Detection of N-RAS and K-RAS in their active GTP-bound form in acute myeloid leukemia without activating RAS mutations.
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Detection of N-RAS and K-RAS in their active GTP-bound form in acute myeloid leukemia without activating RAS mutations. / Ehmann, Falk; Horn, Stefan; Garcia-Palma, Lizet; Wegner, Wiebke; Fiedler, Walter; Giehl, Klaudia; Mayr, Georg W.; Jücker, Manfred.
in: LEUKEMIA LYMPHOMA, Jahrgang 47, Nr. 7, 7, 2006, S. 1387-1391.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Detection of N-RAS and K-RAS in their active GTP-bound form in acute myeloid leukemia without activating RAS mutations.
AU - Ehmann, Falk
AU - Horn, Stefan
AU - Garcia-Palma, Lizet
AU - Wegner, Wiebke
AU - Fiedler, Walter
AU - Giehl, Klaudia
AU - Mayr, Georg W.
AU - Jücker, Manfred
PY - 2006
Y1 - 2006
N2 - RAS genes, predominantly N-RAS and K-RAS, have been implicated in the pathogenesis of acute myeloid leukemia (AML), due to activating RAS mutations detectable in approximately 20% of AML patients. In the present study, RAS proteins were detected in their activated, GTP-bound form, in AML patients (n = 10) not expressing mutated forms of H-RAS, K-RAS and N-RAS. Further analysis revealed the simultaneous presence of N-RAS and K-RAS proteins in the GTP-bound state in seven out of 10 AML samples. In four out of 10 samples the levels of RAS-GTP were comparable to an AML cell line (TF-1) with an activating N-RAS mutation (Q61P). The detection of RAS-GTP in AML patients without RAS mutations further supports a functional role of RAS proteins in the pathogenesis of AML and may explain the observed effects of RAS inhibitors in some AML patients in the absence of activating RAS mutations.
AB - RAS genes, predominantly N-RAS and K-RAS, have been implicated in the pathogenesis of acute myeloid leukemia (AML), due to activating RAS mutations detectable in approximately 20% of AML patients. In the present study, RAS proteins were detected in their activated, GTP-bound form, in AML patients (n = 10) not expressing mutated forms of H-RAS, K-RAS and N-RAS. Further analysis revealed the simultaneous presence of N-RAS and K-RAS proteins in the GTP-bound state in seven out of 10 AML samples. In four out of 10 samples the levels of RAS-GTP were comparable to an AML cell line (TF-1) with an activating N-RAS mutation (Q61P). The detection of RAS-GTP in AML patients without RAS mutations further supports a functional role of RAS proteins in the pathogenesis of AML and may explain the observed effects of RAS inhibitors in some AML patients in the absence of activating RAS mutations.
M3 - SCORING: Zeitschriftenaufsatz
VL - 47
SP - 1387
EP - 1391
JO - LEUKEMIA LYMPHOMA
JF - LEUKEMIA LYMPHOMA
SN - 1042-8194
IS - 7
M1 - 7
ER -