Identification of additional cytogenetic and molecular genetic abnormalities in acute myeloid leukaemia with t(8;21)/AML1‐ETO
F Kuchenbauer, S Schnittger, T Look… - British journal of …, 2006 - Wiley Online Library
British journal of haematology, 2006•Wiley Online Library
AML1‐ETO collaborates with further genetic abnormalities to induce acute myeloid
leukaemia (AML). We analysed 99 patients with an AML1‐ETO rearrangement for additional
aberrations. Frequent genetic abnormalities were, loss of a sex chromosome (56/99, 56· 5%)
and del (9)(q22)(24/99, 24· 2%). The most frequent molecular aberrations were mutations of
KITD816 (3/23, 13%) and NRAS (8/89, 8· 9%). Further molecular abnormalities were FLT3
mutations (3/87, 3· 4%), AML1 (1/26, 3· 8%) and PU1 (1/14, 7· 1%). MLL‐PTD, KRAS and …
leukaemia (AML). We analysed 99 patients with an AML1‐ETO rearrangement for additional
aberrations. Frequent genetic abnormalities were, loss of a sex chromosome (56/99, 56· 5%)
and del (9)(q22)(24/99, 24· 2%). The most frequent molecular aberrations were mutations of
KITD816 (3/23, 13%) and NRAS (8/89, 8· 9%). Further molecular abnormalities were FLT3
mutations (3/87, 3· 4%), AML1 (1/26, 3· 8%) and PU1 (1/14, 7· 1%). MLL‐PTD, KRAS and …
Abstract
AML1‐ETO collaborates with further genetic abnormalities to induce acute myeloid leukaemia (AML). We analysed 99 patients with an AML1‐ETO rearrangement for additional aberrations. Frequent genetic abnormalities were, loss of a sex chromosome (56/99, 56·5%) and del(9)(q22) (24/99, 24·2%). The most frequent molecular aberrations were mutations of KITD816 (3/23, 13%) and NRAS (8/89, 8·9%). Further molecular abnormalities were FLT3 mutations (3/87, 3·4%), AML1 (1/26, 3·8%) and PU1 (1/14, 7·1%). MLL‐PTD, KRAS and CEBPA mutations were not found. These clinical findings support the model that AML1‐ETO collaborates with other genetic alterations, such as mutations of receptor tyrosine kinases, to induce AML.
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