Eneda Toska, PhD
Eneda Toska, PhD
Memorial Sloan Kettering Cancer Center
Mutations in the PIK3CA gene are the most frequent genomic alterations in estrogen receptor (ER)-positive breast cancers. One treatment strategy is the use of drugs that inhibit the gene’s signaling pathway—however, many patients eventually become resistant to this type of therapy. Further, PI3K signaling pathway inhibition has been show to increase ER activity, which then increases cells’ dependency on ER and estrogen—fueling growth. However, very little is known about the molecular basis of the crosstalk between the PI3K pathway and ER function.
To better understand this relationship, we have identified genes that both contribute to PI3K inhibition resistance and are necessary for the ER-PI3K crosstalk. As a Terri Brodeur research fellow, Dr. Toska will explore these newly identified mechanisms of resistance and examine their role on patient biopsies pre-and-on treatment to PI3K inhibitors. With this in mind, she aims to expose new therapeutic targets that could potentially increase treatment success.
Dr. Toska obtained her PhD at University at Buffalo, where she worked under the supervision of Dr. Stefan Roberts. During her doctoral studies, Dr. Toska investigated the mechanisms by which Wilms’ tumor 1 (WT1) regulates transcription and its role in both development and cancer. For her postdoctoral training, she joined Dr. José Baselga’s laboratory, a world leader in breast cancer research, to study the molecular mechanisms that regulate ER function and contribute to resistance to PI3K inhibitors in patients with ER-positive breast cancers.