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1. 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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2. Göthert JR, Brake RL, Smeets M, Dührsen U, Begley CG, Izon DJ: NOTCH1 pathway activation is an early hallmark of SCL T leukemogenesis. Blood; 2007 Nov 15;110(10):3753-62
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  • The acquired activation of stem cell leukemia (SCL) during T lymphopoiesis is a common event in T-cell acute lymphoblastic leukemia (T-ALL).
  • Here, we generated tamoxifen (TAM)-inducible transgenic mice (lck-ER(T2)-SCL) to study the consequences of acquired SCL activation during T-cell development.
  • Aberrant activation of SCL in thymocytes resulted in the accumulation of immature CD4(+)CD8(+) (double-positive, DP) cells by preventing normal surface expression of the T-cell receptor alphabeta (TCRalphabeta) complex.
  • Strikingly, NOTCH1 target gene up-regulation was already observed after short-term SCL induction, implying that enhanced NOTCH signaling is mediated by SCL and is not dependent on secondary genetic events.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / metabolism. Leukemia, T-Cell / genetics. Proto-Oncogene Proteins / genetics. Receptor, Notch1 / metabolism
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / cytology. Cell Survival. Genes, T-Cell Receptor beta. Mice. Mice, Transgenic. Models, Biological. Organ Culture Techniques. Signal Transduction / physiology. Thymus Gland / cytology. Thymus Gland / embryology

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  • (PMID = 17698635.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse
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3. Fenaux P, Raza A, Mufti GJ, Aul C, Germing U, Kantarjian H, Cripe L, Kerstens R, De Porre P, Kurzrock R: A multicenter phase 2 study of the farnesyltransferase inhibitor tipifarnib in intermediate- to high-risk myelodysplastic syndrome. Blood; 2007 May 15;109(10):4158-63
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  • [Title] A multicenter phase 2 study of the farnesyltransferase inhibitor tipifarnib in intermediate- to high-risk myelodysplastic syndrome.
  • This multicenter phase 2 study evaluated the use of tipifarnib (R115777) in patients with poor-risk myelodysplastic syndrome (MDS; French-American-British classification).
  • Patients (n = 82) received tipifarnib 300 mg orally twice daily for the first 21 days of each 28-day cycle.
  • Twenty-six patients (32%) responded to tipifarnib: 12 (15%) complete responses (CRs) and 14 (17%) hematologic improvements; 37 patients (45%) had stable disease (modified International Working Group criteria, 2006).
  • Among the 12 CRs, the median response duration was 11.5 months (range, 2.0-21.9 months), the median time to progression was 12.4 months (range, 3.9-23.8 months), and 7 were still alive at time of analysis (all > 3 years).
  • Median overall survival was 11.7 months (95% CI, 9.4-15.0).
  • Grade 3-4 neutropenia (18%) and thrombocytopenia (32%) were the most common treatment-related adverse events; severe nonhematologic adverse events were rarely reported.
  • In this study, durable responses and acceptable side effects were observed.
  • Tipifarnib is an active agent for the treatment of patients with intermediate- to high-risk MDS.
  • [MeSH-major] Farnesyltranstransferase / antagonists & inhibitors. Myelodysplastic Syndromes / drug therapy. Quinolones / therapeutic use
  • [MeSH-minor] Administration, Oral. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Blood Transfusion. Female. Humans. Male. Middle Aged. Risk. Survival Analysis. Treatment Outcome


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4. 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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5. Wang J, Zhao HP, Lin G, Xie CQ, Nie DS, Wang QR, Lu GX: In vitro hematopoietic differentiation of human embryonic stem cells induced by co-culture with human bone marrow stromal cells and low dose cytokines. Cell Biol Int; 2005 Aug;29(8):654-61
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  • [Title] In vitro hematopoietic differentiation of human embryonic stem cells induced by co-culture with human bone marrow stromal cells and low dose cytokines.
  • Human embryonic stem (hES) cells randomly differentiate into multiple cell types during embryoid body (EB) development and limited studies have focused on directed hematopoietic differentiation.
  • Here, we report that the treatment of hES cells during EBs development with a combination of low dose hematopoietic cytokines, including stem cell factor (SCF), Flt-3 ligand, vascular endothelial growth factor (VEGF) and human bone marrow stromal cells (hBMSCs), generated cell clusters that contained 8.81% KDR-positive hemangioblasts, 9.94% CD34-positive hematopoietic stem cells and 25.7% CD45-positive mature hematopoietic cells, and expressed hematopoietic genes such as KDR, stem cell leukemia (scl) and runt-related transcription factor 1 (Runx1).
  • [MeSH-major] Bone Marrow Cells / physiology. Cell Differentiation / drug effects. Cytokines / pharmacology. Embryo, Mammalian / cytology. Hematopoietic Stem Cells / cytology. Stem Cells / cytology. Stromal Cells / physiology
  • [MeSH-minor] Antigens, CD / metabolism. Basic Helix-Loop-Helix Transcription Factors. Biomarkers / metabolism. Cell Lineage. Coculture Techniques. Colony-Forming Units Assay. Core Binding Factor Alpha 2 Subunit. DNA-Binding Proteins / metabolism. Dose-Response Relationship, Drug. Fetus. Flow Cytometry. Humans. Proto-Oncogene Proteins / metabolism. Stem Cell Factor / metabolism. Transcription Factors / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15950498.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Stem Cell Factor; 0 / Transcription Factors; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 135471-20-4 / TAL1 protein, human
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6. Bandi SR, Brandts C, Rensinghoff M, Grundler R, Tickenbrock L, Köhler G, Duyster J, Berdel WE, Müller-Tidow C, Serve H, Sargin B, Study Alliance Leukemias: E3 ligase-defective Cbl mutants lead to a generalized mastocytosis and myeloproliferative disease. Blood; 2009 Nov 5;114(19):4197-208
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  • Somatic mutations of Kit have been found in leukemias and gastrointestinal stromal tumors.
  • We recently identified the first c-Cbl mutation in human disease in an acute myeloid leukemia patient, called Cbl-R420Q.
  • Primary murine bone marrow retrovirally transduced with c-Cbl mutants and transplanted into mice led to a generalized mastocytosis, a myeloproliferative disease, and myeloid leukemia.
  • Overexpression of these Cbl mutants inhibited stem cell factor (SCF)-induced ubiquitination and internalization of Kit.
  • Importantly, transformation was observed also with kinase-dead forms of Kit and Flt3 in the presence of Cbl-70Z, but not in the absence of Kit or Flt3, suggesting a mechanism dependent on receptor tyrosine kinases, but independent of their kinase activity.
  • [MeSH-minor] Animals. Bone Marrow Transplantation. COS Cells. Cell Transformation, Neoplastic. Cercopithecus aethiops. Disease Models, Animal. Female. Humans. Ligands. Mice. Mice, Inbred BALB C. Mutagenesis, Site-Directed. Proto-Oncogene Proteins c-kit / metabolism. Signal Transduction. Ubiquitination

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  • (PMID = 19734451.001).
  • [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 / Ligands; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Cbl protein, mouse; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Investigator] Aul C; Aulitzky WE; Bentz M; Berdel W; Cetkovsky P; Dörken B; Dührsen U; Dürfeld BM; Dürk HA; Ehninger G; Einsele H; Fauser AA; Fetscher S; Frickhofen N; Frühauf S; Gaska T; Geer T; Geissler M; Görner M; Griesshammer M; Hänel M; Heits F; Hentrich M; Ho A; Höffkes HG; Jakob A; Kaesberger J; Kaiser U; Kiehl M; Klein S; Kozák T; Krause S; Lanska M; Link H; Ludwig L; Mahlberg R; Löffler LM; Mayer J; Neubauer A; Neuhaus T; Pflüger KH; Pfreundschuh M; Pielken HJ; Possinger K; Reichele A; Reinel HH; Repp R; Sandmann M; Schleyer E; Schmidt H; Schmitz N; Schulz-Abelius A; Serve H; Thiel E; Wagner T; Wandt H; Wolf M
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7. 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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8. Sausville J, Molinolo AA, Cheng X, Frampton J, Takebe N, Gutkind JS, Feldman RA: RCAS/SCL-TVA animal model allows targeted delivery of polyoma middle T oncogene to vascular endothelial progenitors in vivo and results in hemangioma development. Clin Cancer Res; 2008 Jun 15;14(12):3948-55
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  • PURPOSE: To recapitulate the generation of cancer stem cells in the context of an intact animal using a retroviral vector capable of in vivo delivery of oncogenes to primitive endothelial and hematopoietic stem cells.
  • EXPERIMENTAL DESIGN: Targeting of these progenitors was achieved using transgenic mice in which the avian TVA retroviral receptor was placed under the control of the stem cell leukemia (scl/tal-1) gene promoter and SCL +19 enhancer.
  • RESULTS: Injection of an avian retrovirus encoding polyoma middle T (PyMT), an oncogene that transforms endothelial cells, caused rapid lethality in all SCL-TVA mice but not in control TVA(-) littermates.
  • The presence of TVA(+) cells in the lesions suggests that the cells originally infected by PyMT retained stem cell characteristics.
  • This animal model should allow the generation of endothelial cancer stem cells in the natural environment of an immunocompetent animal, thereby enabling the recapitulation of genetic alterations that are responsible for the initiation and progression of human malignancies of endothelial origin.
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Cells, Cultured. Chickens. Mice. Mice, Inbred C57BL. Mice, Transgenic. Models, Animal. NIH 3T3 Cells. Oncogenes / physiology. Stem Cells / metabolism. Transgenes

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  • (PMID = 18559617.001).
  • [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] Evaluation Studies; Journal Article; 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 / Antigens, Polyomavirus Transforming; 0 / Avian Proteins; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Virus; 0 / Tva receptor; 135471-20-4 / TAL1 protein, human
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9. Matsuda A, Germing U, Jinnai I, Iwanaga M, Misumi M, Kuendgen A, Strupp C, Miyazaki Y, Tsushima H, Sakai M, Bessho M, Gattermann N, Aul C, Tomonaga M: Improvement of criteria for refractory cytopenia with multilineage dysplasia according to the WHO classification based on prognostic significance of morphological features in patients with refractory anemia according to the FAB classification. Leukemia; 2007 Apr;21(4):678-86
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  • To predict overall survival (OS) and leukemia-free survival (LFS) for patients with refractory anemia (RA) according to the French-American-British (FAB) classification, we investigated prognostic factors based on the morphological features of 100 Japanese and 87 German FAB-RA patients, excluding 5q-syndrome.
  • In the univariate analysis of all patients, pseudo-Pelger-Huet anomalies >or=10% (Pelger+), micromegakaryocytes >or=10% (mMgk+), dysgranulopoiesis (dys G) >or=10% and dysmegakaryopoiesis (dys Mgk) >or=40% were unfavorable prognostic factors for OS and LFS (OS; P<0.001, LFS; P<0.001).
  • However, dys Mgk >or=10% was not correlated with OS and LFS.

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  • (PMID = 17268513.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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10. Fenaux P, Mufti GJ, Hellstrom-Lindberg E, Santini V, Finelli C, Giagounidis A, Schoch R, Gattermann N, Sanz G, List A, Gore SD, Seymour JF, Bennett JM, Byrd J, Backstrom J, Zimmerman L, McKenzie D, Beach C, Silverman LR, International Vidaza High-Risk MDS Survival Study Group: Efficacy of azacitidine compared with that of conventional care regimens in the treatment of higher-risk myelodysplastic syndromes: a randomised, open-label, phase III study. Lancet Oncol; 2009 Mar;10(3):223-32
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  • After a median follow-up of 21.1 months (IQR 15.1-26.9), median overall survival was 24.5 months (9.9-not reached) for the azacitidine group versus 15.0 months (5.6-24.1) for the conventional care group (hazard ratio 0.58; 95% CI 0.43-0.77; stratified log-rank p=0.0001).
  • At 2 years, on the basis of Kaplan-Meier estimates, 50.8% (95% CI 42.1-58.8) of patients in the azacitidine group were alive compared with 26.2% (18.7-34.3) in the conventional care group (p<0.0001).

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  • (PMID = 19230772.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00071799
  • [Grant] United States / NCI NIH HHS / CA / K24 CA111717
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS428850; NLM/ PMC4086808
  • [Investigator] Durrant S; Enno A; Herrmann R; Horvath N; Mills A; Spencer A; Szer J; Gallo J; Dunlop L; Arthur C; Goranov S; Peytchev D; Gercheva L; Cermak J; Voglova J; Vey N; Dreyfus F; Laurent G; Quesnel B; Dombret H; Stamatoullas A; Wattel E; Hunault-Berger M; Aul C; Giagounidis A; Duhrsen U; Gattermann N; Platzbecker U; Schmid M; Hanel M; Haase D; Fiedler W; Schmitz N; Hofmann W; Horst H; Anagnostopoulos N; Pappa V; Papadaki E; Zoumbos N; Borbenyi Z; Masszi T; Baccarani M; Bacigalupo A; Corradini P; Leone G; Sacchi S; Bosi A; Musto P; Muus P; Dmoszynska A; Robak T; Sulek K; Kuliczkowski K; Jedrzejczak W; Zaritsky A; Abdulkadyrov K; Podoltseva E; Afanasiev B; Bargay J; Brunet S; Del Canizo C; Ribera J; Figuera Alvarez A; Diaz-Mediavilla J; Canales M; Ramos y Ortega F; Nilsson L; Olsson A; Cavenagh J; Parker J; Killick S; Kruger A; Vyas P; Dennis M; Cripe L; DiPersio J; Emanuel P
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11. Germing U, Strupp C, Knipp S, Kuendgen A, Giagounidis A, Hildebrandt B, Aul C, Haas R, Gattermann N, Bennett JM: Chronic myelomonocytic leukemia in the light of the WHO proposals. Haematologica; 2007 Jul;92(7):974-7
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  • [Title] Chronic myelomonocytic leukemia in the light of the WHO proposals.
  • Median survival time was 20 months for CMML I, and 15 months for CMML II (p<0.005).
  • [MeSH-major] Leukemia, Myelomonocytic, Chronic / classification. World Health Organization

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  • (PMID = 17606449.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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12. Wang L, Fidler C, Nadig N, Giagounidis A, Della Porta MG, Malcovati L, Killick S, Gattermann N, Aul C, Boultwood J, Wainscoat JS: Genome-wide analysis of copy number changes and loss of heterozygosity in myelodysplastic syndrome with del(5q) using high-density single nucleotide polymorphism arrays. Haematologica; 2008 Jul;93(7):994-1000
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  • Single nucleotide polymorphism array analysis has been shown to detect not only gene deletions but also regions of uniparental disomy that can pinpoint particular regions for mutation analysis.
  • DESIGN AND METHODS: We studied 42 cases of myelodysplastic syndrome with del(5q), comprising 21 patients with 5q- syndrome and 21 with del(5q) (not 5q- syndrome), and 45 healthy controls by genome wide single nucleotide polymorphism analysis with the 50K Affymetrix single nucleotide polymorphism arrays.
  • For eight patients we had T-cell DNA as a germline control and four recurrent regions of uniparental disomy were identified that were present only in the neutrophil and not T-cell DNA.
  • The recurrent regions of uniparental disomy may indicate the position of novel leukemia-associated genes.


13. Qian F, Zhen F, Xu J, Huang M, Li W, Wen Z: Distinct functions for different scl isoforms in zebrafish primitive and definitive hematopoiesis. PLoS Biol; 2007 May;5(5):e132
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  • The stem-cell leukemia (SCL, also known as TAL1) gene encodes a basic helix-loop-helix transcription factor that is essential for the initiation of primitive and definitive hematopoiesis, erythrocyte and megakarocyte differentiation, angiogenesis, and astrocyte development.
  • Functional analysis reveals that while scl-alpha and -beta are redundant for the initiation of primitive hematopoiesis, these two isoforms exert distinct functions in the regulation of primitive erythroid differentiation and definitive hematopoietic stem cell specification.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Expression. Hematopoiesis / physiology. Hematopoietic Stem Cells / cytology. Proto-Oncogene Proteins / metabolism. Zebrafish / genetics. Zebrafish Proteins / metabolism
  • [MeSH-minor] Animals. Base Sequence. Blotting, Northern. Cell Differentiation / physiology. Cloning, Molecular. DNA Primers. Immunohistochemistry. In Situ Hybridization. Molecular Sequence Data. Protein Isoforms / metabolism. Sequence Alignment. Sequence Analysis, DNA

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  • (PMID = 17472439.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; 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 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish
  • [Other-IDs] NLM/ PMC1858710
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14. Bockamp E, Antunes C, Liebner S, Schmitt S, Cabezas-Wallscheid N, Heck R, Ohnngemach S, Oesch-Bartlomowicz B, Rickert C, Sanchez MJ, Hengstler J, Kaina B, Wilson A, Trumpp A, Eshkind L: In vivo fate mapping with SCL regulatory elements identifies progenitors for primitive and definitive hematopoiesis in mice. Mech Dev; 2009 Oct;126(10):863-72
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  • One of the principal issues facing biomedical research is to elucidate developmental pathways and to establish the fate of stem and progenitor cells in vivo.
  • Hematopoiesis, the process of blood cell formation, provides a powerful experimental system for investigating this process.
  • Here, we employ transcriptional regulatory elements from the stem cell leukemia (SCL) gene to selectively label primitive and definitive hematopoiesis.
  • The distinct lineage-restricted potential of SCL-labelled early progenitors demonstrates that primitive erythroid cell fate specification is initiated during mid gastrulation.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / physiology. Cell Lineage. Hematopoiesis. Proto-Oncogene Proteins / physiology. Stem Cells / cytology

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  • (PMID = 19631738.001).
  • [ISSN] 1872-6356
  • [Journal-full-title] Mechanisms of development
  • [ISO-abbreviation] Mech. Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse
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15. Sucić M, Batinić D, Zadro R, Mrsić S, Labar B: [Cytomorphology of acute mixed leukemia]. Acta Med Croatica; 2008 Oct;62(4):379-85
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  • [Title] [Cytomorphology of acute mixed leukemia].
  • Biphenotypic acute leukemias (AL) with blasts expressing both myeloid and lymphoid antigens are grouped with undifferentiated AL and bilineal AL in the group of AL of ambiguous lineage.
  • Not all AL with myeloid and lymphoid antigens (ALMy+Ly) are true biphenotypic AL.
  • RESULTS AND DISCUSSION: In the group of 169 adult AL patients, 116 were cytomorphologically classified as acute myeloblastic leukemias (AML), 35 as acute lymphoblastic leukemias (ALL) and 18 as acute undifferentiated leukemias (ANLM).
  • In one ANLM,My+ out of 169 AL and also one ANLM,My+ out of 102 AL, blasts were cytomorphologically undifferentiated; in 3 ALLMy+ of 102 AL blasts expressed lymphoid morphology.
  • According to EGIL scoring system, among 15 AMLLy+ of 102 AL there were 4 true biphenotypic ALMy+Ly (1 M1, 2 M3, 1 M4), and in 4 ALMy+Ly with undifferentiated and lymphoid morphology there were 2 true biphenotypic AL (1 L2; 1 ANLM).
  • These observations are consistent with other studies and WHO determinations indicating that the majority of true biphenotypic leukemias are associated with immature monoblastic or myeloid cytomorphology or with lymphoid or undifferentiated characteristics, but may also express any AML cytomorphology type.
  • Thus, there is no direct correlation of leukemic cell cytomorphology and biphenotypic AL immunophenotype.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology
  • [MeSH-minor] Acute Disease. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19205415.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
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16. 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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17. 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.


18. 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
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  • [Title] Clonogenic assays measure leukemia stem cell killing not detectable by chromium release and flow cytometric cytotoxicity assays.
  • BACKGROUND AIMS: NK-92, a permanent natural killer (NK) cell line, shows cytotoxicity against a variety of tumors and has been tested in a phase I trial.
  • We tested the toxicity of NK-92 and chemotherapy drugs against the stem cell capacity of the acute leukemia cell line, KG1.
  • METHODS: KG1 was assessed for stem cell frequency by serial dilution, single-cell sorting and colony growth in methylcellulose.
  • RESULTS: The culture-initiating cell frequency of whole KG1 was between 1 in 100 to 1000 by serial dilution and single-cell sorting.
  • The cumulative flow cytotoxicity assay was more sensitive than the chromium-release assay in detecting target cell killing.
  • At a 10:1 ratio NK-92 eliminated the clonogenic capacity of KG1, which was not predicted by the chromium-release assay.
  • CONCLUSIONS: Clonogenic assays provide a more sensitive means of assessing the effect of a cytotoxic agent against putative cancer stem cells within cell lines, provided that they grow well in liquid culture medium or methylcellulose.
  • [MeSH-major] Flow Cytometry. Killer Cells, Natural / metabolism. Leukemia / immunology. Neoplastic Stem Cells / metabolism. Tumor Stem Cell Assay
  • [MeSH-minor] Antigens, CD34 / biosynthesis. Antigens, CD38 / biosynthesis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Culture Techniques. Cell Line, Tumor. Cell Separation. Chromium Isotopes / metabolism. Cytarabine / pharmacology. Cytarabine / therapeutic use. Cytotoxicity Tests, Immunologic / methods. Cytotoxicity, Immunologic. Daunorubicin / pharmacology. Daunorubicin / therapeutic use. Humans. Sensitivity and Specificity

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  • (PMID = 20230219.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Chromium Isotopes; 04079A1RDZ / Cytarabine; EC 3.2.2.5 / Antigens, CD38; ZS7284E0ZP / Daunorubicin
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19. 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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20. 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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21. 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


22. 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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  • [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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23. Jin H, Xu J, Qian F, Du L, Tan CY, Lin Z, Peng J, Wen Z: The 5' zebrafish scl promoter targets transcription to the brain, spinal cord, and hematopoietic and endothelial progenitors. Dev Dyn; 2006 Jan;235(1):60-7
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  • The stem cell leukemia (SCL) gene encodes a basic helix-loop-helix transcription factor and is essential for embryonic angiogenesis, hematopoietic stem cell specification, and erythrocyte maturation.
  • Detailed analysis of the stable transgenic fish reveals that this 5-kb upstream sequence is sufficient to direct the EGFP transcription to the brain, spinal cord, and hematopoietic-endothelial progenitors, possibly the hemangioblast, but not primitive erythrocyte, suggesting that the zebrafish scl transcription in hematopoietic-endothelial progenitors and erythrocyte is regulated by distinct cis element(s).
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Brain / embryology. Endothelium / embryology. Hematopoietic Stem Cells / metabolism. Promoter Regions, Genetic. Proto-Oncogene Proteins / genetics. Spinal Cord / embryology. Zebrafish / genetics. Zebrafish Proteins / genetics

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  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 16258937.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [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 / Proto-Oncogene Proteins; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish
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24. Xia ZB, Popovic R, Chen J, Theisler C, Stuart T, Santillan DA, Erfurth F, Diaz MO, Zeleznik-Le NJ: The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression. Proc Natl Acad Sci U S A; 2005 Sep 27;102(39):14028-33
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  • MLL, involved in many chromosomal translocations associated with acute myeloid and lymphoid leukemia, has >50 known partner genes with which it is able to form in-frame fusions.
  • Characterizing important downstream target genes of MLL and of MLL fusion proteins may provide rational therapeutic strategies for the treatment of MLL-associated leukemia.
  • To this end, we developed inducible MLL-AF4 fusion cell lines in different backgrounds.
  • Overexpression of MLL-AF4 does not lead to increased proliferation in either cell line, but rather, cell growth was slowed compared with similar cell lines inducibly expressing truncated MLL.
  • We found that in the MLL-AF4-induced cell lines, the expression of the cyclin-dependent kinase inhibitor gene CDKN1B was dramatically changed at both the RNA and protein (p27kip1) levels.
  • Further, we confirmed CDKN1B promoter binding by ChIP in MLL-AF4 as well as in MLL-AF9 leukemia cell lines.
  • Our results suggest that CDKN1B is a downstream target of MLL and of MLL-AF4, and that, depending on the background cell type, MLL-AF4 inhibits or activates CDKN1B expression.
  • This finding may have implications in terms of leukemia stem cell resistance to chemotherapy in MLL-AF4 leukemias.

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  • (PMID = 16169901.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA104300; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA78438; United States / NCI NIH HHS / CA / R01 CA104300; United States / NCI NIH HHS / CA / CA81269
  • [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 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC1236570
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25. Heuser M, Sly LM, Argiropoulos B, Kuchenbauer F, Lai C, Weng A, Leung M, Lin G, Brookes C, Fung S, Valk PJ, Delwel R, Löwenberg B, Krystal G, Humphries RK: Modeling the functional heterogeneity of leukemia stem cells: role of STAT5 in leukemia stem cell self-renewal. Blood; 2009 Nov 5;114(19):3983-93
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  • [Title] Modeling the functional heterogeneity of leukemia stem cells: role of STAT5 in leukemia stem cell self-renewal.
  • Although the cancer stem cell (CSC) concept implies that CSCs are rare, recent reports suggest that CSCs may be frequent in some cancers.
  • We hypothesized that the proportion of leukemia stem cells would vary as a function of the number of dysregulated pathways.
  • Leukemia-initiating cell (LIC) number and in vitro expansion potential of LICs were functionally assessed by limiting dilution analyses.
  • LIC expansion potential was 132-fold increased in the 2- compared with the 1-oncogene model, although phenotypically, both leukemias were similar.
  • Interestingly, in 201 acute myeloid leukemia (AML) patients, coexpression of MN1 and HOXA9 was restricted to patients with the poorest prognosis and was associated with highly active STAT signaling.
  • Our data demonstrate the functional heterogeneity of LICs and show that STAT signaling is critical for leukemia stem cell self-renewal in MN1- and HOXA9-expressing leukemias.
  • [MeSH-major] Leukemia, Experimental / metabolism. Leukemia, Experimental / pathology. Models, Biological. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. STAT5 Transcription Factor / metabolism
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Disease Models, Animal. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. In Vitro Techniques. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. MAP Kinase Signaling System / drug effects. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oncogene Proteins / genetics. Oncogene Proteins / metabolism. Oncogenes. Recombinant Proteins. STAT1 Transcription Factor / deficiency. STAT1 Transcription Factor / genetics. STAT1 Transcription Factor / metabolism. Signal Transduction / drug effects

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  • [CommentIn] Blood. 2009 Nov 5;114(19):3976-7 [19892722.001]
  • (PMID = 19667399.001).
  • [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 / Homeodomain Proteins; 0 / Mn1 protein, mouse; 0 / Neoplasm Proteins; 0 / Oncogene Proteins; 0 / Recombinant Proteins; 0 / STAT1 Transcription Factor; 0 / STAT5 Transcription Factor; 0 / Stat1 protein, mouse; 0 / Stat5b protein, mouse; 0 / homeobox protein HOXA9; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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26. Tao S, Cai Y, Sampath K: The Integrator subunits function in hematopoiesis by modulating Smad/BMP signaling. Development; 2009 Aug;136(16):2757-65
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  • Hematopoiesis, the dynamic process of blood cell development, is regulated by the activity of the bone morphogenetic protein (BMP) signaling pathway and by many transcription factors.
  • Antisense morpholino-mediated knockdown of the Integrator subunit 5 (Ints5) in zebrafish embryos affects U1 and U2 snRNA processing, leading to aberrant splicing of smad1 and smad5 RNA, and reduced expression of the hematopoietic genes stem cell leukemia (scl, also known as tal1) and gata1.
  • Blood smears from ints5 morphant embryos show arrested red blood cell differentiation, similar to scl-deficient embryos.
  • Our work establishes a link between the RNA processing machinery and the downstream effectors of BMP signaling, and reveals a new group of proteins that regulates the switch from primitive hematopoietic stem cell identity and blood cell differentiation by modulating Smad function.
  • [MeSH-minor] Animals. Cell Differentiation / physiology. Erythrocytes / cytology. Erythrocytes / physiology. Gene Knockdown Techniques. In Situ Hybridization. Multiprotein Complexes / metabolism. Oligonucleotides, Antisense / genetics. Oligonucleotides, Antisense / metabolism. RNA, Small Nuclear / genetics. RNA, Small Nuclear / metabolism. Stem Cells / cytology. Stem Cells / physiology

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  • (PMID = 19605500.001).
  • [ISSN] 1477-9129
  • [Journal-full-title] Development (Cambridge, England)
  • [ISO-abbreviation] Development
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Morphogenetic Proteins; 0 / Multiprotein Complexes; 0 / Oligonucleotides, Antisense; 0 / Protein Subunits; 0 / RNA, Small Nuclear; 0 / Smad Proteins; 0 / U1 small nuclear RNA; 0 / U2 small nuclear RNA; 0 / Zebrafish Proteins
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27. 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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28. Faber J, Armstrong SA: Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies. Klin Padiatr; 2007 Nov-Dec;219(6):306-11
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  • [Title] Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies.
  • Hematological malignancies and probably many other tumors are dependent on highly proliferating and self-renewing cancer stem cells.
  • An important question in the development of novel, less toxic antileukemic strategies specifically targeting leukemia stem cells is how closely leukemia stem cells are related to normal hematopoietic stem cells.
  • It has been recently demonstrated that leukemia stem cells can be derived from different stages in normal hematopoiesis and have unique phenotypic and genetic features.
  • Introduction of Mixed-lineage leukemia ( MLL)-fusion oncoproteins, frequently found in infant leukemias and therapy-related leukemias, into differentiated hematopoietic progenitor cells results in the generation of leukemias with a high frequency of leukemia stem cells.
  • The progenitor-derived leukemia stem cells ectopically express a limited stem cell program while maintaining the global identity of differentiated myeloid cells.
  • Development of therapeutic strategies that specifically target the leukemia stem cell program while sparing normal hematopoietic stem cells may represent a novel therapeutic approach in human leukemias with high efficacy yet less side effects.
  • [MeSH-major] Leukemia / therapy. Leukemia, Biphenotypic, Acute. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplastic Stem Cells
  • [MeSH-minor] Child. Hematopoietic Stem Cells. Histone-Lysine N-Methyltransferase. Humans. Infant. Oncogene Proteins, Fusion. Phenotype

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  • (PMID = 18050039.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 62
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29. Carter BZ, Mak DH, Cortes J, Andreeff M: The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it? Semin Hematol; 2010 Oct;47(4):362-70
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  • [Title] The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it?
  • Chronic myeloid leukemia (CML) is a clonal multistep myeloproliferative disease originating from and ultimately sustained by a rare population of BCR-ABL(+) cells with multilineage stem cell properties.
  • Despite this achievement, CML is often not curable, largely due to the innate insensitivity of CML stem cells, particularly when in a quiescent state.
  • This failure of not only imatinib but also the second-generation tyrosine kinase inhibitors (TKIs) frequently leads to relapse upon drug discontinuation.
  • Thus, any curative therapy must eliminate CML stem cells.
  • A comprehensive understanding of the biological properties of CML stem cells and an elucidation of the molecular mechanisms and signaling pathways enabling these CML stem cells to self-renew, combined with insight into the regulation of apoptosis signaling and the mechanisms governing the interaction of CML stem cells with their bone marrow microenvironment, will facilitate the development of therapies for targeting these cells.
  • Here, we discuss the biological properties of CML stem cells and potential strategies to eliminate them.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20875553.001).
  • [ISSN] 1532-8686
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA49639
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS219537; NLM/ PMC2948413
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30. Yoshida K, Hirabayashi Y, Wada S, Watanabe F, Watanabe K, Aizawa S, Inoue T: p53 (TRP53) deficiency-mediated antiapoptosis escape after 5 Gy X irradiation still induces stem cell leukemia in C3H/He mice: comparison between whole-body assay and bone marrow transplantation (BMT) assay. Radiat Res; 2007 Jun;167(6):703-10
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  • [Title] p53 (TRP53) deficiency-mediated antiapoptosis escape after 5 Gy X irradiation still induces stem cell leukemia in C3H/He mice: comparison between whole-body assay and bone marrow transplantation (BMT) assay.
  • Interestingly, the present study showed a high frequency of stem cell leukemia, i.e., leukemias characterized by a lack of differentiation due also to p53 deficiency, even after 5 Gy irradiation.
  • The frequencies of stem cell leukemias (and those of total hematopoietic malignancies) were 16% (24%) at 1 Gy and 45% (75%) at 3 Gy.
  • Furthermore, markedly high incidences of stem cell leukemias were observed at 5 Gy in p53(+/-) mice, i.e., 87% (100%) in the transplantation assay and 60% (83.3%) in the whole-body assay, whereas a conventional whole-body assay induced only 14% in wild-type mice.
  • The high incidence of stem cell leukemias observed in this study using heterozygous p53-deficient mice agrees with results of a previous study of homozygous p53-deficient mice and is consistent with the high frequency of loss of heterozygosity in the p53 wild-type allele observed in leukemias.
  • This suggests that the target cells for radiation-induced stem cell leukemias may be p53-deficient hematopoietic stem cells.
  • [MeSH-major] Apoptosis / radiation effects. Bone Marrow Transplantation / methods. Leukemia, Radiation-Induced / physiopathology. Leukemia, Radiation-Induced / surgery. Stem Cells / radiation effects. Tumor Suppressor Protein p53 / deficiency


31. Saito S, Nouno K, Shimizu R, Yamamoto M, Nagata K: Impairment of erythroid and megakaryocytic differentiation by a leukemia-associated and t(9;9)-derived fusion gene product, SET/TAF-Ibeta-CAN/Nup214. J Cell Physiol; 2008 Feb;214(2):322-33
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  • [Title] Impairment of erythroid and megakaryocytic differentiation by a leukemia-associated and t(9;9)-derived fusion gene product, SET/TAF-Ibeta-CAN/Nup214.
  • SET-CAN associated with the t(9;9) in acute undifferentiated leukemia encodes almost the entire sequence of SET and the C-terminal two-third portion of CAN, including the FG repeat region.
  • Characterization of the bone marrow cells of transgenic mice indicated impairment in hematopoietic differentiation of erythroid, megakaryocytic, and B cell lineages by SET-CAN.
  • Our results demonstrate that SET-CAN blocks the hematopoietic differentiation program--one of the characteristics of acute myeloid leukemia.
  • [MeSH-major] Erythroid Precursor Cells / physiology. Hematopoiesis / physiology. Leukemia / physiopathology. Megakaryocytes / physiology. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Animals. Cell Differentiation. Chromosomal Proteins, Non-Histone / genetics. Chromosomes, Human, Pair 9. DNA, Complementary. Histone Chaperones. Humans. Mice. Mice, Transgenic. Nuclear Pore Complex Proteins / genetics. Promoter Regions, Genetic. RNA, Messenger / metabolism. Transcription Factors / genetics. Translocation, Genetic

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17620317.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA, Complementary; 0 / Histone Chaperones; 0 / Nuclear Pore Complex Proteins; 0 / Nup214 protein, mouse; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / SET protein, human; 0 / SET-CAN fusion protein, human; 0 / Transcription Factors
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32. Göthert JR, Gustin SE, Hall MA, Green AR, Göttgens B, Izon DJ, Begley CG: In vivo fate-tracing studies using the Scl stem cell enhancer: embryonic hematopoietic stem cells significantly contribute to adult hematopoiesis. Blood; 2005 Apr 1;105(7):2724-32
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  • [Title] In vivo fate-tracing studies using the Scl stem cell enhancer: embryonic hematopoietic stem cells significantly contribute to adult hematopoiesis.
  • Evidence for the lineage relationship between embryonic and adult hematopoietic stem cells (HSCs) in the mouse is primarily indirect.
  • In order to study this relationship in a direct manner, we expressed the tamoxifen-inducible Cre-ER(T) recombinase under the control of the stem cell leukemia (Scl) stem-cell enhancer in transgenic mice (HSC-SCL-Cre-ER(T)).
  • Strikingly, the proportion of marked cells within the transplanted and the in vivo-remaining HSC compartment was not different, implying that no further HSC generation occurred during late fetal and neonatal stages of development.
  • [MeSH-major] Enhancer Elements, Genetic. Hematopoiesis / physiology. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Integrases / genetics
  • [MeSH-minor] Age Factors. Animals. Antineoplastic Agents, Hormonal / pharmacology. Biomarkers. Cell Lineage. Gene Expression / drug effects. Hematopoietic Stem Cell Transplantation. Lac Operon. Mice. Mice, Inbred C57BL. Mice, Transgenic. Recombination, Genetic. Tamoxifen / pharmacology. Transgenes / physiology


33. Abla O, Gassas A, Stevens R, Grant R, Abdelhaleem M: bcr-abl-positive T-cell acute lymphoblastic leukemia associated with parvovirus B19 infection. J Pediatr Hematol Oncol; 2006 Feb;28(2):98-9
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  • [Title] bcr-abl-positive T-cell acute lymphoblastic leukemia associated with parvovirus B19 infection.
  • The authors report an unusual presentation of a Philadelphia chromosome-positive acute lymphoblastic leukemia with two unusual features: a bcr-abl fusion mRNA coding for p210 protein and a T-cell immunophenotype.
  • The patient was a 16-year-old boy who presented with septic shock and pancytopenia, likely precipitated by an acute parvovirus B19 infection.
  • Management consisted of supportive therapy, followed by chemotherapy for T-cell acute lymphoblastic leukemia and stem cell transplantation.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / etiology. Parvoviridae Infections / complications. Parvovirus B19, Human / pathogenicity. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Preleukemia / complications
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Bone Marrow / virology. Cerebral Hemorrhage / etiology. Combined Modality Therapy. Disseminated Intravascular Coagulation / etiology. Fatal Outcome. Fusion Proteins, bcr-abl / blood. Genes, abl. Hematopoietic Stem Cell Transplantation. Humans. Male. Methotrexate / administration & dosage. Multiple Organ Failure / etiology. Neoplasm Proteins / blood. Pancytopenia / etiology. Pneumonia / etiology. Prednisone / administration & dosage. Shock, Septic / etiology. Staphylococcal Infections / complications. Vincristine / administration & dosage

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  • (PMID = 16462583.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 5J49Q6B70F / Vincristine; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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34. 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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35. Büchner T, Berdel WE, Schoch C, Haferlach T, Serve HL, Kienast J, Schnittger S, Kern W, Tchinda J, Reichle A, Lengfelder E, Staib P, Ludwig WD, Aul C, Eimermacher H, Balleisen L, Sauerland MC, Heinecke A, Wörmann B, Hiddemann W: Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia. J Clin Oncol; 2006 Jun 1;24(16):2480-9
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  • [Title] Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia.
  • PURPOSE: Intensification by high-dose cytarabine in postremission or induction therapy and prolonged maintenance are established strategies to improve the outcome in patients with acute myeloid leukemia (AML).
  • Whether additional intensification can add to this effect has not yet been determined.
  • PATIENTS AND METHODS: A total of 1,770 patients (age 16 to 85 years) with de novo or secondary AML or high-risk myelodysplastic syndrome (MDS) were randomly assigned upfront for induction therapy containing one course with standard dose and one course with high-dose cytarabine, or two courses with high-dose cytarabine, and in the same step received postremission prolonged maintenance or busulfan/cyclophosphamide chemotherapy with autologous stem-cell transplantation.
  • CONCLUSION: The regimen of one course with standard-dose cytarabine and one course with high-dose cytarabine for induction, and prolonged maintenance for postremission chemotherapy in patients with AML is not improved by additional escalation in cytotoxic treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Drug Administration Schedule. Female. Humans. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Mitoxantrone / administration & dosage. Multivariate Analysis. Prognosis. Prospective Studies. Remission Induction. Risk Factors. Transplantation, Autologous. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2006 Dec 1;24(34):5471-2; author reply 5472-3 [17135654.001]
  • [ErratumIn] J Clin Oncol. 2011 Jul 1;29(19):2739
  • (PMID = 16735702.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; EC 1.1.1.27 / L-Lactate Dehydrogenase
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36. Davey ML, Tsuneda A, Currah RS: Pathogenesis of bryophyte hosts by the ascomycete Atradidymella muscivora. Am J Bot; 2009 Jul;96(7):1274-80
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  • Pycnidia of the Phoma anamorph (P. muscivora) and uniloculate pseudothecia were initiated as tightly packed masses of stromatic dematiaceous hyphae within a single host cell.
  • A new microniche among bryophilous fungi is described, whereby A. muscivora supplants the gemmae of Aul. palustre and exploits the normal nutrient-flow of the moss gametophyte.
  • Atradidymella muscivora produced both cellulases and soluble polyphenolic oxidases, allowing it to also function as a saprobe and degrade the cell walls of bryophytes.

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  • (PMID = 21628276.001).
  • [ISSN] 0002-9122
  • [Journal-full-title] American journal of botany
  • [ISO-abbreviation] Am. J. Bot.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. 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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38. 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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39. Torfs CP, Christianson RE, Iovannisci DM, Shaw GM, Lammer EJ: Selected gene polymorphisms and their interaction with maternal smoking, as risk factors for gastroschisis. Birth Defects Res A Clin Mol Teratol; 2006 Oct;76(10):723-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selected gene polymorphisms and their interaction with maternal smoking, as risk factors for gastroschisis.
  • BACKGROUND: Gastroschisis is a severe birth defect in which the infant is born with a portion of the intestines extruding through a small tear in the abdominal wall, usually to the right of the umbilical cord.
  • Its etiology is unknown, but the prevailing hypothesis is that it results from a vascular accident at the time of involution of the right umbilical vein or of the development of the superior mesenteric artery.
  • METHODS: In a case-control study of 57 cases of gastroschisis and 506 controls, we tested DNA for polymorphisms of 32 genes representing enzymes involved in angiogenesis, blood vessel integrity, inflammation, wound repair, and dermal or epidermal strength.
  • RESULTS: In logistic regression, controlling for maternal ethnicity, and using the homozygote wild-type as referent, the following gene polymorphisms were associated with an increased risk for a gastroschisis for heterozygotes: ICAM1 gly241arg (odds ratio [OR], 1.9; 95% confidence interval [CI], 1.1 -3.4); NOS3 glu298asp (OR, 1.9; 95% CI, 1.1-3.4); NPPA 2238T > C (OR, 1.9; 95% CI, 1.0-3.4); and ADD1 gly460trp (OR, 1.5; 95% CI, 0.8-2.8).
  • Additionally, for the NPPA and ADD1 single-nucleotide polymorphisms (SNPs), the homozygote variants had a significantly higher risk than the heterozygotes (OR, 7.5; 95% CI, 1.7-33.5 and OR, 4.9; 95% CI, 1.9-12.9, respectively).
  • Three SNPs showed a strong interaction with maternal smoking.
  • The risk for smokers with 1 or 2 variant alleles compared to nonsmokers with the wild-type allele were: NOS3 (OR, 5.2; 95% CI, 2.4-11.4); ICAM1 (OR, 5.2; 95% CI, 2.1-12.7); and NPPA (OR, 6.4; 95% CI, 2.8-14.6).
  • CONCLUSIONS: These results support the hypothesis of a vascular compromise as part of a multifactorial etiology of gastroschisis involving both genes and environmental factors.
  • [MeSH-major] Gastroschisis / genetics. Genetic Predisposition to Disease / genetics. Polymorphism, Genetic. Smoking / genetics
  • [MeSH-minor] Female. Follow-Up Studies. Genotype. Humans. Infant, Newborn. Male. Maternal Exposure / adverse effects. Maternal-Fetal Exchange / genetics. Mothers. Pregnancy. Retrospective Studies. Risk Factors

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17051589.001).
  • [ISSN] 1542-0752
  • [Journal-full-title] Birth defects research. Part A, Clinical and molecular teratology
  • [ISO-abbreviation] Birth Defects Res. Part A Clin. Mol. Teratol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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40. 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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41. 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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42. 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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43. Germing U, Platzbecker U, Giagounidis A, Aul C: Platelet morphology, platelet mass, platelet count and prognosis in patients with myelodysplastic syndromes. Br J Haematol; 2007 Aug;138(3):399-400
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  • [Title] Platelet morphology, platelet mass, platelet count and prognosis in patients with myelodysplastic syndromes.
  • [MeSH-major] Blood Platelets / pathology. Myelodysplastic Syndromes / blood
  • [MeSH-minor] Humans. Platelet Count. Prognosis. Survival Rate

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  • [CommentOn] Br J Haematol. 2006 Oct;135(2):198-200 [16939490.001]
  • (PMID = 17555472.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
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44. Caciagli L, Bulayeva K, Bulayev O, Bertoncini S, Taglioli L, Pagani L, Paoli G, Tofanelli S: The key role of patrilineal inheritance in shaping the genetic variation of Dagestan highlanders. J Hum Genet; 2009 Dec;54(12):689-94
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  • Isolated mountain villages (auls) in Dagestan still preserve high level of genetic and cultural diversity and have patriarchal societies with a long history of isolation.
  • The aim of this study was to understand the genetic history of five Dagestan highland auls with distinct ethnic affiliation (Avars, Chechens-Akkins, Kubachians, Laks, Tabasarans) using markers on the male-specific region of the Y chromosome.

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  • (PMID = 19911015.001).
  • [ISSN] 1435-232X
  • [Journal-full-title] Journal of human genetics
  • [ISO-abbreviation] J. Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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45. Giagounidis AA, Heinsch M, von Barany RU, Erlemannb R, Aul C: Breast cancer metastasis to the aortic vessel wall. Onkologie; 2005 Jun;28(6-7):369
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  • [Title] Breast cancer metastasis to the aortic vessel wall.
  • [MeSH-major] Aorta, Abdominal / pathology. Breast Neoplasms / pathology. Carcinoma, Lobular / pathology. Carcinoma, Lobular / secondary. Vascular Neoplasms / pathology
  • [MeSH-minor] Female. Humans. Middle Aged. Neoplasm Invasiveness

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  • [CommentOn] Onkologie. 2005 Mar;28(3):141-3 [15772464.001]
  • (PMID = 15973777.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Comment; Letter
  • [Publication-country] Switzerland
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46. 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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47. Vormoor HJ: Malignant stem cells in childhood acute lymphoblastic leukemia: the stem cell concept revisited. Cell Cycle; 2009 Apr 1;8(7):996-9
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  • [Title] Malignant stem cells in childhood acute lymphoblastic leukemia: the stem cell concept revisited.
  • We have recently shown that in childhood acute lymphoblastic leukemia (ALL) blasts at different stages of immunophenotypic maturation possess stem cell properties.
  • Here, we discuss our results in the context of previous investigations of ALL stem cells and recent studies highlighting specific limitations of the xenotransplantation models for human hematopoietic cells.
  • Leukemia-propagating stem cells in ALL may be more frequent than previously thought!
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Neoplastic Stem Cells / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19270513.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD34
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48. 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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49. Saussele S, Berger U, Aul C, Büchner T, Döhner H, Ehninger G, Ganser A, Gökbuget N, Hoelzer D, Uberla K, Hehlmann R: [Clinical research within the German competence net "acute and chronic leukemias"]. Med Klin (Munich); 2006 May 15;101(5):414-20
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  • [Title] [Clinical research within the German competence net "acute and chronic leukemias"].
  • [Transliterated title] Klinische Forschung im Kompetenznetz "Akute und chronische Leukämien".
  • BACKGROUND: Leukemias are a challenge and a cost factor to society because of their frequency in all age groups.
  • Leukemia research and therapy have achieved high standards and even a leading position in Germany with regard to clinical trials, standardization of diagnostics and molecular studies of prognostic factors, signal transduction and gene expression.
  • Progress is hampered, however, by fragmentation of leukemia trial groups, diagnostic approaches and treatment research activities.
  • GOALS: A network was therefore created to integrate the leading leukemia trial groups on chronic myeloid leukemia (CML), acute myeloid leukemia (AML), acute lymphatic leukemia (ALL), myelodysplastic syndromes (MDS) and chronic myeloproliferative diseases (CMPD) and their interdisciplinary partners (diagnostics, treatment research, biometry) in cooperation with basic research and pharmaceutical industry to foster advancements in leukemiarelated research and health care through clinical trials, promotion of translational research, introduction of standards for diagnostics and therapy, and development of evidence-based guidelines.
  • PERSPECTIVES: On the basis of experience with the Competence Network "Acute and chronic leukemias" with its management, communication and information structures, the "European LeukemiaNet" (ELN) has been established within the 6th Framework Program of the European Union.
  • The ELN integrates 78 leading leukemia trial groups (AML, ALL, CML, CLL, MDS, and CMPD), their 83 interdisciplinary partner groups (diagnostics, treatment research, registry, guidelines), industry and SMEs (small- and medium-sized enterprises) across Europe to form a cooperative network for advancements in leukemia-related research and health care.
  • [MeSH-major] Biomedical Research. Leukemia / therapy. Societies, Medical
  • [MeSH-minor] Acute Disease. Chronic Disease. Germany. Humans

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  • (PMID = 16685489.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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50. Miller DR: A tribute to Sidney Farber-- the father of modern chemotherapy. Br J Haematol; 2006 Jul;134(1):20-6
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  • He recognised that folic acid stimulated leukaemic cell growth and enhanced disease progression.
  • His landmark study, published in 1948, demonstrated that a number of folic acid antagonists, including 4-aminopteroyl-glutamic acid (aminopterin) produced temporary remissions in children with acute undifferentiated leukaemia.
  • [MeSH-minor] History, 20th Century. Humans. Leukemia / drug therapy. United States

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  • (PMID = 16803563.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Biography; Historical Article; Journal Article
  • [Publication-country] England
  • [Personal-name-as-subject] Farber S
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51. Feller N, Kelder A, Westra G, Ossenkoppele GJ, Schuurhuis GJ: Positive selection for CD90 as a purging option in acute myeloid leukemia stem cell transplants. Cytometry B Clin Cytom; 2008 Jan;74(1):9-16
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  • [Title] Positive selection for CD90 as a purging option in acute myeloid leukemia stem cell transplants.
  • BACKGROUND: Several studies showed the benefit of purging of acute myeloid leukemia (AML) stem cell transplants.
  • We reported previously that purging by positive selection of CD34+ and CD133+ cells resulted in a 3-4 log tumor cell reduction (TCR) in CD34- and/or CD133- AML, but has been shown to be potentially applicable in only about 50% of cases.
  • Similar to CD34 and CD133, CD90 marks the hematopoietic CD34 positive stem cells capable of full hematopoietic recovery after myeloablative chemotherapy, and therefore, in the present study, we explored whether a similar purging approach is possible using CD90.
  • METHODS: CD90 expression was established by flowcytometry in diagnosis AML on the clonogenic AML CD34+ blast population by flow cytometry.
  • For the calculation of the efficacy of TCR by positive selection, AML blasts were recognized by either prelabeling diagnosis blasts with CD45-FITC in spiking model experiments or using expression of leukemia associated marker combinations both in spiking experiments and in real transplants.
  • [MeSH-major] Antigens, Thy-1 / immunology. Bone Marrow Purging / methods. Flow Cytometry. Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation / methods
  • [MeSH-minor] Antigens, CD34 / immunology. Antigens, CD34 / metabolism. Biomarkers, Tumor / immunology. Female. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / immunology. Hematopoietic Stem Cells / metabolism. Humans. Immunophenotyping. Male. Middle Aged

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  • [Copyright] (c) 2007 Clinical Cytometry Society
  • (PMID = 18061946.001).
  • [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
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, Thy-1; 0 / Biomarkers, Tumor
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52. Aikawa Y, Katsumoto T, Zhang P, Shima H, Shino M, Terui K, Ito E, Ohno H, Stanley ER, Singh H, Tenen DG, Kitabayashi I: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2. Nat Med; 2010 May;16(5):580-5, 1p following 585
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  • [Title] PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2.
  • Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer.
  • Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.
  • Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.
  • Studies using PU.1-deficient mice showed that PU.1 is essential for the ability of MOZ-TIF2 to establish and maintain AML stem cells.
  • Cells expressing high amounts of CSF1R (CSF1R(high) cells), but not those expressing low amounts of CSF1R (CSF1R(low) cells), showed potent leukemia-initiating activity.
  • Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2-induced leukemia.
  • Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1R(high) cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.

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  • (PMID = 20418886.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041456-24; United States / NCI NIH HHS / CA / R01 CA032551; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / 5P30-CA13330; United States / NCI NIH HHS / CA / CA041456-24; United States / NCI NIH HHS / CA / R01-CA41456; United States / NCI NIH HHS / CA / CA32551; United States / NCI NIH HHS / CA / R01 CA041456; United States / NCI NIH HHS / CA / P30 CA013330; United States / NHLBI NIH HHS / HL / R01 HL112719
  • [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 / Colony-Stimulating Factors; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Proto-Oncogene Proteins; 0 / Receptors, Colony-Stimulating Factor; 0 / Recombinant Fusion Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS265702; NLM/ PMC3039870
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53. Afkir S, Nguelefack TB, Aziz M, Zoheir J, Cuisinaud G, Bnouham M, Mekhfi H, Legssyer A, Lahlou S, Ziyyat A: Arbutus unedo prevents cardiovascular and morphological alterations in L-NAME-induced hypertensive rats Part I: cardiovascular and renal hemodynamic effects of Arbutus unedo in L-NAME-induced hypertensive rats. J Ethnopharmacol; 2008 Mar 5;116(2):288-95
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  • The aim of the present study was to investigate whether chronic treatment with Arbutus unedo leaf (AuL) or root (AuR) aqueous extracts can prevent these alterations.
  • Six groups of rats were used: control group received tap water; N(G)-nitro-l-arginine methyl-ester (L-NAME) group treated with L-NAME at 40 mg/kg/day; AuL and AuR groups received simultaneously L-NAME (40 mg/kg/day) and Au leaves or roots extract at the same concentration 250 mg/kg/day; l-arginine and enalapril groups received simultaneously L-NAME (40 mg/kg/day) and l-arginine at 50mg/kg/day or enalapril at 15 mg/kg/day.
  • The co-administration of AuL or AuR extracts with L-NAME reduces the development of increased SBP, ameliorates the vascular reactivity as well as the baroreflex sensitivity and normalizes the renal function.
  • AuR reduces the ventricular hypertrophy but AuL do not.

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  • (PMID = 18191352.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Plant Extracts; V55S2QJN2X / NG-Nitroarginine Methyl Ester
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54. Faber J, Armstrong SA: Mixed lineage leukemia translocations and a leukemia stem cell program. Cancer Res; 2007 Sep 15;67(18):8425-8
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  • [Title] Mixed lineage leukemia translocations and a leukemia stem cell program.
  • Cancer stem cells (CSC) may provide the self-renewal capacity required to sustain a tumor.
  • One possibility is that CSC arise from the stem cell counterparts in normal tissues.
  • In support of this idea, we showed recently that mixed lineage leukemia fusion oncoproteins can convert committed hematopoietic progenitors into leukemias, which include leukemia stem cells expressing a self-renewal associated program in the context of a differentiated myeloid cell.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Leukemia, Biphenotypic, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Humans. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 17875678.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 24
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55. 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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56. 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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57. Salmon JM, Slater NJ, Hall MA, McCormack MP, Nutt SL, Jane SM, Curtis DJ: Aberrant mast-cell differentiation in mice lacking the stem-cell leukemia gene. Blood; 2007 Nov 15;110(10):3573-81
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  • [Title] Aberrant mast-cell differentiation in mice lacking the stem-cell leukemia gene.
  • The stem cell leukemia (SCL) gene encodes a basic helix-loop-helix transcription factor expressed in erythroid, megakaryocyte, and mast-cell lineages.
  • SCL(-/Delta) mice had markedly increased numbers of mast-cell progenitors (MCPs) within the peritoneal fluid, bone marrow, and spleen.
  • Fractionation of bone marrow myeloid progenitors demonstrated that these MCPs were present in the megakaryocyte-erythroid-restricted cell fraction.
  • In contrast, unilineage MCPs from control mice were present in the cell fraction with granulocyte-macrophage potential.
  • The aberrant mast-cell differentiation of SCL(-/Delta) megakaryocyte-erythroid progenitors was associated with increased expression of GATA-2.
  • Despite increased numbers of MCPs in SCL(-/Delta) mice, numbers of mature tissue mast cells were not increased unless SCL(-/Delta) mice were treated with IL-3 and stem-cell factor.
  • In part, this may be due to a requirement for SCL in normal mast-cell maturation: SCL(-/Delta) mast cells had reduced expression of the high-affinity IgE receptor and mast cell proteases, MCP-5 and MCP-6.
  • Together, these studies suggest that loss of SCL leads to aberrant mast-cell differentiation of megakaryocyte-erythroid progenitors.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Differentiation / genetics. Mast Cells / cytology. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Animals. Cell Count. Cells, Cultured. Erythroid Cells / cytology. GATA2 Transcription Factor / genetics. Humans. Leukemia / genetics. Macrophages / cytology. Megakaryocytes / cytology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Stem Cells / cytology. Transfection. Up-Regulation


58. Giagounidis AA, Germing U, Haase S, Aul C: Lenalidomide: a brief review of its therapeutic potential in myelodysplastic syndromes. Ther Clin Risk Manag; 2007 Aug;3(4):553-62
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  • In a clinical trial of patients with a del(5q) chromosomal abnormality, lenalidomide treatment resulted in red blood cell (RBC) transfusion independence in 67% of patients.

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  • (PMID = 18472976.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2374932
  • [Keywords] NOTNLM ; Lenalidomide / clinical trials / myelodysplastic syndromes / therapy
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59. Krug U, Röllig C, Koschmieder A, Heinecke A, Sauerland MC, Schaich M, Thiede C, Kramer M, Braess J, Spiekermann K, Haferlach T, Haferlach C, Koschmieder S, Rohde C, Serve H, Wörmann B, Hiddemann W, Ehninger G, Berdel WE, Büchner T, Müller-Tidow C, German Acute Myeloid Leukaemia Cooperative Group, Study Alliance Leukemia Investigators: Complete remission and early death after intensive chemotherapy in patients aged 60 years or older with acute myeloid leukaemia: a web-based application for prediction of outcomes. Lancet; 2010 Dec 11;376(9757):2000-8
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  • [Title] Complete remission and early death after intensive chemotherapy in patients aged 60 years or older with acute myeloid leukaemia: a web-based application for prediction of outcomes.
  • BACKGROUND: About 50% of patients (age ≥60 years) who have acute myeloid leukaemia and are otherwise medically healthy (ie, able to undergo intensive chemotherapy) achieve a complete remission (CR) after intensive chemotherapy, but with a substantially increased risk of early death (ED) compared with younger patients.
  • METHODS: Multivariate regression analysis was used to develop risk scores with or without knowledge of the cytogenetic and molecular risk profiles for a cohort of 1406 patients (aged ≥60 years) with acute myeloid leukaemia, but otherwise medically healthy, who were treated with two courses of intensive induction chemotherapy (tioguanine, standard-dose cytarabine, and daunorubicin followed by high-dose cytarabine and mitoxantrone; or with high-dose cytarabine and mitoxantrone in the first and second induction courses) in the German Acute Myeloid Leukaemia Cooperative Group 1999 study.
  • Risk prediction was validated in an independent cohort of 801 patients (aged >60 years) with acute myeloid leukaemia who were given two courses of cytarabine and daunorubicin in the Acute Myeloid Leukaemia 1996 study.
  • FINDINGS: Body temperature, age, de-novo leukaemia versus leukaemia secondary to cytotoxic treatment or an antecedent haematological disease, haemoglobin, platelet count, fibrinogen, and serum concentration of lactate dehydrogenase were significantly associated with CR or ED.
  • INTERPRETATION: The scores for acute myeloid leukaemia can be used to predict the probability of CR and the risk of ED in older patients with acute myeloid leukaemia, but otherwise medically healthy, for whom intensive induction chemotherapy is planned.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Internet. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • [CommentIn] Lancet. 2010 Dec 11;376(9757):1967-8 [21131041.001]
  • (PMID = 21131036.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
  • [Investigator] Fuss H; Hennesser D; Potenberg J; Ludwig WD; Schöndube D; Späth-Schwalbe E; Hesse-Amojo S; Mayr A; Grüneisen A; Boewer C; Derwahl M; Englisch HJ; Rick O; Siegert W; Notter M; Uharek L; Thiel E; Dörken B; Arnold R; Huhn D; Knigge O; Kolloch R; Krümpelmann U; Weh AJ; Zumsprekel A; Teschendorf C; Stechstor M; Trenn G; Wörmann B; Pflüger KH; Wolff T; Hertenstein B; Thomssen H; Peyn A; Rasche H; Heidtmann HH; Marquard F; Hähnel M; Fiedler F; Herbst R; Hallek M; Staib P; Heike M; Niederste-Hollenberg A; Pielken H; Hindahl H; Röllig C; Schaich M; Thiede C; Kramer M; Ehninger G; Aul C; Giagounidis A; Lange W; Kuhlemann SE; Flasshove M; Karow J; Gramatzki M; Helm G; Fuchs R; Schlegel F; Saal JG; Serve H; Kiehl M; Höffkes HG; Arland M; Meckenstock G; Giagounidis A; Haase D; Trümper L; Griesinger F; Gropp C; Depenbusch R; Eimermacher H; Schütte W; Haak U; Fasshaür E; Schmitz N; Stuhlmann R; Braumann D; Schmidt H; Buhrmann K; Balleisen L; Schubert J; Dürk H; Burk M; Ho AD; Mahlknecht U; Lange JG; Schmitz-Hübner U; Bartholomäus A; Fauser A; Link H; Hagmann FG; Wolf M; Ritter B; Frieling T; Planker M; Köchling G; Hartmann F; Middeke H; Gründgens C; Constantin C; Schalk KP; Jost KA; Fetscher S; Schmielau J; Wagner T; Uppenkamp M; Hoffmann M; Hehlmann R; Lengfelder E; Neubauer A; Schwonzen M; Spangenberg H; Bodenstein H; Tischler J; Graeven D; Kohl D; Heuer T; Pohlmann H; Brack N; Nibler K; Fleckenstein D; Haferlach T; Haferlach C; Schnittger S; Kern W; Emmerich B; Dengler R; Schlag B; Hiddemann W; Braess J; Spiekermann K; Berdel WE; Büchner T; Kienast J; Mesters R; Müller-Tidow C; Krug U; Koschmieder S; Volpert S; Wieacker P; Sauerland MC; Heinecke A; Köpcke W; Wilhelm M; Wandt H; Schäfer-Eckart K; Hirsch F; Seeber B; Hartlapp J; Hegge T; Peceny R; Koch O; Innig G; Südhoff T; Wagner T; Maschmeyer G; Kreuser ED; Schenk M; Reichle A; Andreesen R; Huff H; Schönberger D; Geer T; Heissmeyer H; Labenz J; Gassmann W; Gaske T; Käsberger J; Aulitzky WE; Leimer L; Clemens MR; Mahlberg R; Frickhofen N; Fuhr HG; Schwerdtfeger R; Augener W; Engberding R; Winter R; Sandmann M; Einsele H; Weissinger F; Rückle-Lanz H; Brugger W; Papakonstantinou G; Kreibich U; Schott G; Sommer S; Zschille W
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60. 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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61. 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
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  • [Other-IDs] NLM/ PMC2710954
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62. 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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63. 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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64. 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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65. 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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66. Giagounidis AA, Aul C: The 5q- syndrome. Cancer Treat Res; 2008;142:133-48
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  • [Title] The 5q- syndrome.
  • [MeSH-major] Chromosome Deletion. Chromosome Disorders. Chromosomes, Human, Pair 5. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Clinical Trials as Topic. Humans

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  • (PMID = 18283785.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 148
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67. Giagounidis AA, Germing U, Strupp C, Hildebrandt B, Heinsch M, Aul C: Prognosis of patients with del(5q) MDS and complex karyotype and the possible role of lenalidomide in this patient subgroup. Ann Hematol; 2005 Sep;84(9):569-71
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  • [Title] Prognosis of patients with del(5q) MDS and complex karyotype and the possible role of lenalidomide in this patient subgroup.
  • The survival of patients with myelodysplastic syndromes is strongly affected by chromosomal abnormalities.
  • Patients with an isolated del(5q31) have a favourable prognosis that worsens with the addition of another chromosomal abnormality.
  • It has been reported that both patients with isolated del(5q31) and those with one single additional chromosomal abnormality achieve hematological and cytogenetic remissions with lenalidomide therapy.
  • Whether this translates into improved overall survival of the patient population is unclear.
  • We analysed data of 25 patients with myelodysplastic syndrome and complex chromosomal abnormalities including del(5q31) and show that their median survival is between 7 and 8 months, irrespective of the medullary blast count.
  • Furthermore, we present data of a patient with complex karyotypic anomalies inclusive of del(5q31) treated with lenalidomide who achieved complete cytogenetic remission.
  • This cytogenetic remission was diagnosed after 6 months, and the hematological response is ongoing at 9 months of therapy at a dose of 5 mg p.o. daily.
  • We conclude that lenalidomide has the potential to induce sustained hematological and cytogenetic remissions in the poor prognosis MDS subgroup of del(5q31) patients with complex chromosomal anomalies and that this is likely to improve overall survival.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 5. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics. Thalidomide / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Humans. Karyotyping. Middle Aged. Prognosis. Remission Induction. Survival Rate

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  • (PMID = 15891887.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
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68. Li F, Zhang L, Li C, Ni B, Wu Y, Huang Y, Zhang G, Wang L, Zhang A, He Y, Fu T, Tong W, Liu B: Adenovirus-mediated stem cell leukemia gene transfer induces rescue of interstitial cells of Cajal in ICC-loss mice. Int J Colorectal Dis; 2010 May;25(5):557-66
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  • [Title] Adenovirus-mediated stem cell leukemia gene transfer induces rescue of interstitial cells of Cajal in ICC-loss mice.
  • OBJECTIVE: Interaction of c-Kit and its ligand stem cell factor (SCF) is necessary for appropriate development and survival of interstitial cells of Cajal (ICC) in the intestine.
  • Stem cell leukemia (SCL) gene acts as a positive regulator of upstream transcription of c-Kit expression.
  • [MeSH-major] Adenoviridae / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Transfer Techniques. Interstitial Cells of Cajal / pathology. Leukemia / pathology. Stem Cells / metabolism
  • [MeSH-minor] Animals. Cell Shape. Colon / pathology. Colon / ultrastructure. Disease Models, Animal. HeLa Cells. Humans. Mice. Mice, Inbred BALB C. Proto-Oncogene Proteins c-kit / metabolism. Recombination, Genetic. Reproducibility of Results. Staining and Labeling

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  • (PMID = 20165856.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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69. 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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70. Oh SH, Park TS, Cho SY, Kim MJ, Huh J, Kim B, Song SA, Lee JY, Jun KR, Shin JH, Kim HR, Lee JN: Acute myeloid leukemia associated with t(10;17)(p13-15;q12-21) and phagocytic activity by leukemic blasts: a clinical study and review of the literature. Cancer Genet Cytogenet; 2010 Oct 1;202(1):43-6
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  • [Title] Acute myeloid leukemia associated with t(10;17)(p13-15;q12-21) and phagocytic activity by leukemic blasts: a clinical study and review of the literature.
  • Translocation (10;17)(p13-15;q12-21) in acute leukemia is rarely reported in the literature.
  • Here, we present both a novel t(10;17) case study and a review of relevant literature on t(10;17) in acute leukemia (10 cases).
  • In summary, we came to the following preliminary conclusions: t(10;17) is associated with poorly differentiated acute leukemia subtype [90%; eight cases of acute myeloid leukemia (AML M0, M1) and one case of acute undifferentiated leukemia], phagocytic activity by blasts occurs (30%), and the survival time was short in three of the seven t(10;17) cases for whom follow-up data were available (median, 8 months).
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 17. Leukemia / drug therapy. Leukemia / genetics. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20804920.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 1.11.1.7 / Peroxidase; ZS7284E0ZP / Daunorubicin
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71. 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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72. Giagounidis AA, Haase S, Heinsch M, Göhring G, Schlegelberger B, Aul C: Lenalidomide in the context of complex karyotype or interrupted treatment: case reviews of del(5q)MDS patients with unexpected responses. Ann Hematol; 2007 Feb;86(2):133-7
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  • [Title] Lenalidomide in the context of complex karyotype or interrupted treatment: case reviews of del(5q)MDS patients with unexpected responses.
  • Lenalidomide has particular activity in patients with transfusion-dependent del(5q) myelodysplastic syndromes (MDS), but mechanistic information is limited regarding the relationship between erythroid and cytogenetic responses.
  • We reviewed medical records from three distinct subgroups of del(5q) MDS patients who had unexpected effects with lenalidomide treatment: 1. two patients with complex karyotypes who achieved both cytogenetic remissions and transfusion independence; 2. two patients with 5q- syndrome who took lenalidomide for less than 12 weeks but remained transfusion independent for 15+ months still displaying del(5q) metaphases after 6 and 12 months; and 3. one patient who was a non-responder on lenalidomide during treatment but became transfusion independent for 13+ months after discontinuation.
  • All but the latter patient in this series had reduction of affected metaphases, suggesting that erythroid responses might be mediated by result from partial or complete suppression of the malignant clone, either directly or indirectly through modulation of the bone marrow microenvironment.
  • These clinical observations illustrate the heterogeneity of del(5q)MDS pathogenesis and the diversity of lenalidomide responses within this patient subset.
  • [MeSH-major] Chromosome Deletion. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics. Thalidomide / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Female. Humans. Karyotyping. Male. Middle Aged. Treatment Outcome

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  • (PMID = 17111142.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Other-IDs] NLM/ PMC1705486
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73. 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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74. 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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75. 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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76. Germing U, Strupp C, Kuendgen A, Isa S, Knipp S, Hildebrandt B, Giagounidis A, Aul C, Gattermann N, Haas R: Prospective validation of the WHO proposals for the classification of myelodysplastic syndromes. Haematologica; 2006 Dec;91(12):1596-604
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  • The study was not population-based, but included all newly diagnosed patients from different regions in Germany.
  • Patients were followed for survival and disease evolution to acute myeloid leukemia (AML) through December 31th, 2005.
  • The median survival of patients with RA or RARS was not reached, the median survival of patients with RCMD was 31 months, that of patients with RCMD-RS was 28 months, that of 5q- patients was 40 months, of RAEB I 27 months and of RAEB II 12 months.
  • The cumulative risk of AML evolution 2 years after diagnosis was 0% in RA and RARS, 8% in 5q-, 9% in RCMD, 12% in RCMD-RS, 13% in RAEB I and 40% in RAEB II.


77. 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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78. 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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79. 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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80. 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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81. Müller-Tidow C, Klein HU, Hascher A, Isken F, Tickenbrock L, Thoennissen N, Agrawal-Singh S, Tschanter P, Disselhoff C, Wang Y, Becker A, Thiede C, Ehninger G, zur Stadt U, Koschmieder S, Seidl M, Müller FU, Schmitz W, Schlenke P, McClelland M, Berdel WE, Dugas M, Serve H, Study Alliance Leukemia: Profiling of histone H3 lysine 9 trimethylation levels predicts transcription factor activity and survival in acute myeloid leukemia. Blood; 2010 Nov 4;116(18):3564-71
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  • [Title] Profiling of histone H3 lysine 9 trimethylation levels predicts transcription factor activity and survival in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is commonly associated with alterations in transcription factors because of altered expression or gene mutations.
  • These changes might induce leukemia-specific patterns of histone modifications.
  • We used chromatin-immunoprecipitation on microarray to analyze histone 3 lysine 9 trimethylation (H3K9me3) patterns in primary AML (n = 108), acute lymphoid leukemia (n = 28), CD34(+) cells (n = 21) and white blood cells (n = 15) specimens.
  • AML-specific H3K9me3 patterns were not associated with known cytogenetic abnormalities.

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  • (PMID = 20498303.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA068822; United States / NCI NIH HHS / CA / U01 CA114810; United States / NCI NIH HHS / CA / U01 CA0114810
  • [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 / Antigens, CD34; 0 / Histones; 0 / Transcription Factors; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ PMC2981478
  • [Investigator] Schulz-Abelius A; Repp R; Klein S; Thiel E; Possinger K; Dörken B; Görner M; Pflüger KH; Mayer J; Hänel M; Pielken HJ; Ehninger G; Aul C; Mackensen A; Dührsen U; Geissler M; Serve H; Kiehl M; Höffkes HG; Schmoll HJ; Schmitz N; Schmidt H; Dürk HA; Ho A; Kaiser U; Pfreundschuh M; Lanska M; Fauser AA; Link H; Bentz M; Wolf M; Dürfeld BM; Löffler LM; Neuhaus T; Fetscher S; Wagner T; Neubauer A; Schleyer E; Griesshammer M; Lutz L; Berdel W; Wandt H; Jakob A; Gaska T; Cetkovsky P; Kozák T; Reichle A; Freund M; Heits F; Geer T; Koch W; Heidemann E; Aulitzky WE; Clemens MR; Frickhofen N; Sandmann M; Einsele H
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82. Aul K: Calling to say good-bye. Nursing; 2006 May;36(5):64hh8
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  • [Title] Calling to say good-bye.

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  • (PMID = 29019846.001).
  • [ISSN] 1538-8689
  • [Journal-full-title] Nursing
  • [ISO-abbreviation] Nursing
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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83. 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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84. Neghina R, Neghina AM, Merkler C, Marincu I, Moldovan R, Iacobiciu I: Intestinal schistosomiasis, importation of a neglected tropical disease in Romania. Case report of a traveler to endemic regions. Travel Med Infect Dis; 2009 Jan;7(1):49-51
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  • CONCLUSIONS: Final diagnosis was established with difficulty in this case.
  • Failure to associate a febrile prolonged syndrome or chronic diarrhea with a history of travel can cause a delayed diagnosis.
  • [MeSH-major] Anthelmintics / therapeutic use. Intestinal Diseases, Parasitic / diagnosis. Praziquantel / therapeutic use. Schistosomiasis / diagnosis. Travel
  • [MeSH-minor] Adult. Diagnosis, Differential. Feces / parasitology. Humans. Male. Parasite Egg Count / veterinary. Retrospective Studies. Romania / epidemiology. Treatment Outcome

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  • (PMID = 19174302.001).
  • [ISSN] 1477-8939
  • [Journal-full-title] Travel medicine and infectious disease
  • [ISO-abbreviation] Travel Med Infect Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anthelmintics; 6490C9U457 / Praziquantel
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85. 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


86. 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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87. 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


88. Wong P, Iwasaki M, Somervaille TC, Ficara F, Carico C, Arnold C, Chen CZ, Cleary ML: The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression. Cancer Res; 2010 May 1;70(9):3833-42
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  • [Title] The miR-17-92 microRNA polycistron regulates MLL leukemia stem cell potential by modulating p21 expression.
  • Despite advances in defining the critical molecular determinants for leukemia stem cell (LSC) generation and maintenance, little is known about the roles of microRNAs in LSC biology.
  • Here, we identify microRNAs that are differentially expressed in LSC-enriched cell fractions (c-kit(+)) in a mouse model of MLL leukemia.
  • Expression of miR-17 family microRNAs was substantially reduced concomitant with leukemia cell differentiation and loss of self-renewal, whereas forced expression of a polycistron construct encoding miR-17-19b miRNAs significantly shortened the latency for MLL leukemia development.
  • Leukemias expressing increased levels of the miR-17-19b construct displayed a higher frequency of LSCs, more stringent block of differentiation, and enhanced proliferation associated with reduced expression of p21, a cyclin-dependent kinase inhibitor previously implicated as a direct target of miR-17 microRNAs.
  • Knockdown of p21 in MLL-transformed cells phenocopied the overexpression of the miR-17 polycistron, including a significant decrease in leukemia latency, validating p21 as a biologically relevant and direct in vivo target of the miR-17 polycistron in MLL leukemia.
  • Thus, microRNAs quantitatively regulate LSC self-renewal in MLL-associated leukemia in part by modulating the expression of p21, a known regulator of normal stem cell function.

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  • (PMID = 20406979.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL081612; United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / CA55029; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NHLBI NIH HHS / HL / R01 HL081612-05; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / CA116606; United States / NHLBI NIH HHS / HL / R01 HL081612-04; United States / NIH HHS / OD / DP1 OD006435; United States / NCI NIH HHS / CA / CA055029-18; 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 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MicroRNAs; 0 / Mirn17 microRNA, mouse; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ NIHMS185039; NLM/ PMC2862107
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89. Malcovati L, Germing U, Kuendgen A, Della Porta MG, Pascutto C, Invernizzi R, Giagounidis A, Hildebrandt B, Bernasconi P, Knipp S, Strupp C, Lazzarino M, Aul C, Cazzola M: Time-dependent prognostic scoring system for predicting survival and leukemic evolution in myelodysplastic syndromes. J Clin Oncol; 2007 Aug 10;25(23):3503-10
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  • We defined a WHO classification-based prognostic scoring system (WPSS) that was able to classify patients into five risk groups showing different survivals (median survival from 12 to 103 months) and probabilities of leukemic evolution (P < .001).
  • WPSS was shown to predict survival and leukemia progression at any time during follow-up (P < .001), and its prognostic value was confirmed in the validation cohort.
  • [MeSH-major] Leukemia / diagnosis. Leukemia / etiology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology


90. Pimanda JE, Silberstein L, Dominici M, Dekel B, Bowen M, Oldham S, Kallianpur A, Brandt SJ, Tannahill D, Göttgens B, Green AR: Transcriptional link between blood and bone: the stem cell leukemia gene and its +19 stem cell enhancer are active in bone cells. Mol Cell Biol; 2006 Apr;26(7):2615-25
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  • [Title] Transcriptional link between blood and bone: the stem cell leukemia gene and its +19 stem cell enhancer are active in bone cells.
  • The stem cell leukemia gene (SCL/tal 1) encodes a basic helix-loop-helix transcription factor that is essential for the normal development of blood progenitors and blood vessels.
  • We have previously characterized a panel of SCL enhancers including the +19 element, which directs expression to hematopoietic stem cells and endothelium.
  • Despite consistent expression in cells of the osteogenic lineage, SCL protein is not required for bone specification of embryonic stem cells.
  • A 644-bp fragment containing the SCL +19 core enhancer was active in both blood and bone cell lines and was bound in vivo by a common array of Ets and GATA transcription factors.

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  • (PMID = 16537906.001).
  • [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 / ELF1 protein, human; 0 / Elf1 protein, mouse; 0 / Fli1 protein, mouse; 0 / GATA2 Transcription Factor; 0 / Gata2 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Protein c-fli-1; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1430329
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91. 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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92. 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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93. Kasumagic-Halilovic E, Prohic A, Karamehic J: Serum concentrations of interferon-gamma (IFN-g) in patients with alopecia areata: correlation with clinical type and duration of the disease. Med Arh; 2010;64(4):212-4
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  • A wide range of clinical presentations can occur-from a single patch of hair loss (alopecia unilocularis, AUl), multiple patches (alopecia multilocularis, AM) to complete loss of hair on the scalp (alopecia totalis, AT) or the entire body (alopecia universalis, AU).
  • The cause ofAA is unknown although most evidence supports the hypothesis that AA is a T-cell mediated autoimmune disease of the hair follicle and that cytokines play an important role.
  • Significantly elevated serum IFN-g were noticed in patients with AU type (11.81 +/- 1.11 pg/mL), expecialy those suffering from AT (12.30 +/- 0.93 pg/mL), compared with both patients with AUl (10.20 +/- 0.59 pg/mL) and patients with AM clinical type (10.21 +/- 0.78 pg/mL).
  • There was no significant difference in serum IFN-g concentration between patients with AUl and AM group, as well as between patients with AT and AU.

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  • (PMID = 21246917.001).
  • [Journal-full-title] Medicinski arhiv
  • [ISO-abbreviation] Med Arh
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Bosnia and Herzegovina
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma
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94. 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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95. 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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96. 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


97. Neukirchen J, Blum S, Kuendgen A, Strupp C, Aivado M, Haas R, Aul C, Gattermann N, Germing U: Platelet counts and haemorrhagic diathesis in patients with myelodysplastic syndromes. Eur J Haematol; 2009 Nov;83(5):477-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: At the time of diagnosis, 43% of the patients had a platelet count lower than 100 000/microL.
  • On multivariate analysis, platelet anisometry, hypocellularity of megakaryopoiesis, maturational defects of megakaryocytes and platelets <20 000/microL were independent variables showing a statistically significant correlation (P < 0.05) with clinical signs of bleeding.
  • Platelets lower than 100 000/microL were associated with significantly shortened survival (P < 0.00005), because of an increased risk of progression to acute myeloid leukaemia (AML) (30% vs. 21%) (P < 0.02) and bleeding (16% vs. 8%) (P = 0.0005).
  • [MeSH-minor] Disease-Free Survival. Female. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Platelet Transfusion. Predictive Value of Tests. Registries. Retrospective Studies. Survival Rate. Thrombocytopenia / blood. Thrombocytopenia / complications. Thrombocytopenia / mortality. Thrombocytopenia / therapy


98. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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