TP53 polymorphism did not contribute to HNC risk alone; however, interaction between the TP53 GC and MDM2 GG genotypes resulted in significant risk (OR=4.9, 95% CI: 0.2-105.1) (p=0.04).
Patient-Derived Head and Neck Cancer Organoids Recapitulate EGFR Expression Levels of Respective Tissues and Are Responsive to EGFR-Targeted Photodynamic Therapy.
Evaluation of our own results and those published in the literature lead us to conclude that absence of the wild-type p53 allele in human head and neck cancer cell lines is associated with increased radiosensitivity.
The objective of this review is to point out the specificity of p53 gene (TP53) alterations in head and neck cancer in relation with chemocarcinogenesis and to discuss whether or not the determination of p53 alterations will be of clinical relevance in the management of head and neck cancer in terms of prognosis and response to treatments.
Interestingly, regardless of their p53 codon 72 genotype, CD8+ T cells stimulated with either p53(72P) or p53(72R) peptide were cross-reactive against T2 cells pulsed with either peptide, as well as HLA-A2(+) head and neck cancer (HNC) cell lines presenting p53(72P) and/or p53(72R) peptides for T cell recognition.
The effect of irradiation on mitotic and apoptotic frequency in head and neck cancer cell lines, the correlation to p53 mutations and clonogenic survival.
The present study was performed to evaluate whether TP53 mutation may influence the clinical outcome of head and neck cancer patients treated with radiotherapy or surgery.
To further evaluate the timing of p53 alterations in the development of head and neck cancer, paired epithelial samples (one pre-invasive and one invasive) from the same patient were evaluated.