posted on 2023-05-22, 14:20authored byRitu Chaudhary, Robbert J.C. Slebos, Leenil C. Noel, Feifei Song, Maria I. Poole, Dirk S. Hoening, Juan C. Hernandez-Prera, Jose R. Conejo-Garcia, Jose A. Guevara-Patino, Xuefeng Wang, Mengyu Xie, Aik Choon Tan, Christine H. Chung
<p>Cetuximab treatment benefits Hypoxia subgroup. <b>A,</b> Heatmap of gene expression data from pre- and post-cetuximab (CTX) treated patient samples. RNA expression data (GSE109756) was z-normalized, each row represents a single gene in the hypoxia-immune signature gene list, each column represents a patient sample. Hierarchical clustering was performed as detailed in Materials and Methods. Samples were reordered according to its molecular subgroup: Immune (blue), mixture (black), and Hypoxia (red) with pre-cetuximab treated samples labeled BC and post-cetuximab labeled OC. TIMEx scores for the Hypoxia gene signature among the 15 patients classified into the three subgroups (<b>B</b>) and GSEA comparing gene expression changes in the pre- and post-cetuximab data using CIBERSORT gene sets: higher in post-cetuximab (red) and higher in pre-ceuximab (blue) (<b>C</b>).</p>
Funding
HHS | NIH | National Institute of Dental and Craniofacial Research (NIDCR)
While the hypoxic and immunosuppressive TME of HNSCC has been well described, comprehensive evaluation of the immune cell components and signaling pathways contributing to immunotherapy resistance has been poorly characterized. We further identified additional molecular determinants and potential therapeutic targets of the hypoxic TME to fully leverage currently available targeted therapies that can be administered with immunotherapy.