My research investigates how adaptive tumor vulnerabilities emerge through interactions between microbial dysbiosis, epigenetic remodeling, and dynamic DNA repair rewiring in women’s cancers, particularly HPV-associated malignancies. By integrating molecular biology, functional genomics, and translational multi-omics approaches, my work seeks to define clinically relevant tumor states that shape treatment response, resistance evolution, and disease progression.
🧬+🧫 Microbiome–Epigenome–Repair-State Interactions
I study how cervicovaginal microbial ecosystem shifts reshape epigenetic regulation, genome stability, inflammatory signaling, and HPV persistence in women’s cancers. My work focuses on how dysbiosis-associated microbial communities influence chromatin organization and repair-state adaptation, thereby altering tumor behavior under therapeutic stress. Through integrated microbiome profiling, epigenetic analysis, and functional DNA repair assays, I investigate mechanistic links between microbial ecology, immune adaptation, and treatment response in HPV-associated malignancies.
🧬Dynamic DNA Repair Vulnerability and Therapy Response
My research focuses on how cancer cells adapt to therapy-induced DNA damage through dynamic rewiring of DNA repair, replication stress, and checkpoint signaling pathways. I investigate how evolving repair states influence genome instability, therapeutic response, and resistance evolution in HPV-associated and other women’s cancers. By combining functional DNA repair assays with molecular and translational analyses, my work aims to identify clinically actionable repair dependencies and biologically informed strategies for therapeutic stratification.
🧪Epigenetic Plasticity and Tumor State Reprogramming
I investigate how epigenetic remodeling drives tumor adaptation, phenotypic plasticity, and stress survival in cervical and other women’s cancers. My work examines how changes in DNA methylation, chromatin accessibility, histone modifications, and non-coding regulatory networks reshape transcriptional programs associated with immune evasion and therapy adaptation. By integrating epigenetic profiling with functional and translational analyses, I aim to uncover reversible epigenetic vulnerabilities and clinically relevant tumor-state biomarkers.
A central goal of my research is to translate molecular and mechanistic insights into clinically meaningful strategies for women’s cancers. By integrating genomic, epigenomic, microbiome, and treatment-response data, I investigate how adaptive tumor states shape therapeutic outcomes during chemoradiotherapy. This work focuses on developing biologically informed biomarkers and translational stratification frameworks that may improve therapeutic precision across diverse and resource-variable patient populations.