TY  - JOUR
A1  - Camgoz, Aylin
A1  - Paszkowski-Rogacz, Maciej
A1  - Satpathy, Shankha
A1  - Wermke, Martin
A1  - Hamann, Martin V.
A1  - Bonin, Malte von
A1  - Choudhary, Chunaram
A1  - Knapp, Stefan
A1  - Buchholz, Frank
T1  - STK3 is a therapeutic target for a subset of acute myeloid leukemias
T2  - OncoTarget
N2  - Acute myeloid leukemia (AML) is characterized by uncontrolled proliferation and accumulation of immature myeloblasts, which impair normal hematopoiesis. While this definition categorizes the disease into a distinctive group, the large number of different genetic and epigenetic alterations actually suggests that AML is not a single disease, but a plethora of malignancies. Still, most AML patients are not treated with targeted medication but rather by uniform approaches such as chemotherapy. The identification of novel treatment options likely requires the identification of cancer cell vulnerabilities that take into account the different genetic and epigenetic make-up of the individual tumors. Here we show that STK3 depletion by knock-down, knock-out or chemical inhibition results in apoptotic cells death in some but not all AML cell lines and primary cells tested. This effect is mediated by a premature activation of cyclin dependent kinase 1 (CDK1) in presence of elevated cyclin B1 levels. The anti-leukemic effects seen in both bulk and progenitor AML cells suggests that STK3 might be a promising target in a subset of AML patients.
KW  - AML
KW  - personalized medicine
KW  - UCN-01
KW  - STK3
KW  - mitosis
Y1  - 2018
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/46601
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-466012
SN  - 1949-2553
N1  - All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
VL  - 9
IS  - 39
SP  - 25458
EP  - 25473
PB  - Impact Journals LLC
CY  - [s. l.]
ER  -