Publications by authors named "A Pasquier"

Introduction: Chemotherapy continues to be the standard treatment for patients noneligible for targeted or immune-based therapies; nevertheless, treatment resistance remains a major clinical challenge. We previously found that expression levels of DSTYK, a poorly explored dual serine/threonine and tyrosine kinase frequently amplified in cancer, identified patients with lung cancer exhibiting poor response to immune checkpoint inhibitors, and found that its inhibition sensitizes to immunotherapy. Seeking to explore the potential of DSTYK targeting in additional indications, we investigated the functional relevance and actionability of DSTYK in lung cancer chemoresistance.

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Background: Clinical data warehouses provide harmonized access to healthcare data for medical researchers. Informatics for Integrating Biology and the Bedside (i2b2) is a well-established open-source solution with the major benefit that data representations can be tailored to support specific use cases. These data representations can be defined and improved via an iterative approach together with domain experts and the medical researchers using the platform.

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A series of biotin-functionalized transition metal complexes was prepared by iClick reaction from the corresponding azido complexes with a novel alkyne-functionalized biotin derivative ([Au(triazolato)(PPh)], [Pt(dpb)(triazolato)], [Pt(triazolato)(terpy)]PF, and [Ir(ppy)(triazolato)(terpy)]PF with dpb = 1,3-di(2-pyridyl)benzene, ppy = 2-phenylpyridine, and terpy = 2,2':6',2''-terpyridine and R = CH, R' = biotin). The complexes were compared to reference compounds lacking the biotin moiety. The binding affinity toward avidin and streptavidin was evaluated with the HABA assay as well as isothermal titration calorimetry (ITC).

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Sharing biomedical data for research can help to improve disease understanding and support the development of preventive, diagnostic, and therapeutic methods. However, it is vital to balance the amount of data shared and the sharing mechanism chosen with the privacy protection provided. This requires a detailed understanding of potential adversaries who might attempt to re-identify data and the consequences of their actions.

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To fulfill their function, pancreatic beta cells require precise nutrient-sensing mechanisms that control insulin production. Transcription factor EB (TFEB) and its homolog TFE3 have emerged as crucial regulators of the adaptive response of cell metabolism to environmental cues. Here, we show that TFEB and TFE3 regulate beta-cell function and insulin gene expression in response to variations in nutrient availability.

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