Cancer researcher with extensive expertise in cellular and molecular oncology and therapeutic drug resistance, with notable contributions to prostate cancer research resulting in high-impact publications and intellectual property filings. Experienced in functional assay design, in vivo cancer models, and target validation supporting preclinical discovery of small molecules. Skilled in translating mechanistic insights into innovative cancer therapies, leveraging transferable skills in experimental design and mechanism-based research to drive cross-disciplinary collaboration and leadership in translational science.
I investigated therapeutic resistance in MGMT-deficient colorectal cancer models, focusing on mechanisms of acquired temozolomide resistance driven by mismatch repair loss. Using the MGMT-deficient, MMR-proficient SK-CO-1 xenograft model, I studied how DNA repair status shapes treatment response and evaluated KL-50, a novel lab-developed DNA interstrand crosslinking agent, as an alternative strategy. This work showed that KL-50 exploits MGMT deficiency while bypassing mismatch repair dependence, resulting in sustained tumor regression and highlighting a biomarker-guided approach to targeting DNA repair vulnerabilities in colorectal cancer.
I studied DNA repair vulnerabilities in prostate cancer by targeting the TLK1-RAD54 axis through a synthetic lethality approach. Using in vitro models and SCID mouse xenografts of PC-3 and C4-2B cells, I evaluated J54, a novel lab-developed TLK1B inhibitor, in combination with cisplatin to inhibit tumor growth with limited toxicity. This work involved experimental design, animal protocol development, tumor regression studies, drug screening, viability assays, protein analysis, and western blotting, and supported the therapeutic potential of disrupting TLK1B-RAD54–mediated DNA repair in prostate cancer. I analyzed data, recommended next-step experiments, maintained compliant study records, managed SOPs and inventory, and mentored junior trainees while contributing to scientific writing.
I studied the role of the mu-opioid receptor in head and neck cancer progression and treatment response, with the goal of evaluating its potential as a therapeutic target. Using methylnaltrexone (Relistor), I investigated receptor-associated signaling mechanisms and biological activity in the context of tumor growth and cancer-related outcomes, addressing an area of mixed clinical evidence regarding opioid effects on cancer biology.
Project 1: High-Throughput Screening for Small Molecules that Reduce ssDNA Gaps in Fanconi Anemia
I investigated therapeutic strategies to address the underlying replication defects that contribute to bone marrow failure in Fanconi anemia. Building on findings that Fanconi anemia cells carrying single-stranded DNA gaps have reduced cellular fitness, this project focused on identifying small molecules that promote continuous DNA replication and suppress gap formation. The goal was to improve cell fitness and proliferative capacity in FA models and to support the development of mechanism-based therapeutic approaches for Fanconi anemia.
Project 2: Development of Selective DNA Ligase III Inhibitors to Overcome PARP Inhibitor Resistance in Breast Cancer
I studied DNA repair vulnerabilities in breast cancer, focusing on overcoming resistance to PARP inhibitors in homologous recombination–deficient settings. Based on evidence that loss of DNA Ligase III increases PARP inhibitor sensitivity in BRCA1-deficient cells by promoting post-replicative single-stranded DNA gaps and chromosomal instability, this project explored DNA Ligase III as a therapeutic target. The work supported the development of selective DNA Ligase III inhibitors as a strategy to enhance PARP inhibitor efficacy and overcome resistance in BRCA1-deficient breast cancer.
I studied DNA damage response vulnerabilities in prostate cancer by evaluating J54, a novel lab-developed phenothiazine derivative, as a TLK1B inhibitor to prevent progression to metastatic castration-resistant disease. Because TLK1B is upregulated during androgen deprivation therapy, this project examined whether targeting the TLK1 pathway could suppress tumor progression and promote apoptosis, particularly in combination with standard therapy. Using in vitro and in vivo models, I demonstrated that J54 has promising therapeutic activity, with low affinity for dopamine receptor 2 and minimal adverse behavioral effects in animal studies, supporting its potential as a translational strategy for prostate cancer treatment.