Analysis of c-kit mutations in acute myeloid leukemia (AML) with t(8 ; 21) (CROSBI ID 511482)
Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | domaća recenzija
Podaci o odgovornosti
Drmić, Irena ; Radnić, Maja ; Zadro, Renata ; Kušec, Rajko ; Grahovac, Blaženka
engleski
Analysis of c-kit mutations in acute myeloid leukemia (AML) with t(8 ; 21)
Acute myeloid leukemia (AML) has been proposed to arise from the cooperation between abnormalities in genes that incode transcription factors (TF) and tyrosine kinases (TK). Disruption of TFs is often a result of recurring chromosomal translocation with inhibition of haematopoietic differentiation, whereas the mutations in receptor TK, c-kit and other provide a proliferative signal. The most common chromosomal translocation, t(8 ; 21)(q22 ; q22), in AML generates AML1/ETO fusion gene. According to recent data, genetic abnormalities that cooperate with AML1/ETO to induce AML remain elusive, as well as clinical significance of c-kit mutations in leukemias with t(8 ; 21). To estimate the prevalence of c-kit mutations in AML, we analyzed several c-kit mutations in coding sequences and promoter region in AML1/ETO positive patients (n=25). Obtained results suggest that further studies with extended number of patients at disease presentation, during therapy and follow-up are required to evaluate significance of c-kit mutations in prognosis and therapy of AML.
c-kit; acute myeloid leukemia
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Podaci o prilogu
46-46.
2005.
nije evidentirano
objavljeno
Podaci o matičnoj publikaciji
3. hrvatski kongres patologije i sudske medicine, 3. hrvatski kongres kliničke citologije, 1. hrvatski kongres citotehnologije s međunardnim sudjelovanjem, Knjiga sažetaka
Jonjić, Nives ; Kardum-Skelin, Ika
Zagreb: HRG
Podaci o skupu
3. hrvatski kongres patologije i sudske medicine, 3. hrvatski kongres kliničke citologije, 1. hrvatski kongres citotehnologije s međunardnim sudjelovanjem
poster
08.05.2005-11.05.2005
Opatija, Hrvatska