Natalia Cestari Moreno, Ph.D.

Dr. Natalia Cestari Moreno is a Research Assistant Professor in Dr. Ryan Barnes’ lab in the Department of Cancer Biology at the University of Kansas Medical Center. She earned her Ph.D. in Genetics from the University of São Paulo, Brazil, studying how oxidative stress induced by UVA light is related to DNA damage and mutagenesis in cells from patients with the skin cancer–prone disease Xeroderma Pigmentosum. She continued her training at the National Institutes of Health (NIH), where she was focused on the regulation of Translesion Synthesis polymerases, including post-translation modification such as ubiquitination and NEDDylation, and their implication in replication stress and cancer. Her research focuses on the DNA damage response, DNA repair, and genome stability in the context of oxidative stress, particularly in rare disorders and cancer. She also serves as co-chair of the Mutagenesis Mechanisms & Assessments Special Interest Group (MMA-SIG) at Environmental Mutagenesis and Genomic Society (EMGS).

DNA is constantly challenged by endogenous and environmental sources of damage that threaten genome stability. Among these, oxidative stress caused by excess reactive oxygen species (ROS) plays a central role in damaging the genome, particularly in tissues exposed to solar ultraviolet radiation (UVR), inflammation, and certain chemotherapeutic agents. Oxidative stress leads to a wide range of DNA lesions, including base modifications, single- and double-strand breaks, and replication stress, all of which can promote mutagenesis and disease.
Our group is particularly interested in how oxidative stress-induced DNA damage is sensed and repaired in human cells. We study patient-derived cells from individuals with syndromes such as Xeroderma Pigmentosum Variant (XP-V), characterized by mutations in the TLS polymerase POLH. These rare disorders serve as powerful models to dissect how the failure to cope with oxidative DNA damage contributes to disease susceptibility, including heightened cancer risk, and to explore potential therapeutic strategies to reduce cancer burden and improve patient care.
To address these questions, we use a range of molecular and cellular biology techniques including DNA repair assays, chromatin analysis, and cell cycle profiling combined with controlled oxidative stress exposure (e.g., UVA radiation and chemoptogenetic tools) and mechanistic dissection of post-translational modifications on key DNA repair factors. Our long-term goal is to understand how the DNA damage response maintains genome integrity under oxidative stress and how its failure contributes to aging, cancer, and inherited disease.

ATR/Chk1 Pathway is Activated by Oxidative Stress in Response to UVA Light in Human Xeroderma Pigmentosum Variant Cells.

DNA polymerase η is regulated by mutually exclusive mono-ubiquitination and mono-NEDDylation.

How do Translesion Polymerases deal with Photodamage?

The key role of UVA-light induced oxidative stress in human Xeroderma Pigmentosum Variant cells.

Whole-exome sequencing reveals the impact of UVA light mutagenesis in xeroderma pigmentosum variant human cells.