Hayley McDaid, PhD
Albert Einstein College of Medicine
Mechanisms of RAS and RAF-mediated Regulation of Cap-dependent Translation in NSCLC
Dr. Hayley McDaid is working on understanding the particular molecular characteristics of lung cancers that may be sensitive to a new drug called a MEK-inhibitor based on its site of action within the cell. By profiling the genetic traits of tumors that respond to this type of drug, Dr. McDaid hopes to be able to identify a subset of lung cancer patients that will benefit from treatment.
Dr. McDaid has shown that the association of mutant LKB1 with mutant K-RAS can predict a greater sensitivity to the MEK inhibitor, and increases cells’ dependence on the RAS-MEK signaling pathway. LKB1 was also shown to play a role in cell shape and orientation, indicating a possible role in progression and metastasis. Additionally, LKB1 also affects cellular metabolism through the AKT-mTOR pathway. Dr. McDaid has also shown that loss of LKB1 in combination with higher levels of mutant RAS confers sensitivity to MEK inhibition, and that higher expression of the tumor suppressor p53 confers resistance.