scholarly journals Lipid Peroxidation and Antioxidant Status in Head and Neck Squamous Cell Carcinoma Patients

2009 ◽  
Vol 2 (2) ◽  
pp. 68-72 ◽  
Author(s):  
Aashita Gupta ◽  
Madan L. B. Bhatt ◽  
Mithilesh K. Misra

Oxidative stress, a consequence of an imbalance between the formation and inactivation of reactive oxygen species, may be involved in the pathogenesis of many diseases including cancer. To evaluate the magnitude of oxidative stress, a study on the plasma levels of superoxide dismutase, total thiols, ascorbic acid and malondialdehyde (MDA) has been done in head and neck squamous cell carcinoma patients before the start of any oncological treatment and compared with healthy controls. The specific activity of superoxide dismutase in cancer patients is decreased significantly when compared to the control (p < 0.05). The total thiol and ascorbic acid levels are significantly reduced (p < 0.005) whereas MDA levels are significantly increased in the patients (p < 0.00005). Our findings show that the oxidative stress is elevated in cancer patients as evidenced by elevated levels of lipid peroxidation products and depletion of enzymatic and non-enzymatic antioxidants.

1990 ◽  
Vol 5 (3) ◽  
pp. 118-120 ◽  
Author(s):  
F. Palermo ◽  
A. Carniato ◽  
A. Fede ◽  
F. Boccaletto ◽  
C. Marchiori

We estimated the serum levels of SCC-Ag, CEA and TPA in 69 patients with head or neck neoplasia and 31 healthy patients using a radioimmunometric method (double antibody). SCC-Ag concentrations were significantly increased in 43.4% cancer patients with respect to the cut-off point value (1.7 ng/ml) of the control group, and the specificity was 96.7%. The data varied according to the evolutive phase of disease. Since the combined evaluation of SCC-Ag, TPA and CEA serum levels increased the sensitivity, that was 71.0%, we thought it opportune to use all these markers in the tumoral pahtology taken into consideration.


Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1670 ◽  
Author(s):  
Wangjie Yu ◽  
Yunyun Chen ◽  
Nagireddy Putluri ◽  
Cristian Coarfa ◽  
Matthew J. Robertson ◽  
...  

Background: Cisplatin (CDDP) is commonly utilized in the treatment of advanced solid tumors including head and neck squamous cell carcinoma (HNSCC). Cisplatin response remains highly variable among individual tumors and development of cisplatin resistance is common. We hypothesized that development of cisplatin resistance is partially driven by metabolic reprogramming. Methods: Using a pre-clinical HNSCC model and an integrated approach to steady state metabolomics, metabolic flux and gene expression data we characterized the interaction between cisplatin resistance and metabolic reprogramming. Results: Cisplatin toxicity in HNSCC was driven by generation of intra-cellular oxidative stress. This was validated by demonstrating that acquisition of cisplatin resistance generates cross-resistance to ferroptosis agonists despite the fact that cisplatin itself does not trigger ferroptosis. Acquisition of cisplatin resistance dysregulated the expression of genes involved in amino acid, fatty acid metabolism and central carbon catabolic pathways, enhanced glucose catabolism and serine synthesis. Acute cisplatin exposure increased intra-tumoral levels of S-methyl-5-thiadenosine (MTA) precursors and metabotoxins indicative of generalized oxidative stress. Conclusions: Acquisition of cisplatin resistance is linked to metabolic recovery from oxidative stress. Although this portends poor effectiveness for directed metabolic targeting, it supports the potential for biomarker development of cisplatin effectiveness using an integrated approach.


Author(s):  
Marina Marques Toledo ◽  
Bruno De Souza Gonçalves ◽  
Natalie Mounteer Colodette ◽  
Aline Lauda Freitas Chaves ◽  
Luciana Vieira Muniz ◽  
...  

2013 ◽  
Vol 22 (6) ◽  
pp. 558-560 ◽  
Author(s):  
Didier Dequanter ◽  
Maureen Van de Velde ◽  
Vincent Nuyens ◽  
Nathalie Nagy ◽  
Paul Van Antwerpen ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Jackie M. Wypij

Despite advances in understanding cancer at the molecular level, timely and effective translation to clinical application of novel therapeutics in human cancer patients is lacking. Cancer drug failure is often a result of toxicity or inefficacy not predicted by preclinical models, emphasizing the need for alternative animal tumor models with improved biologic relevancy. Companion animals (dogs and cats) provide an opportunity to capitalize on an underutilized and biologically relevant translational research model which allows spontaneous disease modeling of human cancer. Head and neck squamous cell carcinoma (HNSCC) is a common cancer with a poor prognosis and limited clinical advancements in recent years. One potential novel spontaneous animal tumor model is feline oral squamous cell carcinoma (FOSCC). FOSCC and HNSCC share similar etiopathogenesis (tobacco and papillomavirus exposure) and molecular markers (EGFR, VEGF, and p53). Both human and feline SCCs share similar tumor biology, clinical outcome, treatment, and prognosis. Future clinical trials utilizing FOSCC as a tumor model may facilitate translation of preclinical cancer research for human cancer patients.


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