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Lithium niobate (LiNbO3, LN) is a ferroelectric crystal of interest for integrated photonics owing to its large second-order optical nonlinearity and the ability to impart periodic poling via an external electric field. However, on-chip device performance based on thin-film lithium niobate (TFLN) is presently limited by propagation losses arising from surface roughness and corrugations. Atomic layer etching (ALE) could potentially smooth these features and thereby increase photonic performance, but no ALE process has been reported for LN. Here, we report an isotropic ALE process for x-cut MgO-doped LN using sequential exposures of H2 and SF6/Ar plasmas. We observe an etch rate of 1.59±0.02 nm/cycle with a synergy of 96.9%. We also demonstrate that ALE can be achieved with SF6/O2 or Cl2/BCl3 plasma exposures in place of the SF6/Ar plasma step with synergies of 99.5% and 91.5%, respectively. The process is found to decrease the sidewall surface roughness of TFLN waveguides etched by physical Ar+ milling by 30% without additional wet processing. Our ALE process could be used to smooth sidewall surfaces of TFLN waveguides as a postprocessing treatment, thereby increasing the performance of TFLN nanophotonic devices and enabling new integrated photonic device capabilities. 

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer without effective treatments. It is characterized by activating KRAS mutations and p53 alterations. However, how these mutations dysregulate cancer-cell-intrinsic gene programs to influence the immune landscape of the tumor microenvironment (TME) remains poorly understood. Here, we show that p53^(R172H) establishes an immunosuppressive TME, diminishes the efficacy of immune checkpoint inhibitors (ICIs), and enhances tumor growth. Our findings reveal that the upregulation of the immunosuppressive chemokine Cxcl1 mediates these pro-tumorigenic functions of p53^(R172H). Mechanistically, we show that p53^(R172H) associates with the distal enhancers of the Cxcl1 gene, increasing enhancer activity and Cxcl1 expression. p53^(R172H) occupies these enhancers in an NF-κB-pathway-dependent manner, suggesting NF-κB’s role in recruiting p53^(R172H) to the Cxcl1 enhancers. Our work uncovers how a common mutation in a tumor-suppressor transcription factor appropriates enhancers, stimulating chemokine expression and establishing an immunosuppressive TME that diminishes ICI efficacy in PDAC.