P16 is a protein coded by the INK4A gene that belongs to INK4 gene family. They have a tumor suppressor role and negatively regulate the pRb-E2F signal pathway. When a genetic mutation appears in INK4A, it leads to inactivation of the protein p16 or its improper function. Head and neck carcinomas can occur in the oral cavity, pharynx, larynx or in the salivary glands. In 50-70% of head and neck cancers the inactivation of INK4A was found. In this graduation thesis I studied the influence of p16 protein expression in head and neck cell lines A253, FaDU and Detroit 562 on the expression of target genes and its effect of the treatment with chemotherapeutic drugs. I found that chemotherapeutics induce expression of INK4A gene in some cell lines and that additional treatment with p16 amplifies that effect. Following the expression of the p16 target genes I found that the protein and gene expression of BIRC5 gene (survivin protein) is lowered under the influence of p16. Gene expression of the BIRC5 gene was lowered with chemotherapeutics treatment. Treatment with doxorubicin increased the E2F1 gene expression in some cell lines, but the treatment with etoposide and p16 lowered E2F1 expression. Treatment with chemotherapeutics and p16 influenced the cell cycle, DNA damage, apoptosis, and cell death. Combined treatment of p16 and chemotherapeutics did not show consistent results in cell lines, so I could not make a conclusion if p16 has any additional influence.