Abstract
Epidermal growth factor receptor (EGFR) overexpression is common in head and neck squamous cell carcinoma. Targeted therapy specifically directed towards EGFR has been an area of keen interest in head and neck cancer research, as EGFR is potentially an integration point for convergent signaling. Despite the latest advancements in cancer diagnostics and therapeutics against EGFR, the survival rates of patients with advanced head and neck cancer remain disappointing due to anti-EGFR resistance. This review article will discuss recent multilateral efforts to discover and validate actionable strategies that involve signaling pathways in heterogenous head and neck cancer and to overcome anti-EGFR resistance in the era of precision medicine. Particularly, this review will discuss in detail the issue of cancer metabolism, which has recently emerged as a novel mechanism by which head and neck cancer may be successfully controlled according to different perspectives.
Highlights
Head and neck cancer (HNC) is the sixth most common cancer worldwide, as 40,000 new patients are diagnosed every year in the United States, and over 600,000 are diagnosed worldwide[1]
Overexpression or upregulated activity of epidermal growth factor receptor (EGFR) is an important molecular characteristic that has been noted in numerous epithelial solid tumors such as colorectal cancer (CRC), non-small cell lung cancer (NSCLC), HNC, pancreatic cancer, breast cancer, and brain cancer
In this article, studies concerning targeted therapies that involve central EGFR signaling in HNC have been comprehensively reviewed
Summary
Byeon et al Experimental & Molecular Medicine (2019) 51:8 agent for HNC. treatment results were quite disappointing, unlike the initial expectations for this agent, as monotherapy responses were shown in only 10–30%, which suggests some form of intrinsic resistance. EGFR can enter the nucleus where it can serve several roles, be returned to the cell surface to continue its signaling function in its membrane-bound form, be directed to lysosomes for degradation, or remain active in endosomal compartments by mammary-derived growth factor inhibitor (MDG1), which leads to the activation of various downstream signals Among these routes, the nuclear translocation of EGFR can play several important roles in antiEGFR resistance[10]. Nuclear EGFR can directly cause PCNA and DNAPK phosphorylation due to its intrinsic tyrosine kinase activity This increased EGFR activity can induce cell proliferation and promote the repair of DNA damage caused by chemoradiotherapy, which results in therapeutic resistance and cancer progression (Fig. 1)
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