The Davis Laboratory studies how cells preserve genomic and cellular integrity in response to genotoxic, metabolic, and environmental stress. Our research seeks to understand how stress-response pathways coordinate DNA repair, genome maintenance, cellular signaling, metabolic adaptation, and radiation responses, and how defects in these processes drive cancer development, therapeutic resistance, and radiation susceptibility.
We combine molecular, cellular, biochemical, and genomic approaches that define the signaling networks that govern cellular adaptation to stress. By integrating studies of genome stability, radiobiology, metabolism, and cancer biology, we aim to uncover fundamental mechanisms that maintain cellular fitness and identify vulnerabilities that emerge when these pathways are disrupted.
Our long-term goal is to translate these discoveries into new strategies for precision radiotherapy, cancer therapy, and radiation risk prediction, ultimately improving outcomes for patients with cancer and individuals exposed to environmental or occupational radiation.
Genome integrity is continuously challenged by endogenous and exogenous sources of DNA damage. Our laboratory seeks to define the molecular mechanisms that defect DNA lesions, coordinate cellular signaling responses, and preserve genome stability. We are particularly interested in how DNA damage response pathways regulate DNA repair, replication stress responses, cell cycle progression, and chromatin dynamics, and how dysregulation of these processes contributes to genomic instability and cancer development.
Many proteins classically associated with the DNA damage response also regulate fundamental aspects of cellular physiology. Our research investigates how these proteins influence cellular signaling networks, metabolism, mitochondrial function, and cell fate decisions independent of their canonical roles in genome maintenance. By defining these broader biological functions, we seek to uncover new mechanisms of cellular regulation and identify opportunities for therapeutic intervention in cancer and other diseases.
The biological response to radiation varies substantially among individuals, tumors, and normal tissues. Our laboratory investigates the molecular determinants of intrinsic radiosensitivity, radiation-induced genomic instability, and carcinogenesis following exposure to low- and high-linear energy transfer (LET) radiation. We are particularly interested in understanding how biological responses differ between conventional radiotherapy, particle therapy, and space radiation exposures, with the goal of developing biomarkers and biologically informed approaches for precision radiotherapy and radiation risk assessment.
Cancer cells rely on stress response pathways to survive genomic instability, metabolic stress, and therapeutic challenge. Our laboratory combines mechanistic studies, functional genomics, and chemical biology approaches to identify vulnerabilities that arise when these pathways are disrupted. By defining the signaling networks that govern cellular adaptation to stress, we aim to develop mechanism-based therapeutic strategies that improve the efficacy of radiotherapy, targeted therapies, and emerging precision oncology approaches.