scholarly journals ASSESSMENT OF SERUM TOTAL SIALIC ACID AND LIPID BOUND SIALIC ACID LEVELS IN PATIENTS WITH LEUKOPLAKIAAND ORAL SQUAMOUS CELL CARCINOMA-A CASE CONTROL STUDY

2020 ◽  
pp. 1-3
Author(s):  
Daneshwari Koshti

Background and objectives: Oral cancer (OC) is the eleventh most common cancer worldwide. The reason for high prevalence of Oral cancer in India is primarily attributed to tobacco consumption in the form of gutkha, quid, snuff or misri. The most common diagnostic method is biopsy followed by analysis of serum and saliva that are an effective approach for screening and monitoring the patients. Tumor markers are substances which change quantitatively in serum during tumor development. Various tumor markers are identified in oral cancer, one such tumor marker is sialic acid. The objective of the study was to evaluate clinical value of circulatory levels of total and lipid bound sialic acid for the early diagnosis and management of OC. Method: A total of 90 patients were included in the study were further divided into three groups with 30 subjects each. Group 1 - leukoplakia. Group 2- oral squamous cell carcinoma(OSCC). Group 3- healthy age and sex matched individuals. All the three groups were subjected to determination of Serum total and lipid bound sialic acid. Statistical analysis was done using Student t- test, One way ANOVAwas used to compare between the three groups. Multi variate analysis was performed to determine the alterations in TSAand LSAlevels. Results Mean value of serum TSA in Group 1 - 53.18±9.03 mg/dl ,Group 2 -91.58±19.26 mg/dl Group 3 -36.74±5.94 mg/dl. Mean value of serum LSA in Group 1-19.50±3.87 mg/dl , Group 2-33.64±8.05mg/dl, Group 3-14.10±2.86 mg/dl Mean value of serum TSAand LSAin OSCC were significantly higher than leukoplakia and control group (P=0.0001). When multivariate analysis was done it was observed that there is progressive rise in TSAand LSA Conclusion: In the present study there were significant elevations in sialic acid levels in OSCC. This finding can be used as adjunct diagnostic marker in head and neck cancer

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 15070-15070
Author(s):  
N. P. Rizk ◽  
L. Tang ◽  
B. J. Park ◽  
R. Flores ◽  
E. Venkatraman ◽  
...  

15070 Background: Our recent analyses (JCO, in press) showed that residual nodal disease but not T-stage predicted survival after chemo-radiotherapy (CRT) and surgery for esophageal adenocarcinoma (AC). In this study, we investigated prognostic factors for esophageal squamous cell carcinoma (SCC) after CRT. Methods: Retrospective review of patients with esophageal SCC who had CRT and esophagectomy. Data collected: demographics, CRT details, pathologic findings, and survival. Statistical methods included recursive partitioning (RP) and Kaplan-Meier (KM) analyses. Results: Patients included in the study were treated between 1/1996 and 2/2006. Follow up was thru 5/06. 91 patients were appropriate for analysis. There were 56 men (61.5%) and 35 women (38.5%). 72 (79.1%) patients had clinical regional disease prior to treatment, while the rest had locally advanced disease. Median radiation dose was 5040 cGy, and 78 (85.7%) patients received cisplatin based chemotherapy. 49 (53.8%) patients had a complete local pathologic response (pCR), including 10/91 (10.9%) who had a pCR with residual nodal disease. 42 (46.2%) patients had residual local disease. RP analysis identified 3 prognostic groups: a) Group 1 (n=52), patients with minimal residual local disease (pCR & T1- regardless of nodal status), b) Group 2 (n=28), patients with residual T2 disease (N0 and N1) as well as patients with T3–4N0 disease, and c) Group 3 (n=11), patients with residual T3–4N1 disease. 3-year survival by KM analysis was 68.4% in group 1, 45.6% in group 2, and 0 % in group 3 (p<0.001). Conclusions: Unlike adenocarcinoma of the esophagus where residual nodal disease after CRT is the most significant predictor of survival, in SCC of the esophagus, the presence of minimal residual local disease after CRT, regardless of nodal status, predicts the best survival. The implications of these findings might include establishing different endpoints to assess response to treatment and prognostic criteria. No significant financial relationships to disclose.


2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e14597-e14597
Author(s):  
Luis Carlos Moreira Antunes ◽  
Antonio de Barros Lopes ◽  
Luisa Silva Pacheco ◽  
Patricia Chaves Brites ◽  
Leandro Bizarro Muller ◽  
...  

e14597 Background: The highest rates of esophageal cancer in Brazil occur in Rio Grande do Sul (18/100,000/year for men and 6/100,000/year for women). Furthermore, the incidence of head and neck squamous cell carcinoma (HNSCC) is significant in this region (11/100,000/year for cancer of the oral cavity and 10/100,000/year for laryngeal cancer in men). Tobacco smoking and alcohol consumption are the major risk factors for esophageal squamous cell carcinoma (ESCC) and HNSCC. The role of HPV in the development of ESCC remains controversial. Otherwise, there are some evidence that HPV-related HNSCC is a distinct entity compared with HNSCC associated with smoking and alcohol consumption. Methods: In order to investigate the association of HPV infection with ESCC and HNSCC in smokers/alcoholics in southern Brazil, we evaluated, prospectively, samples from three groups. Group 1 was formed by patients with ESCC where we evaluated esophageal samples from tumor and from non-tumoral areas. Group 2 was formed by HNSCC patients. We assessed biopsies from primary tumor and esophageal biopsies from either iodine negative or positive areas. Group 3 was formed by dyspeptic patients, no smokers/non alcoholics, with normal appearing esophageal mucosa in Upper GI Endoscopy. Biopsies were taken from middle esophagus. With extreme care to prevent DNA contamination, we used nested PCR with the general primer sets MY09/11 and GP5/GP6 for HPV L1 in formalin fixed paraffin-embedded tissue. We planned to genotype the final PCR product for 73 HPV types. Results: Group 1 included 48 samples from ESCC and 48 samples of esophageal non-tumoral areas. In Group 2, there were 37 patients with 35 biopsies taken from primary tumor, 32 from iodine positive esophageal areas and 17 from unstained esophageal areas (15 normal and 2 esophagitis). In this group, 1 patient had synchronous tumors of HNSCC and ESCC. Group 3 included 37 patients, 35 with normal esophageal mucosa and 2 with mild esophagitis. HPV DNA was negative in all samples. Therefore, we did not carry out the genotyping. Conclusions: In smokers/alcoholics patients from Southern Brazil, there is no evidence that HPV is involved in upper aerodigestive carcinogenesis.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e15083-e15083
Author(s):  
Luis Carlos Moreira Antunes ◽  
Antonio de Barros Lopes ◽  
Leandro Bizarro Muller ◽  
Renato Borges Fagundes

e15083 Background: The highest rates of esophageal cancer in Brazil occur in Rio Grande do Sul (18/100,000/year for men), where squamous cell carcinoma is the most common. Furthermore, the incidence of head and neck squamous cell carcinoma (HNSCC) is significant in this region (11/100,000/year for cancer of the oral cavity and 10/100,000/year for laryngeal cancer in men). Tobacco smoking and alcohol consumption are the major risk factors for esophageal squamous cell carcinoma (ESCC) and HNSCC. The role of HPV in the development of ESCC remains controversial. Otherwise, there is some evidence that HPV-related HNSCC is a distinct entity compared with HNSCC associated with smoking and alcohol consumption. Methods: Polymerase chain reaction (PCR) was used to evaluate the presence of HPV from 218 samples from three groups of patients. Group 1 comprised 51 patients with ESCC who underwent esophagectomy, in which two samples from each patient were analyzed: one tumor sample and another from normal esophageal mucosa. Group 2 comprised 37 patients with HNSCC who underwent Lugol chromoendoscopy. In this group, we took biopsies from the primary tumor and from esophageal mucosa (unstained areas and middle esophagus when the esophageal mucosa was evenly stained). Thirty-seven dyspeptic patients, non-smokers and without alcohol consumption who underwent endoscopy, comprised Group 3, in which we took one biopsy from middle esophagus. All samples were fixed in formalin and stored in paraffin blocks. Nested-PCR with MY09/11 and GP5/6 primers was used to detect HPV L1 in those samples. Results: Of a total of 224 samples fixed in formalin and stored in paraffin, only 6 samples had insufficient material for PCR analysis: one sample from normal distal epithelium in Group 1, one sample from a stained area and 2 samples from unstained areas in Group 2 and 2 samples from normal esophageal mucosa in Group 3. PCR was positive for one of conserved genes GAPDH, G3PDH or B-globin in 218 samples, showing that DNA was adequate for analysis. The PCR results were negative for HPV DNA in all esophageal samples, as well as in all biopsies from the primary tumor of HNSCC. Conclusions: There is no evidence that HPV is involved in carcinogenesis of the upper aerodigestive tract in southern Brazil.


2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 47-47
Author(s):  
Luis Carlos Moreira Antunes ◽  
Leandro Bizarro Muller ◽  
Antonio de Barros Lopes ◽  
Renato Borges Fagundes

47 Background: The highest rates of esophageal cancer in Brazil occur in Rio Grande do Sul (18/100,000/year for men), where squamous cell carcinoma is the most common. Furthermore, the incidence of head and neck squamous cell carcinoma (HNSCC) is significant in this region (11/100,000/year for cancer of the oral cavity and 10/100,000/year for laryngeal cancer in men). Tobacco smoking and alcohol consumption are the major risk factors for esophageal squamous cell carcinoma (ESCC) and HNSCC. The role of HPV in the development of ESCC remains controversial. Otherwise, there are some evidence that HPV-related HNSCC is a distinct entity compared with HNSCC associated with smoking and alcohol consumption. Methods: Polymerase chain reaction (PCR) was used to evaluate the presence of Human Papillomavirus from 218 samples from three groups of patients. Group 1 comprised 51 patients with ESCC who underwent esophagectomy, in which two samples from each patient were analyzed: one sample of the tumor and another of normal esophageal mucosa distant from the tumor. Group 2 comprised 37 patients with HNSCC who underwent Lugol chromoendoscopy. In this group, samples were analyzed from the primary tumor, the stained areas of mucosa from the middle esophagus, and, when present, discolored and tumoral areas of the esophageal mucosa. Thirty-seven dyspeptic patients, not exposed to smoking or alcohol consumption, comprised Group 3, in which one sample per patient of mucosa with normal appearance from the middle esophagus was evaluated. Nested-PCR with MY09/11 and GP5/6 L1 primers was used to detect HPV L1 in samples fixed in formalin and stored in paraffin blocks. Results: Of a total of 224 samples fixed in formalin and stored in paraffin, only 6 samples had insufficient material for PCR analysis: one sample from normal distal epithelium in Group 1, one sample from a stained area and 2 samples from unstained areas in Group 2 and two samples from normal esophageal mucosa in Group 3. PCR was positive for one of conserved genes GAPDH, G3PDH or B-globin and negative for HPV DNA in all the 118 samples tested. Conclusions: There is no evidence that HPV is involved in carcinogenesis of the upper aerodigestive tract in southern Brazil.


2021 ◽  
Vol 30 (1) ◽  
pp. 29-33
Author(s):  
Nazish Fatima ◽  
◽  
Sidra Mohiuddin ◽  
Salim Hosein ◽  
Mervyn Hosein

OBJECTIVE: To determine the association among betel nut, betel quid or smoking alone, and betel quid combined with smoking in subjects reporting with oral sub mucous fibrosis, oral submucous fibrosis with malignant transformation in to cancer and oral squamous cell carcinoma. METHODOLOGY: An analytical cross sectional, multi centric study of n = 1009 cases collected through non-probability convenience sampling. These n=1009 subjects were subdivided into four groups: group 1, who consumed areca nut only; group 2, who chewed betel quid along with areca nut; group 3, who used betel quid and smoked; and group 4, who had no chewing habits history but were smokers. These changes were further confirmed with the help of biopsy reports of the subjects with OSMFCa and OSCC. Chi square test was performed to find out association of chewing habits with the progression of disease state. Level of significance was kept at p<0.05. RESULTS: The mean age of the sample (n=1009) were 42.79±1.31 years (range: 10-70 years). Statistically significant difference was (p<0.00) found among all four groups in terms of initiation, propagation and progression of oral squamous cell carcinoma. Furthermore, statistically insignificant difference (p=0.40) was found between group 2 and group 3 as similar number of cases (OSCC) was seen among them. CONCLUSION: Current study concluded that patients who have combined habits of chewing betel quid with areca nut and betel quid with smoking were at highest risk of initiation and progression of oral cancer. However, smoking cigarettes alone was the weakest risk factor. KEYWORDS: Betel quid; Areca nut; Smoking; Oral squamous cell carcinoma, Oral submucous fibrosis HOW TO CITE: Fatima N, Mohiuddin S, Hosein S, Hosein M. Association of carcinogenic oral habits with oral squamous cell carcinoma. J Pak Dent Assoc 2021;30(1):29-33.


2013 ◽  
Vol 3 (5) ◽  
pp. 379-385
Author(s):  
S Dahal ◽  
K Bozaz ◽  
N Srikant ◽  
K Reshma ◽  
N Agrawal

Background: Carcinogens and co-carcinogens act in an additive, synergistic and antagonistic manner. Tobacco is the most common carcinogen related to oral cancer. The aim of this study was to assess the effect of tobacco on the oral epithelium by evaluating genotoxic damage to cells as quantitated by micronuclei and also the alterations to the cell membrane were correlated by the measurement of free sialic acid and protein-bound sialic acid in saliva and in serum. Materials and Methods: Blood samples collected from 15 untreated oral squamous cell carcinoma patients, 15 patients with oral precancerous conditions, 15 tobacco chewers without clinically evident lesion and 15 non-tobacco chewers. Serum and salivary sialic acid levels both in free and bound form were measured spectrophotometrically. Smear was taken from the same patient from the suspicious site and assessment of micronuclei was done by acridine orange method. Results: Serum free sialic acid and micronuclei assessment showed greater level of signifi cance (P=?0.05) between all other groups. This implies it’s potential use as an indicator of oral cancer. Predictability of occurrence of oral Cancer = 0.561+ 0.005× serum protein-bound sialic acid+ 0.244 serum free sialic acid + 0.71 M, where M=mean of micronuclei in 500 exfoliated oral cells. Predictability of occurrence of oral Premalignancy = 0.13+ 0.909× serum free sialic acid+ 0.045 M, where M=mean of micronuclei in 500 exfoliated oral cells. Conclusion: Micronuclei, serum and salivary sialic acid levels may be a good marker for prediction of premalignancy and oral squamous cell carcinoma transformation. Journal of Pathology of Nepal (2013) Vol. 3, No.1, Issue 5, 379-385 DOI: http://dx.doi.org/10.3126/jpn.v3i5.7862


2012 ◽  
Vol 13 (3) ◽  
pp. 339-344 ◽  
Author(s):  
MD Prasanna ◽  
K Shailaja Yadav ◽  
Sudhir Gonuguntla ◽  
Surekha Reddy Velidandla ◽  
CR Charan Reddy ◽  
...  

ABSTRACT Mitotic counting is often used for classification, grading and prognosis of tumors. The count usually stands as a decision point for treatment as well. The easiest way of counting the number of mitoses is done by screening routine H&E stained slides. However, for proper mitotic counting, certain strict protocols should be taken into consideration. This study on 30 cases of different grades of oral squamous cell carcinoma was undertaken to determine the interobserver variations in two different groups: Group1 (A1, A2), who were given certain criteria to be followed during the counting of the mitotic figures and group 2 investigators (B1, B2) who were unaware of such criteria. The paired t-test gives a correlation of 0.988 and a significant difference of 0.000 between the two investigators in group 1. The correlation was 0.650 with a significant difference of 0.058 between two investigators in-group 2, indicating that group 1 observers exhibit good interobserver agreement. The results emphasize that following of strict protocols are of great help in determining the accuracy of mitotic counting. How to cite this article Yadav KS, Gonuguntla S, Ealla KKR, Velidandla SR, Reddy CRC, Prasanna MD, Bommu SR. Assessment of Interobserver Variability in Mitotic Figure Counting in Different Histological Grades of Oral Squamous Cell Carcinoma. J Contemp Dent Pract 2012;13(3):339-344.


Author(s):  
Mehwish Feroz Ali

Oral cancer, the most challenging and life threatening disease in the field of dentistry, may start as a reactive lesion due to constant stimulus from tobacco consumption, transform into a pre-malignant lesion (dysplastic lesion) and ultimately develop into a cancerous lesion (Invasive carcinoma). There is a fundamental revolution taking place in the analyzing methods; extraction of biological protein from the saliva rather than from tissues or blood. Several of the biomarkers have been studied with pro-carcinogenic effects like Interleukins (ILs), tumor necrosis factor (TNF) and leptin, but only a few have been stated in the literature, which show anti-cancer characteristics like adiponectin and zinc alpha-2 glycoprotein. This review explored the diagnostic and prognostic values of a biomarkers zinc alpha-2 glycoprotein (ZAG) in adults suspected of oral squamous cell carcinoma (OSCC). The PubMed, EMBASE and Google Scholar were searched for scientific studies reported on the potential mechanism of zinc alpha-2 glycoprotein. All the research articles were selected in which ZAG is applied solely or in conjunction with other biomarkers in oral cancer and other cancers. These literatures were carefully assessed to find out and compile the diagnostic and prognostic values and to inquire therapeutic action of ZAG in the process of carcinogenesis.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Wen Chen ◽  
Chenzhou Wu ◽  
Yafei Chen ◽  
Yuhao Guo ◽  
Ling Qiu ◽  
...  

AbstractC18 ceramide plays an important role in the occurrence and development of oral squamous cell carcinoma. However, the function of ceramide synthase 1, a key enzyme in C18 ceramide synthesis, in oral squamous cell carcinoma is still unclear. The aim of our study was to investigate the relationship between ceramide synthase 1 and oral cancer. In this study, we found that the expression of ceramide synthase 1 was downregulated in oral cancer tissues and cell lines. In a mouse oral squamous cell carcinoma model induced by 4-nitroquinolin-1-oxide, ceramide synthase 1 knockout was associated with the severity of oral malignant transformation. Immunohistochemical studies showed significant upregulation of PCNA, MMP2, MMP9, and BCL2 expression and downregulation of BAX expression in the pathological hyperplastic area. In addition, ceramide synthase 1 knockdown promoted cell proliferation, migration, and invasion in vitro. Overexpression of CERS1 obtained the opposite effect. Ceramide synthase 1 knockdown caused endoplasmic reticulum stress and induced the VEGFA upregulation. Activating transcription factor 4 is responsible for ceramide synthase 1 knockdown caused VEGFA transcriptional upregulation. In addition, mild endoplasmic reticulum stress caused by ceramide synthase 1 knockdown could induce cisplatin resistance. Taken together, our study suggests that ceramide synthase 1 is downregulated in oral cancer and promotes the aggressiveness of oral squamous cell carcinoma and chemotherapeutic drug resistance.


2013 ◽  
Vol 420 ◽  
pp. 45-53 ◽  
Author(s):  
Yi-Ting Chen ◽  
Yi-Min Chong ◽  
Chu-Wen Cheng ◽  
Chung-Liang Ho ◽  
Hung-Wen Tsai ◽  
...  

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