About this trial
Based on the recently identified mutations in HNSCCs, the major pathologic pathways implicated in the tumorigenesis of HNSCC include dysregulation of four processes:
1. cellular survival and proliferation (e.g., TP53, EGFR, MET, and PIK3CA); 2. cell-cycle control (e.g., CDKN2A and CCND1); 3. cellular differentiation (e.g., NOTCH1); and 4. Adhesion and invasion signaling (e.g., FAT1).7 TP53, EGFR, PIK3CA, CDKN2A, CCND1, and MET participate in several common signaling pathways.
Alterations of these genes are most frequently seen in alcohol and tobacco-related HNSCC. However their role in prognostication and selection of therapeutics is not known
Eligibility criteria
Qualifiers
Histologically proven cases of primary head and neck cancers.
Disqualifiers
Patients under 18 years of age
Pregnant and lactating women
Multiple cancers or patients with cancer of other sites.
Trial design
Treatments tested in this trial
- Next generation Sequencing