Relationship between head and neck cancer therapy and some genetic endpoints.

Abstract

Head and neck cancer (HNC) is the sixth most common human malignancy worldwide. The main forms of treatment for HNC are surgery, radiotherapy (RT) and chemotherapy (CT). However, the choice of therapy depends on the tumor staging and approaches, which are aimed at organ preservation. Because of systemic RT and CT genotoxicity, one of the important side effects is a secondary cancer that can result from the activity of radiation and antineoplastic drugs on healthy cells. Ionizing radiation can affect the DNA, causing single and double-strand breaks, DNA-protein crosslinks and oxidative damage. The severity of radiotoxicity can be directly associated with the radiation dosimetry and the dose-volume differences. Regarding CT, cisplatin is still the standard protocol for the treatment of squamous cell carcinoma, the most common cancer located in the oral cavity. However, simultaneous treatment with cisplatin, bleomycin and 5-fluorouracil or treatment with paclitaxel and cisplatin are also used. These drugs can interact with the DNA, causing DNA crosslinks, double and single-strand breaks and changes in gene expression. Currently, the late effects of therapy have become a recurring problem, mainly due to the increased survival of HNC patients. Herein, we present an update of the systemic activity of RT and CT for HNC, with a focus on their toxicogenetic and toxicogenomic effects. © 2014 Baishideng Publishing Group Co., Limited. All rights reserved. Key words: Chemotherapy; Head and neck cancer; Radiotherapy; Toxicogenetic; Toxicogenomic Core tip: The main therapies for head and neck cancer (HNC) are surgery, radiotherapy (RT) and chemotherapy. Considering that both RT and chemotherapeutical drugs can interact with the DNA, one of the important, late-occurring complications is a therapy-related secondary tumor resulting from the genotoxic effects of the therapy on the healthy cells. This review presents an update of the toxicogenetic and toxicogenomic effects of HNC treatments, highlighting the main mechanisms evolved in the secondary damage caused by RT and chemotherapies.