Delineating MYC-Mediated Escape Mechanisms from Conventional and T Cell-Redirecting Therapeutic Antibodies.

In B-cell malignancies, the overexpression of MYC is associated with poor prognosis, but its mechanism underlying resistance to immunochemotherapy remains less clear. In further investigations of this issue, we show here that the pharmacological inhibition of MYC in various lymphoma and multiple myeloma cell lines, as well as patient-derived primary tumor cells, enhances their susceptibility to NK cell-mediated cytotoxicity induced by conventional antibodies targeting CD20 (rituximab) and CD38 (daratumumab), as well as T cell-mediated cytotoxicity induced by the CD19-targeting bispecific T-cell engager blinatumomab. This was associated with upregulation of the target antigen only for rituximab, suggesting additional escape mechanisms.

Supramolecular tunnelling junctions with robust high rectification based on assembly effects.

The performance of large-area molecular diodes can in rare cases approach the lower limit of commercial semiconductor devices but predictive structure-property design remains difficult as the rectification ratio () achieved by self-assembled monolayer (SAM) based diodes depends on several intertwined parameters. This paper describes a systematic approach to achieve high rectification in bisferrocenyl-based molecular diodes, HSCFc-CC-Fc ( = 9-15) immobilised on metal surfaces (Ag, Au and Pt). Experiments supported by molecular dynamics simulations show that the molecular length and bottom electrode influence the SAM packing, which affects the breakdown voltage (), the associated maximum (), and the bias at which the is achieved ().

Evaluation of Sézary cell marker expression and cell death behaviour upon in vitro treatment by flow cytometry in Sézary syndrome patients.

The diagnosis of Sézary syndrome (SS) relies on the identification of blood Sézary cells (SC) by different markers via flow cytometry. Treatment of SS is challenging since its pathogenesis is characterized by cell death resistance rather than hyperproliferation. In this study, we establish an integrated approach that considers both the expression of SC markers and sensitivity to cell death both spontaneously and upon in vitro treatment.