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Sorafenib treatment of FLT3-ITD(+) acute myeloid leukemia: favorable initial outcome and mechanisms of subsequent nonresponsiveness associated with the emergence of a D835 mutation.
The results suggest that sorafenib have selected more aggressive sorAFenib-resistant subclones carrying both FLT3-ITD and D835 mutations, and might provide important leads to further improvement of treatment outcome with FLT 3 inhibitors. Expand
Cyclin A in cell cycle control and cancer
Consistent with its role as a key cell cycle regulator, expression of cyclin A is found to be elevated in a variety of tumors. Expand
Synthetic lethal targeting of oncogenic transcription factors in acute leukemia by PARP inhibitors
It is demonstrated that AML driven by repressive transcription factors, including AML1-ETO and PML-RARα fusion oncoproteins, are extremely sensitive to poly (ADP-ribose) polymerase (PARP) inhibition and a novel molecular mechanism governing PARPi sensitivity in AML is revealed. Expand
A roller coaster ride with the mitotic cyclins.
Central to the knowledge is the understanding of how APC/C is turned on from anaphase to early G1 phase, and turned off from late G1 till the spindle-assembly checkpoint is deactivated in metaphase. Expand
Targeting Aberrant Epigenetic Networks Mediated by PRMT1 and KDM4C in Acute Myeloid Leukemia
Experimental evidence for the functional involvement and therapeutic potential of targeting PRMT1, an H4R3 methyltransferase, in various MLL and non-MLL leukemias is provided and Pharmacological inhibition of KDM4C/PRMT1 suppresses transcription and transformation ability of MLL fusions and MOZ-TIF2, revealing a tractable aberrant epigenetic circuitry in acute leukemia. Expand
Specialized roles of the two mitotic cyclins in somatic cells: cyclin A as an activator of M phase-promoting factor.
It is shown that down-regulation of cyclin A induces a G2 phase arrest through a checkpoint-independent inactivation ofcyclin B-CDC2 by inhibitory phosphorylation, and a critical role of Cyclin A as a trigger for MPF activation is underscore. Expand
Cyclin F Is Degraded during G2-M by Mechanisms Fundamentally Different from Other Cyclins*
- T. Fung, W. Y. Siu, C. Yam, A. Lau, R. Poon
- Biology, Medicine
- The Journal of Biological Chemistry
- 20 September 2002
Although cyclin F is degraded at similar time as the mitotic cyclins, the underlying mechanisms are entirely distinct and appear to involve metalloproteases. Expand
Suppression of SOX7 by DNA methylation and its tumor suppressor function in acute myeloid leukemia.
It is shown that SOX7 expression was regulated by DNA hypermethylation in AML but not in acute lymphoblastic leukemia or normal bone marrow cells, and the antileukemia effects ofSOX7 in THP-1 cells were significantly reduced by deletion of its β-catenin binding site. Expand
The N-terminal Regulatory Domain of Cyclin A Contains Redundant Ubiquitination Targeting Sequences and Acceptor Sites
A novel approach involving in vitro cleavage of cyclin A after ubiquitination found that several lysine residues proximal to the D-box were ubiquitin acceptor sites and revealed that ubiquitinations does not occur randomly on Cyclin A and open up questions on the precise function of the D -box. Expand
Overcoming treatment resistance in acute promyelocytic leukemia and beyond
The underlying mechanisms and the potential avenue of targeting a critical histone demethylase PHF8 in overcoming the treatment resistance in APL and beyond are discussed. Expand