • Although the radiographic spectrum of bony changes in leukemia have been well characterized, skeletal X-ray abnormalities in the setting of AML M7 in pediatric patients have been described in few reports that were associated with bone marrow fibrosis.
  • [MeSH-major] Hyperostosis / etiology. Leukemia, Megakaryoblastic, Acute / complications. Paraneoplastic Syndromes. Periosteum / pathology. Primary Myelofibrosis / etiology

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  • (PMID = 18045316.001).
  • [ISSN] 1328-8067
  • [Journal-full-title] Pediatrics international : official journal of the Japan Pediatric Society
  • [ISO-abbreviation] Pediatr Int
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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88. Estrov Z: The leukemia stem cell. Cancer Treat Res; 2010;145:1-17
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  • [Title] The leukemia stem cell.
  • [MeSH-major] Leukemia / pathology. Neoplastic Stem Cells / cytology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Differentiation. Cell Transformation, Neoplastic. Clone Cells / cytology. Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / cytology. Humans. Leukemia, Myeloid, Acute / pathology. Mice. Mice, Inbred NOD. Mice, SCID. Mice, Transgenic. Models, Biological. Recurrence. Transcription Factors / physiology

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  • (PMID = 20306242.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Transcription Factors
  • [Number-of-references] 125
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89. Hall MA, Slater NJ, Begley CG, Salmon JM, Van Stekelenburg LJ, McCormack MP, Jane SM, Curtis DJ: Functional but abnormal adult erythropoiesis in the absence of the stem cell leukemia gene. Mol Cell Biol; 2005 Aug;25(15):6355-62
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  • [Title] Functional but abnormal adult erythropoiesis in the absence of the stem cell leukemia gene.
  • Previous studies have indicated that the stem cell leukemia gene (SCL) is essential for both embryonic and adult erythropoiesis.
  • We have examined erythropoiesis in conditional SCL knockout mice for at least 6 months after loss of SCL function and report that SCL was important but not essential for the generation of mature red blood cells.
  • The unexpected finding that SCL-independent erythropoiesis can proceed in the adult suggests that alternate factors can replace the essential functions of SCL and raises the possibility that similar mechanisms also explain the relatively minor defects previously observed in SCL-null hematopoietic stem cells.

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  • (PMID = 16024775.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL053749; United States / NHLBI NIH HHS / HL / R01 HL069232; United States / NHLBI NIH HHS / HL / P01 HL53749-03; United States / NHLBI NIH HHS / HL / R01 HL69232-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1190361
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90. Carlson A, Berkowitz JM, Browning D, Slamon DJ, Gasson JC, Yates KE: Expression of c-Fes protein isoforms correlates with differentiation in myeloid leukemias. DNA Cell Biol; 2005 May;24(5):311-6
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  • [Title] Expression of c-Fes protein isoforms correlates with differentiation in myeloid leukemias.
  • Increased c-Fes expression is associated with differentiation in normal myeloid cells and cell lines.
  • Our hypothesis was that primary leukemia cells would show a similar pattern of increased expression in more differentiated cells.
  • Therefore, we compared c-Fes expression in cells with an undifferentiated, blast phenotype (acute myelogenous leukemia--AML) to cells with a differentiated phenotype (chronic myelogenous leukemia--CML).
  • Using mRNA from mouse and human cell lines, we found deletion of one or more exons in the c-fes mRNA.
  • This may be a mechanism to direct the c-Fes kinase domain to different subcellular locations and/or substrates at specific stages of myeloid cell differentiation.
  • [MeSH-major] Cell Differentiation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelomonocytic, Acute / metabolism. Protein Isoforms / metabolism. Proto-Oncogenes
  • [MeSH-minor] Animals. Antigens, CD34 / metabolism. Cell Line. Cell Line, Tumor. Fluorescent Antibody Technique, Indirect. HL-60 Cells. Hematopoietic Stem Cells / enzymology. Hematopoietic Stem Cells / metabolism. Humans. Immunoblotting. K562 Cells. Mice. NIH 3T3 Cells. Neutrophils / enzymology. Neutrophils / metabolism. Polymerase Chain Reaction. RNA, Messenger / genetics. U937 Cells

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  • (PMID = 15869408.001).
  • [ISSN] 1044-5498
  • [Journal-full-title] DNA and cell biology
  • [ISO-abbreviation] DNA Cell Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA32737
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Protein Isoforms; 0 / RNA, Messenger
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91. Stubbs MC, Armstrong SA: Therapeutic implications of leukemia stem cell development. Clin Cancer Res; 2007 Jun 15;13(12):3439-42
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  • [Title] Therapeutic implications of leukemia stem cell development.
  • Acute myelogenous leukemias, and perhaps many other cancers, are maintained by a population of cancer stem cells that can regenerate themselves as well as give rise to more differentiated and less proliferative cells that constitute the bulk of the disease.
  • Recent discoveries have shed light on both the nature of leukemia stem cells (LSC) and their cells of origin.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Hematopoietic Stem Cells / physiology. Leukemia / physiopathology. Neoplastic Stem Cells / physiology
  • [MeSH-minor] Animals. Cell Differentiation. Cell Lineage. Humans