Second hit mutations in the RTK/RAS signaling pathway in acute myeloid leukemia with inv(16)

Valk, P.J.M.; Bowen, D.T.; Frew, M.E.; Goodeve, A.C.; Löwenberg, B.; Reilly, J.T.; Valk, P.J.M; Bowen, D.T; Frew, M.E; Goodeve, A.C; Löwenberg, B; Reilly, J.T

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Second hit mutations in the RTK/RAS signaling pathway in acute myeloid leukemia with inv (16)

Valk, P.J.M.; Bowen, D.T.; Frew, M.E.; Goodeve, A.C.; Löwenberg, B.; Reilly, J.T.

Haematologica 89(1): 106

2004

ISSN/ISBN: 0390-6078

PMID: 14754614

Document Number: 568026

We report that 69% of patients with acute myeloid leukemia (AML) and inv(16) possess either a RAS or receptor tyrosine kinase (RTK) mutation (e.g. C-KIT or FLT3). These findings, together with the fact that 90% of the mutations were mutually exclusive, lend support for the two-hit model of leukemogenesis and suggest possibilities of targeted therapy for patients with AML and inv(16).