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Leukemia-Related Protein 16 (LRP16), a member of the macro domain family, plays a crucial role in orchestrating genotoxicity-initiated NF-κB signaling in the colon and the pathophysiological relevance of NF-κB activation induced by LRP16 in colonic cell survival/recovery from extrinsic DNA damage.

A geneome-scale shRNA screen identifies five genes whose suppression promotes cell death upon PI3K inhibition both in vitro and in vivo, thus suggesting potential combination therapies involving PI3K inhibition.

Targeted therapies induce an aberrant fucosylation of complex tumor secretomes stimulating the expansion of minority drug-resistant clones and promoting therapy resistance.

RNF43 interacts with receptor complexes of the Wnt/PCP signaling and its enzymatic activity results in the reduced cells sensitivity to WNT5A what translates in melanoma into decreased invasive properties and increased response to targeted therapies of this skin cancer.

A periosteal Bmp2 signaling center couples bone length to bone width during development and must be reactivated by clinical bone anabolic therapies to reduce fracture risk and accelerate fracture repair.

Classification of MET mutations allows a better understanding of sensitivity and resistance to targeted therapies used in cancer.

A gene expression data-informed model reveals that a small fraction of interferon-producing cells can effectively constrain early virus spread in epithelial tissue, elucidating connections between critical dynamics and infection heterogeneity.

The ability of cartilaginous fishes to generate new cartilage through adulthood, and to spontaneously repair damaged cartilage, could shed light on novel cell-based therapies for cartilage injury in mammals.

A model based on empirical parameter estimates predicts that arresting cancer cell growth by less than 1% per day will produce optimal outcomes in preventing life-threatening cancers, and that such preventive measures are generally more successful than post-diagnostic interventions.

In triple-drug-treated HIV, partially resistant viruses can spread and resistance to specific drugs evolves in a predictable order, potentially a result of spatial or temporal heterogeneity in drug concentrations.