My long-term career goal is to acquire leadership in cancer research and contribute to breakthrough discoveries that result in improved treatment strategies. Throughout my graduate school and postdoctoral training, and following my research fellow training at NIH, I have gained multidisciplinary experience in cardiovascular cell biology, cancer biology, molecular biology, and several animal models. As a graduate student, I focused on the regulative mechanism of endothelial biology and the diverse mechanisms of atherosclerosis progression, especially in macrophage-foam cell formation. After one year of mandatory military service, I explored the integral role of calcium channels in the regulation of endothelial pathophysiology in my first postdoctoral training. I also collaborated with my colleagues to understand the molecular mechanism of atherosclerosis in cardiovascular biology. During my second postdoctoral training in The Jackson Laboratory and subsequently as a Research Fellow at the National Cancer Institute, NIH, I studied the complex mechanism of heat shock factor 1 (HSF1)-mediated proteostasis in the regulation of tumor growth. Specifically, I found that HSF1 combats stress and maintains cell growth by directly interacting with c-Jun N-terminal kinase (JNK) and titrating it away from the mechanistic target of rapamycin complex 1 (mTORC1), and I published the results as first author in Nature Cell Biology. In addition, I found that HSF1 reciprocally inhibits AMPK-activated protein kinase (AMPK) via a transcription-independent mechanism leading to AMPK secondary structure conformational change. I published these findings as first author in Molecular Cell. I became an expert in genetically-modified mouse models of cancer and a wide range of biomedical techniques. My research at The University of Toledo focuses on the role of HSF1 in cholesterol trafficking, lipid metabolic reprogramming, and the autophagy process in pancreatic tumorigenesis via in vitro, in vivo, and preclinical models. Our studies aim to reveal novel clinical therapeutic strategies to address these fundamental processes in current cancer therapies.