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Academic literature on the topic 'Fli-1'

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Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Fli-1"

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Peterlin, Pierre, Joelle Gaschet, Thierry Guillaume, Alice Garnier, Marion Eveillard, Amandine Le Bourgeois, Michel Cherel, et al. "A New Cytokine-Based Stratification Is Highly Predictive of Survivals in AML Patients." Blood 134, Supplement_1 (November 13, 2019): 1412. http://dx.doi.org/10.1182/blood-2019-125774.

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Introduction: Recently, a significant impact of the kinetics of Fms-like tyrosine kinase 3 ligand concentration (FLc) during induction (day[D]1 to D22) has been reported on survivals in first-line acute myeloid leukemia (AML) patients (pts) (Peterlin et al, 2019). Three different FLc profiles were disclosed i) sustained increase of FLc (FLI group, good-risk), ii) increase from D1 to D15, then decrease at D22 (FLD group, intermediate-risk) and iii) stagnation of low levels (<1000 pg/mL, FLL group, high-risk). An update of this prospective monocentric study (www.ClinicalTrials.gov NCT02693899) is presented here evaluating also retrospectively the impact on outcomes of 6 other cytokine level profiles during induction. Methods: Between 05/2016 and 01/2018, 62 AML pts at diagnosis (median age 59 yo [29-71], <60 yo n=33) eligible for first intensive induction were included and provided informed consent. They received standard of care first-line chemotherapy. Serum samples collected on D1, 8, 15 & 22 of induction were frozen-stored until performing ELISA for FL, TNFa, SCF, IL-1b, IL-6, IL-10, GM-CSF. Normal values were assessed in 5 healthy controls. Pts outcomes considered were relapse/leukemia-free (LFS) and overall (OS) survivals. Results: FLI, FLD and FLL profiles were observed for 26, 22 and 14 pts respectively. A total of 372 samples were assayed for the 6 other cytokines. Median concentrations at D1, D8, D15, D22 for these 6 cytokines were as follows, considering the whole cohort (and healthy donors): TNFa: 0.53, 0, 0, 0 (0); SCF: 5.91, 0, 0, 0 (3); IL-1b : 0, 0, 0, 0 (0); IL-6: 4.85, 16.28, 10.11, 7.1 (0), IL-10: 0, 0, 0, 0 (0) and GM-CSF:1.63, 1.8, 0.67, 1.34 (9.98). Median IL-6 and GM-CSF levels, compared to healthy controls, were respectively higher and lower during induction. No significant difference was observed in terms of median cytokine concentrations at any time when comparing the three FL sub-groups or FLI vs FLD pts. With a median follow-up of 28 months (range: 17-37), FLI and FLD pts show now similar 2-y LFS (62.9% vs 59%, p=0.63) and OS (69.2% vs 63.6%, p=0.70). FLL pts have a significantly higher rate of relapse (85,7% vs FLI 19,2% vs FLD 32%, p=0,0001). Comparing FLL vs FLI+FLD pts disclosed significantly different LFS (7.1% vs 61.1%, p<0.001) but not OS (36.7% vs 66.6%, p=0.11). In univariate analysis, 2y LFS and OS were not affected by the concentration (< or > median) of the 7 cytokines studied except for LFS and GM-CSFc at D8 (p=0,04) and D15 (p=0,08), for LFS and FLc at D1 (p=0.06), D8 (p=0,03), D15 (p=0,04) and D22 (p=0,03) and for OS and GM-CSF at D15 (p=0.08). A significant association between LFS was observed with ELN 2017 risk stratification (2-y LFS: favorable: 68,1% vs intermediate: 48,1% vs unfavorable: 30,7%, p=0.03) but not OS (2 y: 77% vs 55,5% vs 46,1%, p=0.09). Multivariate analysis showed that no factor was independently associated with OS while LFS remained significantly associated with the FLc profile (FLL vs others, HR: 5.79. 95%CI: 2.48-13.53, p<0.0001) and GM-CSF at D15 (HR: 0.45; 95%CI: 0.20-0.98, p=0.04) but not with ELN 2017 risk stratification (p=0.06). Cytokine levels were then assessed to try to better discriminate FLI and FLD pts. A significant higher IL-6 level at D22 was found in relapsed or deceased FLI/FLD pts (median:15,34 vs 5,42 pg/mL, p=0,04). FLI/FLD pts with low IL-6 at D22 (< median, 15.5 pg/mL, n=35 vs n=14 with high level) had significant better 2y LFS and OS (74,2% vs 38,4%, p=0,005 and 77,1% vs 38,4%, p=0,009, respectively). A new prognostic risk-stratification could thus be proposed, i.e. FLI/FLD with IL-6 <15.5 pg/mL (favorable), FLI/FLD with IL-6 >15.5 pg/mL (intermediate) and FLL (unfavorable). This new classification was considered for a second multivariate analysis, showing that it is the strongest factor associated with OS (p=0.006, ELN p=0.03, FL profile p=0.04) and LFS (p<0.0001, ELN p=0.005, GM-CSFc D15 p=0.03) (figure 1). Conclusion: This study confirms stagnation of low FLc during AML induction as a strong poor prognosis factor. Moreover, IL-6 levels at D22 further discriminate FLI/FLD pts. Thus, a new cytokine-based risk-stratification integrating FL kinetics and IL-6 levels during induction may help to better predict outcomes in first-line AML patients. These results need to be validated on a larger cohort of AML patients while anti-IL-6 therapy should be tested in combination with standard 3+7 chemotherapy. Figure 1 Disclosures Peterlin: AbbVie Inc: Consultancy; Jazz Pharma: Consultancy; Daiichi-Sankyo: Consultancy; Astellas: Consultancy. Moreau:Janssen: Consultancy, Honoraria; Amgen: Consultancy, Honoraria; Takeda: Consultancy, Honoraria; AbbVie: Consultancy, Honoraria; Celgene: Consultancy, Honoraria. Chevallier:Jazz Pharmaceuticals: Honoraria; Incyte: Consultancy, Honoraria; Daiichi Sankyo: Honoraria.
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Olubamwo, Olubunmi O., Jyrki K. Virtanen, Jussi Pihlajamaki, Pekka Mantyselka, and Tomi-Pekka Tuomainen. "Fatty liver index as a predictor of increased risk of cardiometabolic disease: finding from the Kuopio Ischaemic Heart Disease Risk Factor Study Cohort." BMJ Open 9, no. 9 (September 2019): e031420. http://dx.doi.org/10.1136/bmjopen-2019-031420.

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ObjectiveFatty liver disease (FLD), a global epidemic, is also a predictor of cardiometabolic disease (CMD) (type 2 diabetes or cardiovascular disease). Our objective was to examine whether progressive FLD, as assessed by fatty liver index (FLI), predicts increasing future CMD risk compared with relatively stable FLD, among middle-aged men.DesignProspective epidemiological study.SettingUniversity affiliated research centre in Kuopio, Eastern Finland.ParticipantsOur subjects were 501 men without CMD during the initial 4-year follow-up in the Kuopio Ischaemic Heart Disease Risk Factor Study cohort.Outcome measureOver the initial 4-year follow-up, 135 men (26.9%) had a significant (≥10) FLI increase. The association of 4-year FLI increase with incident CMD was analysed in multivariable-adjusted Cox regression models, adjusting for baseline constitutional and lifestyle factors (model 1) and, in addition, metabolic and inflammation biomarker factors (model 2).ResultsDuring a mean follow-up of 15 years, 301 new CMD cases occurred. We used subjects with low baseline FLI and no significant 4-year FLI increase as the reference. For subjects with intermediate baseline FLI and significant 4-year FLI increase, the HRs and 95% CIs for incident CMD in model 1 (2.13 (1.45 to 3.13)) and model 2 (1.73 (1.13 to 2.66)) exceeded values for subjects with similar baseline FLI without a significant 4-year change (HRs (95% CIs) were 1.36 (0.94 to 1.97) for model 1 and 1.18 (0.81 to 1.70) for model 2). They approached HRs (95% CI) for subjects who maintained high FLI over the 4 years (HRs (95% CIs) were 2.18 (1.54 to 3.10) in model 1 and 1.85 (1.21 to 2.82) in model 2).ConclusionPersons with significant FLI increase are likely with increasing CMD risk. Such persons should be evaluated for progressive FLD and CMD and managed to reduce CMD risk.
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May, W. A., S. L. Lessnick, B. S. Braun, M. Klemsz, B. C. Lewis, L. B. Lunsford, R. Hromas, and C. T. Denny. "The Ewing's sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1." Molecular and Cellular Biology 13, no. 12 (December 1993): 7393–98. http://dx.doi.org/10.1128/mcb.13.12.7393.

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EWS/FLI-1 is a chimeric protein formed by a tumor-specific 11;22 translocation found in both Ewing's sarcoma and primitive neuroectodermal tumor of childhood. EWS/FLI-1 has been shown to be a potent transforming gene, suggesting that it plays an important role in the genesis of these human tumors. We now demonstrate that EWS/FLI-1 has the characteristics of an aberrant transcription factor. Subcellular fractionation experiments localized the EWS/FLI-1 protein to the nucleus of primitive neuroectodermal tumor cells. EWS/FLI-1 specifically bound in vitro an ets-2 consensus sequence similarly to normal FLI-1. When coupled to a GAL4 DNA-binding domain, the amino-terminal EWS/FLI-1 region was a much more potent transcriptional activator than the corresponding amino-terminal domain of FLI-1. Finally, EWS/FLI-1 efficiently transformed NIH 3T3 cells, but FLI-1 did not. These data suggest that EWS/FLI-1, functioning as a transcription factor, leads to a phenotype dramatically different from that of cells expressing FLI-1. EWS/FLI-1 could disrupt normal growth and differentiation either by more efficiently activating FLI-1 target genes or by inappropriately modulating genes normally not responsive to FLI-1.
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May, W. A., S. L. Lessnick, B. S. Braun, M. Klemsz, B. C. Lewis, L. B. Lunsford, R. Hromas, and C. T. Denny. "The Ewing's sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1." Molecular and Cellular Biology 13, no. 12 (December 1993): 7393–98. http://dx.doi.org/10.1128/mcb.13.12.7393-7398.1993.

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EWS/FLI-1 is a chimeric protein formed by a tumor-specific 11;22 translocation found in both Ewing's sarcoma and primitive neuroectodermal tumor of childhood. EWS/FLI-1 has been shown to be a potent transforming gene, suggesting that it plays an important role in the genesis of these human tumors. We now demonstrate that EWS/FLI-1 has the characteristics of an aberrant transcription factor. Subcellular fractionation experiments localized the EWS/FLI-1 protein to the nucleus of primitive neuroectodermal tumor cells. EWS/FLI-1 specifically bound in vitro an ets-2 consensus sequence similarly to normal FLI-1. When coupled to a GAL4 DNA-binding domain, the amino-terminal EWS/FLI-1 region was a much more potent transcriptional activator than the corresponding amino-terminal domain of FLI-1. Finally, EWS/FLI-1 efficiently transformed NIH 3T3 cells, but FLI-1 did not. These data suggest that EWS/FLI-1, functioning as a transcription factor, leads to a phenotype dramatically different from that of cells expressing FLI-1. EWS/FLI-1 could disrupt normal growth and differentiation either by more efficiently activating FLI-1 target genes or by inappropriately modulating genes normally not responsive to FLI-1.
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Itkin, Tomer, Chaitanya R. Badwe, Sean Houghton, Yang Lin, Ying Liu, Peipei Guo, Jesus M. Gomez-Salinero, et al. "Fli-1 Transcriptionally Integrates Microenvironmental Cues Sensing By Self-Renewing Hematopoietic Stem and Progenitor Cells." Blood 134, Supplement_1 (November 13, 2019): 725. http://dx.doi.org/10.1182/blood-2019-126190.

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During adulthood and embryogenesis, fate decisions of hematopoietic stem and progenitor cells (HSPCs), such as specification, self-renewal, and differentiation are tightly regulated by their neighboring niche cells. Moreover, distinct types of niches supply differential cues to direct alternative cell fates for HSPCs. Yet, currently the intrinsic mechanisms balancing HSPC response obliqueness to microenvironmental signals are unknown. Friend Leukemia integration-1 (Fli-1), is an ETS transcription factor expressed by vascular beds and hematopoietic lineages. Fli-1 belongs to the "heptad factors" which are hypothesized to specify and sustain a hematopoietic cell fate. While Fli-1 overexpression is linked to leukemia, the functional role Fli-1 plays in HSPC specification and maintenance remains undefined. We show that inducible deletion of Fli-1 using a Rosa-CreERT2 transgenic adult mice (Fli-1ROSAΔ), results in a rapid thrombocytopenia-associated mortality. Transplantation of Fli-1ROSAΔ bone marrow (BM) cells into WT recipients, to exclude vascular-mediated defects, followed by induction of Fli-1 deletion, resulted with the same phenotype. In a set of modulated competitive transplantation experiments (differential induction time points pre- or post-transplant), we observed defective ability of Fli-1ROSAΔ HSPCs to lodge, engraft, and to sustain hematopoiesis post repopulation. Fli-1 deficient HSPCs exhibited reduced quiescent cell cycling status, a hallmark of stemness, and displayed enhanced apoptosis. Thus, Fli-1 is essential for previously unrecognized cell-autonomous HSPC functions. To determine whether Fli-1 modulates HSPC specification, Fli-1 was conditionally deleted using a developmental VE-cadherin (CDH5)-Cre transgenic model (Fli-1CDH5Δ). This resulted with premature mortality of Fli-1CDH5Δ embryos, accompanied with a hemorrhagic phenotype. Reduced numbers of hematopoietic cells were still detected in the AGM of e10.5 Fli-1CDH5Δ embryos. Conditional Fli-1 deletion using a developmental hematopoietic Vav-1 Cre transgenic model (Fli-1Vav-1Δ) resulted again with premature mortality. Reduced presence of embryonic Fli-1Vav-1Δ liver HSPCs was observed at e12.5. We also applied two in vitro co-culture systems, to study Fli-1 in endothelial to hematopoietic transition (EHT). First, isolated hemogenic endothelial cells (HEC) from WT and Fli-1ROSAΔ embryos were co-cultured with AGM-derived vascular niche. HECs isolated from Fli-1ROSAΔ AGM were still able to convert to CD45+ cells, however these cells did not expand on a vascular niche. Secondly, we have applied an endothelial to hematopoietic reprogramming system in which isolated lung ECs are virally introduced with DOX inducible FosB, Gfi1, Runx1, and Spi1 (FGRS) factors and co-cultured with vascular niche cells. Both WT and Fli-1ROSAΔ ECs were able to acquire a hemogenic like state resulting with a final capacity to convert into hematopoietic cells. Again, Fli-1ROSAΔ cells displayed lesser numbers of CD45+ cells at the end point, presumably due to impaired interaction with the vascular niche. Indeed, reduced expansion capacity was observed both for mature CD45+ and for HSPC derived from Fli-1CDH5Δ AGM region. Adult Fli-1ROSAΔ HSPCs exhibited the same niche-dependent expansion defect. Induction of Fli-1 deletion in vitro in adult HSPCs revealed loss of dependency on vascular niche inductive signals, as no additive expansion effect was observed for Fli-1ROSAΔ HSPCs in the presence of a vascular niche. Hence, Fli-1 is essential for HSPC expansion rather than hematopoietic specification. Differential RNA-seq analysis combined with epigenetic studies of expanding WT and Fli-1ROSAΔ HSPCs, revealed dysregulation of Fli-1-controlled pathways involved in transduction of microenvironmental signals for self-renewal. Unexpectedly, H3K27Ac analysis, a marker for transcriptional priming, revealed increased global acetylation of Fli-1ROSAΔ HSPCs' chromatin. Therefor, Fli-1 may not only perform as transcription activator, but foremostly as a genomic suppressor via modulation of histone acetylation status. Decrypting the mechanism(s) by which Fli-1 orchestrates HSPC self-renewal, may promote an improved expansion protocol of human HSPC pre-transplantation, and provide additional insights for microenvironmental sensing by Fli-1-dependent leukemic cells. Disclosures No relevant conflicts of interest to declare.
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Schutt, Steven Douglas, David Bastian, Hee-Jin Choi, Yongxia Wu, Mohammed Hanief Sofi, Hung Nguyen, Xian Zhang, and Xue-Zhong Yu. "Fli-1 Regulates Multiple T-Cell Subsets during Inflammatory Responses and Experimental Graft-Versus-Host Disease." Blood 134, Supplement_1 (November 13, 2019): 3201. http://dx.doi.org/10.1182/blood-2019-127577.

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Allogeneic hematopoietic stem cell transplantation (allo-HCT) is a procedure undertaken to cure hematological malignancies, especially leukemia. Graft-Versus-Host Disease (GVHD) is a serious condition that often appears following allo-HCT. Friend Leukemia Virus Integration 1 (Fli-1) is a transcription factor highly expressed in cancers including erythroleukemia and acute myeloid leukemia while also implicated in pathogenesis of systemic lupus. We have interrogated the role of Fli-1 in T-cell responses by generating a novel T-cell specific conditional disruption of fli-1 where essential exons 3 and 4 of the gene are floxed and excised in the presence of CD4-Cre recombinase. Models of acute GVHD (aGVHD) and chronic GVHD (cGVHD) were tested utilizing hematopoietic cells from mice with a heterozygous (fli-1-/+ or Het) or homozygous (fli-1-/-or Null) disruption of the fli-1 gene, or from wild-type (fli-1+/+ or WT) littermate controls. At baseline, T cells among each of these three mouse strains showed no significant difference in CD44/CD62L expression or CD4+FoxP3+ (nTreg) frequencies. In the cGVHD model, BALB/c (H2Kd) recipients were infused with allogeneic B6 (H2Kb) genotype-respective bone marrow and splenocytes in order to induce cGVHD. Recipients that received fli-1-/+CD4Cre+ marrow and splenocytes demonstrated improved survival and mild cGVHD, whereas those that received fli-1-/-CD4Cre+ or WT donor cells developed serve cGVHD (Fig. 1 a-f). Cellular studies from lymphoid organs of cGVHD allo-HCT recipients revealed that disruption of fli-1 was associated with decreased frequencies of donor CD4+ cells expressing IL-17A, IFN-γ, T follicular-like (TFH-like) cell markers, and CD8+ cells expressing PD-1. In aGVHD settings, donor fli-1-/+CD4Cre+ T cells had a decreased ability to induce aGVHD compared to WT donor T cells and fli-1-/- donor T cells (Fig. 2 a-b). When investigating cellular mechanisms in aGVHD settings, we found that fli-1-/+CD4Cre+ T cells produced significantly lower IFN-γ early after T-cell activation in vivo compared to WT and fli-1-/-CD4Cre+ T cells (Fig. 2 c). To then investigate the role of Fli-1 in T cells beyond GVHD, we utilized a colitis model by transferring naïve CD4+ T cells (CD44-CD25-) into Rag2-/- syngeneic recipients. While fli-1+/+ T cells induced severe colitis as expected, fli-1-/- and fli--/+ T cells caused moderate and mild colitis, respectively. These results were consistent with those observed in GVHD models. To elucidate underlying mechanisms, we tested the effects of Fli-1 on antigen-specific T-cells using a MHC-II restricted TCR transgenic (Tg) mouse strain specific for HY-peptide. CD4+CD25- T cells from fli-1+/+, fli-1-/+, or fli-1-/- CD4Cre+ TCR-Tg mice were polarized in vitro with endogenous antigen presenting cells from spleen in presence of HY-peptide under iTreg- or Th17-polarizing conditions. Both fli-1-/+ and fli-1-/- TCR-tg T cells exhibited significant increases in iTreg (CD4+FoxP3+) frequencies and surface expression of iTreg functional markers (CD25, CD39, CD73, NRP-1), while also having significantly decreased frequencies of IL-17A producing T cells compared to WT-TCR-tg T cells. To further explore the molecular mechanisms, we retrieved fli-1+/+, fli-1-/+, or fli-1-/- donor T cells from recipient spleens after allo-HCT and did RNAseq analysis on these cells. RNAseq data reveals significant differences in mRNA expression within acute inflammatory response and positive regulation of the immune response enrichment pathways between fli-1-/+ T cells and littermate fli-1+/+ T cells, and to a lesser extent in fli-1-/- T cells (Fig. 2 d-f). Thus, reducing Fli-1 transcriptional activity represents a potential therapeutic concept toward ameliorating GVHD after allo-HCT, while simultaneously targeting cancers such as leukemia which typically overexpress Fli-1. Disclosures No relevant conflicts of interest to declare.
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Eisbacher, Michael, Melissa L. Holmes, Anthea Newton, Philip J. Hogg, Levon M. Khachigian, Merlin Crossley, and Beng H. Chong. "Protein-Protein Interaction between Fli-1 and GATA-1 Mediates Synergistic Expression of Megakaryocyte-Specific Genes through Cooperative DNA Binding." Molecular and Cellular Biology 23, no. 10 (May 15, 2003): 3427–41. http://dx.doi.org/10.1128/mcb.23.10.3427-3441.2003.

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ABSTRACT Friend leukemia integration 1 (Fli-1) is a member of the Ets family of transcriptional activators that has been shown to be an important regulator during megakaryocytic differentiation. We undertook a two-hybrid screen of a K562 cDNA library to identify transcription factors that interacted with Fli-1 and were potential regulators of megakaryocyte development. Here we report the physical interaction of Fli-1 with GATA-1, a well-characterized, zinc finger transcription factor critical for both erythroid and megakaryocytic differentiation. We map the minimal domains required for the interaction and show that the zinc fingers of GATA-1 interact with the Ets domain of Fli-1. GATA-1 has previously been shown to interact with the Ets domain of the Fli-1-related protein PU.1, and the two proteins appear to inhibit each other's activity. In contrast, we demonstrate that GATA-1 and Fli-1 synergistically activate the megakaryocyte-specific promoters GPIX and GPIbα in transient transfections. Quantitative electrophoretic mobility shift assays using oligonucleotides derived from the GPIX promoter containing Ets and GATA binding motifs reveal that Fli-1 and GATA-1 exhibit cooperative DNA binding in which the binding of GATA-1 to DNA is increased approximately 26-fold in the presence of Fli-1 (from 4.2 to 0.16 nM), providing a mechanism for the observed transcriptional synergy. To test the effect on endogenous genes, we stably overexpressed Fli-1 in K562 cells, a line rich in GATA-1. Overexpression of Fli-1 induced the expression of the endogenous GPIX and GPIbα genes as measured by Northern blot and fluorescence-activated cell sorter analysis. This work suggests that Fli-1 and GATA-1 work together to activate the expression of genes associated with the terminal differentiation of megakaryocytes.
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Juban, Gaëtan, Guillaume Giraud, Boris Guyot, Stéphane Belin, Jean-Jacques Diaz, Joëlle Starck, Christel Guillouf, Françoise Moreau-Gachelin, and François Morlé. "Spi-1 and Fli-1 Directly Activate Common Target Genes Involved in Ribosome Biogenesis in Friend Erythroleukemic Cells." Molecular and Cellular Biology 29, no. 10 (March 16, 2009): 2852–64. http://dx.doi.org/10.1128/mcb.01435-08.

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ABSTRACT Spi-1 and Fli-1 are ETS transcription factors recurrently deregulated in mouse erythroleukemia induced by Friend viruses. Since they share the same core DNA binding site, we investigated whether they may contribute to erythroleukemia by common mechanisms. Using inducible knockdown, we demonstrated that Fli-1 contributes to proliferation, survival, and differentiation arrest of erythroleukemic cells harboring an activated fli-1 locus. Similarly, we used inducible Fli-1 knockdown and either hexamethylenebisacetamide (HMBA)- or small interfering RNA-mediated Spi-1 knockdown to investigate their respective contributions in erythroleukemic cells harboring an activated spi-1 locus. In these cells, simple or double knockdown of both Spi-1 and Fli-1 additively contributed to induce proliferation arrest and differentiation. Transcriptome profiling revealed that virtually all transcripts affected by both Fli-1 knockdown and HMBA are affected in an additive manner. Among these additively downregulated transcripts, more than 20% encode proteins involved in ribosome biogenesis, and conserved ETS binding sites are present in their gene promoters. Through chromatin immunoprecipitation, we demonstrated the association of Spi-1 and Fli-1 on these promoters in Friend erythroleukemic cells. These data lead us to propose that the oncogenicity of Spi-1, Fli-1, and possibly other ETS transcription factors may involve their ability to stimulate ribosome biogenesis.
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Starck, Joëlle, Alexandre Doubeikovski, Sandrine Sarrazin, Colette Gonnet, Govinda Rao, Arthur Skoultchi, Jacqueline Godet, Isabelle Dusanter-Fourt, and François Morle. "Spi-1/PU.1 Is a Positive Regulator of the Fli-1 Gene Involved in Inhibition of Erythroid Differentiation in Friend Erythroleukemic Cell Lines." Molecular and Cellular Biology 19, no. 1 (January 1, 1999): 121–35. http://dx.doi.org/10.1128/mcb.19.1.121.

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ABSTRACT Spi-1/PU.1 and Fli-1 are two members of the ETS family of transcription factors whose expression is deregulated by proviral insertion in most erythroleukemic cell lines induced by the spleen focus-forming virus (SFFV) and Friend murine leukemia virus (F-MuLV) components of the Friend viral complex, respectively. In this study, we present evidence that transcription of the Fli-1 gene is positively regulated by Spi-1/PU.1 in SFFV-transformed cell lines: (i) all SFFV-transformed cell lines expressing Spi-1/PU.1 are characterized by a specific pattern of Fli-1 gene transcripts initiated in the −200 region instead of position −400 as reported for F-MuLV-transformed cell lines; (ii) these Fli-1 transcripts initiated in the −200 region are downregulated in parallel with that of Spi-1/PU.1 during hexamethylenebisacetamide (HMBA) induced differentiation; and (iii) Fli-1 transcription is upregulated in SFFV cells lines following stable transfection of a Spi-1/PU.1 expression vector. Furthermore, we found by transient transfection assays that the −270/−41 region of the Fli-1 gene displays promoter activity which is transactivated by Spi-1/PU.1. This promoter is strictly dependent on the integrity of two highly conserved ETS DNA binding sites that bind the Spi-1/PU.1 protein in vitro. Finally, we show that transfection of constitutive or inducible Fli-1 expression vectors in SFFV-transformed cells inhibits their erythroid differentiation induced by HMBA. Overall, these data indicate that Fli-1 is a target gene of the Spi-1/PU.1 transcription factor in SFFV-transformed cell lines. We further suggest that deregulated synthesis of Fli-1 may trigger a common mechanism contributing to erythroleukemia induced by either SFFV or F-MuLV.
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Lakhanpal, Gurpreet K., Laura M. Vecchiarelli-Federico, You-Jun Li, Jiu-Wei Cui, Monica L. Bailey, David E. Spaner, Daniel J. Dumont, Dwayne L. Barber, and Yaacov Ben-David. "The inositol phosphatase SHIP-1 is negatively regulated by Fli-1 and its loss accelerates leukemogenesis." Blood 116, no. 3 (July 22, 2010): 428–36. http://dx.doi.org/10.1182/blood-2009-10-250217.

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Abstract The activation of Fli-1, an Ets transcription factor, is the critical genetic event in Friend murine leukemia virus (F-MuLV)–induced erythroleukemia. Fli-1 overexpression leads to erythropoietin-dependent erythroblast proliferation, enhanced survival, and inhibition of terminal differentiation, through activation of the Ras pathway. However, the mechanism by which Fli-1 activates this signal transduction pathway has yet to be identified. Down-regulation of the Src homology 2 (SH2) domain-containing inositol-5-phosphatase-1 (SHIP-1) is associated with erythropoietin-stimulated erythroleukemic cells and correlates with increased proliferation of transformed cells. In this study, we have shown that F-MuLV–infected SHIP-1 knockout mice display accelerated erythroleukemia progression. In addition, RNA interference (RNAi)-mediated suppression of SHIP-1 in erythroleukemia cells activates the phosphatidylinositol 3-kinase (PI 3-K) and extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) pathways, blocks erythroid differentiation, accelerates erythropoietin-induced proliferation, and leads to PI 3-K–dependent Fli-1 up-regulation. Chromatin immunoprecipitation and luciferase assays confirmed that Fli-1 binds directly to an Ets DNA binding site within the SHIP-1 promoter and suppresses SHIP-1 transcription. These data provide evidence to suggest that SHIP-1 is a direct Fli-1 target, SHIP-1 and Fli-1 regulate each other in a negative feedback loop, and the suppression of SHIP-1 by Fli-1 plays an important role in the transformation of erythroid progenitors by F-MuLV.
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Dissertations / Theses on the topic "Fli-1"

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Eisbacher, Michael School of Medical Science UNSW. "The regulation of megakaryocyte-specific genes by Fli-1 and GATA-1." Awarded by:University of New South Wales. School of Medical Science, 2003. http://handle.unsw.edu.au/1959.4/19171.

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The successive activation of tissue-specific genes during cellular differentiation is orchestrated by the formation of transcriptional complexes consisting of cellspecific and ubiquitous transcription factors. Understanding the molecular events associated with normal megakaryocyte (Mk) differentiation is an issue of central importance to haematology. The aims of this study were therefore to: (i) define the transcription factors responsible for regulating the expression of Mkspecific genes such as Glycoprotein IX, (ii) identify the protein partners of such important Mk-regulatory transcription factors and (iii) examine the mechanisms utilised by these factors to regulate gene expression. First, the regulatory elements in the GPIX promoter required for basal and inducible expression were examined in megakaryoblastic Dami cells stimulated to undergo differentiation. The resulting data suggested that an Ets site in the GPIX promoter binding the Ets-family member Fli-1 was crucial in regulating both constitutive and inducible GPIX expression. Second, a two-hybrid screen of a K-562 cDNA library was used to identify transcription factors that interacted with Fli-1 and were potential regulators of Mk development. Results of this screen identified a novel protein-protein interaction with GATA-1, a previously well-characterised zinc finger transcription factor also implicated in erythroid and Mk development. Mapping of the domains required for the interaction show that the zinc fingers of GATA-1 interact with the Ets domain of Fli-1. The biological significance of the Fli-1/GATA-1 interaction was demonstrated in transient transfection assays, which resulted in synergistic activation of Mkspecific promoters. Analysis of Fli-1 and GATA-1 expression in a series of erythroleukaemic and megakaryoblastic cell lines demonstrated that the Fli- 1/GATA-1 combination correlates with a Mk-phenotype. Moreover, expression of Fli-1 in K-562 cells (a line rich in GATA-1 but normally lacking Fli-1) induces endogenous GPIX expression. Quantitative mobility shift assays reveal that Fli- 1 and GATA-1 exhibit cooperative DNA-binding in which the binding of GATA-1 to DNA is increased approximately 26 fold in the presence of Fli-1. This data provides a mechanism for the observed transcriptional synergy. In conclusion, this work suggests that Fli-1 and GATA-1 work together through protein-protein interaction and cooperative DNA-binding to activate the expression of genes associated with the terminal differentiation of Mks.
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Barbeau, Benoit. "Caractérisation des promoteurs des gènes fli-1 murin et humain." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0007/NQ32578.pdf.

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PEREIRA, RUI. "Etude des proprietes transformantes de fli-1 et spi-1/pu. 1 dans les erythroblastes primaires." Paris 11, 2001. http://www.theses.fr/2001PA112021.

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Les proteines ets sont souvent impliquees dans des processus oncogeniques chez l'homme et l'animal. Les erythroleucemies induites chez la souris par le virus de friend est un modele classique d'un processus leucemogene multi-etape caracterise par differentes alterations moleculaires dont la surexpression de genes de la famille ets, spi-1 et fli-1. Spi-1 est specifiquement surexprime dans les erythroleucemies causees par le virus sffv. Chez la souris nouveau-nee, c'est fli-1 qui est surexprime par mutagenese insertionelle dans les erythroleucemies induites par le f-mulv. Par l'utilisation d'un systeme heterologue d'erythroblastes primaires, nous avons analyse et compare les consequences de l'expression forcee des proteines spi-1 et fli-1 sur le controle de la survie, la proliferation et la differenciation des erythroblastes primaires, afin de mieux apprecier leur contribution dans les erythroleucemies de friend. Nous avons montre l'existence d'une cooperation entre spi-1 et le recepteur a l'erythropoietine active anormalement (epor/gp55), amenant a une inhibition de la differenciation erythroide et a la conversion de la reponse normale a l'erythropoietine (differenciation) en une reponse proliferative. Par contre, l'expression de fli-1 est, a elle seule, suffisante pour inhiber le processus normal de differenciation des erythroblastes primaires et induire la survie accrue et la proliferation de ces cellules. Pour aborder les mecanismes d'actions de fli-1 et spi-1 dans la transformation erythroblastique, differents mutants de fli-1 ont ete construits et compares a la proteine fli-1 sauvage pour leur capacite a transformer les erythroblastes. Les resultats obtenus montrent que l'integrite du domaine ets de fli-1 est requise pour que celle-ci transforme les erythroblastes. D'autre part, l'echange du domaine ets de fli-1 par celui de ets-1 conserve les proprietes transformantes de fli-1 ; par contre l'echange par celui de spi-1 genere une proteine non transformante. Ces resultats indiquent que fli-1 et spi-1 transforment les erythroblastes par des mecanismes moleculaires distincts. Nos resultats indiquent aussi que la difference d'activite in vivo entre fli-1 et spi-1 pourrait resulter de la deregulation de genes cibles differents ou/et de leur interaction en trans avec des proteines distinctes.
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Kayali, Samer. "Spi-1,Fli-1et miR-17-92 contribuent au même réseau oncogénique impliqué dans le contrôle de la prolifération dans l’érythroleucémie de Friend." Thesis, Lyon 1, 2012. http://www.theses.fr/2012LYO10100.

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Plus de 90% des érythroleucémies induites par le virus de Friend sont associées à l'activation récurrente de l’un ou l’autre des facteurs de transcription ETS Spi-1 ou Fli-1, ou du cluster miR-17-92. La contribution de ces trois oncogènes à la prolifération des clones érythroleucémiques correspondant a déjà été indépendamment démontrée. De plus, il a été montré dans l’équipe que Spi-1 active de façon directe l’expression de Fli-1 et que les deux facteurs activent des gènes cibles communs. Dans cette thèse, j’ai montré que Spi-1 et Fli-1 activent l’expression du cluster miR-17-92 en se liant sur un motif ETS conservé dans le promoteur de ce cluster. J’ai montré que la réexpression de miR-17 et miR-20a est suffisante pour contrebalancer partiellement la baisse de la prolifération et la survie cellulaire induite par l’inhibition de l’expression de Fli-1. De plus, j’ai identifié Hbp1 comme une cible de ces miARNs dans les cellules érythroleucémiques. Ces résultats montrent que les trois oncogènes activés de façon récurrente par le virus de Friend constituent un seul réseau oncogénique contrôlant la prolifération. Ces résultats suggèrent également un rôle potentiel de réseaux ETS-miR-17-92 dans d’autres contextes normaux ou pathologiques
Clonal erythroleudemia developing in susceptible mice infected by Friend virus complex are associated with higly recurrent orviral insertinons at one of three loci called Spi-1, Fli-1 or Fli-3, leading to deregulated expression of oncogenic Spi-1 or Fli-1 transcription factors or miR-17-92 miRNA cluster, respectively. Deregulated expression of each of these here ocongenes has been independently shown to contribute to cell profileration of erythroleukemic clones. Previous studies showed close relationship between Spi-1 and Fli-1, which belong te the seame ETS family, Spi-1 activating fli-1 gene and both Spi-1 and Fli-1 activating multiple common target genes involved in ribosome biogenesis. In this tehesis, we habe also demonstrated that physiological re-expression of exogenous miR-17 and MiR-20a are able to partially rescue proliferation arrest induced by Fli-1 knock down and we identified Hbp1 as a tarteg of these miRNAs in erythroleukemia cell line.These results establish that three of the most recurrently activated oncogenes in Friend erythroleukemia are arctually involved in the same oncogenic network controlling proliferation . The putative contribution of similar ETS-MiR-17-92 network in other normal or hyper
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Johnson, Lacey Nicole St George Clinical School UNSW. "Molecular regulation of Megakaryopoiesis: the role of Fli-1 and IFI16." Awarded by:University of New South Wales. St George Clinical School, 2006. http://handle.unsw.edu.au/1959.4/26819.

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Megakaryocytes (Mks) are unique bone marrow cells, which produce platelets. Dysregulated Mk development can lead to abnormal platelet number and the production of functionally defective platelets, causing bleeding, thrombotic events, and leukaemia. Understanding the molecular mechanisms driving megakaryopoiesis may yield insights into the molecular genetics and cellular pathophysiology of a diversity of disorders. The primary aim of this thesis was to gain insight into the molecular events required for normal Mk development. As transcription factors and cytokines play a central role in driving Mk development, both of these processes were investigated. Fli-1 and GATA-1 are key transcription factors regulating Mk-gene expression, alone and co-operatively. To understand the mechanism of transcriptional synergy exerted by Fli-1 and GATA-1, in vitro assays were carried out investigating the interactions between Fli-1, GATA-1 and DNA that mediate synergy. A novel mechanism of synergy was identified, where Fli-1 DNA binding is not required, although an interaction between Fli-1 and GATA-1, and GATA-1 DNA binding is required. Importantly, the results demonstrate that Fli-1 DNA binding is not essential for promoting Mk-gene expression in primary murine bone marrow cells. Thrombopoietin (TPO) is the primary cytokine responsible for Mk and platelet development. Identifying novel TPO gene-targets may provide invaluable information to aid the understanding of the complex and unique processes required for Mk development. Using microarray technology, IFI16 was identified as a TPO-responsive gene that has not previously been studied in the Mk lineage. This work demonstrated that IFI16 is expressed in CD34+ HSC-derived Mks, and that the Jak/STAT pathway is essential for the activation of IFI16 by both TPO and IFN-??. Of biological significance, IFI16 was found to regulate both the proliferation and differentiation of primary Mks, suggesting that IFI16 may control the balance between these two essential processes. In conclusion, the data in this thesis presents a novel mechanism through which Fli-1 and GATA-1 regulate the synergistic activation of Mk genes. The identification and functional characterisation of a novel TPO-inducible gene, IFI16, involved in regulating the proliferation and differentiation of Mks is also described. These findings have implications for several congenital and malignant conditions affecting Mk and platelet development, and possibly a mechanism for IFN-induced thrombocytopaenia.
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Chan, David Wai 1968. "The role of EWS/FLI-1 fusion gene in Ewing's sarcoma." Monash University, Institute of Reproduction and Development, 2001. http://arrow.monash.edu.au/hdl/1959.1/8307.

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Lebigot, Ingrid. "Recherche des gènes dérégulés dans les érythroblastes transformés par FLI-1." Paris 11, 2003. http://www.theses.fr/2003PA11TO40.

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Ano, Sabine. "Etude du facteur de transcription FLI-1 dans la transformation érythroblastique." Paris 7, 2004. http://www.theses.fr/2004PA077200.

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Mateo, Lozano Silvia. "Sarcoma de Ewing: nuevas aproximaciones terapéuticas y búsqueda de dianas biológicas del oncogén EWS/FLI-1." Doctoral thesis, Universitat Autònoma de Barcelona, 2007. http://hdl.handle.net/10803/3571.

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La familia de tumores del sarcoma de Ewing (ESFT) incluye un grupo heterogéneo de neoplasias caracterizadas por la presencia de células redondas de pequeño tamaño con mínima evidencia morfológica de diferenciación. ESFT es el segundo tumor óseo más frecuente, afectando fundamentalmente a niños y adolescentes. A pesar del uso de terapias agresivas combinando quimioterapia, radioterapia y cirugía, la supervivencia de pacientes con metástasis es aproximadamente del 30%, mientras que en ausencia de enfermedad metastásica alcanza valores del 70 %. Debido a esto, son necesarias nuevas aproximaciones terapéuticas dirigidas a reducir la morbilidad relacionada con el tratamiento y a mejorar el índice de supervivencia. Afortunadamente, los ESFT presentan una diana molecular perfecta que resulta de la translocación cromosómica t(11;22)(q24;q12), que ocurre en aproximadamente un 95% de los casos, e involucra al gen EWS y a un miembro de la familia de factores de transcripción ETS, fundamentalmente FLI-1 o ERG. La translocación más común genera la formación de la oncoproteína de fusión EWS/FLI-1 que actúa como factor de transcripción y regula de forma aberrante la expresión de genes diana, favoreciendo el proceso tumorigénico. De esta forma la inactivación de la proteína de fusión EWS/FLI-1 se convierte en una estrategia atractiva, no sólo debido su papel fundamental en la tumorigénesis de ESFT, sino también por su especificidad en células transformadas. En este estudio se evaluaron diferentes estrategias dirigidas a reducir los niveles expresión de EWS/FLI-1 in vitro e in vivo. La primera estrategia utilizada para inhibir los niveles de expresión de la proteína de fusión EWS/FLI-1 se basó en el uso de la rapamicina, un antifúngico e inmunosupresor con propiedades anticancerígenas. La rapamicina inhibió la vía de señalización de mTOR/p70s6K y la proliferación de células de ESFT. Estos resultados sugirieron el uso de esta droga como agente citostático en el tratamiento de este tipo de tumores. La segunda aproximación terapéutica se basó en la inhibición simultánea de EWS/FLI-1 a nivel transcripcional y post-transcripcional. El tratamiento combinado de oligonucleótidos antisentido y rapamicina resultó en un incremento en la muerte de células de ESFT, a través de un proceso que involucra la restauración de la vía de señalización pro-apoptótica del TGF?1/TGF?-RII. In vivo, la administración del tratamiento combinado causó un retraso en el crecimiento de los tumores. Estos datos aportan la base para una mayor exploración del potencial del tratamiento combinado como una nueva estrategia en el tratamiento de este tipo de tumores. Los análisis moleculares mostraron que ESFT presentan alteraciones en proteínas reguladoras del ciclo celular, incluyendo la sobreexpresión de proteínas quinasas ciclina-dependientes (CDK2) y la pérdida o baja expresión de sus inhibidores. Basándonos en ésto, la tercera estrategia se basó en la reversión de alguna de estas alteraciones, mediante el uso de la roscovitina, un potente inhibidor de la actividad quinasa de las CDKs. El tratamiento con roscovitina resultó en un incremento de los niveles de apoptosis en células de ESFT in vitro e in vivo, por un mecanismo dependiente de la activación de caspasas. Estos resultados sugieren que la roscovitina puede ser un agente terapéutico efectivo en el tratamiento de ESFT, sola o en combinación con otras drogas potencialmente sinérgicas. Con el objetivo de identificar y evaluar nuevas proteínas que interactúan con EWS/FLI-1 y contribuir de esta forma a la comprensión de los mecanismos de transformación, identificamos como una diana transcripcional directa de EWS/FLI-1 a la caveolina-1, proteína involucrada en gran variedad de procesos celulares, tales como endocitosis, homeostasis del colesterol, transducción de señales y tumorigénesis. Los resultados de este trabajo mostraron que caveolina-1 juega un papel determinante en la tumorigénesis de células de ESFT y su inhibición podría permitir el desarrollo de nuevas estrategias terapéuticas moleculares dirigidas a mejorar el tratamiento de los pacientes de ESFT.
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Cohet, Nathalie. "Mécanismes de répression de la transcription par l'oncoprotéine FLI-1 dans les érythroleucémies." Lyon 1, 2005. http://www.theses.fr/2005LYO10137.

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Le proto-oncogène FLI-1 est impliqué de manière récurrente dans les érythroleucémies induites par le virus de Friend chez la souris. Sa surexpression constitutive, suite à l'insertion du provirus, participe au blocage de la différenciation érythrocytaire. Ayant montré que FLI-1 est capable de réprimer la transcription des gènes de globine β, l'objectif de ma thèse a été d'éclaircir son mode d'action dans ce contexte. Nos résultats ont d'abord révélé que l'activité répresseur de FLI-1 passait par des interactions protéine-protéine avec des facteurs activateurs de la différenciation érythrocytaire. Ainsi un antagonisme fonctionnel a été mis en évidence entre FLI-1 et le facteur EKLF. Puis, des études par immunoprécipitation de chromatine directement sur le locus des gènes de globine β ont montré que FLI-1 était recruté sur les séquences régulatrices de globine β et qu'il pouvait aussi interférer avec l'activité du facteur de transcription NF-E2 en empêchant son recrutement sur l'ADN
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Books on the topic "Fli-1"

1

Rossi, Derrick James. Characterization of the genomic structure of Fli-1 and the generation of mice bearing a Fli-1 null allele. Ottawa: National Library of Canada, 1993.

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Fly by Night: Fly by Night #1. New York, NY: HarperCollinsPublishers, 2006.

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Hardinge, Frances. Fly by Night: Fly by Night #1. New York, NY: HarperCollinsPublishers, 2006.

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Bruce, J. M. Sopwith 1 1. Hertfordshire: Albatros Productions, 1992.

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The Girl Who Could Fly: Piper McCloud #1. New York: Scholastic, 2010.

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Crandall, David. Fly free, as easy as 1-2-3. Boise, Idaho: Legendary Pub., 1998.

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Kreh, Lefty. Lefty's favorite fly fishing waters, volume 1: United States. Birmingham, AL: Odysseus Editions, 1993.

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Bhimani, Munsif Ali. Detecting mediators of the Flk-1 signalling pathway by mRNA differential display. Ottawa: National Library of Canada, 1998.

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Bruce, J. M. Vickers Vimy. Hertfordshire: Albatros Productions, 1994.

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Rimell, Raymond L. Pfalz DIII. 2nd ed. Berkhamsted, Hertz: Albatros Productions, 1996.

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Book chapters on the topic "Fli-1"

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Ortéga, Nathalie, and Jean Plouët. "Determination of the Functions Mediated by each of the Two VEGF Receptors KDR/FLK-1 and FLT-1." In Vascular Endothelium, 272. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0_34.

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Starczewski, Janusz T. "What Differs Interval Type-2 FLS from Type-1 FLS?" In Lecture Notes in Computer Science, 381–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-24844-6_55.

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Golanbari, Mohammad Saber, Mojtaba Ebrahimi, Saman Kiamehr, and Mehdi B. Tahoori. "Selective Flip-Flop Optimization for Circuit Reliability." In Dependable Embedded Systems, 337–64. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-52017-5_14.

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AbstractThis chapter proposes a selective flip-flop optimization method (Golanbari et al., IEEE Trans Very Large Scale Integr VLSI Syst 39(7):1484–1497, 2020; Golanbari et al., Aging guardband reduction through selective flip-flop optimization. In: IEEE European Test Symposium (ETS) (2015)), in which the timing and reliability of the VLSI circuits are improved by optimizing the timing-critical components under severe impact of runtime variations. As flip-flops are vulnerable to aging and supply voltage fluctuation, it is necessary to address these reliability issues in order to improve the overall system lifetime. In the proposed method, we first extend the standard cell libraries by adding optimized versions of the flip-flops designed for better resiliency against severe Bias Temperature Instability (BTI) impact and/or supply voltage fluctuation. Then, we optimize the VLSI circuit by replacing the aging-critical and voltage-drop critical flip-flops of the circuit with optimized versions to improve the timing and reliability of the entire circuit in a cost-effective way. Simulation results show that incorporating the optimized flip-flops in a processor can prolong the circuit lifetime by 36.9%, which translates into better reliability.This chapter is organized as follows. Section 1 introduces wide-voltage operation reliability issues and motivates the proposed selective flip-flop optimization approach. The impacts of runtime variations on flip-flops are explained in Sect. 2. Consequently, Sect. 3 presents cell-level optimization of the flip-flops. The proposed selective flip-flop optimization methodology is described in Sect. 4, and optimization results are discussed in Sect. 5. Finally, Sect. 7 concludes the chapter.
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Benckert, C., S. Jonas, T. Cramer, B. Wiedenmann, S. Rosewicz, and P. Neuhaus. "Die Expression des vaskulären endothelialen Wachstumsfaktors (VEGF) sowie seiner Rezeptoren KDR/flk-1 und flt-1 im humanen cholangiozellulären Karzinom." In Deutsche Gesellschaft für Chirurgie, 75–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57295-1_17.

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Foley, Caitríona. "‘This Revived Old Plague’1: Coping with Flu." In Cultures of Care in Irish Medical History, 1750–1970, 141–67. London: Palgrave Macmillan UK, 2010. http://dx.doi.org/10.1057/9780230304628_8.

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Preu, Merle, Johannes L. Frieß, Broder Breckling, and Winfried Schröder. "Case Study 1: Olive Fruit Fly (Bactrocera oleae)." In Gene Drives at Tipping Points, 79–101. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-38934-5_4.

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Li, Ning, Lanshi Zheng, David B. Bogy, and Yonggang Meng. "Fly-Ability and Durability Test of Dynamic Fly Height Heads at 1 nm Clearance." In Advanced Tribology, 533–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03653-8_170.

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Domínguez-Rodrigo, M., and R. Barba. "FLK North North 1: “living floor” or natural accumulation?" In Deconstructing Olduvai: A Taphonomic Study of the Bed I Sites, 217–28. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-6152-3_12.

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Starczewski, Janusz T. "A Type-1 Approximation of Interval Type-2 FLS." In Fuzzy Logic and Applications, 287–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02282-1_36.

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Li, Kwai Hei. "1-μm Micro-Lens Array on Flip-Chip LEDs." In Nanostructuring for Nitride Light-Emitting Diodes and Optical Cavities, 81–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-48609-2_5.

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Conference papers on the topic "Fli-1"

1

Marques, Michelle, Bethsaida Nieves, Ron Chen, Dideepya Vaka, Charles Chan, Grace Zheng, Howard Chang, Irv Weissman, and Alejandro Sweet-Cordero. "Abstract 1427: Signal rewiring induced by EWS/FLI-1 in mouse and human mesenchymal stem cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1427.

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Rorie, C. J., and B. E. Weissman. "Ews/Fli-1 Chimeric Oncogene: Role in Neuronal Differentiation and Abrogation of p53 A Two-Year Study." In Minority Trainee Research Forum, 2004. TheScientificWorld Ltd, 2004. http://dx.doi.org/10.1100/tsw.2004.147.

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Cohen-Gogo, Sarah, Franck Tirode, and Olivier Delattre. "Abstract A59: Deciphering the role(s) of the FET family of proteins in the Ewing sarcoma model: Is EWS-FLI-1 crashing the party?" In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-a59.

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Johnson, Kirsten M., Cenny Taslim, and Stephen L. Lessnick. "Abstract 3509: EWS/FLI regulates transcriptional activation via length-dependent GGAA microsatellites." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3509.

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Balboni, Amanda L., Bjorn Stolte, Amy Saur Conway, Gabriela Alexe, Emily Jue Wang, Nicholas Kwiatkowski, Tinghu Zhang, et al. "Abstract 1118: Synthetic lethality of CDK12 inhibition in tumors with EWS/FLI rearrangements." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1118.

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Bordas, M. L., A. Cartellier, and P. Se´chet. "A One Dimensional Two-Fluid Model for Bubbly Flows in Fixed Beds." In ASME 2002 Joint U.S.-European Fluids Engineering Division Conference. ASMEDC, 2002. http://dx.doi.org/10.1115/fedsm2002-31382.

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Pressure drop and gas void fraction are important parameters for the design of multiphase packed bed reactors which are widely used in petrochemical industry. Several experimental studies have been devoted to the hydrodynamics of two-phase cocurrent upflow or downflow through fixed beds, and various correlations of limited range of validity are available in the literature. However, there is not yet a clear agreement on the form of the momentum equations to be used in such systems. Early attempts devoted to the pressure drop estimate were based on an extension of the Lockhart-Martinelli approach (Sweeney 1967), Rao et al. 1983). More recently, Attou at al. (1999) proposed the first serious attempt to adapt the Eulerian two-fluid model to cocurrent bubbly flows through packed beds. From an analysis of their proposal, it happens that the basic mechanical equilibrium for the gas phase needs to be reconsidered. In this scope, we derived a new model on the basis of the so-called hybrid approach initially developed for bubbly flows in ducts in absence of shear-induced turbulence (Achard and Cartellier 2000). As a first application, we considered a mean unidirectional flow of a bubbly mixture through a porous medium composed of beads uniform in size. For steady and fully established flows, and assuming a flat void fraction (α) profile, the resulting momentum equations for each phase write: Liquidphase:−dpdz=ρLg+fLS−fLG1−α(1)Gasphase:−dpdz=ρGg+fLS+fLGα(2) where fLS is the resultant of the liquid shear stress exerted on beads surface and on exterior walls, and where the quantity fLG = α F* / Vp represents the interaction force density between the gas and the liquid (F* is the mean force on bubbles and Vp = 4πa3/3 denotes the bubble volume, a being the bubble radius). The main difference with the model derived by Attou et al. is the presence of the fLS term in the gas phase equation. Without this term, the relative velocity of bubbles would be controlled by the axial pressure gradient dP/dz even in non accelerating flows which is unphysical. On the opposite, in the present model (1–2) the relative movement of bubbles is simply due to buoyancy. The set of equations (1–2) provides a mean to exploit the experimental data to derive the required closures, namely the evolution of the friction fLS with the gas content and that of the momentum exchange between phases fLG. Notably, from (1) and (2), one gets fLG=α(1−α)(ρL−ρG)g(3) In order to establish reliable closures, available experimental data of the literature are currently revisited under this framework. For the friction term, which is the principal contribution to the pressure drop, the usual closure law for fLS as given by an Ergun equation adapted to two-phase flows is under analysis. For the interfacial momentum transfer, the objective is to evaluate an “apparent” drag coefficient defined as Cd = F*/[ρL Ur2 π a2 / 2] where the mean relative velocity Ur is defined as the difference between the mean gas and liquid velocities averaged over a volume. Indeed, paralleling an approach already exploited for bubbly flows in ducts (Riviere and Cartellier 1999), it happens that the mean void fraction can be derived from equations (1) and (2) assuming a flat void fraction profile: β(1−β)−α(1−α)=(4π/3)α(1−α)[gδ2VSLνc](aδ)2fd(4) where δ is the typical size of the pores and where fd = (π/2) Rep Cd is expected to be a function of the bubble size, the porosity ε and the void fraction. To extract fd or Cd from (4), a characteristic bubble size must be specified. As shown Fig.1, the bubble size is controlled by the bed geometry and evolves between 0.2 δ and 3 δ in the dilute limit (Bordas et al. (2001)). Analysis of the existing data will be presented based on these size estimates, and comparison will be performed of this “apparent” drag with values measured for isolated bubbles in fixed beds (Fig.2).
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Hedditch, J. N., B. G. Lasscock, D. B. Leinweber, A. G. Williams, W. Kamleh, and J. M. Zanotti. "1−+ Exotic on the Lattice with FLIC Fermions." In Proceedings of the 3rd Asia-Pacific Conference. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812706881_0030.

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Hagras, Hani. "Developing a type-2 FLC through embedded type-1 FLCs." In 2008 IEEE 16th International Conference on Fuzzy Systems (FUZZ-IEEE). IEEE, 2008. http://dx.doi.org/10.1109/fuzzy.2008.4630358.

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Williams, Anthony, J. N. Hedditch, B. G. Lasscock, Derek Leinweber, Waseem Kamleh, and J. M. Zanotti. "Light-Quark FLIC Fermion Simulations of the 1-+ Exotic Meson." In XXIIIrd International Symposium on Lattice Field Theory. Trieste, Italy: Sissa Medialab, 2005. http://dx.doi.org/10.22323/1.020.0040.

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Fischer, Robert E., and Thomas U. Kampe. "Actively controlled 5:1 afocal zoom attachment for common module FLIR." In Aerospace Sensing, edited by David M. Aikens, Victor L. Genberg, Gary C. Krumweide, and Michael J. Thomas. SPIE, 1992. http://dx.doi.org/10.1117/12.137989.

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Reports on the topic "Fli-1"

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Kleinerman, Eugenie S. Hypoxia induces lineage modulation of Ewing’s sarcoma tumor cells into EWS-FLI-1 + vascular pericytes. Science Repository, March 2019. http://dx.doi.org/10.31487/j.cor.2019.01.006.

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Harwood, Charlotte M. Flt-1 Function and Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada496327.

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Harwood, Charlotte M. Flt-1 Function and Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada482556.

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Self, S. A. Optical properties of fly ash. Volume 1, Final report. Office of Scientific and Technical Information (OSTI), December 1994. http://dx.doi.org/10.2172/82031.

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Page, Gregory, and Chris Bovias. AIAA Student Aircraft Design, Build & Fly Competition. Volume 1. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada424278.

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Baral, Aniruddha, Jeffrey Roesler, M. Ley, Shinhyu Kang, Loren Emerson, Zane Lloyd, Braden Boyd, and Marllon Cook. High-volume Fly Ash Concrete for Pavements Findings: Volume 1. Illinois Center for Transportation, September 2021. http://dx.doi.org/10.36501/0197-9191/21-030.

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High-volume fly ash concrete (HVFAC) has improved durability and sustainability properties at a lower cost than conventional concrete, but its early-age properties like strength gain, setting time, and air entrainment can present challenges for application to concrete pavements. This research report helps with the implementation of HVFAC for pavement applications by providing guidelines for HVFAC mix design, testing protocols, and new tools for better quality control of HVFAC properties. Calorimeter tests were performed to evaluate the effects of fly ash sources, cement–fly ash interactions, chemical admixtures, and limestone replacement on the setting times and hydration reaction of HVFAC. To better target the initial air-entraining agent dosage for HVFAC, a calibration curve between air-entraining dosage for achieving 6% air content and fly ash foam index test has been developed. Further, a digital foam index test was developed to make this test more consistent across different labs and operators. For a more rapid prediction of hardened HVFAC properties, such as compressive strength, resistivity, and diffusion coefficient, an oxide-based particle model was developed. An HVFAC field test section was also constructed to demonstrate the implementation of a noncontact ultrasonic device for determining the final set time and ideal time to initiate saw cutting. Additionally, a maturity method was successfully implemented that estimates the in-place compressive strength of HVFAC through wireless thermal sensors. An HVFAC mix design procedure using the tools developed in this project such as the calorimeter test, foam index test, and particle-based model was proposed to assist engineers in implementing HVFAC pavements.
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Woychik, C. G. Electrically conductive adhesive Flip Chip Attach Project. Annual report, October 1, 1994--October 1, 1995. Office of Scientific and Technical Information (OSTI), November 1995. http://dx.doi.org/10.2172/149988.

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Kearney, Joseph B., and Victoria L. Bautch. Flt-1 (VEGFR-1) as an Angiogenic Inhibitor: Implications for a Novel Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417967.

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Brown, P. W. Hydrothermal reactions of fly ash. [Progress report], October 1, 1991--December 31, 1991. Office of Scientific and Technical Information (OSTI), December 1991. http://dx.doi.org/10.2172/10146550.

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Park, John W. Development of Anti-VEGF Receptor/Flk-1 Immunoliposomes for Cytotoxic Anti-Angiogenesis Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada394052.

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