Kelsey P. Pendleton

TL;DR: Analysis of whole-exome sequencing data from 151 tumors revealed the phosphoinositide 3-kinase (PI3K) pathway to be the most frequently mutated oncogenic pathway, suggesting that PI3K pathway mutations may serve as predictive biomarkers for treatment selection.

TL;DR: It is demonstrated that receptor-like protein tyrosine phosphatases, encoded by PTPR genes, including PTPRT, are commonly mutated in HNSCC where PTPR mutations are associated with increased phosphorylation of STAT3 in tumors, providing a mechanistic basis for tumor-specific STAT3 hyperactivation in head and neck squamous cell carcinoma.

TL;DR: Current research is focused on molecular targeting therapies inhibiting epidermal growth factor receptor, phosphoinositide-3-kinase/Akt/mammalian target of rapamycin, and vascular endothelial growth factor pathways, which may enhance response to cisplatin therapy.

TL;DR: Selective erlotinib use in HNSCC may be informed by precision oncology approaches and Hypotheses were formulated regarding enhanced erlot inib response in preclinical models harboring the patient tumor somatic variant MAPK1 E322K following the identification of tumor somatics variants.

TL;DR: Cumulative findings implicate increased AREG secretion and EGFR activation as contributing to increased erlotinib sensitivity in MAPK1E322K HNSCC.