Nuri A. Temiz

This study examines the relationship between APOBEC3B mRNA expression and mutational signatures in breast cancer, finding that high APOBEC3B expression correlates with specific genetic and metabolic changes affecting drug response.

The paper identifies mutational signatures in cancer genomes caused by tobacco-specific nitrosamines NNN and NNK, showing their unique contribution to specific cancer types.

The paper uses Sleeping Beauty mutagenesis to identify BACH2 and other genes that enhance CD8+ T cell persistence and function under chronic antigen stimulation, improving engineered T cell therapies.

This study shows that progesterone receptors (PR) interact with mutant ESR1 variants in ER+ breast cancer, driving CSC expansion and UPR activation, which can be targeted therapeutically.

The paper develops two murine TNBC models with differing immunotherapy responses for studying treatment mechanisms and therapies.

This study shows that carcinogen-induced DNA adducts enhance APOBEC3B-mediated mutagenesis, leading to increased mutation rates in cancer genomes.

This study shows that overexpressing human APOBEC3B in mice causes lethality through RNA editing and organ dysfunction.