Head and neck squamous cell carcinoma (HNSCC) represents the seventh most common cancer globally with approximately 47,000 new cases reported every year . Cigarette smoking/tobacco consumption is a major cause of HNSCC [2- 4]. Around 50% of the 10.9 million people diagnosed with cancer worldwide each year require RT, 60 % of which are treated with curative intent. RT is the most important non-surgical modality for the curative treatment of cancer.
Ionizing radiation is an ubiquitous, environmental physical agent whose DNA damaging effects are fairly well established. Although the exposure of patients to radiation during radiotherapy is beneficial to improve the health of the individuals, ionizing radiation may also induce genetic damage in the neighbouring/adjacent non-target cells. Genetic damage induced by radiation or other mutagens in non-target cells is most frequently monitored in peripheral blood leukocytes . A key challenge in RT is to maximize radiation doses to cancer cells while minimizing damage to the surrounding non-target healthy tissue. Recent literature in the field of clinical oncology and RT still does not explain sufficiently the question of damages to non-target cells and tissues after chemo-radiation treatment [6-8].
In order to obtain information concerning the extent of radiation exposure, its distribution and dose assessment, various biological methods have been developed. Human bio-monitoring can be performed using various genetic markers which detect early biological effects, including evaluation of DNA mutations, CAs, the induction of micronuclei and sister chromatid exchanges . Among the various cytogenetic parameters employed, the most reliable biological indicators of ionizing radiation exposure are CAs in peripheral blood lymphocytes [10, 11]. The CA assay is often employed for monitoring the populations exposed to genotoxic agents because it allows the evaluation of the entire genome to identify mutagenic and carcinogenic agents . Quantification of CAs in circulating lymphocytes is being used to estimate the dose received by individuals exposed to ionising radiation during RT and also the genetic damage prevailing in the whole body [13, 14]. The number of peripheral lymphocytes exposed to irradiation during RT will vary in various HNSCC patients depending upon the exact target area and the quantum of radiation absorbed. Studies on HNSCC patients is of great significance as this part of human body covers a large number of blood vessels, lymph nodes and is a very sensitive region to irradiation.
Cytogenetic assessment of the lymphocytes of cancer patients undergoing localised fractionated therapeutic irradiation would evaluate the clastogenic effect induced by such treatment in the patient’s circulating blood. The analysis of CAs in peripheral blood lymphocytes is often being used as a biomarker of health outcome, measuring genetic damage due to radiation that results from non-repaired primary lesions. Hence, in order to know the quantum of genetic damage induced by various doses of gamma rays in the non-target cells of cancer patients and their inter-patient variability, HNSCC patients receiving fractionated RT were selected as the subjects for the present study and further analysis was carried out.
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