Past Trainees

 

Monica Akre, PhD

Monica AkreMy work focusses on the use of cell line expression data and corresponding drug responsiveness with the goal of identifying predictive expression profiles that will better direct use of effective therapeutics and avoid ineffective options.

Samuel Callisto

Samuel CallistoSamuel was a PhD Candidate in the Experimental and Clinical Pharmacology department. During his time in the program Samuel pursued various avenues of research related to precision medicine in neuropharmacology with a focus on anti-seizure drugs. Projects included the effect of patient demographics on likelihood of experiencing side effects from topiramate, the pharmacogenomic underpinnings of lamotrigine clearance changes during pregnancy, and clinical applications of pharmacogenomics to epilepsy treatment.

Seenae Eum

Seenae EumMedications with high anticholinergic activity have adverse effects on neuropsychological performance. During her time with PUMA, Dr. Eum word on quantifying neuropsychological performance relationships with anticholinergic burden and genetic factors in patients with psychotic disorders, first degree relatives, and controls with the goal of identifying key genetic variants associated with anticholinergic effects on cognitive phenotypes.

Taylor Harding, PhD

Taylor HardingUsing pre-clinical modeling to identify transcriptomic signatures that accurately predict drug resistance in multiple myeloma. Additionally, we are testing new chemotherapeutic approaches to target unique features of the myeloma epigenome and improve the efficacy of current therapies.

Gregory Laffen, PharmD

Gregory LaffenPharmacogenomic determinants of the serum uric acid lowering effects of the drug fenofibrate. We aim to determine if there are genetic markers that can be used as predictors of both drug response and serum uric acid levels that can be used to help guide clinical decision making in order to improve treatment of gout and help ease the burden of comorbid cardiovascular disease.

Marissa Nolan

marissa nolanDuring my time with PUMA, my research project involved studying Multiple Myeloma and the long-term effects of an epigenetic modifying drug called EPZ-6438 on human myeloma cell lines. This drug is an EZH2 inhibitor; EZH2 is a protein complex in the cell attributed with oncogenic activity in Multiple Myeloma. We concluded EPZ-6438 to be a potential novel therapy in treating Multiple Myeloma.

Malek Okour, PhD

Malek OkourPharmacokinetics and pharmacodynamics analysis of mycophenolic acid (MPA) in kidney transplant recipients. We aim into individualizing therapy while keeping in mind exposure relation to acute rejection and side effects.

Christopher Olson

Christopher OlsonThe current lifetime prevalence of psychotic disorders is approximately 4.1% with non-response to standard treatments being in the range of 40-50%. This reveals a need for improvements in current treatment practices and the use of pharmacogenomics can help to improve the precision of individual patient treatments; therefore, we are aiming to analyze various dopamine receptor and transporter single nucleotide polymorphisms (SNPs) in relation to participant’s antipsychotic dosing.

Rebecca Pulk, PharmD

Rebecca PulkTacrolimus is a calcineurin inhibitor immunosuppressant that widely used in kidney transplant. I am working to improve our ability to select an optimized tacrolimus dose for kidney transplant patients based on their individual clinical and genetic factors to decrease time to optimal coverage and improve clinical outcomes.

Youssef Roman, PharmD, PhD

youssef romanThe contribution of genetic polymorphisms in select genes responsible for uric acid disposition and the drugs used to treat hyperuricemia and gout. My ultimate goal is to identify key genetic variants to be used for guided drug selection to optimally manage patients with gout, hyperuricemia, and their associated comorbidities.

Kinjal Sanghavi, PhD

Kinjal SanghaviImproving immunosuppressive therapy in transplantation using population pharmacokinetic and pharmacogenetic approach. These approaches were used to optimize dosing for tacrolimus (for kidney transplant recipients) and fludarabine (for hematopoietic stem cell transplant recipients).

Aileen Scheibner

Aileen ScheibnerFludarabine and cyclophosphamide are chemotherapeutics  used in hematopoietic cell transplant (HCT) preparative regimens for their anticancer and immunosuppressive properties. We are investigating the relationship between fludarabine and cyclophosphamide pharmacokinetics, single nucleotide polymorphisms (SNPs), and non-relapse mortality, neutrophil engraftment, overall survival and acute graft-versus-host disease in patients undergoing allogeneic nonmyeloablative HCT. Understanding the relationships between target SNPs, pharmacokinetics, and clinical outcomes will facilitate the development of a personalized approach to HCT preparative regimens that improves safety and overall survival while minimizing the risk of acute graft-versus-host disease.

Stephan Seibert

Stephan SeibertTacrolimus is the cornerstone immunosuppressive agent after kidney transplantation, but its high pharmacokinetic variability is a well-known problem which contributes to adverse effects and poor outcomes. We are investigating the associations between intra-patient tacrolimus pharmacokinetic variability, CYP3A5 loss of function alleles, and acute rejection in a large cohort of African American and European American kidney transplant recipients.

Sofia Shrestha

Sofia ShresthaMicroRNAs regulate gene expression, participate in normal neuro developmental and physiological processes, and have recently been implicated in the pathogenesis of several psychiatric disorders. My project aims to examine the relationship between microRNA genetic variants and antipsychotic treatment response outcomes in patients with psychosis. We hope that this project will enhance our understanding of miRNAs as therapeutic biomarkers in psychiatric disorders.

Tyler Stevens

tyler stevens bioMethylphenidate is the most commonly prescribed medication to treat ADHD and it is metabolized to its inactive form by the CES1 protein.  We are looking for variants within the CES1 gene that may explain differences in clinical response, side effect profile and dosing requirements in pediatric patients with ADHD.