Loris Mularoni

This study maps uterine remodeling postpartum using single-cell transcriptomics, revealing a novel homeostatic state that does not revert to pre-pregnancy cellular architecture.

This study shows that STAU2 regulates human neurogenesis by affecting transcription factors, miRNA control, and progenitor maintenance, leading to changes in neural differentiation and organoid development.

This study identifies ceruloplasmin deficiency in mutant astrocytes as a driver of iron toxicity and neurodegeneration in a Parkinson's tri-culture model.

This study shows that reducing RhoA activity in aged HSCs lowers nuclear tension, restores chromatin structure, and improves regenerative capacity and lineage balance.

This study identifies 15 novel ductal cell populations in the mouse pancreas using scRNA-seq and investigates their roles in regeneration and exocrine pathogenesis.

This study compares preservation methods for scRNA-seq of neural cells, finding that methanol fixation best preserves cellular composition and expression profiles.

The paper introduces the Cancer LncRNA Census (CLC), a curated resource of lncRNAs with causative roles in cancer, and shows their genomic and evolutionary features.

ActivePathways integrates multivariate omics data to identify enriched pathways, revealing cancer driver genes and prognostic pathways in breast cancer.

OncodriveCLUSTL identifies cancer drivers by detecting mutation clustering signals in genomic data, outperforming existing methods across tumor whole-exomes.

The paper identifies and characterizes coding and non-coding driver mutations across 2,500 cancer genomes, revealing new candidates and questioning previous findings.

This paper identifies driver mutations across 2,500 tumors from 37 cancer types, revealing a whole-genome panorama of genomic events that underlie tumor development.

The paper identifies 15 high-confidence cancer driver lncRNAs across 1112 tumour genomes using a mutational pattern analysis approach.

The paper shows that DNA-binding proteins reduce nucleotide excision repair activity, leading to higher mutation rates at their binding sites in melanoma.