Angel Noble
Research Mentor(s): Abdullah Saeed
Department or Program: MM-Internal Medicine
Authors: Angel Thomas Noble and Abdullah Saeed, PhD
Session: Session 2: 1:00pm-1:50pm
Poster: 37
Abstract
EML4-ALK is a fusion protein that causes abnormal cellular signaling leading to excessive cell growth and proliferation to develop lung cancer. Similarly, it is responsible for 5% of non-small cell lung cancer (NSCLC) cases globally. Cancers often take advantage of regulatory T cells (Tregs) for progression through immunosuppression and immune evasion but need further understanding. Tyrosine kinase inhibitors (TKIs) are FDA-approved drugs for treating Alk+ NSCLC. Here, we used Alectinib and Lorlatinib in EML4-Alk+ mice tumors to analyze Treg immune modulation. Tregs were analyzed using the CD4+ lineage markers i.e., CD25, and FOXP3 in the mouse spleen using spectral immunophenotyping. We observed that the frequency of Tregs altered in the spleen with progressing tumors as compared to the control. Likewise, Tregs showed varied frequencies when TKIs were administrated to treat mice tumors. Modulating the Tregs in the tumor microenvironment (TME), and thus preventing immune evasion using TKI drugs offers potential therapeutic advances to improve human health.
