L. Magnani

This study identifies VGLL1 as a driver of resistance to endocrine therapy in ER+ breast cancer and shows that targeting VGLL1/TEAD interaction can inhibit resistant cell growth.

The paper shows how epigenetic heritability of cell plasticity contributes to cancer drug resistance through a one-to-many genotype-to-phenotype mapping.

This study investigates phenotypic plasticity and genetic control in colorectal cancer by analyzing gene expression and genetic variation across multiple tumor regions.

This study examines the co-evolution of genome and epigenome in colorectal cancer using single-clone spatial multi-omic profiling, revealing epigenetic changes and their impact on mutation accumulation.

This study identifies non-coding DNA alterations in hormone-dependent breast cancer that contribute to endocrine therapy resistance and disease progression.

This study identifies oncogenic regulatory circuits driven by chromosome 1q amplification in cancer and proposes targeted therapy strategies using a systems medicine approach.

This study uses spatial multiomic data to assess the evolutionary impact of putative driver mutations in colorectal cancer, identifying both genetic and non-genetic factors influencing subclonal expansion.

This study investigates dormancy and awakening in endocrine-treated breast cancer cells, revealing stochastic awakening strategies and the role of epigenetic decay.

This study identifies ATF3 as a novel mediator of endocrine resistance in breast cancer through time-resolved profiling and validates its role in key signaling pathways and clinical relevance.

This study identifies magnesium-containing spherical nano and micro particles in invasive breast cancers using nano-analytical methods, showing their concentration increases with cancer progression.

This study uses single-cell transcriptomics to identify pre-adapted cells that undergo reprogramming to develop resistance to endocrine therapy in breast cancer.

This study identifies SREBP1-driven KRT80 upregulation as a mechanism promoting invasion in endocrine-resistant ERα breast cancer through cytoskeletal changes and increased tumor stiffness.

This study maps enhancers in luminal breast cancer to reveal phenotypic heterogeneity and its evolutionary dynamics during treatment.