Simone Bruno

This study identifies BRD2 as a co-targetable vulnerability with PI3K/AKT inhibitors in breast cancer, showing that BRD2 phosphorylation is required for chromatin binding and that targeting BRD2 enhances drug efficacy.

This paper develops a digital twin model to optimize epigenetic therapies in triple-negative breast cancer by simulating treatment responses and identifying effective drug combinations.

This study reveals analog epigenetic memory through graded DNA methylation, showing its temporal stability and role in gene expression regulation.

BESTDR quantifies drug response mechanisms using Bayesian modeling of cell state transitions, improving accuracy in dose-response analysis across cell lines.

The paper investigates how p21 transcription variability arises through an incoherent feedforward loop involving p53 and MDM2, showing it enables rapid p21 induction and treatment-tolerant cell states.

The paper identifies OCT4 trajectories critical for reprogramming human fibroblasts to iPSCs and develops a synthetic genetic circuit to enforce these trajectories, improving reprogramming efficiency.

This paper compares three reprogramming approaches by modeling the Oct4 gene regulatory network and finds that overexpressing eraser enzymes accelerates and stabilizes reprogramming, with TET outperforming JMJD2 under specific conditions.

The paper models how chromatin modification circuits enable epigenetic memory through time-scale separation and bistability in gene expression states.