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1. Chen YC, Sheen JM, Huang LT, Wu KS, Hsiao CC: Disseminated tuberculous myositis in a child with acute myelogenous leukemia. Pediatr Neonatol; 2009 Apr;50(2):74-7
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  • [Title] Disseminated tuberculous myositis in a child with acute myelogenous leukemia.
  • We present a case of disseminated tuberculous myositis in a girl with secondary acute myelogenous Leukemia following successful chemotherapy for undifferentiated sarcoma of the maxillary sinus.
  • The diagnosis was established by direct visualization of acid-fast bacilli in the biopsied nodule and by typical pathologic findings.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Myositis / complications. Tuberculosis / complications


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. 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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4. 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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5. 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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6. 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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7. 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


8. 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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9. Yamaguchi K, Koga Y, Suminoe A, Saito Y, Matsuzaki A, Kanno S, Takimoto T, Suda M, Oda Y, Muto T, Takatsuki H, Hara T: [Alveolar rhabdomyosarcoma of unknown origin mimicking acute leukemia at the initial presentation]. Rinsho Ketsueki; 2007 Apr;48(4):315-20
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  • [Title] [Alveolar rhabdomyosarcoma of unknown origin mimicking acute leukemia at the initial presentation].
  • Laboratory examination of the peripheral blood revealed white blood cells 11,300/microl, hemoglobin 10.4 g/dl, platelets 45,000/microl, fibrinogen < 50 mg/dl, fibrin/fibrinogen degradation products 536 microg/ml and lactate dehydrogenase 1,684 U/l.
  • A bone marrow aspirate contained 89.6% of undifferentiated tumor cells.
  • Reverse transcriptase polymerase chain reaction demonstrated PAX3/FKHR fusion transcripts, confirming the diagnosis of alveolar rhabdomyosarcoma.
  • The patient received an allogeneic bone marrow transplantation eight months after diagnosis, although he died of hepatic veno-occlusive disease on day 21.
  • Alveolar rhabdomyosarcoma often develops in older children and younger adults, and its bone marrow infiltration may mimic acute leukemia.
  • [MeSH-major] Rhabdomyosarcoma, Alveolar / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Antigens, CD56 / analysis. Biomarkers, Tumor / analysis. Bone Marrow / pathology. Diagnosis, Differential. Disseminated Intravascular Coagulation / etiology. Fatal Outcome. Forkhead Transcription Factors / genetics. Humans. Leukemia. Male. Paired Box Transcription Factors / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic

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  • (PMID = 17515123.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Biomarkers, Tumor; 0 / FOXO1 protein, human; 0 / Forkhead Transcription Factors; 0 / PAX3 protein, human; 0 / Paired Box Transcription Factors
  • [Number-of-references] 28
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10. 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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11. Liu ML, Kallakury B, Kessler C, Hartmann DP, Azumi N, Ozdemirli M: Chronic idiopathic myelofibrosis terminating in extramedullary anaplastic plasmacytoma. Leuk Lymphoma; 2006 Feb;47(2):315-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Similar to other CMPDs, the stem cell in CIMF has the potential to differentiate into myeloid or lymphoid lineages, and thus CIMF can culminate in acute leukemia of myeloid or, rarely, lymphoid lineage.
  • Lymph node biopsy revealed a diffuse undifferentiated infiltrate in the background of extramedullary hematopoiesis.
  • Flow cytometric and immunohistochemical analysis demonstrated plasma cell-related antigens (CD138, CD38, cytoplasmic kappa light chain), epithelial membrane antigen and CD43 in the tumor cells.
  • The myeloid, B-cell or T-cell markers were negative.
  • The plasma cell origin was further confirmed by electron microscopic examination, which revealed stacks of rough endoplasmic reticulum.
  • Monoclonal gammopathy may occur in CIMF, and rare cases of simultaneous plasma cell myeloma and CIMF have been reported in the literature.
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Chronic Disease. Diagnosis, Differential. Disease Progression. Fatal Outcome. Humans. Lymph Nodes / pathology. Male. Middle Aged. Spleen / pathology


12. 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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13. 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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14. 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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15. 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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16. 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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17. 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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18. 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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  • (PMID = 19321862.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [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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19. 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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20. 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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21. 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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22. 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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23. 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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24. 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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25. 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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26. 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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27. 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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28. 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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29. 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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30. 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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31. 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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32. 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


33. 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


34. 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


35. 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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36. 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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37. 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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38. 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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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. 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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41. 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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42. 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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43. 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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44. 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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  • 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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45. 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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46. 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


47. Ozbek U, Kandilci A, van Baal S, Bonten J, Boyd K, Franken P, Fodde R, Grosveld GC: SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice. Am J Pathol; 2007 Aug;171(2):654-66
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  • [Title] SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice.
  • Leukemia-specific chromosome translocations involving the nucleoporin CAN/NUP214 lead to expression of different fusion genes including DEK-CAN, CAN-ABL, and SET-CAN.
  • DEK-CAN and CAN-ABL1 are associated with acute myeloid leukemia and T-cell acute lymphoblastic leukemia, respectively, whereas SET-CAN was identified in a patient with acute undifferentiated leukemia.
  • Although SET-CAN mice showed expansion of an early progenitor cell pool and partial depletion of lymphocytes, the animals were not leukemia-prone and did not show shortening of disease latency after retroviral tagging.
  • This suggests that SET-CAN expression in acute undifferentiated leukemia might determine the primitive phenotype of the disease, whereas secondary genetic lesions are necessary for disease development.

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  • (PMID = 17569777.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-76480
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / Ki-67 Antigen; 0 / Nuclear Pore Complex Proteins; 0 / Nup214 protein, mouse; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC1934515
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48. 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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49. 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.


50. 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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51. 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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52. 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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53. 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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54. 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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55. 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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56. 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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57. 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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  • (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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58. 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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59. 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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60. Manola KN, Georgakakos VN, Stavropoulou C, Spyridonidis A, Angelopoulou MK, Vlachadami I, Katsigiannis A, Roussou P, Pantelias GE, Sambani C: Jumping translocations in hematological malignancies: a cytogenetic study of five cases. Cancer Genet Cytogenet; 2008 Dec;187(2):85-94
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  • Jumping translocations (JT) are rare cytogenetic aberrations in hematological malignancies that include unbalanced translocations involving a donor chromosome arm or chromosome segment that has fused to two or more different recipient chromosomes in different cell lines.
  • These cases involve JT of 1q in a case of acute myeloblastic leukemia (AML)-M1, a case of Burkitt lymphoma, and a case of BCR/ABL-positive acute lymphoblastic leukemia, as well as a JT of 13q in a case of AML-M5, and a JT of 11q segment in a case of undifferentiated leukemia.
  • To our knowledge, with regard to hematologic malignancies, this study presents the first case of JT associated with AML-M1, the first case of JT involving 13q as a donor chromosome, and the first report of JT involving a segment of 11q containing two copies of the MLL gene, jumping on to two recipient chromosomes in each cell line and resulting in six copies of the MLL gene.
  • Our investigation suggests that JT may not contribute to the pathogenesis but rather to the progression of the disease, and it demonstrates that chromosome band 1q10 as a breakpoint of the donor chromosome 1q is also implicated in AML, not only in multiple myeloma as it has been known until now.
  • [MeSH-minor] Adult. Aged. Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / genetics. Cytogenetic Analysis. Female. Humans. Karyotyping. Leukemia / diagnosis. Leukemia / genetics. Leukemia, Monocytic, Acute / diagnosis. Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Young Adult

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  • (PMID = 19027489.001).
  • [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
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61. 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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62. Wang YL, Wang T, Xu F, Gang Y, Wang J: [Analysis of Flt-3 expression and Flt-3/ITD mutation in acute myeloid leukemia cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):446-9
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  • [Title] [Analysis of Flt-3 expression and Flt-3/ITD mutation in acute myeloid leukemia cells].
  • This study was aimed to explore the relationship between Flt-3 expression, Flt-3/ITD mutation in acute leukemia (AL) cell line and pathogenesis of AL, especially AML.
  • The Flt-3 expression and Flt-3/ITD mutation were detected by RT-PCR and sequencing method in 82 leukemia cell lines including 20 AML, 57 ALL and 5 CML cell lines.
  • The results indicated that positive results of Flt-3 expression were obtained in 48 out of 77 AL cell line, the positive rate was 62%; 12 cell lines were positive in 20 AML cell lines, the positive rate was 60%; 33 cell lines was positive in 57 ALL cell lines, the positive rate was 58%; 3 cell lines were positive in 5 CML cell lines, the positive rate was 60%.
  • There was abnormal gene product in 1 AMOL cell line out of 12 AML cell lines with Flt-3 positive expression (positive rate 8.3%).
  • The positive rate of Flt-3 expression in undifferentiated cell line was prominently higher than that in mature B cell ALL (P < 0.05).
  • It is concluded that the Flt-3 expression is different in various leukemia cells.
  • Flt-3/ITD duplication was found in one AML cell line.
  • The detection of Flt-3 gene and Flt-3/ITD mutation may contribute to the diagnosis of ALL, especially to AML.

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  • (PMID = 16800917.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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63. 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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64. 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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65. 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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66. 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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67. 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

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  • (PMID = 17575205.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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68. 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


69. Deshpande AJ, Buske C: Knocking the Wnt out of the sails of leukemia stem cell development. Cell Stem Cell; 2007 Dec 13;1(6):597-8
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  • [Title] Knocking the Wnt out of the sails of leukemia stem cell development.
  • Tumor propagation by cancer stem cells (CSCs) requires their ability to self-renew, and yet the signal pathways involved in this process remain poorly defined.
  • In the December issue of Cancer Cell, Zhao et al. (2007) provide compelling evidence that Wnt/beta-catenin signaling is crucial for the maintenance of chronic myelogenous leukemia (CML) stem cells.
  • [MeSH-major] Leukemia. Stem Cells / physiology. Wnt Proteins / genetics. Wnt Proteins / physiology. beta Catenin / physiology

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  • (PMID = 18371398.001).
  • [ISSN] 1875-9777
  • [Journal-full-title] Cell stem cell
  • [ISO-abbreviation] Cell Stem Cell
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin
  • [Number-of-references] 10
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70. 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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71. Rodríguez-Rodríguez CE, Marco-Urrea E, Caminal G: Degradation of naproxen and carbamazepine in spiked sludge by slurry and solid-phase Trametes versicolor systems. Bioresour Technol; 2010 Apr;101(7):2259-66
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  • Detectable laccase activity levels were found in the 10 and 25%-cultures (up to 1308 and 2588 AUL(-1), respectively) while it was negligible in the 38%-culture.

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20031398.001).
  • [ISSN] 1873-2976
  • [Journal-full-title] Bioresource technology
  • [ISO-abbreviation] Bioresour. Technol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Sewage; 33CM23913M / Carbamazepine; 57Y76R9ATQ / Naproxen; EC 1.10.3.2 / Laccase; IY9XDZ35W2 / Glucose
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72. Niebuhr B, Fischer M, Täger M, Cammenga J, Stocking C: Gatekeeper function of the RUNX1 transcription factor in acute leukemia. Blood Cells Mol Dis; 2008 Mar-Apr;40(2):211-8
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  • [Title] Gatekeeper function of the RUNX1 transcription factor in acute leukemia.
  • The RUNX1 gene encodes the alpha subunit of the core binding factor (CBF) and is a common target of genetic mutations in acute leukemia.
  • This pool of "escaped" cells is the target of secondary mutations, accumulating over time to induce the aggressive manifestation of acute leukemia.
  • Evidence from patient and animal studies supports the concept that RUNX1 mutations are the initiating event in different leukemia subtypes, but also suggests that diverse mechanisms are used to subvert RUNX1 function.
  • A number of different approaches have led to the identification of secondary events that lead to the overt acute phase; however, the majority is unknown.
  • Finally, the concept of the "leukemia stem cell" and its therapeutic importance is discussed in light of the RUNX1 gatekeeper function.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. Leukemia, Myeloid, Acute / metabolism. Oncogene Proteins, Fusion / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Animals. Cell Differentiation / genetics. Cell Transformation, Neoplastic. Hematopoiesis / genetics. Humans. Mutation. Neoplastic Stem Cells / metabolism. Transcription, Genetic

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  • (PMID = 17920312.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors
  • [Number-of-references] 81
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73. Wang Z, Iwasaki M, Ficara F, Lin C, Matheny C, Wong SH, Smith KS, Cleary ML: GSK-3 promotes conditional association of CREB and its coactivators with MEIS1 to facilitate HOX-mediated transcription and oncogenesis. Cancer Cell; 2010 Jun 15;17(6):597-608
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  • Acute leukemias induced by MLL chimeric oncoproteins are among the subset of cancers distinguished by a paradoxical dependence on GSK-3 kinase activity for sustained proliferation.
  • We demonstrate here that GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, a critical component of the MLL-subordinate program, which in turn facilitates HOX-mediated transcription and transformation.
  • This mechanism also applies to hematopoietic cells transformed by other HOX genes, including CDX2, which is highly expressed in a majority of acute myeloid leukemias, thus providing a molecular approach based on GSK-3 inhibitory strategies to target HOX-associated transcription in a broad spectrum of leukemias.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20541704.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE21842
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009151; United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / T32 CA009151-37; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / T32 CA09151; United States / NCI NIH HHS / CA / CA009151-37; United States / NCI NIH HHS / CA / CA116606; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [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 / CRTC1 protein, human; 0 / CRTC2 protein, human; 0 / Cdx4 protein, mouse; 0 / Cyclic AMP Response Element-Binding Protein; 0 / DNA-Binding Proteins; 0 / HOXB1 homeodomain protein; 0 / Homeodomain Proteins; 0 / Hoxb4 protein, mouse; 0 / Indoles; 0 / Maleimides; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Pbx1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / SB 216763; 0 / Transcription Factors; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; 0 / pbx1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.11.26 / Glycogen Synthase Kinase 3
  • [Other-IDs] NLM/ NIHMS203816; NLM/ PMC2919232
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74. 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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75. Li X, Xiong JW, Shelley CS, Park H, Arnaout MA: The transcription factor ZBP-89 controls generation of the hematopoietic lineage in zebrafish and mouse embryonic stem cells. Development; 2006 Sep;133(18):3641-50
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  • [Title] The transcription factor ZBP-89 controls generation of the hematopoietic lineage in zebrafish and mouse embryonic stem cells.
  • Hematopoietic development is closely linked to that of blood vessels and the two processes are regulated in large part by transcription factors that control cell fate decisions and cellular differentiation.
  • Both blood and blood vessels derive from a common progenitor, termed the hemangioblast, but the factor(s) specifying the development and differentiation of this stem cell population into the hematopoietic and vascular lineages remain ill defined.
  • Injection of ZBP-89 mRNA into cloche zebrafish embryos, which lack both the hematopoietic and endothelial lineages, rescues hematopoiesis but not vasculogenesis.
  • Injection of mRNA for Stem Cell Leukemia (SCL), a transcription factor that directs hemangioblast development into blood cell precursors, rescues the bloodless phenotype in ZBP-89 zebrafish morphants.
  • Forced expression of ZBP-89 induces the expansion of hematopoietic progenitors in wild-type zebrafish and in mouse embryonic stem cell cultures but inhibits angiogenesis in vivo and in vitro.

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  • (PMID = 16914492.001).
  • [ISSN] 0950-1991
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG019676-04; United States / NIDDK NIH HHS / DK / R01 DK081920; United States / NIA NIH HHS / AG / AG19676; United States / NIA NIH HHS / AG / K01 AG019676-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Transcription Factors; 0 / ZBP-89 protein, zebrafish; 0 / Zebrafish Proteins; 0 / Zfp148 protein, mouse
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76. Gekas C, Rhodes KE, Gereige LM, Helgadottir H, Ferrari R, Kurdistani SK, Montecino-Rodriguez E, Bassel-Duby R, Olson E, Krivtsov AV, Armstrong S, Orkin SH, Pellegrini M, Mikkola HK: Mef2C is a lineage-restricted target of Scl/Tal1 and regulates megakaryopoiesis and B-cell homeostasis. Blood; 2009 Apr 9;113(15):3461-71
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  • [Title] Mef2C is a lineage-restricted target of Scl/Tal1 and regulates megakaryopoiesis and B-cell homeostasis.
  • The basic helix-loop-helix transcription factor stem cell leukemia gene (Scl) is a master regulator for hematopoiesis essential for hematopoietic specification and proper differentiation of the erythroid and megakaryocyte lineages.
  • Here, we identified a novel Scl target gene, transcription factor myocyte enhancer factor 2 C (Mef2C) from Scl(fl/fl) fetal liver progenitor cell lines.
  • Analysis of Mef2C(-/-) embryos showed that Mef2C, in contrast to Scl, is not essential for specification into primitive or definitive hematopoietic lineages.
  • Chromatin immunoprecipitation microarray hybridization analysis revealed that Mef2C is directly regulated by Scl in megakaryocytic cells, but not in erythroid cells.
  • In addition, an Scl-independent requirement for Mef2C in B-lymphoid homeostasis was observed in Mef2C-deficient mice, characterized as severe age-dependent reduction of specific B-cell progenitor populations reminiscent of premature aging.

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  • (PMID = 19211936.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM007185; United States / NIGMS NIH HHS / GM / GM07185
  • [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 / MEF2 Transcription Factors; 0 / Mef2c protein, mouse; 0 / Myogenic Regulatory Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse
  • [Other-IDs] NLM/ PMC2945827
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77. Sumanas S, Lin S: Ets1-related protein is a key regulator of vasculogenesis in zebrafish. PLoS Biol; 2006 Jan;4(1):e10
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  • During embryonic development, multiple signaling pathways control specification, migration, and differentiation of the vascular endothelial cell precursors, angioblasts.
  • No single gene responsible for the commitment of mesenchymal cells to the angioblast cell fate has been identified as yet.
  • Angioblasts in etsrp-morpholino-injected embryos (morphants) failed to undergo migration and differentiation and did not coalesce into functional blood vessels.
  • Expression of all vascular endothelial molecular markers tested was severely reduced in etsrp morphants, whereas hematopoietic markers were not affected.
  • Overexpression of etsrp RNA caused multiple cell types to express vascular endothelial markers. etsrp RNA restored expression of vascular markers in cloche mutants, defective in hematopoietic and endothelial cell formation, arguing that etsrp functions downstream of cloche in angioblast formation. etsrp gene function was also required for endothelial marker induction by the vascular endothelial growth factor (vegf) and stem cell leukemia (scl/tal1).

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  • (PMID = 16336046.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ DQ021472
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK054508; United States / NHLBI NIH HHS / HL / T32 HL069766; United States / NIDDK NIH HHS / DK / R01 DK54508
  • [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 / Etsrp protein, zebrafish; 0 / GATA1 Transcription Factor; 0 / Proto-Oncogene Proteins; 0 / Zebrafish Proteins; 0 / gata1 protein, zebrafish; 0 / tal1 protein, zebrafish; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC1310653
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78. Koschmieder S, Göttgens B, Zhang P, Iwasaki-Arai J, Akashi K, Kutok JL, Dayaram T, Geary K, Green AR, Tenen DG, Huettner CS: Inducible chronic phase of myeloid leukemia with expansion of hematopoietic stem cells in a transgenic model of BCR-ABL leukemogenesis. Blood; 2005 Jan 1;105(1):324-34
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  • [Title] Inducible chronic phase of myeloid leukemia with expansion of hematopoietic stem cells in a transgenic model of BCR-ABL leukemogenesis.
  • To develop murine models of leukemogenesis, a series of transgenic mice expressing BCR-ABL in different hematopoietic cell subsets was generated.
  • Here we describe targeted expression of P210 BCR-ABL in stem and progenitor cells of murine bone marrow using the tet-off system.
  • The transactivator protein tTA was placed under the control of the murine stem cell leukemia (SCL) gene 3' enhancer.
  • Autopsy of sick mice demonstrated splenomegaly, myeloid bone marrow hyperplasia, and extramedullary myeloid cell infiltration of multiple organs.
  • Fluorescence-activated cell sorter (FACS) analysis demonstrated a significant increase in mature and immature myeloid cells in bone marrow and spleen, together with increased bilineal B220+/Mac-1+ cells in the bone marrow. tTA mRNA was expressed in FACS-sorted hematopoietic stem cells expanded 26-fold after BCR-ABL induction.
  • Thirty-one percent of the animals demonstrated a biphasic phenotype, consisting of neutrophilia and subsequent B-cell lymphoblastic disease, reminiscent of blast crisis.
  • In summary, this mouse model recapitulates many characteristics of human chronic myeloid leukemia (CML) and may help elucidate basic leukemogenic mechanisms in CML stem cells during disease initiation and progression.
  • [MeSH-major] Disease Models, Animal. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Hematopoietic Stem Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Animals. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Transformation, Neoplastic / genetics. Disease Progression. Leukocytosis / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Mice, Transgenic. Myeloid Cells / metabolism. Myeloid Cells / pathology. Neoplasm Invasiveness. Neutrophils / metabolism. Neutrophils / pathology. Phenotype. Spleen / metabolism. Spleen / pathology. Stem Cell Transplantation. Survival Rate. Transcriptional Activation / genetics


79. Zhang L, Liu BH, Tong WD, Li CX: [Distribution and efficiency of recombinant adenovirus mediated human stem cell leukemia gene transfer in mice with interstitial cells of Cajal loss]. Zhonghua Wei Chang Wai Ke Za Zhi; 2007 Mar;10(2):119-23
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  • [Title] [Distribution and efficiency of recombinant adenovirus mediated human stem cell leukemia gene transfer in mice with interstitial cells of Cajal loss].
  • OBJECTIVE: To investigate the construction of the green fluorescent protein (GFP) labeled recombinant adenovirus containing human stem cell leukemia (hSCL) and its distribution and efficiency in mice with interstitial cells of Cajal (ICC) loss.
  • [MeSH-major] Adenoviridae / genetics. Genetic Therapy. Green Fluorescent Proteins / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 17380448.001).
  • [ISSN] 1671-0274
  • [Journal-full-title] Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery
  • [ISO-abbreviation] Zhonghua Wei Chang Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 147336-22-9 / Green Fluorescent Proteins
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80. Cheng QS, Wang XB: [CD47 and leukemia stem cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Aug;18(4):1088-91
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  • [Title] [CD47 and leukemia stem cells].
  • The expression of CD47 on normal hematopoietic stem cells (HSCs) is useful for maintaining the stability of HSCs in body, but the high expression of CD47 existed on leukemia stem cell (LSCs) of AML patients which can reduce the macrophage-induced phagocytosis to LSCs and decrease the clearance of innate immune system of organism to LSCs.

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  • (PMID = 20723335.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD47
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81. Silberstein L, Sánchez MJ, Socolovsky M, Liu Y, Hoffman G, Kinston S, Piltz S, Bowen M, Gambardella L, Green AR, Göttgens B: Transgenic analysis of the stem cell leukemia +19 stem cell enhancer in adult and embryonic hematopoietic and endothelial cells. Stem Cells; 2005 Oct;23(9):1378-88
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  • [Title] Transgenic analysis of the stem cell leukemia +19 stem cell enhancer in adult and embryonic hematopoietic and endothelial cells.
  • Appropriate transcriptional regulation is critical for the biological functions of many key regulatory genes, including the stem cell leukemia (SCL) gene.
  • As part of a systematic dissection of SCL transcriptional regulation, we have previously identified a 5,245-bp SCL +18/19 enhancer that targeted embryonic endothelium together with embryonic and adult hematopoietic progenitors and stem cells (HSCs).
  • This enhancer is proving to be a powerful tool for manipulating hematopoietic progenitors and stem cells, but the design and interpretation of such transgenic studies require a detailed understanding of enhancer activity in vivo.
  • Moreover, activity in a proportion of thymocytes and other SCL-negative cell types suggests the existence of a silencer elsewhere in the SCL locus.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Enhancer Elements, Genetic / genetics. Hematopoietic Stem Cells / cytology. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Cell Lineage. Endothelial Cells / cytology. Endothelial Cells / enzymology. Female. Gene Expression Regulation, Developmental / genetics. Gene Expression Regulation, Enzymologic / genetics. Male. Mast Cells / cytology. Mast Cells / enzymology. Megakaryocytes / cytology. Megakaryocytes / enzymology. Mice. Mice, Inbred C57BL. Mice, Inbred CBA. Mice, Transgenic. beta-Galactosidase / biosynthesis. beta-Galactosidase / blood. beta-Galactosidase / genetics

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  • (PMID = 16051983.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [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 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; EC 3.2.1.23 / beta-Galactosidase
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82. Dekel B, Metsuyanim S, Garcia AM, Quintero C, Sanchez MJ, Izraeli S: Organ-injury-induced reactivation of hemangioblastic precursor cells. Leukemia; 2008 Jan;22(1):103-13
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  • Early in mammalian development, the stem cell leukemia (SCL/TAL1) gene and its distinct 3' enhancer (SCL 3'En) specify bipotential progenitor cells that give rise to blood and endothelium, thus termed hemangioblasts.
  • [MeSH-major] Endothelium, Vascular / cytology. Hematopoietic Stem Cells / metabolism. Kidney Diseases / metabolism. Reperfusion Injury / metabolism. Vascular Endothelial Growth Factor Receptor-2 / genetics

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  • (PMID = 17898790.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Antigens, CD34; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Tal1 protein, mouse; EC 2.7.10.1 / Flt1 protein, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.1.3.48 / Antigens, CD45
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83. Ellison DA, Parham DM, Sawyer JR: Cytogenetic findings in pediatric T-lymphoblastic lymphomas: one institution's experience and a review of the literature. Pediatr Dev Pathol; 2005 Sep-Oct;8(5):550-6
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  • Six children (2 to 20 years old) had LL that presented as mediastinal or cervical masses and had a T-cell immunophenotype and clonal abnormalities.
  • Eleven chromosome breakpoints in 6 of our patients (7q11, 12p13, 16p13, 18q21, 9q11, 2p11, 2q13, 7q32, and 7q23) have been reported in other patients with acute lymphoblastic leukemia or LL and involved regions containing TEL, ABL, E2A, MLL, and T-cell receptor-alpha genes.
  • A review of the cytogenetic findings of these and other cases of LL reveals that clonal aberrations are common and most frequently involve T-cell receptor gene regions.
  • The aberrations show some features similar to those of acute lymphoblastic leukemia and are not unique to LL, thus furnishing additional evidence of the equivalence of these two diseases.
  • The cytogenetic features of LL may be helpful in the diagnosis of pediatric lymphomas and undifferentiated neoplasms.
  • [MeSH-major] Chromosome Aberrations. Cytogenetic Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16211447.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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84. Wilson NK, Miranda-Saavedra D, Kinston S, Bonadies N, Foster SD, Calero-Nieto F, Dawson MA, Donaldson IJ, Dumon S, Frampton J, Janky R, Sun XH, Teichmann SA, Bannister AJ, Göttgens B: The transcriptional program controlled by the stem cell leukemia gene Scl/Tal1 during early embryonic hematopoietic development. Blood; 2009 May 28;113(22):5456-65
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  • [Title] The transcriptional program controlled by the stem cell leukemia gene Scl/Tal1 during early embryonic hematopoietic development.
  • The basic helix-loop-helix transcription factor Scl/Tal1 controls the development and subsequent differentiation of hematopoietic stem cells (HSCs).
  • In this study, we have used ChIP-Seq technology (coupling chromatin immunoprecipitation with deep sequencing) to generate a genome-wide catalog of Scl-binding events in a stem/progenitor cell line, followed by validation using primary fetal liver cells and comprehensive transgenic mouse assays.
  • By coupling ChIP-Seq in model cell lines with in vivo transgenic validation and sophisticated bioinformatic analysis, we have identified a widely applicable strategy for the reconstruction of stem cell regulatory networks in which biologic material is otherwise limiting.
  • Moreover, in addition to revealing multiple previously unrecognized links to known HSC regulators, as well as novel links to genes not previously implicated in HSC function, comprehensive transgenic analysis of regulatory elements provided substantial new insights into the transcriptional control of several important hematopoietic regulators, including Cbfa2t3h/Eto2, Cebpe, Nfe2, Zfpm1/Fog1, Erg, Mafk, Gfi1b, and Myb.


85. 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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86. Jordan CT: The potential of targeting malignant stem cells as a treatment for leukemia. Future Oncol; 2005 Apr;1(2):205-7
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  • [Title] The potential of targeting malignant stem cells as a treatment for leukemia.
  • Malignant stem cells have recently been described as the source of several types of human cancer.
  • These unique cell types are typically rare and possess properties that are distinct from most other tumor cells.
  • In leukemia, the natural properties of cancer stem cells indicate that current chemotherapy drugs will not be effective.
  • Consequently, new strategies are required that specifically and preferentially target the cancer stem cell population, whilst sparing normal stem cells.
  • This perspective article summarizes recent findings in the leukemia stem cell field and discusses new directions for therapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Leukemia / drug therapy. Neoplastic Stem Cells / drug effects

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  • (PMID = 16555992.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
  • [Number-of-references] 22
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87. Nicholson E, Holyoake T: The chronic myeloid leukemia stem cell. Clin Lymphoma Myeloma; 2009;9 Suppl 4:S376-81
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  • [Title] The chronic myeloid leukemia stem cell.
  • Chronic myeloid leukemia (CML) is a clonal stem cell disorder that is characterized by the acquired chromosomal translocation BCR-ABL.
  • This gives rise to a constitutively active tyrosine kinase deregulation of the normal mechanisms of cell cycle control.
  • In the normal hematopoietic system, hematopoietic stem cells (HSC) self-renew to form identical daughter cells but also differentiate to mature blood cells.
  • Leukemic stem cells (LSC) share these properties of self-renewal and also differentiate to mature leukemic cells.
  • LSC have been isolated from patients with CML: these cells give rise to leukemia following transplantation into NOD-SCID mice models.
  • Further characterization of CML stem cells has demonstrated that a small percentage of these cells are quiescent despite culture with growth factors.
  • The CML stem cell arises from a normal HSC that has acquired the Philadelphia chromosome.
  • Quiescent stem cells are resistant to treatment with imatinib in vitro and are thought also to show resistance in vivo.
  • The properties of the stem cells that lead to this drug resistance are still being characterized.
  • Newer molecular therapies are in development that act to specifically target and eradicate the stem cell pool.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Neoplastic Stem Cells / pathology


88. López-Jiménez J, Martín-Ballesteros E, Sureda A, Uralburu C, Lorenzo I, del Campo R, Fernández C, Calbacho M, García-Belmonte D, Fernández G: Chemotherapy-induced nausea and vomiting in acute leukemia and stem cell transplant patients: results of a multicenter, observational study. Haematologica; 2006 Jan;91(1):84-91
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  • [Title] Chemotherapy-induced nausea and vomiting in acute leukemia and stem cell transplant patients: results of a multicenter, observational study.
  • DESIGN AND METHODS: This was a multicenter, prospective, observational follow-up study including: (i) acute myeloid leukemia patients treated with moderately to highly emetogenic chemotherapy and (ii) hematopoietic stem cell transplant recipients, without reduced intensity conditioning.
  • RESULTS: One hundred consecutive transplant and 77 acute myeloid leukemia patients were studied.
  • Transplant conditioning was the most important risk factor for CINV: complete response occurred in only 20% of transplant patients (vs. 47% for leukemia patients).
  • Among patients with emesis, the mean percentage of days with emesis and the mean (+/-SD) total number of emetic episodes were 61% and 9.4+/-8.9 (transplant recipients), and 53.6% and 6.2+/-7.3 (leukemia patients), respectively.
  • CINV control was lower in the delayed than in the acute phase.
  • [MeSH-minor] Acute Disease. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation / adverse effects. Hematopoietic Stem Cell Transplantation / methods. Humans. Leukemia / complications. Leukemia / therapy. Male. Middle Aged. Prospective Studies. Serotonin Antagonists / therapeutic use. Transplantation Conditioning / adverse effects. Transplantation Conditioning / methods

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  • (PMID = 16434375.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Serotonin Antagonists
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89. Kim J, Lee SG, Song J, Kim SJ, Rha SY, Lee KA, Park TS, Choi JR: Molecular characterization of alternative SET-NUP214 fusion transcripts in a case of acute undifferentiated leukemia. Cancer Genet Cytogenet; 2010 Sep;201(2):73-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular characterization of alternative SET-NUP214 fusion transcripts in a case of acute undifferentiated leukemia.
  • The SET-NUP214 fusion gene has been rarely reported in acute myeloid leukemia, acute undifferentiated leukemia, and recurrently in T-cell acute lymphoblastic leukemia.
  • Herein we present a novel case of acute undifferentiated leukemia with SET-NUP214 rearrangement due to the cryptic deletion of the 9q34 region producing two different types of fusion transcripts by alternative splicing and molecular characterization of the fusion transcripts by fluorescence in situ hybridization, reverse transcriptase-polymerase chain reaction, and array comparative genomic hybridization analyses.
  • [MeSH-major] Leukemia / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Comparative Genomic Hybridization. Female. Gene Deletion. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Sequence Analysis, RNA. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20682390.001).
  • [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 / Oncogene Proteins, Fusion; 0 / SET-CAN fusion protein, human
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90. Radzhabov MO, Mamaev IA, Shamov IA, Gasaev DG, Shneĭder IuV: [The dagestan gene pool: the genetic structure of the nine largest ethnic groups: analysis based on data on the ABO and Rhesus blood groups]. Genetika; 2009 Feb;45(2):263-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A total of 32101 representatives of the nine largest ethnic groups of Dagestan (from 682 auls in 46 raions) have been examined.

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  • (PMID = 19334622.001).
  • [ISSN] 0016-6758
  • [Journal-full-title] Genetika
  • [ISO-abbreviation] Genetika
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / ABO Blood-Group System; 0 / Rh-Hr Blood-Group System
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91. Sun XL, Fang MY, Jiang F, Jing Y: [Immunologic classification used in typing of 68 cases of acute leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Feb;14(1):39-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Immunologic classification used in typing of 68 cases of acute leukemias].
  • To evaluate the significance of immunologic classification for typing of acute leukemia (AL).
  • In conclusion, immunologic classification can improve the accuracy in acute leukemia diagnosis.
  • The diagnosis of some special AL, such as acute unidentified leukemia (AUL), AML-M(0) and so on, must rely on immunologic classification.

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  • (PMID = 16584588.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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92. Guzman ML, Jordan CT: Lessons learned from the study of JunB: new insights for normal and leukemia stem cell biology. Cancer Cell; 2009 Apr 7;15(4):252-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lessons learned from the study of JunB: new insights for normal and leukemia stem cell biology.
  • JunB is important in maintaining normal hematopoietic stem cell functions, but the mechanisms underlying its activity are not well understood.
  • In the current issue of Cancer Cell, a study by Santaguida et al. provides new insights into JunB's function and the genesis of myeloid disease.
  • [MeSH-major] Leukemia / pathology. Neoplastic Stem Cells / pathology. Proto-Oncogene Proteins c-jun / physiology
  • [MeSH-minor] Animals. Cell Differentiation

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  • [CommentOn] Cancer Cell. 2009 Apr 7;15(4):341-52 [19345332.001]
  • (PMID = 19345324.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-jun
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93. Williams BA, Wang XH, Keating A: Clonogenic assays measure leukemia stem cell killing not detectable by chromium release and flow cytometric cytotoxicity assays. Cytotherapy; 2010 Nov;12(7):951-60