Significance of salivary phosphodiesterase level in oral squamous cell carcinoma patients

Yousef Rezaei Chianeh, Krishnananda Prabhu, Rashmi M, Donald J. Fernandes

Abstract


Oral cancer, more specifically oral squamous cell carcinoma (OSCC) consider as common cancer that 300,000 people diagnosed per year worldwide. The only effective treatment for OSCC is surgical intervention. Over the past two decades, overall disease condition has not improved although advancement of treatment has considerably increased. The phosphodiesterase (PDEs) are responsible for the hydrolysis of the second messengers with a fundamental role in the transduction of the intracellular signals. In numerous pathological conditions such as cellular differentiation, apoptosis, and tumor invasivity the different PDF activity has been observed that shown role in pathophysiological mechanism. The role of PDEs as an intervention factor for activation of angiogenesis by influencing a tumor growth has been shown. The objective of this study was to estimate and compare salivary PDEs levels in healthy controls and biopsy-proven oral cancer patients before definitive therapy. Study was done in patients age between 25-65 years biopsy proven oral cancer patients and control group. After obtaining prior consent from biopsy-proven oral cancer patients (n=26) (before onset of any definitive treatment) and age- and sex-matched healthy controls (n=29), salivary sample was collected for estimation of the activity of phosphodiesterases (PDEs).


Keywords


Oral cancer, Oral squamous cell carcinoma (OSCC), Phosphodiesterases (PDEs)

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References


Sudbo J. Novel management of oral cancer: a paradigm of predictive oncology. Clin Med Res 2004;2:233-242.

Ries LAG, Harkins D, Krapcho M, et al. Cancer Statistics Review 1975–2003. National Cancer Institute; 2006.

Mehrotra R, Yadav S (2006) Oral squamous cell carcinoma: etiology, pathogenesis and prognostic value of genomic alterations. Indian J Cancer 43:60-66.

Macfarlane GJ, Zheng T, Marshall JR, Boyle P, et al. Alcohol, tobacco, diet and the risk of oral cancer: a pooled analysis of three case-control studies. Oral Oncol. 1995;31:181-187.

Mashberg A, Boffetta P, Winkelman R, Garfinkel L. Tobacco smoking, alcohol drinking, and cancer of the oral cavity and oropharynx among U.S. veterans. Cancer. 1993;72:1369-1375.

Warnakulasuriya S, Sutherland G, Scully C. Tobacco, oral cancer, and treatment of dependence. Oral Oncol. 2005;41:244-260.

Shafer WG, Levy BM, Hine MK, Rajendran R, Sivapathasundharam B (2006) Shafer’s textbook of oral pathology. Elsevier, New Delhi.

Groschl M, Kohler H, Topf HG, Rupprecht T, Rauh M (2008) Evaluation of saliva collection devices for the analysis of steroids, peptides and therapeutic drugs. J Pharm Biomed Anal 47:478–486.

Zimmermann BG, Wong DT (2008) Salivary mRNA targets for cancer diagnostics. Oral Oncol 44:425–429.

Spoto G, Fioroni M, Rubini C, Di Nicola M, Di Pietrantonio F, Di Matteo E, et al. Cyclic AMP phosphodiesterase activity in human gingival carcinoma. J Oral Pathol Med 2004;33:269-73.

Prosperi C, Scali C, Barba M, Bellucci A, Giovannini MG, Pepeu G, et al. Comparison between flurbiprofen and its nitric oxide-releasingderivatives HCT-1026 and NCX-2216 on Abeta(1-42)-induced braininflammation and neuronal damage in the rat. Int J Immunopathol Pharmacol 2004;17:317-30.

Ptaszynska MM, Pendrak ML, Bandle RW, Stracke ML, Roberts DD. Positive feedback between vascular endothelial growth factor-A and autotaxin in ovarian cancer cells. Mol Cancer Res 2008;6:352-63.

Grossman L, Moldave K. Purification and properties of Venom Phosphodiesterase. In: Laskowski M, editor. Methods in enzymology, Nucleic acids. Part I, vol 65. New York: Academic press; 1974. p. 279-80.

Massano J, Regateiro FS, Januário G, Ferreira

A. Oral squamous cell carcinoma: review of prognostic and predictive factors. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006 Jul; 102(1):67-76.

Genden EM, Ferlito A, Bradley PJ, Rinaldo A, Scully C. Neck disease and distant metastases. Oral Oncol. 2003;39:207–212.

Sabichi AL, Demierre MF, Hawk ET, Lerman CE, Lippman SM. Frontiers in cancer prevention research. Cancer Res. 2003;63:5649–5655.

Spafford MF, Koch WM, Reed AL, et al. Detection of head and neck squamous cell carcinoma among exfoliated oral mucosal cells by microsatellite analysis. Clin Cancer Res. 2001;7:607–612.

Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell. 1990;61:759-767.

Marshall CJ. Tumor suppressor genes. Cell. 1991; 64:313-326.

Prosperi C, Scali C, Barba M, Bellucci A, Giovannini MG, Pepeu G, et al. Comparison between flurbiprofen and its nitric oxide-releasingderivatives HCT-1026 and NCX-2216 on Abeta(1-42)-induced braininflammation and neuronal damage in the rat. Int J ImmunopatholPharmacol 2004;17:317-30.

Spoto G, della Malva M, Rubini C, Fioroni M, Piattelli A, Serra E, et al. cAMP phosphodiesterase activity evaluation in human carcinomaof salivary glands. Nucleosides Nucleotides Nucleic Acids 2006;25:1113-7.

Chougule A, Hussain S, Agarwal DP. Prognostic and diagnostic value of serum pseudocholinesterase, serum aspartate transaminase, and serum alinine transaminase in malignancies treated by radiotherapy. J Cancer Res Ther 2008;4:21-5.

Savai R, Pullamsetti SS, Banat GA, Weissmann N, Ghofrani HA, Grimminger F, et al. Targeting cancer with phosphodiesterase inhibitors. Expert Opin Investig Drugs 2010;19:117-31.

Dou AX, Wang X. Cyclic adenosine monophosphate signal pathway in targeted therapy of lymphoma. Chin Med J (Engl) 2010;123:95-9.

Safa M, Zand H, Mousavizadeh K, Kazemi A, Bakhshayesh M, Hayat P. Elevation of cyclic AMP causes an imbalance between NFkappaB and p53 in NALM-6 cells treated by doxorubicin. FEBS Lett 2010;584:3492-8.