Research Areas

My research integrates genetics, epigenetic regulation, DNA damage and repair biology, and the cervicovaginal microbiome to understand the molecular drivers of women’s cancers, particularly HPV-associated disease. I focus on how genetic variation, epigenetic instability, and microbial dysbiosis converge to shape tumor evolution, immune signaling, and therapeutic response, with the goal of identifying mechanism-driven biomarkers and precision treatment strategies.

🧬+🧫 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.

🎗️Translational Oncology & Precision Medicine for Women’s Health

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.