Publications by authors named "Kelly Jacques"

Inhibiting the tribological failure of mechanical assemblies which rely on fuels for lubrication is an obstacle to maintaining the lifetime of these systems with low-viscosity and low-lubricity fuels. In the present study, a MoVN-Cu nanocomposite coating was tribologically evaluated for durability in high- and low-viscosity fuels as a function of temperature, load, and sliding velocity conditions. The results indicate that the MoVN-Cu coating is effective in decreasing wear and friction relative to an uncoated steel surface.

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  • Deregulation of the PRC2 complex, which is important for gene regulation, leads to abnormal cancer growth due to hypermethylation of histone H3K27.
  • Despite promising results from EZH2 inhibitors, resistance can develop from mutations in EZH2 that escape drug effects.
  • The newly designed PROTACs target EED for degradation, effectively inhibiting PRC2 activity and reducing the growth of cancer cells dependent on PRC2, showcasing a novel therapeutic approach.
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BRD4 is a transcriptional co-activator functioning to recruit regulatory complexes to acetylated chromatin. A subset of High-grade Serous Ovarian Cancer (HGSOC) patients are typified by focal, recurrent BRD4 gene amplifications. Despite previously described cancer dependencies, it is unclear whether BRD4 amplification events are oncogenic in HGSOC.

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  • Exogenous expression of AKT1(E17K) in breast epithelial cells leads to increased AKT activation, colony formation, and tumor growth in mice, which can be inhibited by AKT inhibitors MK-2206 and AZD5363.
  • Clinical studies indicate that AZD5363 shows promise in treating breast and ovarian cancers with AKT1(E17K) mutations, but may require combination therapies for effective treatment in tumors with additional oncogenic mutations.
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Centrosome amplification is observed in many human cancers and has been proposed to be a driver of both genetic instability and tumorigenesis. Cancer cells have evolved mechanisms to bundle multiple centrosomes into two spindle poles to avoid multipolar mitosis that can lead to chromosomal segregation defects and eventually cell death. KIFC1, a kinesin-14 family protein, plays an essential role in centrosomal bundling in cancer cells, but its function is not required for normal diploid cell division, suggesting that KIFC1 is an attractive therapeutic target for human cancers.

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