Association of angiotensin-converting enzyme gene insertion/deletion polymorphism with decreased risk for basal cell carcinoma.

The incidence of basal cell carcinoma (BCC) is significantly reduced in individuals treated with inhibitors of angiotensin I-converting enzyme (ACE) that produces angiotensin II. The objective of this study was to investigate the possible association of a functional polymorphism in the ACE gene, which affects its transcription, with risk for BCC. In DNA samples of 92 patients with BCC and 103 healthy controls of Greek origin and comparable age and gender, we studied the ACE gene insertion/deletion (I/D) polymorphism.

A common 9 bp deletion in the ataxia-telangiectasia-mutated gene is not associated with oral cancer.

Background: The ataxia-telangiectasia-mutated gene (ATM) product is a well-characterized tumour suppressor that plays a key role in the maintenance of genomic stability. Given the fact that the loss of heterozygosity at the ATM locus is common in head and neck tumours, we investigated the possible association of 7636del9, which is the most frequent ATM deletion, with risk for oral cancer.

Patients And Methods: The 7636del9 9nt deletion was investigated in DNA samples of 67 German and Greek patients with oral cancer and 57 healthy controls of equivalent ethnicity, age and gender, by polymerase chain reaction (PCR) followed by electrophoretic analysis.

Diabetes enhances the expression of H-ras and suppresses the expression of EGFR leading to increased cell proliferation.

EGFR kinase activity triggers numerous signaling pathways, such as the Ras/Raf/MAPK cascade, leading to the activation of various mitogen activated protein kinases, which are implicated in cell proliferation through induction of several genes, including c-fos. The possible effect of diabetes on the expression of the oncogenes EGFR, H-ras and c-fos was investigated in an experimental model of chemically induced oral oncogenesis in normal and diabetic (type I) Sprague-Dawley rats. Thirteen diabetic and twelve normal rats developed cancer after 4NQO treatment, while six diabetic and six normal animals were used as controls.

H-ras and c-fos exhibit similar expression patterns during most stages of oral oncogenesis.

Background: H-ras and c-fos oncogenes interact in signalling pathways but their level and time course of expression during oral cancer development are unclear. The present study used an animal model for the simultaneous investigation of H-Ras and c-Fos expression in sequential stages of oral oncogenesis.

Materials And Methods: Three experimental groups of Syrian golden hamsters (A, B and C; 10 animals each) and one control group (7 animals) were used.

The interleukin-10 (-1082A/G) polymorphism is strongly associated with increased risk for oral squamous cell carcinoma.

Background: Increased levels of interleukin-10 (IL-10) have been observed in patients with oral cancer, possibly as a result of suppression of the immune response. Based on this, the -1082A/G polymorphism, which influences IL-10 gene expression level, was investigated in regard to its possible association with risk for oral cancer.

Patients And Methods: The polymorphism was examined in DNA samples of 144 patients with oral squamous cell carcinoma and 141 healthy controls of equivalent gender, age and ethnicity.

Gene expression polymorphisms of interleukins-1 beta, -4, -6, -8, -10, and tumor necrosis factors-alpha, -beta: regression analysis of their effect upon oral squamous cell carcinoma.

Purpose: Functional DNA polymorphisms affecting gene expression and serum or saliva levels of interleukins IL-1 beta,-4,-6,-8,-10 and tumor necrosis factors TNF-alpha,-beta have been associated with increased risk for the development of oral squamous cell carcinoma (OSCC). The present retrospective case-control study examines possible interactions between seven cytokine genotype polymorphisms and their combinatory effect in predicting the occurrence of OSCC in Caucasians.

Methods: Three hundred and thirty Greeks and Germans were studied, consisting of 162 OSCC cases and 168 healthy controls of comparable age, gender, and ethnicity.

Diabetes and oral oncogenesis.

Oral squamous cell carcinoma (OSCC) is the sixth most common malignancy in humans including type I diabetic and normal rats. Tobacco and alcohol, as well as dysregulation of oncogenes and tumor suppressor genes, epigenetic changes and mitochondrial mutations have been implicated in OSCC development. Recent epidemiological studies have incriminated diabetes mellitus as a risk factor for the development of OSCC, as well as oral premalignant lesions.

The interleukin-18 -607A/C polymorphism is not associated with risk for oral cancer.

Background: The purpose of the present study was to investigate the association of angiogenesis-inhibitor interleukin-18 (IL-18) with risk for oral cancer, with regard to the recently found contribution of cytokines to carcinogenesis.

Patients And Methods: The -607A/C polymorphism in the promoter region of the IL-18 gene, which affects transcription, was studied in 149 patients with oral squamous cell carcinoma and 89 matched healthy controls.

Results: The detected carrier and allele frequencies of the low transcription A allele were not significantly different in patients in comparison with controls (63.

Increased risk of oral cancer in diabetic animals is not associated with c-jun activation pathway.

Purpose: The expression of oncogenic protein c-jun was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats.

Material And Methods: Thirteen diabetic and twelve normal rats developed cancer after 4-nitroquinoline-N-oxide treatment, while six diabetic and six normal animals were used as controls. The biopsies were classified pathologically from oral mucosal dysplasia to moderately differentiated oral squamous cell carcinoma (OSCC) and studied immunohistochemically using monoclonal antibody against c-jun protein.

EGFR and c-Jun exhibit the same pattern of expression and increase gradually during the progress of oral oncogenesis.

Background: Epidermal growth factor receptor (EGFR) and c-Jun oncogenes are implicated in the same pathway of signal transduction affecting cell differentiation. In order to investigate their possible correlation with sequential histological stages of OSCC formation, we established an experimental model of induced oral carcinogenesis in Syrian golden hamsters.

Materials And Methods: Thirty-seven animals were divided into one control group (n=7) and three experimental groups (n = 10 each), which were treated with a carcinogen and sacrificed at 10, 14 and 19 weeks after treatment.

Expression of cell cycle regulator p16 is not affected by diabetes during oral oncogenesis.

Background: The tumor suppressor protein p16 plays a vital role in the regulation of the cell cycle. The expression of p16 was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats.

Materials And Methods: Tissue sections ranging from normal oral mucosa to moderately differentiated oral squamous cell carcinoma (OSCC) were studied immunohistochemically.

Increased risk for oral cancer is associated with coagulation factor XIII but not with factor XII.

In light of recently found contribution of factors associated with thrombosis and inflammation to carcinogenesis, we investigated the possible association of coagulation factors XII and XIII with increased risk for oral cancer. In DNA samples of patients with oral squamous cell carcinoma and healthy controls of comparable ethnicity, age and sex, we studied the C46T polymorphism in FXII gene which affects gene transcription and the V34L polymorphism in FXIII gene which affects enzyme activity resulting in alteration of the fibrin network structure. No significant differences were observed in genotype and mutant allele frequencies of the FXII C46T polymorphism between patients and healthy controls.

Association of angiotensin-converting enzyme gene insertion/deletion polymorphism with increased risk for oral cancer.

Introduction: In light to recently found contribution of factors associated with thrombosis and inflammation to carcinogenesis, we investigated the possible association of angiotensin I- converting enzyme (ACE) with increased risk for oral cancer.

Materials And Methods: In DNA samples of 160 patients with oral squamous cell carcinoma and 153 healthy controls of comparable ethnicity, age and sex, we studied the insertion/deletion (I/D) polymorphism in the ACE gene, which affects its transcription.

Results: The I allele frequencies were significantly increased in patients compared to controls, 40.

Diabetes does not influence oral oncogenesis through fibroblast growth factor receptors.

Background: Increased expression of fibroblast growth factors and their receptors (FGFRs) has recently been described in oral squamous cell carcinoma. In addition, we have previously described a molecular basis for an association between oral cancer and diabetes. The expression of FGFR-2 and FGFR-3 investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) rats.

Diabetes increases both N-ras and ets-1 expression during rat oral oncogenesis resulting in enhanced cell proliferation and metastatic potential.

Background: The expression of N-ras and ets-1 proteins was investigated in an experimental model of chemically-induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats.

Materials And Methods: Tissue sections ranging from normal mucosa to moderately-differentiated oral squamous cell carcinoma were studied using monoclonal antibodies against N-ras and ets-1 proteins.

Results: In diabetic rats, N-ras expression increased with tumor advancement, while in normal rats N-ras was not detected in initial stages of oral oncogenesis and increased only in well-differentiated OSCC.

Enhancement of erbB2 and erbB3 expression during oral oncogenesis in diabetic rats.

Purpose: The expression of erbB2 and erbB3 receptors was investigated in an experimental model of chemically induced oral carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats.

Methods: Thirteen diabetic and twelve normal rats developed precancerous and cancerous lesions after 4-nitroquinoline-N-oxide treatment, while six diabetic and six normal animals were used as controls. Sections of biopsies from all animals were classified histologically in the following categories: normal mucosa, hyperplasia, dysplasia, early invasion, well- and moderately-differentiated squamous cell carcinoma.

Coagulation-related factors, thrombomodulin and protein Z, are not associated with risk for oral cancer.

Background: The link between thrombosis and cancer has been well established. Levels of protein Z and thrombomodulin indirectly regulate thrombin productionl and therefore may affect cancer susceptibility.

Patients And Methods: The functional polymorphisms -13A/G and -33G/A in protein Z and thrombomodulin genes (respectively) influence transcription.

The 1040C/T polymorphism influencing thermal stability and activity of thrombin activatable fibrinolysis inhibitor is associated with risk for oral cancer.

No studies thus far have investigated the contribution of thrombin activatable fibrinolysis inhibitor (TAFI) to oral oncogenesis. We studied the activity-related 1040C/T polymorphism in 150 patients with oral cancer and 138 healthy controls matched by age, gender, and ethnicity. The increased-activity T allele frequency was significantly reduced in patients compared with controls (28.

Diabetes alters expression of p53 and c-myc in different stages of oral oncogenesis.

Background: The expression of tumour suppressor p53 and oncogene c-myc was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats.

Materials And Methods: Tissue sections ranging from normal mucosa to moderately differentiated oral squamous cell carcinoma were studied using monoclonal antibodies against mutant p53 and c-myc proteins.

Results: From hyperplasia to later stages of oral oncogenesis, mutant p53 expression was at higher levels in diabetic rats in comparison to normal animals, although the pattern of expression was similar.

Loss of tumour suppressor p16 expression in initial stages of oral oncogenesis.

Background: The p16 tumour suppressor gene is known to be involved in regulation of the cell cycle. p16 expression in sequential histological stages of oral squamous cell carcinoma (OSCC) formation was investigated using an experimental model of induced oral carcinogenesis in Syrian golden hamsters.

Materials And Methods: Thirty-seven animals were divided into one control group (N = 7) and three experimental groups (N = 10 each) which were treated with a carcinogen and sacrificed at 10, 14 and 19 weeks after treatment.

Association of matrix metalloproteinase-1 (-1607 1G/2G) polymorphism with increased risk for oral squamous cell carcinoma.

Background: The purpose of this study was to investigate the possible relation of matrix metalloproteinase-1 (MMP-1) to increased risk for oral cancer, in light of recently found contribution of angiogenesis and thrombosis-related factors to the development of malignancies.

Materials And Methods: The 1G/2G polymorphism in the MMP-1 gene, which influences its expression, was examined in 156 patients with oral squamous cell carcinoma and 141 healthy controls of comparable ethnicity (Greeks and Germans), gender and age.

Results: In comparison to controls, the detected 2G allele frequency was significantly lower in the patient group and in subgroups with early cancer stages, with positive family history of thrombophilia, with tobacco abuse and without alcohol abuse (p < 0.

FGFR-2 and -3 play an important role in initial stages of oral oncogenesis.

Background: FGFR-2 and FGFR-3 (fibroblast growth factor receptors) have been shown to play an important role in several processes including carcinogenesis. This study was designed to determine gradual FGFR-2 and FGFR-3 expression in sequential stages of oral carcinogenesis in an experimental animal system of Syrian golden hamsters.

Materials And Methods: Tissue sections ranging from normal mucosa to squamous cell carcinoma were studied using monoclonal antibodies against FGFR-2 and FGFR-3 proteins.

Expression of ets-1 is not affected by N-ras or H-ras during oral oncogenesis.

Purpose: To determine whether ras-activated cascades lead to activation of ets-1 expression in sequential histological stages of oral oncogenesis in an experimental animal model.

Methods: Thirty-seven Syrian golden hamsters were divided into three experimental groups (A, B, C) and one control group. The hamsters' buccal pouches in experimental groups were treated with 0.

The co-expression of c-myc and p53 increases and reaches a plateau early in oral oncogenesis.

Background: The balance between cell proliferation and apoptosis plays a significant role in cancer development. The expressions of the p53 and c-myc genes, both strongly related to cell proliferation and apoptosis, were studied in sequential histological grades of oral carcinogenesis in an animal model.

Materials And Methods: Thirty-seven hamsters were divided into three groups (A,B,C), which were treated with 9,10-dimethyl-1,2-benzanthracene and sacrificed at 10,14 or 19 weeks, respectively, after treatment.