Doc. MUDr. Tomáš Stopka, Ph.D.

Publikovaná abstrakta

• 5-Azacytidine and G-CSF Derepressed Chromatin Structure of PU.1 and Its Targets Cebpa and Cbfb In Myelodysplastic Syndrome (MDS)
• Activation of Chromatin Structure Upstream PU.1 Gene and in Vitro Differentiation in High Risk Myelodysplastic Syndrome Following 5-Azacytidine
• Active Chromatin Structure near MYB Occupancy at the Mir-155 Host Gene Promoter Coincides with Increased Mir-155 and MYB Levels In Chronic Lymphocytic Leukemia
• Activity Determines Fate of Myeloid Progenitor Cells during Lineage Commitment
• Disruption of a Functional Relationship Between PU.1 and Mir-155 during the Pathogenesis of Chronic Lymphocytic Leukemia (CLL)
• Divalent Metal Transporter 1 (DMT1) Regulates EPO Receptor Gene Expression Via GATA-1
• Epigenetic regulation of miR155 expression - insights into pathogenesis of CLL
• Erythroid Transcription Factor GATA-1 Binds and Represses PU.1 Gene – Candidate Mechanism Of Epigenetic Repression Of PU.1 and Inefficient Erythropoiesis In MDS
• EXPRESSION LEVELS OF MIR-150 AND TRANSCRIPTION FACTORS PU.1, EGR2 INVERSELY CORRELATE WITH MYB AND MYCN IN CHRONIC MYELOID LEUKEMIA
• Fog1 and Cebpa Are DNA Targets of GATA-1/PU.1 Antagonism during Leukemia Differentiation.
• Gata1 Regulates Erythroid Transcription by Cooperating with Chromatin Remodeling Protein Snf2h
• ISWI ATPase Snf2h Is Required for Both Heterochromatin and Euchromatin Structure in ES Cells.
• ISWI Chromatin Remodeling ATPase Smarca5 (Snf2h) Is Required for Murine Erythroid Development and Globin Gene Regulation
• MicroRNA Analysis in the Cerebrospinal Fluid and Blood Serum of Lymphoma Patients At Diagnosis and in Response to Therapy
• MicroRNA Mir-155 and Myb Proto-Oncogene Family Members Cooperate in Pathogenesis of Chronic Lymphocytic Leukemia
• MikroRNA polycistrony miR-17-92, miR-106b-25 and miR-106a-363 asociované s lymfoidním vývojem jsou přímé cíle transkripčního faktoru PU.1
• Mutation Of The Divalent Metal Transporter (Dmt1) Gene Results In Inefficient Induction Of The Erythroid Transcriptional Program Due To Latter Onset Of GATA-1 and Epor Expression
• Oncogenic Micrornas In Cerebrospinal Fluid and Sera Reflect Therapy Efficacy and Their Reappearance Precedes Clinical Relapse In Primary and Secondary CNS Lymphoma
• Patients with Chronic Myeloid Leukemia Show Different Modulation of MYB-Dependent Oncogenic Pathway in the Course of Hematopoietic Differentiation upon Sensitivity to the TKI Treatment
• Porušení rovnováhy vzájemné regulace mezi PU.1 a miR-155 je kandidátním mechanizmem leukemogeneze CLL
• PU.1 and p53 Double Mutant Mice Develop Aggressive AML with Dysplastic Features
• PU.1 Dose-Dependently Induces Granulocyte or Macrophage Commitment by Targeting Lineage Restricted Genes and by Regulating Transcription Factors Egr2, Nab2, Cebpa and Gfi1.
• PU.1 Relieves Its GATA-1-Mediated Repression near Cebpa and Cbfb During Transdifferentiation of Murine Erythroleukemia - Tool of Inducing Leukemic Blasts to Differentiate
• Retroviral rescue with PU.1 induces derepression of both PU.1 and miR155 target genes - possible therapeutic implications for CLL
• Smarca5 Regulates Ctcf Recruitment to Chromatin, Including to Regulatory Loci Involved In Control of Globin Gene Expression In Erythroleukemia
• Snf2h regulates heterochromation structure and global transcription in blood cells
• The Oncogenic Mir-17-92 MicroRNA Cluster Is Inhibited by EGR2 During Macrophage Differentiation Via JARID1b-Mediated Histone 3 Lysine 4 Demethylation
• Tracking the Somatic Mutations in Azacitidine-Treated MDS Patients Documents Clonal Development and AZA Responsiveness
• Transcription Factor CTCF Inhibits Effects of 5-Azacitidine in MDS/AML Cells
• Transcription Factors PU.1 and EGR2 Inhibits the Oncogenic Microrna Cluster Mir-17-92 during Macrophage Differentiation