My interest in translational research as it relates to cancer therapy was sparked in the lab I joined as an undergraduate. It focused on synthesizing and studying taxol derivatives conjugated to cancer-targeting factors. My later work as a research technician in a gene therapy lab further bolstered my desire to pursue a research career in therapeutics, with a focus on improving cancer treatments. Joining GSK was the obvious choice because Memorial Sloan Kettering is the premier cancer institute. The exceptional GSK program is distinguished by several unique features. Chief among them is the core course, which enables students to gain a broad look into many fields of biology from area experts. This exposure provides an opportunity for students to find, and potentially pursue, new research interests. Overall, it’s an excellent program, populated by amazing faculty, students, and staff. I’m pursuing my thesis work in the lab of pharmacologist Neal Rosen, where I study the RAS/ERK and PI3K/AKT/mTOR pathways in colon cancer and other lineages. My goal is to understand certain mutation mechanisms with an eye towards improving treatment strategies.
Understanding the Role of KRAS in KRAS G12C Mutant Cancers (with and without PI3K/AKT/mTOR Pathway Alterations) towards Improving Treatment Strategies
The goal of this project involves delineating the role of KRAS G12C in KRAS G12C mutant cancers. In particular, we wish to understand the function of KRAS G12C, as well as the dependency upon this specific oncogenic mutation, in various models – both in vitro and in vivo. How does this dependency change in the presence or absence of PI3K/AKT/mTOR pathway alterations? How can we improve targeting of these cancers through combination strategies? What is the interplay between RAS/ERK and PI3K/AKT/mTOR signaling in KRAS G12C mutant cells? How is this interplay modulated upon pathway inhibition (with RAS/ERK and/or PIK3/AKT/mTOR inhibitors) or stimulation in both single mutants and double mutants bearing a PI3K/AKT/mTOR alteration alongside the KRAS G12C mutation? How does RAS/ERK and PI3K/AKT/mTOR regulate apoptosis in these cells? Using various inhibitors alone, and in combination, to target diverse nodes of one or both pathways, as well as various in vitro and in vivo models, we hope to make discoveries surrounding these and other questions.
- Geoffrey Beene Graduate Student Fellowship (2018-2019)