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Results for “oral oncogenesis”

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At least 19 recordsLinked to original sources

PubMed2006

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 0.5% 9, 10-dimethyl-1, 2-benzanthracene (DMBA) for 14 weeks and were excised at 10, 14, 19 weeks, respectively. The biopsies were classified pathologically (normal mucosa, hyperkeratosis, hyperplasia, dysplasia, early invasion, well and moderately differentiated carcinoma) and studied immunohistochemically. The two-tailed Student's t test was performed for each animal group and for each histological category. RESULTS: The ets-1 expression increased in early stages of oral tumor formation and invasion. The expression of N-ras gradually decreased during oral oncogenesis, as previously observed with H-ras. CONCLUSIONS: Neither N-ras nor H-ras affects ets-1 expression in contrast to other types of cancer in which N-ras and ets-1 are implicated in the same signalling pathway. Therefore, the existing pathway implicating these proteins might be somehow altered in oral cancer. It seems that ets-1 is a good prognostic marker for invasiveness and progression of oral cancer.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1997

Evaluation of P-glycoprotein expression in human oral oncogenesis: correlation with clinicopathological features.

To determine whether the multidrug-resistance-gene product phospho-glycoprotein (P-gp) is implicated in progression of oral tumours and/or drug resistance, the expression of P-gp was examined in different stages of oral oncogenesis using monoclonal antibody C-219. Cryosections from normal (41 cases), dysplastic lesions (32 cases), untreated primary SCCs (50 cases) and recurrent tumours (31 cases) were used for immunostaining, and the results were corroborated by immunoblotting. Chi-square test for trend analysis showed a significant increase in P-gp immunopositivity across the normal, leukoplakia, primary oral SCC and recurrent SCC groups (p < 0.01). Expression of P-gp in dysplastic lesions showed significant association with severity of dysplasia, the level of P-gp protein being higher in severe and moderate dysplasia. Among the primary tumours, significant correlation was observed between P-gp positivity as well as level of P-gp expression and tumour stage. The recurrent tumours showed significant increase in P-gp expression as compared with untreated primary oral tumours. We conclude that differential expression of P-gp may be an index of the disease prognosis in oral-cancer patients in the context of the Indian population.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMedDate not supplied

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. The histological status of the oral lesions in the experimental groups corresponded well with tumour advancement (from dysplasia to moderately-differentiated carcinoma). Tumour sections were studied immunohistochemically. RESULTS: The expressions of both p53 and c-myc increased significantly in precancer stages and then reached a plateau. The same pattern was observed in the animal groups with the culmination of expression of both genes in group A. CONCLUSION: The coexpression of p53 and c-myc proteins in the earlier stages of oral oncogenesis may be used for the early detection of premalignant lesions.

Animals↗

PubMed1998

Prognostic significance of p53 protein overexpression in betel- and tobacco-related oral oncogenesis.

We have previously reported overexpression of p53 protein in tobacco-related oral dysplasia and squamous cell carcinoma (SCC) in the Indian population. A follow-up study was carried out to determine the prognostic significance of an accumulation of p53 protein during oral tumorigenesis. One hundred and two of 145 (70%) of oral SCCs and 39/75 (52%) of oral dysplasias showed overexpression of p53 protein, while only 3 of 107 (3%) normal oral tissues showed a detectable level of the protein. Follow-up studies of these patients suggest that an accumulation of p53 protein may be involved in the early phases of oral SCC development and indicate the predisposition of a particular premalignant lesion towards malignancy. In patients with premalignant lesions, the median transition time (premalignancy to malignancy) was significantly shorter in p53 positive cases than in p53 negative cases (p = 0.013). Among the oral cancer patients, univariate analysis showed that alteration in p53 expression was associated with significantly decreased disease-free survival. The p53 positive cases showed decreased median disease-free survival time (no recurrence/metastasis) compared with the p53 negative cases (p = 0.013), indicating that p53 accumulation may serve as a prognostic indicator in oral cancer patients.

Adult↗

PubMed2006

Cell proliferation and apoptosis culminate in early stages of oral oncogenesis.

Markers of cell proliferation (Ki-67 antigen) and apoptosis (Bax, Bcl-2) were studied in an experimental system of induced oral carcinogenesis in Syrian golden hamsters. Thirty-seven animals were divided into one control group and three experimental groups, which were treated with a carcinogen and sacrificed at 10, 14 and 19 weeks after treatment. The histological status of the lesions in the three experimental groups corresponded well with tumour advancement (from oral mucosal dysplasia to moderately differentiated squamous cell carcinoma). Tumour sections were studied using monoclonal antibodies against Bax, Bcl-2 and Ki-67 proteins. Pro-apoptotic Bax expression maintained high levels during all stages of oral carcinogenesis. Anti-apoptotic Bcl-2 expression decreased significantly in dysplastic and early invasion lesions and consequently increased almost to normal tissue level in consequent stages. Finally, Ki-67 expression increased sharply in initial stages of oral carcinogenesis, but significantly decreased in later stages.

Animals↗

PubMedDate not supplied

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. RESULTS: A significant elevation was revealed in both FGFR-2 and FGFR-3 expression during the stages of dysplasia and early invasion, while in the later stages of oral carcinogenesis the expression of both FGFR-2 and FGFR-3 decreased although not significantly. CONCLUSION: Our findings indicate that FGFR-2 and FGFR-3 seem to play an important role in the initial stages of oral cancer progression.

Animals↗

PubMedDate not supplied

Evidence of multi-step oncogenesis of oral squamous cell carcinoma.

We examined biopsy samples from one oral cancer and three precancerous lesions of the tongue of an 81-year old woman by polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) and sequence analyses using 18 oligonucleotide primer pairs of adenomatous polyposis coli (APC) gene and 5 primers of p53 gene. Normal tongue epithelium adjacent to lesions was used as a control. The four lesions harbored the common mutation of APC gene that was not detected in the control. At codon 1621 in exon 15 of the APC gene there was a C to G substitution resulting in serine (TCA) to stop codon (TGA). No mutation of p53 gene was detected in any samples of the control and three precancerous lesions of the tongue. On the other hand, an A to G substitution at codon 170 in exon 5 of p53 gene resulting in glutamic acid (ACG) to glycine (GCG) was detected in the DNA of her tongue cancer. These results may suggest that the four lesions have the same origin, and that multi-step oncogenesis had occurred, the APC gene alteration being one of the early events in the process of tumorigenesis and p53 gene alteration involved in the late events.

Aged↗

PubMed2006

Plasminogen activator inhibitor-1 polymorphism is associated with increased risk for oral cancer.

In light of the recently observed contribution of thrombosis-related factors to carcinogenesis, we investigated the possible association of plasminogen activator inhibitor-1 (PAI-1) with increased risk for oral cancer. In DNA samples of 104 patients with oral squamous cell carcinoma and 106 healthy controls of comparable ethnicity, age and sex, we studied the 4G/5G polymorphism in the PAI-1 gene, which affects its expression. The mutant 4G allele and carrier frequencies were significantly increased in patients compared to controls (65.9% versus 49.5%; 88.5% versus 69.8% respectively, P<0.01). That increase was even higher in patients with a positive family history for thrombophilia or without one for cancer (P<0.001). Interestingly, significant difference from controls was observed only in patients with cancer stages I and II. These findings suggest that the 4G allele, by resulting in higher PAI-1 expression, is a major contributing factor in early stages of oral oncogenesis. Possibly, increased PAI-1 promotes initial development of oral cancer through regulation of cell detachment and delays further tumor progression by inhibiting vascularization.

Adult↗

PubMed1998

Expression of cyclin dependent kinase inhibitor p21waf1/cip1 in premalignant and malignant oral lesions: relationship with p53 status.

p21waf1/cip1 protein, an inhibitor of cyclin dependent kinases, is a critical downstream target in the p53-specific pathway of growth control, and can also be induced by p53 independent pathways in relation to terminal differentiation. p21waf1 is also a putative tumour suppressor. Hence, we sought to determine whether this protein is abnormally expressed during betel- and tobacco-related oral oncogenesis. The aim was to determine whether a correlation exists between the expression profile of p21 and clinicopathological parameters of the patients, as well as with their p53 status. Immunohistochemical analysis showed that the expression of p21 protein in premalignant lesions was consistently elevated in the superficial, differentiated cells of the epithelium, while overexpression of the p53 tumour suppressor gene was observed in the basal proliferating layers of the epithelium. Our study demonstrated that p21 overexpression is associated with differentiation in proliferating dysplasias and squamous cell carcinomas (SCCs). The expression of p21 and p53 proteins was observed in 11/25 premalignant lesions. In 7 of these 11 cases, a heterogenous pattern of expression of p21 and p53 was observed. Four of these 11 premalignant and 30/51 malignant lesions showed concordant expression of both p21 and p53 proteins. The discordant p21 +/p53- phenotype was observed in 4/25 premalignant lesions and 5/51 oral SCCs. The p21-/p53+ phenotype was observed in 5/25 premalignant lesions and 7/51 oral SCCs. These results suggest that induction of p21 occurs by both p53 dependent and independent mechanisms during oral tumorigenesis.

Adult↗

PubMed2003

Elevated expression of cyclooxygenase (COX)-2 in oral squamous cell carcinoma--evidence for COX-2 induction by areca quid ingredients in oral keratinocytes.

BACKGROUND: Elevated expression of cyclooxygenase (COX)-2 has been demonstrated in several human cancers. Whether COX-2 is up-regulated in areca quid (AQ) related oral squamous cell carcinoma (OSCC) is unknown and the potential of AQ ingredients to induce COX-2 expression has not been studied. METHODS: COX-2 expression was analyzed by immunohistochemistry and RT-PCR in oral tissues. The COX-2 mRNA and protein induction potential of AQ ingredients were analyzed by real-time RT-PCR and Western blotting in normal human oral keratinocyte (NHOK). RESULTS: COX-2 protein expression was significantly higher (P < 0.01) in OSCC (n = 27) as compared to their adjacent non-cancerous matched tissue (NCMT). COX-2 protein was nearly undetectable in control normal oral mucosa. The level of COX-2 mRNA was markedly elevated in 63% (12/19) of OSCC compared to NCMT. Hydroxychavicol induced COX-2 mRNA and protein expression in NHOK. CONCLUSIONS: COX-2 protein as well as mRNA expression were significantly enhanced in OSCC as compared to NCMT. Hydroxychavicol, a unique ingredient in AQ, induced COX-2 expression in NHOK, which highlighted early involvement of COX-2 in AQ-associated oral oncogenesis.

Areca↗

PubMedDate not supplied

Strong association of interleukin-6 -174 G>C promoter polymorphism with increased risk of oral cancer.

In view of the recently found contribution of factors associated with thrombosis and inflammation to carcinogenesis, we investigated the possible association of interleukin-6 (IL-6) with an increased risk of oral cancer. In DNA samples of 162 patients with oral squamous cell carcinoma and 156 healthy controls of comparable ethnicity, age and sex, we studied the -174 G>C polymorphism in the IL-6 gene, which affects its transcription. C allele frequencies were significantly increased in patients compared to controls, 42.6% versus 23.1% (p<0.001). The CC homozygotes had a 7-fold greater risk of developing oral cancer (odds ratio 7.39, 95% CI 2.61-20.92), while the GC heterozygotes had a 4-fold greater risk (odds ratio 3.74, 95% CI 2.29-6.11). A significant increase in C alleles was observed in patients regardless of their smoking or alcohol consumption habits, early or advanced stage of cancer, and presence or absence of a family history for cancer or thrombophilia (p<0.001; Fisher's exact test). These findings suggest that the -174 G>C polymorphism, by affecting IL-6 gene expression, is strongly associated with oral oncogenesis.

Adult↗

PubMed1998

Circulating p53 antibodies as early markers of oral cancer: correlation with p53 alterations.

p53 aberrations are early events in the pathogenesis of betel- and tobacco-related oral malignancies. Accumulation of p53 protein in oral lesions may elicit a humoral immune response against p53 protein in these patients. p53 antibodies (Abs) were analyzed in 183 sera obtained from patients with premalignant or malignant oral lesions and normal individuals by enzyme-linked immunoassay using recombinant p53 protein as antigen. These results were correlated with accumulation of p53 protein in patients' matched oral tissue specimens. Circulating p53 Abs were observed in 24 of 70 (34%) cancer patients and 15 of 50 (30%) patients with premalignant oral lesions. p53 Abs showed a significant association with increase in tumor size and dedifferentiation of tumors, factors indicative of poor prognosis. Expression of p53 protein was analyzed in 43 matched oral lesions (18 premalignant and 25 malignant cases). All the p53-seropositive patients (7 leukoplakia and 11 squamous cell carcinoma) showed elevated levels of p53 protein in matched oral lesions. However, the total number of patients seropositive for p53 Abs was lesser than that of patients exhibiting p53 protein accumulation in oral lesions. Four of the 63 normal healthy individuals who were heavy consumers of tobacco (smoking/chewing) and betel were found to be positive for p53 Abs. Detection of circulating p53 Abs in patients with premalignant oral lesions suggests that humoral immune response against p53 protein is an early event in oral oncogenesis and may be a surrogate marker for both p53 alteration and preclinical cancer.

Adult↗

PubMed1982

[Effect of FT-207 on bladder cancer in rats induced by BBN. II: The effect of oral administration of FT-207 during oncogenesis of bladder cancer].

The effect of Tegafur (FT-207) by oral administration on the development of urinary bladder tumors in Wistar strain male rats induced by N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) was studied. Urinary bladder tumors were induced in 18 of 20 rats (90.0%) when rats were given 0.05% BBN in the drinking water for 8 weeks and then given water without BBN for 12 weeks. When FT-207 100mg/kg B. W./day was given in their diet after treatment with 0.05% BBN for 8 weeks, tumors developed in the urinary bladder with low incidence (9 of 16 rats: 56.3%). Hematotoxicity was not observed in all animals treated with FT-207. These results shows that FT-207 also inhibited the development of urinary bladder tumors treated with BBN in rats by oral administration, which were similar those our previous results showed by intraperitoneal administration of FT-207.

Administration, Oral↗

PubMed2004

Involvement of viral and chemical factors with oral cancer in Taiwan.

BACKGROUND: The association between oral squamous cell carcinoma (OSCC) and viral and chemical factors is uncertain. Therefore the correlation of viral and chemical factors with oral cancer in Taiwan was investigated. METHODS: Thirty-seven paraffin-embedded oral cancer biopsies and 36 normal oral tissue specimens were examined by the polymerase chain reaction method for six viruses: HPV, CMV, EBV, HSV-1, HSV-2 and HHV-8. To elucidate the role of arecoline in the oncogenesis of oral cancer, human buccal fibroblasts, oral submucosal fibroblasts and three cancer cell lines KB, GNM and TSCCa were used for MTT cytotoxity assay and flow cytometry DNA content analysis. RESULTS: Two (5.4%) HSV-1-positive and four (10.8%) HPV-positive cases were recognized in oral cancer biopsies. Among the four HPV-positive tissues, two were further typed as HPV-16, one was identified as HPV-18- and HSV-1-positive; and one contained both HPV-16 and HPV-18. One sample presented HSV-1 only. Arecoline, at a concentration lower than 0.8 micro g/ml, increased cell growth (all cell types); at higher concentrations (25-400 micro g/ml) it was cytotoxic. The cell cycle was demonstrated to be altered either by low or high concentrations of arecoline treatment, depending on the cells treated. CONCLUSIONS: The data demonstrated that HPV, HSV-1 and betel quid chewing were significantly associated with OSCC, but HSV-2, CMV, EBV and HHV-8 were not. We suggest that the most determinative factor for oral cancer may be chemical in nature rather than viral infection.

Arecoline↗

PubMed2006

[Expression of tumor suppressor gene PTEN, PIP3 and cyclin D1 in oral squamous cell carcinoma and their correlations].

OBJECTIVE: To detect the expression of PTEN, PIP3 and cyclin D1 in oral squamous cell carcinoma and precancerous lesions and analyze their correlation. METHODS: Immunohistochemistry SP method was used to detect the expression of PTEN, PIP3 and cyclin D1 in 63 cases of oral squamous cell carcinoma, 29 cases of simple hyperplasia, 33 cases of dysplasia, and 25 cases of normal oral mucosa. RESULTS: The negative or low expression of PTEN in oral squamous cell carcinoma was 25%, which was remarkably lower than that in other groups. The positive expression of PIP3 in simple hyperplasia, dysplasia and oral squamous cell carcinoma was 66%, 64%, and 76% respectively, which were much higher than those in normal oral mucosa. The positive expression of cyclin D1 in oral squamous cell carcinoma was 49%, which was significantly higher than that in other groups. The negative correlation between PTEN with PIP3, cyclin D1 and the positive correlation between PIP3 and cyclin D1 were observed. CONCLUSIONS: PTEN may play a role in the oncogenesis of oral squamous cell carcinoma, and PTEN may down-regulate the expression of PIP3, and then down-regulate the expression of cyclin D1, which leads to the suppression of cell growth.

Carcinoma, Squamous Cell↗

PubMed1999

[Study and detection of telomerase activity in oral squamous cell carcinomas and precancerous lesions].

OBJECTIVE: To find out the expression of telomerase activity in oral squamous cell carcinomas (SCC) and oral precancerous lesions. METHODS: Telomerase activity was examined by telomerase PCR ELISA assay and telomere repeat amplification protocol (TRAP) electrophoresis. 60 fresh oral specimens were selected, including 20 oral SCC, 30 oral precancerous lesions (10 oral leukoplakia, LK, 20 oral lichen planus, LP) and 10 normal mucosa (NM). RESULTS: Telomerase activity detected in SCC (0.128) was highest among all of the tissues(LK: 0.054, LP: 0.0094, NM: 0.0014). Statistical difference was notable between SCC and LK, LP, NM (P < 0.01). A little difference was detected between LK, LP and NM. No difference was found between LK, and LP (P > 0.05). CONCLUSION: Telomerase may play an important role during oncogenesis of oral precancerous lesions, and may be a good molecular biomarker for observing the cancerization ability of precancerous lesion and estimating its prognosis.

Carcinoma, Squamous Cell↗

PubMed1984

Oral carcinoma: evidence for viral oncogenesis.

Since early this century, when Rous (1911) first demonstrated the association of a tumour (chicken sarcoma) with a transmissible agent, evidence has accumulated on possible associations between viruses and various neoplasms. There is now conclusive evidence linking some RNA viruses (Temin, 1972) and DNA viruses (Rapp, 1973) with tumours in animals--including sub-human primates (Leading article, 1982). Indeed, a serious complication of hepatitis B infection in man is now recognised to be hepatocellular carcinoma. (Editorial, 1982). The evidence association other viruses with human neoplasms is not unequivocal but there are strong associations between, for example, herpesviruses and some human malignant neoplasms (Klein, 1972; Rapp, 1973; zur Hausen, 1975).

Animals↗

PubMed2004

Presence of human papillomavirus-18 and Epstein-Barr virus in a squamous cell carcinoma of the tongue in a 20-year-old patient. Case report and review of the current literature.

We report on a squamous cell carcinoma of the tongue in a 20-year-old woman with co-infection of the tumor with human papilloma virus type 18 and Epstein-Barr virus. To our knowledge, this is the first case of co-infection in carcinoma of the tongue to be reported. We review the present data and theories concerning viral oncogenesis of oral carcinomas.

Adult↗