Fogorvosi szemle, 2007 (100. évfolyam, 1-6. szám)

2007-10-01 / 5. szám

256 FOGORVOSI SZEMLE ■ 100. évf. 5. sz. 2007. was characteristic in the control group: 37 of the 52 cases (71.2%) (Table IV). The histological results re­vealed a more aggressive tumor invasion in the type- 2 diabetes group as compared with the control group; the difference between the two groups was significant (p<01). OC has a poor prognosis, with a 5-year survival rate of 50% to 55% [41]. Local recurrence typically occurs relatively early, most often within 1 to 2 years. Because tumor progression is considerably influenced by TNM stage, our cases were homogenized, and only T2-T3 cases were included. Presumably, the more rapid tumor progression in DM may be caused by different factors [43]. The main promoting factor of tumor spread in DM may be the hy­perglycemia, as a result of which the tissue responses may change. It has been confirmed that the oxidation equilibrium is also disturbed in DM2 [3]. In response to the chronic hyperglycemia, increased amounts of AGEs may be formed, which promote the delibera­tion of further free radicals, induce the production of cytokines and growth factors and damage the struc­ture and function of various extracellular matrix mate­rials [51]. All these processes facilitate tumor invasion. Elevated matrix metalloproteinase level in DM2 plays an important role in both direct and metastatic tumor spread [9], Increased RAGE expression appears to be closely associated with the invasiveness of OC [5]. In DM there is an excessive glucose supply in the serum, an increased Glut-1 expression and glucose transport activity as compared with physiologic glucose concentrations [37], Glut-1 has an important correla­tion with human malignancies. In OC cases, a signif­icant relationship between disease-related death and Glut-1 expression was observed; a high Glut-1 level predicted shorter survival [27, 42]. Smoking has well-known harmful effects in terms of both OC and DM2 [24, 25]. In the present study, the percentage of smokers was not higher in the DM2 group than in the control group. This suggests that in our gingival cancer cases the diabetic tissue derange­ment seems to be stronger factor than smoking for the progression of OC. All these data permit a supposition that DM2 may be considered a prognostic factor in cases of gingival cancer, suggesting an unfavorable course. Conclusions The literary data and our results on OC cases support the strong association of DM2 with increased cancer risk at several sites. Moreover, DM2 has a significant impact on the local spread and metastatic progression of cancer. Among OC patients DM2 has a close cor­relation with a higher rate of overall mortality, local tu­mor recurrence and metastatic spread. The associations between insulin resistance and malignancies reveal new possibilities in the prevention and treatment of cancer. Healthy diet, physical activ­ity and weight loss increase insulin sensitivity, and de­crease the risk for both cardiovascular diseases and malignancies. In patients with cancers at several sites (breast, colon, prostate, oral mucosa, etc.) tumor pro­gression may be hampered by maintenance of the euglycemia and a healthy lifestyle. References 1. Adami HO, Chow WH, Nyren O: Excess risk of primary liver can­cer in patients with diabetes mellitus. J Natl Cancer Inst 1996; 88: 1472-1476. 2. Albrecht M, Bánóczy J, Dinya E, Tamás G: Occurrence of oral leu­koplakia and lichen planus in diabetes mellitus. J Oral Pathol Med 1992; 21: 364-366. 3. Baynes JW, Thorpe SR: Role of oxidative stress in diabetic com­plications: a new perspective on an old paradigm. Diabetes 1999; 48: 1-9. 4. Bánóczy J, Bakó A, Dombi C, Ember I, Kosa Z, Sándor J, Szabo G: Stomato-oncological screening examinations: possibilities for early diagnosis. Magy Onkol 2001; 45: 143-148. 5. 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Dietrich T, Reichart PA, Scheifele C: Clinical risk factors of oral leukoplakia in a representative sample of the US population. Oral Oncology 2004; 40: 158-163. 13. Dikshit RP, Ramadas K, Hashibe M, Thomas G, Somanathan T, Sankaranarayanan R: Association between diabetes mellitus and pre-malignant oral diseases: a cross sectional study in Kerala, India. Int J Cancer 2006; 118:453-457. 14. Dobrössy L: Cancer mortality in central-eastern Europe: Facts behind the figures. Lancet Oncol2002; 3: 374-381. 15. Gibson J, Lamey PJ, Lewis MAO, Frier BM: Oral manifestations of previously undiagnosed non-insulin dependent diabetes mellitus. J Oral Pathol Med 1990; 19: 284-287. 16. Goutzanis L, Vairaktaris E, Yapijakis C, Kavantzas N, Nkenke E, Derka S, Vassiliou S, Acyl Y, Kessler P, Stavrianeas N, Perrea D, Donta I, Skandalakis P, Patsouris E: Diabetes may increase risk for oral cancer through the insulin receptor substrate-1 and focal adhe­sion kinase pathway. Oral Oncol 2007; 43: 165-173. 17. Guggenheimer J, Moore PA, Rossie K, Myers D, Mongelluzzo MB, Block HM, Weyant R, Orchard T: Insulin-dependent diabetes melli­tus and oral soft tissue pathologies. II. Prevalence and characteris­tics of Candida and candidal lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 89: 507-576. 18. Hammarsten J, Hogstedt B: Hyperinsulinaemia: A prospective risk factor for lethal clinical prostate cancer. Eur J Cancer 2005; 41 : 2887-2895.

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