<p>Novel genetic alterations and their impact on target therapy response in head and neck squamous cell carcinoma</p>

Abstract

Head and neck squamous cell carcinoma (HNSCC) is highly variable by tumor site, histologic type, molecular characteristics, and clinical outcome. During recent years, emerging targeted therapies have been focused on driver genes. HNSCC involves several genetic alterations, such as co-occurrence, multiple feedback loops, and cross-talk communications. These different kinds of genetic alterations interact with each other and mediate targeted therapy response. In the current review, it is emphasized that future treatment strategy in HNSCC will not solely be based on “synthetic lethality” approaches directed against overactivated genes. More importantly, biologic, genetic, and epigenetic alterations of HNSCC will be taken into consideration to guide the therapy. The emerging genetic alterations in HNSCC and its effect on targeted therapy response are discussed in detail. Hopefully, novel combination regimens for the treatment of HNSCC can be developed.

Outcome of Targeted Therapy Recommendations for Metastatic and Recurrent Head and Neck Cancers

“…The observed mutations and expressions in R/M HNC patients were in keeping with previous studies [ 20 , 21 ]. The ten most frequent mutations ( TP53, CDKN2A, PIK3CA, NOTCH1, PTEN, ATM, BRCA2, CREBBP, EGFR, and MET ) together accounted for more than 50% percent of all detected mutations.…”

Prognostic Correlation of an Autophagy-Related Gene Signature in Patients with Head and Neck Squamous Cell Carcinoma

“…The results of immunohistochemistry suggest that oropharyngeal tumors with p16INK4a protein expression demonstrate better prognosis than p16-negative oropharyngeal tumors [ 35 ]. Meanwhile, HPV-positive patients with p16INK4a expression have better response to chemotherapy and radiotherapy compared with HPV-negative patients, during the standard multimodality treatments [ 36 ]. FADD is originally described as an adapter molecule mediating apoptosis, which has been newly revealed to engage in cell survival and tumor development [ 37 , 38 ].…”

PYHIN Proteins and HPV: Role in the Pathogenesis of Head and Neck Squamous Cell Carcinoma

“…The prevalence of loss-of-function mutations of NOTCH1 in HNSCC has led to the hypothesis that this protein acts as a tumor suppressor rather than as an oncogene in this type of tumor [34]. Other genes involved in HPV − HNSCC include the epidermal growth factor receptor (EGFR), often amplified in HNSCCs and related to cell cycle control [35], and Met, a receptor tyrosine kinase often associated with enhanced migration, invasion, and angiogenesis when overexpressed in cancer [36].…”