Ana Janic

The paper identifies a p53-FBXO44-RAD18 axis that limits mutagenesis by terminating translesion DNA synthesis after replication stress.

The paper identifies a metabolic vulnerability in TP53-deficient cells linked to nuclear adenosine metabolism and histone methylation, showing its role in DNA damage response and tumor growth.

This study shows that inhibiting nonsense-mediated mRNA decay enhances tumour immunogenicity, drives immunoediting, and improves checkpoint blockade efficacy in preclinical models.

This study compares immunotherapy responses in subcutaneous and orthotopic dMMR LUAD models, finding that orthotopic models show better anti-PD1 response with increased immune infiltration and CD4+ memory T cells.

The paper identifies PRDX1 as essential for DNA damage repair by scavenging nuclear ROS and regulating aspartate synthesis during the DNA damage response.