A biomimetic and patient-specific Glioblastoma-on-a-Chip microphysiological system provides an avenue for personalized screening of PD-1 immunotherapy and novel combinational therapies that maximize therapeutic outcomes in Glioblastoma patients.

Novel human models of the lung and intestine are described and validated as preclinical in vitro tools for predictive profiling of T-cell-bispecific antibodies with expected on-target off-tumor risk.

YAP and TAZ, the ultimate targets of the Hippo signaling pathway, are transcriptional co-activators of AP-1 proteins and STAT3 through which they are important for breast cellular transformation.

In fusion-positive rhabdomyosarcoma, CHD4 positively regulates super-enhancer-mediated gene expression by allowing a chromatin architecture at these cis-regulatory regions, which is permissive to the binding of the transcription factor PAX3-FOXO1.

CausalXtract is a computational tool to discover causal effects, beyond classical Granger and Schreiber causality approaches, from live-cell imaging data for a range of fundamental and translational research applications.

The HOXB13 binding partner MEIS1 suppresses prostate cancer proliferation, invasion, and metastasis by promoting expression of the anti-oncogenic extracellular proteoglycan Decorin.

MYF5 and MYOD regulate rhabdomyosaroma growth and tumor-propagating potential, acting more than as passive markers retained from the target cell-of-origin during transformation.

Binding of the translation initiation factor eIF3 to the messenger RNAs encoding the T cell receptor subunits alpha and beta is required to drive a short burst in their translation and promote a strong T cell response.

NFATc2 maintains the drug-induced TIC phenotypes through trans-activating SOX2/ALDH1A1 expression and scavenging stress from ROS.

G9a regulates chromatin-bound b-catenin enabling cell-intrinsic control of WNT signaling-mediated cell fate decisions.