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We have designed and synthesized a helical cysteamine-terminated oligourea foldamer composed of ten urea residues featuring side carboxyl and amine groups. The carboxyl group is located in proximity to the C-terminus of the oligourea and hence at the negative pole of the helix dipole. The amine group is located close to the N-terminus and hence at the positive pole of the helix dipole. Beyond the already remarkable dipole moment inherent in oligourea 2.5 helices, the incorporation of additional charges originating from the carboxylic and amine groups is supposed to impact the overall charge distribution along the molecule. These molecules were self-assembled into monolayers on a gold substrate, allowing us to investigate the influence of an electric field on these polar helices. By applying surface-enhanced infrared reflection–absorption spectroscopy, we proved that molecules within the monolayers tend to reorient themselves more vertically when a negative bias is applied to the surface. It was also found that surface-confined oligourea molecules affected by the external electric field tend to rearrange the electron density at urea groups, leading to the stabilization of the resonance structure with charge transfer character. The presence of the external electric field also affected the nanomechanical properties of the oligourea films, suggesting that molecules also tend to reorient in the ambient environment without an electrolyte solution. Under the same conditions, the helical oligourea displayed a robust piezoresponse, particularly noteworthy given the slender thickness of the monolayer, which measured approximately 1.2 nm. This observation demonstrates that thin molecular films composed of oligoureas may exhibit stimulus–responsive properties. This, in turn, may be used in nanotechnology systems as actuators or functional films, enabling precise control of their thickness in the range of even fractions of nanometers.

Introduction: Immune checkpoint inhibitors are highly effective in treating various cancers. We analyzed the significance of the KRAS/STK11co-mutation in relation to the efficacy of immune checkpoint inhibitors in pan-cancer patient cohort.Methods: We analyzed data from open-access research: MSK-IMPACT (molecular profiling data from patients receiving systemic antitumor therapy) and MSK-TMB (molecular profiling data from patients receiving immune checkpoint inhibitors). In both studies, high throughput sequencing was used for molecular profiling.Results: A total of 10,336 patients receiving antitumor therapy (MSK-IMPACT study) and 1661 patients receiving immune checkpoint inhibitors (MSK-TMB study) were included in the analysis. Co-mutation STK11/KRASwas found in 156 (1.5%) and 46 (2.8%) patients in the two studies, respectively. Most patients with the STK11/KRASco-mutation had non-small cell lung cancer (83% and 85% in the two studies, respectively). Among non-small cell lung cancer patients, the STK11mutation was associated with a worse outcome for patients receiving systemic antitumor therapy, but not immune checkpoint inhibition therapy (HR for OS 1.90 [95% CI 1.36-2.65] and 1.44 [95% CI 0.88-2.37]). Co-mutation STK11/KRASwas also not associated with patient outcome in any of the studies (HR for OS 0.93 [95% CI 0.56-1.52] and 1.09 [95% CI 0.54-2.19]). High tumor mutational burden was associated with better outcome in the cohort of patients receiving immune checkpoint inhibitors. An analogous analysis among patients in the pan-cancer cohort (excluding patients with non-small cell lung cancer) showed STK11mutations and high tumor mutational burden have a predictive role for the efficacy of immune checkpoint inhibitors, but not STK11/KRASco-mutation.Conclusions: Co-mutation STK11/KRASis common among patients with non-small cell lung cancer and is not an independent predictive marker for the efficacy of immune checkpoint inhibitors. Further studies are required to clarify the role of STK11mutations in immune checkpoint inhibitor treatment response.