Primary Faculty Mentor Name

David J. Seward

Project Collaborators

Hailey Sarausky

Status

Undergraduate

Student College

College of Arts and Sciences

Program/Major

Biology

Primary Research Category

Biological Sciences

Secondary Research Category

Health Sciences

Presentation Title

Investigation of molecular pathway and pathology of Non-Small Lung Cell Cancer mutations

Time

3:40 PM

Location

Williams Family Room

Abstract

There are ~200,000 new lung cancer diagnoses each year is the US, 85% of which are non-small cell lung carcinomas (NSCLC). To date, NSCLCs are relatively resistant to immunotherapy—roughly 20-30% of NSCLC patients will respond well to immunotherapy, but we cannot yet predict who those patients will be (Ventola 2017). Specifically for the adenocarcinoma NSCLC, serine/threonine kinase 11 (STK11), also known as liver kinase B1 (LKB1) is the third most commonly mutated gene (Larsen 2015). STK11 variants resulting in loss of function (LoF) have recently been highlighted as predicting resistance to immunotherapy in NSCLC by preventing lymphocyte recruitment into the tumor microenvironment. Immunotherapies are contingent upon the ability to recruit/activate cytotoxic T-lymphocytes within the tumor microenvironment. It is currently hypothesized that STK11 LoF variants confer immunotherapy resistance, but the mechanism is unclear and, thus, represents an ongoing gap in knowledge in attempting to treat NSCLC patients (Leliefeld et al. 2015). This research is focused specifically on elucidating the mechanistic function and downstream effects linking several STK11 mutations and clinical outcomes in NSCLC, especially concerning their potential metabolic significance. Detecting and analyzing cancer genetic variation and metabolism for STK11 mutations in NSCLC will allow us to increase our understanding of the biology of STK11 mutations and will be relevant to immunotherapy approaches and consequent insurance policy strategies needed to NSCLC incidence.

This document is currently not available here.

Share

COinS
 

Investigation of molecular pathway and pathology of Non-Small Lung Cell Cancer mutations

There are ~200,000 new lung cancer diagnoses each year is the US, 85% of which are non-small cell lung carcinomas (NSCLC). To date, NSCLCs are relatively resistant to immunotherapy—roughly 20-30% of NSCLC patients will respond well to immunotherapy, but we cannot yet predict who those patients will be (Ventola 2017). Specifically for the adenocarcinoma NSCLC, serine/threonine kinase 11 (STK11), also known as liver kinase B1 (LKB1) is the third most commonly mutated gene (Larsen 2015). STK11 variants resulting in loss of function (LoF) have recently been highlighted as predicting resistance to immunotherapy in NSCLC by preventing lymphocyte recruitment into the tumor microenvironment. Immunotherapies are contingent upon the ability to recruit/activate cytotoxic T-lymphocytes within the tumor microenvironment. It is currently hypothesized that STK11 LoF variants confer immunotherapy resistance, but the mechanism is unclear and, thus, represents an ongoing gap in knowledge in attempting to treat NSCLC patients (Leliefeld et al. 2015). This research is focused specifically on elucidating the mechanistic function and downstream effects linking several STK11 mutations and clinical outcomes in NSCLC, especially concerning their potential metabolic significance. Detecting and analyzing cancer genetic variation and metabolism for STK11 mutations in NSCLC will allow us to increase our understanding of the biology of STK11 mutations and will be relevant to immunotherapy approaches and consequent insurance policy strategies needed to NSCLC incidence.