Matches in SemOpenAlex for { <https://semopenalex.org/work/W2765454716> ?p ?o ?g. }
- W2765454716 endingPage "103639" @default.
- W2765454716 startingPage "103626" @default.
- W2765454716 abstract "// Carolina Yaeko Namasu 1 , Christiane Katzerke 1 , Daniela Bräuer-Hartmann 1 , Alexander Arthur Wurm 1 , Dennis Gerloff 2 , Jens-Uwe Hartmann 1 , Sebastian Schwind 1 , Carsten Müller-Tidow 3 , Nadja Hilger 4 , Stephan Fricke 4 , Maximilian Christopeit 5 , Dietger Niederwieser 1 and Gerhard Behre 1 1 Division of Hematology and Oncology, University Hospital Leipzig, Leipzig, Germany 2 Division of Dermatology and Venereology, University Hospital Halle, Halle, Germany 3 Division of Hematology and Oncology, University Hospital Heidelberg, Heidelberg, Germany 4 Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany 5 Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany Correspondence to: Gerhard Behre, email: gerhard.behre@medizin.uni-leipzig.de Keywords: acute myeloid leukemia, ABR, C/EBPα, myelopoiesis, prognostic Received: April 04, 2017 Accepted: September 22, 2017 Published: October 26, 2017 ABSTRACT Active BCR related ( ABR ) gene deactivates ras-related C3 botulinum toxin substrate 1 (RAC1), which plays an essential role in regulating normal hematopoiesis and in leukemia. BCR gene, closely related to ABR, acts as a tumor suppressor in chronic myeloid leukemia and has overlapping functions with ABR . Evidence for a putative tumor suppressor role of ABR has been shown in several solid tumors, in which deletion of ABR is present. Our results show downregulation of ABR in AML. A block of ABR prevents myeloid differentiation and leads to repression of the myeloid transcription factor C/EBPα, a major regulator of myeloid differentiation and functionally impaired in leukemia. Conversely, stable overexpression of ABR enhances myeloid differentiation. Inactivation of the known ABR target RAC1 by treatment with the RAC1 inhibitor NSC23766 resulted in an increased expression of C/EBPα in primary AML samples and in AML cell lines U937 and MV4;11. Finally, AML patients with high ABR expression at diagnosis showed a significant longer overall survival and patients who respond to azacitidine therapy showed a significant higher ABR expression. This is the first report showing that ABR expression plays a critical role in both myelopoiesis and AML. Our data indicate the tumor suppressor potential of ABR and underline its potential role in leukemia therapeutic strategies." @default.
- W2765454716 created "2017-11-10" @default.
- W2765454716 creator A5003617360 @default.
- W2765454716 creator A5004233773 @default.
- W2765454716 creator A5007132946 @default.
- W2765454716 creator A5013003322 @default.
- W2765454716 creator A5019502130 @default.
- W2765454716 creator A5028388949 @default.
- W2765454716 creator A5031660112 @default.
- W2765454716 creator A5037877971 @default.
- W2765454716 creator A5042734609 @default.
- W2765454716 creator A5052562050 @default.
- W2765454716 creator A5056932736 @default.
- W2765454716 creator A5064722914 @default.
- W2765454716 creator A5085103227 @default.
- W2765454716 date "2017-10-26" @default.
- W2765454716 modified "2023-09-24" @default.
- W2765454716 title "ABR, a novel inducer of transcription factor C/EBPα, contributes to myeloid differentiation and is a favorable prognostic factor in acute myeloid leukemia" @default.
- W2765454716 cites W137827881 @default.
- W2765454716 cites W1502074492 @default.
- W2765454716 cites W1526134400 @default.
- W2765454716 cites W1586732387 @default.
- W2765454716 cites W1904660196 @default.
- W2765454716 cites W1976915376 @default.
- W2765454716 cites W1980860344 @default.
- W2765454716 cites W1981860701 @default.
- W2765454716 cites W1987598864 @default.
- W2765454716 cites W1990120418 @default.
- W2765454716 cites W1996441871 @default.
- W2765454716 cites W2006131936 @default.
- W2765454716 cites W2006771034 @default.
- W2765454716 cites W2011177881 @default.
- W2765454716 cites W2018995007 @default.
- W2765454716 cites W2019308110 @default.
- W2765454716 cites W2023449786 @default.
- W2765454716 cites W2025978850 @default.
- W2765454716 cites W2035228126 @default.
- W2765454716 cites W2035665330 @default.
- W2765454716 cites W2038802455 @default.
- W2765454716 cites W2040257851 @default.
- W2765454716 cites W2040304029 @default.
- W2765454716 cites W2045027881 @default.
- W2765454716 cites W2053603004 @default.
- W2765454716 cites W2058761715 @default.
- W2765454716 cites W2071199281 @default.
- W2765454716 cites W2071981907 @default.
- W2765454716 cites W2079625864 @default.
- W2765454716 cites W2082461806 @default.
- W2765454716 cites W2083483484 @default.
- W2765454716 cites W2083973772 @default.
- W2765454716 cites W2085213378 @default.
- W2765454716 cites W2085774571 @default.
- W2765454716 cites W2086418945 @default.
- W2765454716 cites W2094425604 @default.
- W2765454716 cites W2095659935 @default.
- W2765454716 cites W2100211224 @default.
- W2765454716 cites W2102752941 @default.
- W2765454716 cites W2103043828 @default.
- W2765454716 cites W2106185171 @default.
- W2765454716 cites W2110807341 @default.
- W2765454716 cites W2118771330 @default.
- W2765454716 cites W2121173249 @default.
- W2765454716 cites W2123719503 @default.
- W2765454716 cites W2143835472 @default.
- W2765454716 cites W2163337149 @default.
- W2765454716 cites W2164396922 @default.
- W2765454716 cites W2165787335 @default.
- W2765454716 cites W2166599801 @default.
- W2765454716 cites W2276580523 @default.
- W2765454716 cites W2289820450 @default.
- W2765454716 cites W2319322696 @default.
- W2765454716 cites W2415047932 @default.
- W2765454716 cites W2419140434 @default.
- W2765454716 cites W2471743272 @default.
- W2765454716 cites W4253702721 @default.
- W2765454716 doi "https://doi.org/10.18632/oncotarget.22093" @default.
- W2765454716 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5732755" @default.
- W2765454716 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29262589" @default.
- W2765454716 hasPublicationYear "2017" @default.
- W2765454716 type Work @default.
- W2765454716 sameAs 2765454716 @default.
- W2765454716 citedByCount "12" @default.
- W2765454716 countsByYear W27654547162018 @default.
- W2765454716 countsByYear W27654547162019 @default.
- W2765454716 countsByYear W27654547162020 @default.
- W2765454716 countsByYear W27654547162021 @default.
- W2765454716 countsByYear W27654547162022 @default.
- W2765454716 countsByYear W27654547162023 @default.
- W2765454716 crossrefType "journal-article" @default.
- W2765454716 hasAuthorship W2765454716A5003617360 @default.
- W2765454716 hasAuthorship W2765454716A5004233773 @default.
- W2765454716 hasAuthorship W2765454716A5007132946 @default.
- W2765454716 hasAuthorship W2765454716A5013003322 @default.
- W2765454716 hasAuthorship W2765454716A5019502130 @default.
- W2765454716 hasAuthorship W2765454716A5028388949 @default.
- W2765454716 hasAuthorship W2765454716A5031660112 @default.
- W2765454716 hasAuthorship W2765454716A5037877971 @default.
- W2765454716 hasAuthorship W2765454716A5042734609 @default.