Publication details

Increased level of malondialdehyde as negative prognostic factor for recurrent HNSCC

Authors

SALZMAN Richard KOSTŘICA Rom PÁCAL Lukáš KAŇKOVÁ Kateřina TOMANDL Josef HORÁKOVÁ Zuzana ROTTENBERG Jan

Year of publication 2006
Type Article in Proceedings
Conference Otorinolaryngologie a foniatrie, Supplementum 1
MU Faculty or unit

Faculty of Medicine

Citation
Field ORL, ophthalmology, stomatology
Keywords malondialdehyde; prognostic factor; head and neck cancer; oxidative stress
Description Introduction:Oxidative status plays an important role in cancer development. Our aim is to investigate relationship between genetic variants encoding for antioxidant enzymes; activity of the expressed enzyme and clinical stage of head and neck squamous cell carcinoma (HNSCC). Material and Methods:prospective study of 65 patients with HNSCC. PCR-based methodology was used to detect genotype of the manganese superoxide dismutase (MnSOD) Ala16Val polymorphism. We measured activity of superoxide dismutase in plasma (pSOD) and in erythrocytes (ercSOD). Using high performance liquid chromatography we analyzed malondialdehyde (MDA) in plasma. Tumor necrosis factor a (TNF) in plasma was measured by the ultrasensitive ELISA. Results: The mean activities of pSOD, resp. ercSOD, were 11117U/g, resp. 4137U/g. The mean levels of MDA, resp. TNF, were 2.27nmol/g, resp. 2.48ng/L. Val/Val variant manifested higher TNF than other two variants (p<0.05). Increased plasmatic MDA was found in patients with recurrent disease (p<0.05). Patients with negative neck (N0) had lower pSOD activity than those with locoregional metastatic spread (N+) (p<0.0005). Activity of ercSOD and plasmatic level of MDA tended to increase in N+ with no significant difference. Conclusions: Increased MDA resulting from elevated oxidative burden correlates with negative prognosis of a recurrent disease. Similarly, SOD is predisposed to become a prognostic factor in HNSCC since it is significantly increased in N+ patients. This might be caused by stronger tendency to breaks in DNA, resp. formation or progression of HNSCC, in patients with decreased antioxidative defenses or in patients who had encountered massive doses of reactive oxygen species in their previous lives. Homozygotes with Val in MnSOD Ala16Val polymorphism manifested increased TNF. Hence, they were more sensitive to conditions leading to higher TNF levels, e.g. oxidative stress.
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