My work sits at the intersection of genetics, epigenetics, DNA repair biology, the cervicovaginal microbiome, and cancer therapeutics, with a strong focus on women’s cancers. I’m especially interested in how disruptions across these layers—from gene variants and epigenetic drift to microbial imbalance—reshape tumor behavior, immune regulation, and treatment response. The goal is simple: understand these molecular conversations well enough to design better diagnostics and more precise therapies for patients.
🧬+🧫 Microbiome–Epigenome–DNA Repair Axis
I investigate how shifts in the cervicovaginal microbiome—especially the transition from Lactobacillus dominance to Gardnerella-driven dysbiosis—reshape host epigenetic states, DNA repair efficiency, inflammation, and HPV persistence.
Aim: To uncover microbial drivers of therapy response and identify multi-layered biomarkers for cervical cancer.
What I study:
Microbiome signatures and microbial imbalance
Microbiome-driven epigenetic reprogramming
Microbial metabolites influencing genome stability
Host–microbial interactions affecting HPV biology
Approach: Microbiome profiling → epigenetic mapping → DNA repair readouts → integrated modeling
A mechanistic framework connecting microbial ecology to drug sensitivity and disease progression in women’s cancers.
🧬DNA Damage Response (DDR) & Repair Pathways in Treatment Sensitivity
My work focuses on how tumors detect, process, and repair therapy-induced DNA damage. Genes like MGMT, XRCC1, XRCC4, and OGG1 play decisive roles in determining whether cancer cells die or evolve resistance.
Aim: To define DNA repair pathway defects that can predict or modulate chemoradiotherapy response.
What I study:
Methylation and expression of DNA repair genes
Base excision repair & homologous recombination efficiency
MGMT-mediated resistance mechanisms
Genome instability signatures
Approach: Gene expression profiling → promoter methylation → functional DDR assays → survival correlations
Identification of actionable DNA repair biomarkers that can guide treatment intensification or sensitization strategies.
🧪Epigenetic Reprogramming in Tumor Evolution & Therapy Response
Cancer cells constantly remodel their epigenetic landscape to survive stress, evade immunity, and resist treatment. I study how methylation changes, histone modifications, and ncRNA networks influence phenotypic plasticity in cervical and other women’s cancers.
Aim: To map epigenetic states that predict therapeutic response and highlight epigenetic vulnerabilities.
What I study:
Promoter methylation & chromatin accessibility
Histone modification shifts under therapy
Non-coding RNA–mediated regulatory networks
Stress-induced epigenetic remodeling
Approach: Methylation profiling → chromatin analysis → ncRNA/miRNA mapping → functional reprogramming assays
Epigenetic markers and targets that can be leveraged for therapy sensitization or risk stratification.
My overarching goal is to bridge molecular discoveries with clinical decision-making. By integrating genomics, epigenomics, microbiome data, and treatment outcomes, I work toward building predictive tools that support personalized therapy planning in cervical cancer.
Aim: To develop clinically useful biomarkers and predictive models that improve treatment accuracy and reduce therapy failure.
What I study:
Pharmaco-genetic and pharmaco-epigenetic regulators
Clinical treatment response signatures
HPV–host molecular interactions
Predictors of chemoradiotherapy success or failure
Approach: Multi-omics integration → biostatistics & ML modeling → clinical validation
Risk prediction frameworks and precision oncology tools tailored for women’s cancers, especially in Indian and global underserved populations.