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Sang-Heng Kok

Publications and source records attributed to Sang-Heng Kok.

At least 19 recordsLinked to original sources
PubMed2006

Establishment and characterization of a tumorigenic cell line from areca quid and tobacco smoke-associated buccal carcinoma.

A cell line, TW2.6, has been established from the surgically resected specimen of an untreated primary squamous cell carcinoma of the buccal mucosa from a 48-year-old man who was an areca quid chewer and tobacco smoker. TW2.6 cells exhibited morphological features of keratinocytes and replicated rapidly in culture with a doubling time of 24h. The karyotype showed human chromosomes with high hyperdiploidy and complex rearrangements. Western blotting showed pronounced expression of p53 and moderate expression of p21(CIP1). The baseline expressions of p27(KIP1) and p16(INK4a) were barely detectable. Low levels of Bax and Fas were found in TW2.6 cells but Bcl-2 expression was more readily observed. Mutational analysis of p53 gene revealed an A-->G transition at the second base of codon 220, resulting in amino acid substitution from tyrosine to cysteine in the protein. Functional analysis showed that TW2.6 was unable to activate the p53-specific PUMA promoter. Lipofectamine 2000 and calcium phosphate precipitation technique offer good transfection efficiencies for TW2.6 cells and may be used in future transfection experiments. A xenograft-SCID mouse tumor model was established for TW2.6. Histological examination demonstrated that the engrafted tumors maintained the morphological features of a squamous cell carcinoma. It is thought that the establishment of tumorigenic TW2.6 cell line provides a valuable model for AQ and tobacco smoke-associated buccal carcinoma.

Areca↗
PubMed2006

Evaluation of mandibular block using a standardized method.

The purpose of this prospective randomized study was to investigate the manifestations and efficiency of mandibular block (MB) using a standardized method. In this study, 123 patients requiring MB were randomly assigned to receive MB using a repeated measures design. Mandibular block was administered in each patient by using 2.1 mL of 2% lidocaine with 1:100 000 epinephrine for the inferior alveolar nerve, lingual nerve, and/or buccal nerve. Clinical parameters including the electric pulp test and test for soft tissue sensation using a sharp dental explorer were assessed on both the operated side and contralateral side before and 5, 10, and 15 minutes after injection, and at the end of surgical procedure. Results of the test of the contralateral tooth served as the control group. No response to the electric pulp test at a maximum output (80 readings) was used as the criterion for pulpal anesthesia. Results obtained with electric pulp test and sharp explorer test were not significantly different during various intervals on the contralateral side, indicating the reliability of this standardized method for assessing MB. The MB technique achieved a high rate of subjective numbness (100%) according to the perception of the patients of overall numbness and lip numbness. Overall anesthetic success rates of pulpal anesthesia were 5.7% for the central incisor, 38.2% for the canine, 55.3% for the first premolar, and 90.2% for the first molar. No significant difference was found in the efficiency of anesthesia related to sex or age of the patients. A slower onset of pulpal anesthesia after MB was found for the anterior teeth than for the posterior teeth. This study suggests that the use of a standardized method might produce a clearer and more comprehensive evaluation of the efficiency and manifestations of MB.

Adolescent↗
PubMed2006

Carcinoma and dysplasia in oral leukoplakias in Taiwan: prevalence and risk factors.

OBJECTIVES: The issue of existence of malignancy within oral leukoplakia has seldom been addressed in Taiwan. The aims of this study were to investigate the prevalence of carcinoma and dysplasia within oral leukoplakia at the time of clinical diagnosis and to identify the associated risk factors in Taiwan. STUDY DESIGN: The prevalence rate of malignancy and dysplasia in 1046 oral leukoplakias at a university hospital was calculated. Univariate and multivariate analyses by the Mantel-Haenszel method and multiple logistic regression model were performed to examine risk factors associated with the presence of carcinoma and dysplasia within the lesions. RESULTS: The prevalence rate of carcinoma was 12.9%. The relative risks for the presence of malignancy in leukoplakias on the tongue/floor of mouth and with nonhomogeneous appearance were 2.72- and 28.13-fold by multivariate logistic regression analysis, when compared with those on buccal mucosa and lesions having homogeneous surface (both P < .05). In contrast, patients who both smoked and chewed betel quid had a significantly lower risk for carcinoma than the abstainers (P < .05). A synergistic effect between the 2 major risk factors of clinical appearance and lesion site was evident. Nonhomogeneous leukoplakia on tongue/floor of mouth had a 43.10-fold higher risk compared to homogeneous lesions located on buccal mucosa or other sites (P < .05). However, homogeneous leukoplakia in buccal mucosa or other sites of the oral cavity still had the possibility of having carcinoma within the lesion. The prevalence of dysplasia was 45.6% among the noncancerous leukoplakias with risk factors similar to those for carcinoma. CONCLUSIONS: Our results demonstrate that some leukoplakias contain a malignant component. Lesions with certain features are more prone to carcinoma, but no clinical attributes can bring certitude. Therefore, all oral leukoplakias should be submitted to microscopic analysis before any definite treatment or long-term follow-up.

Adult↗
PubMed2005

A clinical staging system and treatment guidelines for maxillary osteoradionecrosis in irradiated nasopharyngeal carcinoma patients.

PURPOSE: To develop a clinical staging system for maxillary osteoradionecrosis (ORN) in irradiated nasopharyngeal carcinoma (NPC) patients. METHODS AND MATERIALS: The data of maxillary ORN cases among 1,758 irradiated NPC patients were analyzed. A staging system based on the degrees of bone exposure (E), infection (I), and bleeding (B) was developed. Correlations between various clinical parameters and stages of maxillary ORN and relationships between treatment modalities and outcomes at each stage were evaluated. Cumulative success of treatment and risk factors that affect treatment outcomes were analyzed. RESULTS: The incidence of maxillary ORN was 2.7% (48/1,758). TNM stage of NPC (p < 0.001), radiation dose (p = 0.029), and tooth extraction (p < 0.001) appeared to have significant influences on disease severity. Success rates between conservative therapy and surgical treatment were not significantly different for Stage I ORN but differed significantly for Stage II (p = 0.013) and Stage III (p = 0.008) lesions. Grade 3 infection and bleeding significantly jeopardized treatment success (p = 0.043 and 0.015, respectively). The risk ratios of treatment failure for Grade 3 infection and bleeding were 2.523 (p = 0.034) and 3.141 (p = 0.027), respectively. CONCLUSIONS: More serious maxillary ORN tended to occur in cases with more advanced NPC, higher radiation dose, and history of tooth extraction. Surgical treatment was usually required in Stage II and III ORN. The grades of infection and bleeding are important factors in guidance of treatment and prediction of outcomes.

Female↗
PubMed2005

Extensive maxillary sequestration resulting from mucormycosis.

Mucormycosis is an invasive and potentially lethal infection caused primarily by fungi of the order mucorales. An ulcer or extraction in the mouth can be the port of fungal invasion, particularly when the patient is immunocompromised. Early recognition and aggressive treatment have reduced the mortality and morbidity. We present a case of oral mucormycosis with extensive maxillary osteonecrosis that is of interest because the patient ignored the initial warning signs and was rescued from the fulminating stage by thorough debridement and medical treatment.

Follow-Up Studies↗
PubMed2005

Univariate and multivariate analysis of prognostic significance of betel quid chewing in squamous cell carcinoma of buccal mucosa in Taiwan.

BACKGROUND AND OBJECTIVES: While betel quid (BQ) chewing is clearly the most avoidable risk factor of squamous cell carcinoma of buccal mucosa (BMSCC), little is known about the influence of this habit on the prognosis of BMSCC. METHODS: We surveyed 280 patients with BMSCC who were treated during an 8-year period in a cohort study to assess the independent predictive value of pretreatment BQ chewing habit on the prognosis by univariate and multivariate analysis. RESULTS: We found by univariate analysis that sex, age, clinical stage, smoking, and BQ chewing significantly affected the patients' prognosis and only age, clinical stage, and BQ chewing had significant influence on prognosis by multivariate analysis (P < 0.05). Further analysis revealed that the prognostic effect of BQ chewing changed in a dose- and time-dependent manner. The risk of death was 31.4-fold higher in heavy user (duration >30 years, daily consumption >30 quids, age of start <20 years old) when compared to those who chewed BQ to a milder degree (duration <10 years, daily consumption <15 quids, age of start > or =20 years old ) (P < 0.001). CONCLUSIONS: Pretreatment BQ chewing habit worsens the prognosis of BMSCC in Taiwan. BQ chewing is a prognostic indicator that can be used in conjunction with clinical staging to help plan the treatment for the patients.

Adult↗
PubMed2005

Norcantharidin-induced apoptosis in oral cancer cells is associated with an increase of proapoptotic to antiapoptotic protein ratio.

Norcantharidin (NCTD), the demethylated analogue of cantharidin, has been used to treat human cancers in China since 1984. It was recently found to be capable of inducing apoptosis in human colon carcinoma, hepatoma and glioblastoma cells by way of an elusive mechanism. In this study, we demonstrated that NCTD also induces apoptosis in human oral cancer cell lines SAS (p53 wild-type phenotype) and Ca9-22 (p53 mutant) as evidenced by nuclear condensation, TUNEL labeling, DNA fragmentation and cleavage of PARP. Apoptosis induced by NCTD was both dose- and time-dependent. We found NCTD did not induce Fas and FasL, implying that it activated other apoptosis pathways. Our data showed that NCTD caused accumulation of cytosolic cytochrome c and activation of caspase-9, suggesting that apoptosis occurred via the mitochondria mediated pathway. NCTD enhanced the expression of Bax in SAS cells consistent with their p53 status. Moreover, we showed that NCTD downregulated the expression of Bcl-2 in Ca9-22 and Bcl-XL in SAS. Our results suggest that NCTD-induced apoptosis in oral cancer cells may be mediated by an increase in the ratios of proapoptotic to antiapoptotic proteins. Since oral cancer cells with mutant p53 or elevated Bcl-XL levels showed resistance to multiple chemotherapeutic agents, NCTD may overcome the chemoresistance of these cells and provide potential new avenues for treatment.

Apoptosis↗
PubMed2005

Higher expressions of p53 and proliferating cell nuclear antigen (PCNA) in atrophic oral lichen planus and patients with areca quid chewing.

OBJECTIVE: The aim of the study was to examine the expressions of p53 and proliferating cell nuclear antigen (PCNA) in oral lichen planus (OLP) in relation to its clinical behavior and the patients' oral habits. STUDY DESIGN: Immunohistochemical study was carried out to investigate the expressions of p53 and PCNA in 56 OLP specimens. The results were correlated with the clinical behavior of the disease and the patients' oral habits. The expression rates were further compared with those of normal oral mucosa (NOM), epithelial hyperkeratosis (EH), epithelial dysplasia (ED), and squamous cell carcinoma (SCC). RESULTS: The staining rate of p53 (28.6%) and PCNA labeling index (LI) (27.6 +/- 8.8%) in OLP were similar to those in EH ( P = .868, .074, respectively), but higher than those of NOM and lower than those of ED and SCC (all P < .05). In OLP, no significant correlations were found between p53 or PCNA expression and the patients' age, gender, lesion duration, location, size, number of site, presence of pain, presence of local irritant, and the habits of alcohol drinking and cigarette smoking (all P > .05). In addition, the mean PCNA LI of p53+ cases was close to that of p53- cases (P = .38). However, the staining rate of p53 in OLP was higher in areca quid (AQ) chewers compared to abstainers (P = .001), and the mean PCNA LI in atrophic cases was higher than that in hypertrophic cases (P = .029). Interestingly, the staining rate of p53 and mean PCNA LI were significantly increased in AQ chewers with atrophic OLP (100%, 36.7% +/- 9.0%, respectively), which were similar to those in ED and SCC (all P > .05). CONCLUSIONS: Although this study could not confirm the precancerous nature of OLP by the relatively low p53 and PCNA expression, the results do suggest that atrophic form OLP and patients with AQ chewing habit may have a higher disease activity in view of higher expression rates of p53 and PCNA in the lesions.

Adolescent↗
PubMed2005

C-C chemokine ligand 2 gene expression in nasal polyp fibroblasts: possible implication in the pathogenesis of nasal polyposis.

OBJECTIVES: Recruitment of macrophages is essential to the pathogenesis of nasal polyps (NP), since this disease is inflammation-related. In this study, the effects of tumor necrosis factor alpha (TNF-alpha) on the expression of C-C chemokine ligand 2 (CCL2) in fibroblasts derived from nasal polyps (NPFs) were investigated. The roles of cyclooxygenase (COX) 2 and prostaglandins in the mediation of TNF-alpha-stimulated CCL2 gene expression were also investigated. METHODS: Northern blot analysis was used to study the expression of CCL2 and c-Fos in cultured NPFs. An electrophoretic mobility shift assay was used to explore the interactions between activator protein 1 (AP- 1) and DNA. Immunohistochemistry was used to explore the in vivo expressions of COX-2, CCL2, and CD68 in NPs. RESULTS: The Northern blot analysis showed that TNF-alpha stimulated the expression of CCL2 and COX-2 genes, and the synthesis of CCL2 messenger RNA was COX-2-dependent. A transient elevation of c-Fos and c-Jun messenger RNAs was induced by TNF-alpha, whereas COX-2 inhibitors NS-398 and meloxicam abolished the up-regulation of c-Fos. The electrophoretic mobility shift assay revealed that TNF-alpha triggered AP-1 and DNA binding and again, NS-398 and meloxicam inhibited this reaction via reducing c-Fos synthesis. Curcumin (AP-1 inhibitor) markedly suppressed the TNF-alpha-induced CCL2 expression. The immunohistochemical staining of NP surgical specimens also revealed an intimate alignment between CCL2-positive fibroblasts and CD-68-positive macrophages. CONCLUSIONS: These data suggest that NPFs may contribute to NP development by synthesizing CCL2 to promote macrophage recruitment. Furthermore, COX-2 facilitates CCL2 transcription in NPFs via a c-Fos and AP-1 signaling pathway.

Cells, Cultured↗
PubMed2004

MEK/ERK and signal transducer and activator of transcription signaling pathways modulate oncostatin M-stimulated CCL2 expression in human osteoblasts through a common transcription factor.

OBJECTIVE: To analyze the effects of oncostatin M (OSM), a gp130-type cytokine, on CCL2 expression in MG-63 cells, a human osteosarcoma cell line with a characteristic osteoblastic phenotype, and to investigate the signaling pathway involved. METHODS: The expression of messenger RNA (mRNA) for CCL2 and c-Fos was analyzed by Northern blotting. Amounts of CCL2 released into the supernatant were measured by enzyme-linked immunosorbent assay. Western blotting was used to examine the activation of MAPK signaling pathways. Interactions between activator protein 1 (AP-1) and DNA were evaluated by electrophoretic mobility shift assay. RESULTS: OSM stimulated CCL2 expression at both the mRNA and the protein levels. Cyclooxygenase 2 (COX-2) was also induced by OSM. However, the up-regulation of CCL2 mRNA was COX-2-independent but required tyrosine kinase and protein kinase C (PKC). OSM stimulated the phosphorylation of MEK-1/2 and ERK-1/2 but not p38 and JNK. A transient elevation of c-Fos mRNA was induced by OSM, but PD 98059 (MEK inhibitor), fludarabine (signal transducer and activator of transcription 1 [STAT-1] inhibitor), and piceatannol (STAT-3 and STAT-5 inhibitor) abolished this effect. Electrophoretic mobility shift assay revealed that OSM stimulated AP-1-DNA binding, which was also abolished by PD 98059, fludarabine, and piceatannol. Supershift study further confirmed the role of c-Fos in the above interaction. PD 98059, fludarabine, piceatannol, and curcumin (AP-1 inhibitor) inhibited the OSM-induced expression of CCL2. CONCLUSION: OSM induces CCL-2 expression in osteoblasts. Activation of the MEK/ERK and STAT pathways, which leads to c-Fos expression and AP-1-DNA binding, is involved in the process. The signaling requires tyrosine kinase and PKC but not COX-2.

Cells, Cultured↗
PubMed2004

Intrusion and reversal of a free-standing natural tooth bounded by two implant-supported prostheses: a clinical report.

Although intrusion of natural tooth abutments in tooth-implant connected fixed prostheses has been reported, it can also occur to a free-standing natural tooth bounded by implant prostheses. For the patient described in this article, intrusion was noted with a natural tooth bounded by 2 implant-supported prostheses 5 months after insertion of the prostheses. The intrusion was reversed completely after 5 months with appropriate management. The course of treatment and possible mechanisms of intrusion are provided.

Bicuspid↗
PubMed2004

Effectiveness of an educational program in reducing the incidence of wrong-site tooth extraction.

OBJECTIVES: The aim of the study was to investigate the effectiveness of an educational program on the reduction of the incidence of wrong-site tooth extraction at the outpatient department of a university hospital in Taiwan. STUDY DESIGN: Data collected from cases of wrong-site tooth extraction during 1996 to 1998 were used to develop a specific educational intervention that was implemented from 1999 to 2001. The annual incidence of erroneous extraction was compared between the preintervention and intervention periods. The factors contributing to wrong tooth extraction were also analyzed. RESULTS: The annual incidence rates of erroneous extraction from 1996 to 1998 were 0.026%, 0.025%, and 0.046%, respectively. During the intervention period from 1999 to 2001, wrong-site tooth extraction did not occur at the department. There was a significant difference in the incidence of erroneous extraction between the preintervention and intervention periods (P<.01). Cognitive failure was the most frequent form of active failure responsible for wrong-site tooth extraction, whereas communication and training were found to be major latent factors contributing to these errors. CONCLUSIONS: Our results suggest the effectiveness of an educational program comprising case-based materials, information feedback, and clinical guidelines in reducing the incidence of wrong-site tooth extraction.

Adolescent↗
PubMed2004

Intrusion of the overerupted upper left first and second molars by mini-implants with partial-fixed orthodontic appliances: a case report.

Overeruption of maxillary molar(s) because of loss of the opposing teeth creates occlusal interference and functional disturbances. To restore proper occlusion, intrusion of the overerupted molars becomes essential before reconstruction can be initiated. A plausible procedure is orthodontic intrusion, which demands calibrated anchorage support from intraoral multiunit teeth and from headgear wear. In this report, we present a simplified and localized version of the orthodontic appliances in conjunction with mini-implants to intrude the overerupted molars. The purpose of using implants as skeletal anchorage was to eliminate the need for patient compliance for headgear wear and to overcome the difficulty resulting from the shortage of anchor teeth. The results showed that the biological responses of the teeth and the surrounding bony structures to the intrusion appeared normal and acceptable. Furthermore, the periodontal health and vitality of the teeth were well maintained even after a one-year follow-up.

Adult↗
PubMed2004

The role of lipopolysaccharide in infectious bone resorption of periapical lesion.

BACKGROUND: The role of lipopolysaccharide (LPS) in periapical lesion-induced bone resorption was investigated. Polymyxin B (PMB), a specific inhibitor of LPS, was evaluated to treat the apical lesion. METHODS: Lipopolysaccharide isolated from two common endodontic pathogens, Fusobacterium nucleatum and Porphyromonas endodontalis, stimulated mouse macrophage (J774) to release interleukin-1alpha (IL-1 alpha) and tumor necrosis factor-alpha (TNF-alpha) in a time-dependent manner. RESULTS: Combination of LPS further enhanced the stimulation. PMB inhibited these effects significantly. LPS also stimulated matrix metalloproteinase-1 (MMP-1) gene expression in J774, whereas anti-IL-1 alpha and anti-TNF-alpha antibodies, as well as PMB, diminished this effect. A disease model of periapical lesion was established in Wistar rat. Administration of PMB reduced the extent of lesion-associated bone resorption by 76% to approximately 80%, and simultaneously reduced the numbers of MMP-1-producing macrophages. CONCLUSIONS: It is suggested that LPS released from the infected root canal triggers the synthesis of IL-1 alpha and TNF-alpha from macrophages. These pro-inflammatory cytokines up-regulate the production of MMP-1 by macrophages to promote periapical bone resorption.

Alveolar Bone Loss↗
PubMed2003

Nitric oxide promotes infectious bone resorption by enhancing cytokine-stimulated interstitial collagenase synthesis in osteoblasts.

This experiment was undertaken to determine the role of macrophage-derived nitric oxide (NO) in mediating lipopolysaccharide (LPS)-induced bone resorption by using an in vitro co-culture system and an in vivo model of infectious bone resorption. Our results demonstrated that LPS stimulated the expression of inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF)-a mRNAs and nitrite synthesis in the J774 mouse macrophage cell line but not in the UMR-106 (rat) and MC3T3-E1 (mouse) osteoblast cell lines. Conditioned media (CM) from LPS-stimulated J774 triggered only low to moderate levels of iNOS mRNAs in MC3T3-E1 and a trivial effect in UMR-106. On the other hand, CM induced matrix metalloproteinase-1 (MMP-1) gene expression in both osteoblast cell lines. The NOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA) did not alter this effect in MC3T3-E1 and UMR-106, whereas TNF-a antibody diminished the CM-induced MMP-1 gene expression in both cell lines. Interestingly, SNAP, a NO donor, although by itself is not a MMP-1 stimulator for UMR-106, augmented the TNF-alpha-stimulated MMP-1 mRNA production in UMR-106. In a J774/UMR-106 co-culture system, LPS stimulated significant MMP-1 gene expression in UMR-106, and this upregulation was abolished by L-NMMA and TNF-alpha antibodies. Immunohistochemical analysis in a rat model of infectious bone resorption (periapical lesion) showed co-distributions of iNOS+ macrophages and MMP-1+ osteoblasts around the osteolytic areas. Administration of L-NMMA markedly reduced the extent of bone loss and the percentage of MMP-1-synthesizing osteoblasts. These data suggest that NO derived from macrophages after LPS stimulation may enhance bone loss by augmenting the cytokine-induced MMP-1 production in osteoblasts.

3T3 Cells↗
PubMed2002

Prognostic role of p27(Kip1) expression in oral squamous cell carcinoma in Taiwan.

The cyclin-dependent kinase inhibitor p27(Kip1) can inhibit the G1 to S transition of the cell cycle and is a putative tumor suppressor. Decreased expression of p27(Kip1) protein has been correlated with poor prognosis in a variety of human tumors. We examined the expression of p27(Kip1) in oral squamous cell carcinoma (SCC), epithelial dysplasia (ED) and normal oral mucosa (NOM) using antibodies to p27(Kip1). Positive p27(Kip1) nuclear staining was detected in all the specimems from ED and NOM, whereas positive p27(Kip1) staining was observed in 16 of the 63 (25%) cases of oral SCC. The labeling index for p27(Kip1) protein was significantly reduced from NOM through ED to oral SCCs, indicating that changes of p27(Kip1) protein expression may be an early event in oral carcinogenesis in Taiwan. The Kaplan-Meier analysis showed patients with p27(Kip1)-positive tumors had significantly higher overall survival than those with p27(Kip1)-negative tumors in a total of 63 patients (P=0.015) and 47 patients with areca quid chewing habit (P=0.026). Multivariate analysis showed decreased p27(Kip1) protein expression was an independent significant predictor of poor overall survival in the patients with oral SCCs. These results indicate that p27(Kip1) protein expression may serve as a putative new adjuvant prognostic marker for routine assessment of oral SCC patients.

Adult↗
PubMed2002

Mutations of the adenomatous polyposis coli gene in areca quid and tobacco-associated oral squamous cell carcinomas in Taiwan.

BACKGROUND: Adenomatous polyposis coli (APC) gene mutations have been demonstrated not only in colorectal tumors but also in a variety of human cancers. METHODS: To elucidate the possible roles of APC gene mutations in oral squamous cell carcinomas (OSCCs), we examined 40 untreated human primary OSCCs using polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and DNA sequencing assays. RESULTS: By screening nearly one-half of the coding region (codons 279-1673, including the MCR) of the APC gene, five missense mutations and a 1-base pair deletion were detected in five (12.5%) tumors, resulting in five amino-acid substitutions or a truncation of the APC protein. All patients with APC mutations were both areca quid chewers and tobacco smokers (P = 0.049). CONCLUSIONS: These results suggest that APC mutations may also contribute to the carcinogenesis of at least some OSCCs in Taiwan, especially for the users of areca quid and tobacco.

Adenomatous Polyposis Coli Protein↗
PubMed2002

Prognostic role of p21WAF1 expression in areca quid chewing and smoking-associated oral squamous cell carcinoma in Taiwan.

BACKGROUND: Alterations in p21WAF1 protein expression have been observed in a wide variety of human cancers by immunohistochemistry, and both decreased and increased levels of p21WAF1 protein expression have been shown to correlate with poor prognosis. METHOD: To examine the relation between p21WAF1 protein expression and prognosis in oral squamous cell carcinomas (SCCs), we performed an immunohistochemical study with antip21WAF1 antibody on 43 oral SCCs. Immunostaining results were then correlated with p53 protein levels, clinicopathological parameters of the tumors and overall patient survival. RESULTS: Of the 43 patients, 31 (72%) had tumors with positive p21WAF1 nuclear staining and 27 (63%) had tumors with p53 nuclear staining. There was no significant correlation between p21WAF1 and p53 protein expressions and both mutant p53-containing oral SCCs overexpressed p21WAF1 protein. In addition, no significant correlation was found between the p21WAF1 expression and the patients' age, sex, oral habit, cancer location, or primary tumor TNM status at the time of initial presentation. The Kaplan-Meier analysis showed a significant correlation between p21WAF1 protein overexpression and poor patient overall survival (P = 0.049). When p53 and p21WAF1 were evaluated together, the 5-year overall survival was lowest in p53(+)-p21WAF1(+) patients and highest in p53(-)-p21WAF1(-) patients (P = 0.057). CONCLUSION: Combined evaluation of p21WAF1 and p53 expressions may be useful in estimating the prognosis of patients with oral SCCs in Taiwan.

Adult↗