STK3 is a therapeutic target for a subset of acute myeloid leukemias
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STK3 is a therapeutic target for a subset of acute myeloid leukemias. / Camgoz, Aylin; Paszkowski-Rogacz, Maciej; Satpathy, Shankha; Wermke, Martin; Hamann, Martin V.; von Bonin, Malte; Choudhary, Chunaram; Knapp, Stefan; Buchholz, Frank.
In: OncoTarget, Vol. 9, No. 39, 2018, p. 25458-25473.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - STK3 is a therapeutic target for a subset of acute myeloid leukemias
AU - Camgoz, Aylin
AU - Paszkowski-Rogacz, Maciej
AU - Satpathy, Shankha
AU - Wermke, Martin
AU - Hamann, Martin V.
AU - von Bonin, Malte
AU - Choudhary, Chunaram
AU - Knapp, Stefan
AU - Buchholz, Frank
PY - 2018
Y1 - 2018
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.
AB - 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.
U2 - 10.18632/oncotarget.25238
DO - 10.18632/oncotarget.25238
M3 - Journal article
C2 - 29876001
VL - 9
SP - 25458
EP - 25473
JO - Oncotarget
JF - Oncotarget
SN - 1949-2553
IS - 39
ER -
ID: 197764925