Matches in SemOpenAlex for { <https://semopenalex.org/work/W2164873768> ?p ?o ?g. }
- W2164873768 endingPage "1379" @default.
- W2164873768 startingPage "1372" @default.
- W2164873768 abstract "Background Myelodysplastic syndromes are a heterogeneous group of clonal hematopoietic stem cell disorders characterized by ineffective hematopoiesis. Survivin is a member of the inhibitor of apoptosis family and suppresses apoptosis. Survivin also functions as a subunit of the chromosomal passenger complex for regulating mitosis with Aurora-B. Survivin and Aurora-B play an important role in maintaining genome stability. The aim of this study was to determine the role of Survivin and Aurora-B kinase in disease progression and prognosis of myelodysplastic syndromes.Design and Methods We evaluated the expression levels of these two genes in CD34+ cells prepared from 64 patients with myelodysplastic syndrome or leukemic blasts from 50 patients with de novo acute myeloid leukemia using quantitative real-time PCR.Results Survivin and Aurora-B expression levels were highly correlated with the type of myelodysplastic syndrome, were much higher in refractory anemia with excess blasts-1, refractory anemia with excess blasts-2, and secondary acute myeloid leukemia following myelodysplastic syndrome than in normal control, and increased during disease progression. There was a significant correlation between these expression levels and the International Prognostic Scoring System. Interestingly, these levels were remarkably higher in patients with secondary acute myeloid leukemia following myelodysplastic syndromes than in those with de novo acute myeloid leukemia.Conclusions This is the first report showing that high levels of Survivin and Aurora-B kinase expression in CD34+ cells are distinctive molecular features of high-risk myelodysplastic syndromes and secondary acute myeloid leukemia following myelodysplastic syndrome. Marked upregulation of Survivin and Aurora-B kinase may contribute to genetic instability and disease progression of myelodysplastic syndromes. Our data may explain why patients with high-risk myelodysplastic syndromes frequently show complex chromosomal abnormality." @default.
- W2164873768 created "2016-06-24" @default.
- W2164873768 creator A5004676245 @default.
- W2164873768 creator A5011340584 @default.
- W2164873768 creator A5013873963 @default.
- W2164873768 creator A5042047703 @default.
- W2164873768 creator A5054372643 @default.
- W2164873768 creator A5059400008 @default.
- W2164873768 creator A5059412860 @default.
- W2164873768 creator A5062355927 @default.
- W2164873768 creator A5077635586 @default.
- W2164873768 creator A5080736574 @default.
- W2164873768 date "2012-03-14" @default.
- W2164873768 modified "2023-10-04" @default.
- W2164873768 title "Marked upregulation of Survivin and Aurora-B kinase is associated with disease progression in the myelodysplastic syndromes" @default.
- W2164873768 cites W1004685331 @default.
- W2164873768 cites W1523461418 @default.
- W2164873768 cites W1540060031 @default.
- W2164873768 cites W1556655356 @default.
- W2164873768 cites W1768187423 @default.
- W2164873768 cites W1918156452 @default.
- W2164873768 cites W1961680179 @default.
- W2164873768 cites W1970445062 @default.
- W2164873768 cites W1974586741 @default.
- W2164873768 cites W1979015094 @default.
- W2164873768 cites W1982384929 @default.
- W2164873768 cites W1991865867 @default.
- W2164873768 cites W2002125670 @default.
- W2164873768 cites W2005068236 @default.
- W2164873768 cites W2006240263 @default.
- W2164873768 cites W2006613051 @default.
- W2164873768 cites W2007010211 @default.
- W2164873768 cites W2013722663 @default.
- W2164873768 cites W2016531290 @default.
- W2164873768 cites W2032448172 @default.
- W2164873768 cites W2035523654 @default.
- W2164873768 cites W2040754722 @default.
- W2164873768 cites W2041053820 @default.
- W2164873768 cites W2047893179 @default.
- W2164873768 cites W2055407691 @default.
- W2164873768 cites W2062194101 @default.
- W2164873768 cites W2073359373 @default.
- W2164873768 cites W2075971408 @default.
- W2164873768 cites W2094842968 @default.
- W2164873768 cites W2126776706 @default.
- W2164873768 cites W2130236734 @default.
- W2164873768 cites W2144878135 @default.
- W2164873768 cites W2147223587 @default.
- W2164873768 cites W2149982846 @default.
- W2164873768 cites W2155225188 @default.
- W2164873768 cites W2155660862 @default.
- W2164873768 cites W2155961719 @default.
- W2164873768 cites W2168881161 @default.
- W2164873768 cites W2278431283 @default.
- W2164873768 cites W2326501676 @default.
- W2164873768 cites W2461711455 @default.
- W2164873768 cites W251630186 @default.
- W2164873768 cites W2035982561 @default.
- W2164873768 cites W2138215232 @default.
- W2164873768 doi "https://doi.org/10.3324/haematol.2011.055681" @default.
- W2164873768 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3436238" @default.
- W2164873768 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22419576" @default.
- W2164873768 hasPublicationYear "2012" @default.
- W2164873768 type Work @default.
- W2164873768 sameAs 2164873768 @default.
- W2164873768 citedByCount "13" @default.
- W2164873768 countsByYear W21648737682012 @default.
- W2164873768 countsByYear W21648737682013 @default.
- W2164873768 countsByYear W21648737682014 @default.
- W2164873768 countsByYear W21648737682015 @default.
- W2164873768 countsByYear W21648737682016 @default.
- W2164873768 countsByYear W21648737682017 @default.
- W2164873768 crossrefType "journal-article" @default.
- W2164873768 hasAuthorship W2164873768A5004676245 @default.
- W2164873768 hasAuthorship W2164873768A5011340584 @default.
- W2164873768 hasAuthorship W2164873768A5013873963 @default.
- W2164873768 hasAuthorship W2164873768A5042047703 @default.
- W2164873768 hasAuthorship W2164873768A5054372643 @default.
- W2164873768 hasAuthorship W2164873768A5059400008 @default.
- W2164873768 hasAuthorship W2164873768A5059412860 @default.
- W2164873768 hasAuthorship W2164873768A5062355927 @default.
- W2164873768 hasAuthorship W2164873768A5077635586 @default.
- W2164873768 hasAuthorship W2164873768A5080736574 @default.
- W2164873768 hasBestOaLocation W21648737681 @default.
- W2164873768 hasConcept C109159458 @default.
- W2164873768 hasConcept C121608353 @default.
- W2164873768 hasConcept C126322002 @default.
- W2164873768 hasConcept C203014093 @default.
- W2164873768 hasConcept C2775975398 @default.
- W2164873768 hasConcept C2778461978 @default.
- W2164873768 hasConcept C2778729363 @default.
- W2164873768 hasConcept C2779282312 @default.
- W2164873768 hasConcept C2780007613 @default.
- W2164873768 hasConcept C2780817109 @default.
- W2164873768 hasConcept C28328180 @default.
- W2164873768 hasConcept C502942594 @default.
- W2164873768 hasConcept C54355233 @default.
- W2164873768 hasConcept C71924100 @default.