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
This trial does not accept healthy volunteersQualifiers
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 population
Histologically proven cases of Head and neck cancer undergoing treatment will be included, Next generation sequencing will be done and cohort will be followed up for 10 years
Trial design
Cohort
Prospective
Treatments tested in this trial
Next generation Sequencing
Other interventionNext generation sequencing for 161 genes
Treatment groups
Trial outcomes
Primary outcomes
Over all survival
Survival time from the diagnosis to death
Relapse free survival
survival time from diagnosis to recurrence or metastasis
Secondary outcomes
Progression free survival
The time from the diagnosis to progression of disease
Sponsors and contacts
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