Filippo Beleggia

This study identifies Miz1/Myc complexes at enhancers as key regulators of neuroendocrine identity in SCLC, showing their role in gene expression and chemosensitivity.

This study benchmarks preprocessing strategies for single-cell transformer models and finds that simple log-transformed counts outperform complex methods, leading to a more efficient foundation model.

This study identifies NMD inhibition as a therapeutic strategy for SCLC by enhancing immunogenicity and improving immunotherapy efficacy through increased neoantigen presentation.

This paper investigates Cav1.2-dependent excitation-transcription coupling in nociceptors, showing it modulates pain sensitivity by affecting gene expression and neuronal function.

This study shows oncogenic RAS signaling suppresses ferroptosis by upregulating GCH1 and BH4, making RAS-driven cancers resistant to ferroptosis-inducing agents.

The paper identifies ferroptosis sensitivity as a distinguishing feature of non-neuroendocrine SCLC subtypes and shows that combining ferroptosis induction with TRX pathway inhibition can selectively kill both non-NE and NE SCLC tumors.