Vito Quaranta

This study identifies a novel intermediate cell state and a regulatory network in SCLC that drives lineage plasticity and immunogenicity.

This study identifies YAP1-positive cells in relapsed SCLC that exhibit drug tolerance and transition from SCLC to LCNEC-like features, losing some targets but gaining others.

This study identifies three distinct DDR phenotypes in SCLC associated with chemotherapy response and tumor evolution.

The paper uses Bayesian multimodel inference to analyze tumor growth mechanisms in SCLC, finding that high lineage plasticity, not rare stem-like populations, drives tumor evolution.

This study shows that cooperative RNA degradation via microRNA binding sites can stabilize intermediate EMT states without transcriptional feedback, supporting a phenotypic continuum in EMT.

This study shows SCLC cells exist in a continuum of plastic states rather than discrete subtypes, with gene expression patterns linked to cancer hallmarks and potential therapeutic targets.

This paper introduces a method using real-time luminescence to estimate drug response in cell lines, avoiding the need for cell counting and fluorescent labeling.

The paper identifies heterogeneous drug-tolerant persisters (DTPs) as population-level states with distinct division and death rates, showing increased ferroptosis susceptibility.

This study disentangles genetic, epigenetic, and stochastic factors contributing to drug-response variability in an in vitro tumor heterogeneity model using PC9 cell lines.

ACDC automates cell detection and counting in time-lapse microscopy images, achieving high accuracy without large annotated datasets.

The paper identifies a drug-tolerant metabolic state in melanoma cells that reduces both glycolysis and oxidative phosphorylation, supporting survival but limiting growth.

The paper identifies four SCLC subtypes using a systems approach, with NEv2 being a new subtype, and finds master regulators and destabilizers using BooleaBayes.

The paper shows that increased antioxidant capacity in BRAF-mutated melanoma cells reduces sensitivity to BRAF inhibitors and suggests targeting redox pathways could improve treatment outcomes.