Abstract

In the last two decades, there have been several changes in the field of head and neck surgery. Reconstructions using microvascular free flaps completely replaced earlier methods. More significantly, there has been a paradigm change toward attempting to re-establish normal function and appearance in addition to reliable wound closure to safeguard key structures. Using an evidence-based strategy whenever possible, the current research will propose an algorithmic approach to head and neck reconstruction of diverse subsites.

In contrast to typical cytotoxic therapies, which often cause cell loss, molecular therapeutics are a targeted approach to treating malignancies that express the epidermal growth factor receptor (EGFR). However, the early excitement for this focused treatment has been dampened by the discovery that resistance to such therapy is widespread in clinical studies. However, a deeper knowledge of the molecular mechanisms underlying various receptor tyrosine kinases that are known to be active in cancer has shown a rich network of cross-talk between receptor pathways, with a crucial discovery being shared downstream signalling pathways. Such interactions could be a major factor in the resistance to EGFR-directed treatment. In the context of squamous cell cancer of the head and neck, a tumour that is known to be primarily driven by EGFR-related oncogenic signals, we review the interaction between EGFR and Met and the type 1 insulin-like growth factor receptor (IGF-1R) tyrosine kinases as well as their contribution to anti-EGFR therapeutic resistance in this article.