Eros Lazzerini Denchi

MUTYH activity maintains telomere stability in response to chronic telomeric 8-oxoguanine damage in cancer cells

This study shows MUTYH prevents telomere shortening and genomic instability in cancer cells under chronic 8-oxoG damage by resolving BER intermediates.

SMARCAL1 is a candidate therapeutic target for ALT-positive tumors

The paper identifies SMARCAL1 as a key regulator of ALT metabolism and a potential therapeutic target for ALT-positive tumors.

Conserved and Unique Features of Terminal Telomeric Sequences in ALT-Positive Cancer Cells

The paper uses END-seq to analyze telomere sequences in ALT-positive cancer cells, revealing conserved and unique features of terminal telomeric sequences.

Optical Pooled Screening for the Discovery of Regulators of the Alternative Lengthening of Telomeres Pathway

The paper develops an Optical Pooled Screen (OPS) assay using telomeric native DNA FISH to measure ALT pathway activity and identifies regulators of the ALT pathway.

Identification of Novel Modulators of the ALT Pathway Through a Native FISH-Based Optical Screen

This study identifies novel genes that modulate the ALT pathway using a high-throughput imaging screen, revealing both promoting and inhibiting factors and demonstrating pharmacological modulation potential.

CTCF is a Barrier for Totipotent-like Reprogramming

This study identifies CTCF as a barrier to 2C-like reprogramming in ESCs, showing its role in maintaining chromatin structure and that its depletion promotes totipotent-like state conversion.

Telomere relocalization to the nuclear pore complex in response to replication stress

The paper investigates how mutant POT1 alleles cause replication stress and telomere fragility, revealing a role for the nuclear pore complex in resolving these defects and telomere repositioning to the nuclear periphery.

POT1a depletion in the developing brain leads to p53-dependent neuronal cell death and ataxia.

This study shows that POT1a depletion in neural progenitors causes p53-dependent neuronal death and ataxia, while p53 inactivation rescues lethality, highlighting distinct DNA damage response pathways in neurological disorders.