Theranostic Potential of for Cetuximab Resistance in Head and Neck Cancer.

Indian J Otolaryngol Head Neck Surg

Department of Medical Oncology, K.S. Hegde Medical Academy (KSHEMA), Justice K.S. Hegde Charitable Hospital, Nitte (Deemed to be University), Deralakatte, Mangaluru, Karnataka 575018 India.

Published: September 2023

Unlabelled: Only 13% of head and neck cancer (HNC) patients respond to cetuximab therapy despite its target (EGFR) is expressed in about 80-90% of HNC patients. However, this problem remained unresolved till date despite of numerous efforts. Thus, the current study aimed to establish hub genes involved in cetuximab resistance via series of bioinformatics approach. The GSE21483 dataset was analysed for differentially expressed genes (DEGs) using GEO2R and enrichment analysis was carried out using DAVID. STRING 11.5 and Cytoscape 3.7.2 were used for protein-protein interactions and hub genes respectively. The significant hub genes ( < 0.05) were validated using ULCAN and Human protein atlas. Validated genes were further queried for tumor infiltration using TIMER2.0. Out of total 307 DEGs, 38 hub genes were identified of which and were the significant hub genes associated with both mRNA expression and overall survival. and were found to be downregulated whereas and were found to be upregulated in our study. However, using UALCAN, we found that high expression of negatively affects overall survival whereas high expression of and positively affects overall survival. Protein level for and expression was significant in tumor HNC tissue as compared to normal HNC tissue. was found to be a key regulator of CTX resistance among HNC patients. Targeting and associated PPI circuits might improve the response rate to CTX. Thus, EFNB2 has potential to be theranostic marker for CTX resistance.

Supplementary Information: The online version contains supplementary material available at 10.1007/s12070-023-03739-9.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10447808PMC
http://dx.doi.org/10.1007/s12070-023-03739-9DOI Listing

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