The translational nature of the PEMM program allowed me to discover that the driving force behind my passion for cancer research is the continuous improvement of patient outcome. In the lab of Dr. Todd Miller, I was able to develop expertise in a variety of in vitro and in vivo techniques as well as experience the design and downstream evaluation of clinical trials. The PEMM lab rotation structure also gave me the opportunity to spend time in multi-disciplinary labs and complete coursework that helped me to build a valuable skill set in immunology. This, combined with my expertise in cancer biology, were instrumental in obtaining my current position in the immuno-oncology industry.
Hosford SR, Dillon LM, Bouley SJ, Rosati R, Yang W, Chen VS, Demidenko E, Morra RP, Miller TW. Combined inhibition of both p110α and p110β isoforms of phosphatidylinositol 3-kinase is required for sustained therapeutic effect in PTEN-deficient, ER+ breast cancer. Clin Cancer Res. 2016 Nov 30.
Yang W, Hosford SR, Dillon LM, Shee K, Liu SC, Bean JR, Salphati L, Pang J, Zhang X, Nannini MA, Demidenko E, Bates DJ, Lewis LD, Marotti JD, Eastman A, Miller TW. Strategically timing inhibition of phosphatidylinositol 3-kinase to maximize therapeutic index in estrogen receptor alpha-positive, PIK3CA-mutant breast cancer. Clin Cancer Res. 2016.
Bean JR, Hosford SR, Symonds LK, Owens P, Dillon LM, Yang W, Shee K, Schwartz GN, Marotti JD, Muller KE, Rosenkranz KM, Barth RJ, Chen VS, Agarwal VR, Miller TW. The PI3K/mTOR dual inhibitor P7170 demonstrates potent activity against endocrine-sensitive and endocrine-resistant ER+ breast cancer. Breast Cancer Res Treat. 2015;149:69-79.
Hosford SR, Miller TW. Clinical potential of novel therapeutic targets in breast cancer: CDK4/6, Src, JAK/STAT, PARP, HDAC, and PI3K/AKT/mTOR pathways. Pharmgenomics Pers Med. 2014;7:203-15.