Journal of Cancer Research and Treatment
ISSN (Print): 2374-1996 ISSN (Online): 2374-2003 Website: https://www.sciepub.com/journal/jcrt Editor-in-chief: Jean Rommelaere
Open Access
Journal Browser
Go
Journal of Cancer Research and Treatment. 2014, 2(1), 10-15
DOI: 10.12691/jcrt-2-1-3
Open AccessArticle

Study of p53, Pcna, Ki67 and Micronuclei Related to Genotoxic Damage for Risk Categorization in Pre-Malignant Oral Lesions

Asoke Roy1, , Satyendra Prakash Bhatnagar2, Malay Chatterjee3, Dipanwita Ghosh1, Goutam Mandal4, Shyamsundar Mondal5 and Shyamal Goswami6

1Department of Pathology and Cervical Screening, Chittaranjan National Cancer Institute, Kolkata, India

2Department of Pharmaceutical Sciences, Birla Institute of Technology, Mesra, Ranchi, India

3Department of Pharmaceutical Technology, Jadavpur University, Kolkata, India

4Department of Pathology, Hospital wing, Chittaranjan National Cancer Institute, Kolkata, India

5Department of Statistics and Records, Chittaranjan National Cancer Institute, Kolkata, India

6Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute, Kolkata, India

Pub. Date: January 03, 2014

Cite this paper:
Asoke Roy, Satyendra Prakash Bhatnagar, Malay Chatterjee, Dipanwita Ghosh, Goutam Mandal, Shyamsundar Mondal and Shyamal Goswami. Study of p53, Pcna, Ki67 and Micronuclei Related to Genotoxic Damage for Risk Categorization in Pre-Malignant Oral Lesions. Journal of Cancer Research and Treatment. 2014; 2(1):10-15. doi: 10.12691/jcrt-2-1-3

Abstract

In this prospective study, search for high risk cases of premalignant oral lesions were attempted through evaluation of oncoprotein expression, cell proliferation and micronuclei. Materials and methods: A total 50 cases of oral leukoplakia were diagnosed and adequate controls along with detailed history were included in this study. Study of tumour markers like p53, PCNA and Ki-67 were done immunohistochemically on tissue sections. Study of micronuclei was performed by feulgen staining method. Results: The mean age of the 50 cases were 44.48 ± 9.76 and median age was 50 years. There were 45 male cases (90%) and 5 female cases (10%). There were 26 non dysplastic (52%) and 24 dysplastic cases (48%). The smokers consist of 25 cases (50%) and other addictions (betel quid chewers, ghutka, khaini, alcohol etc.) had 24 cases (48%) and 1 case was non addict (2%). Out of 25 cases of smokers, 20 (80%) were positive in case of p53, 19 (76%) were positive in case of PCNA and 17 (68%) were positive in case of Ki67. Out of 24 cases of other addictions, 16 (66.67%) cases were positive in case of p53, 13 (54.17%) positive cases in case of PCNA and16 cases (66.67%) were positive in case of Ki67.The smokers had 0.51 ± 0.21 micronuclei frequency whereas other addiction groups had 0.24 ± 0.10. Conclusion: The histopathological risk assessment of these cases is inconclusive and thus p53, PCNA, Ki67 and micronuclei evaluation are needed for risk categorization.

Keywords:
oral leukoplakia oral squamous cell carcinoma immunohistochemistry molecular-markers p53 PCNA Ki67 micronuclei epithelial dysplasia

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Figures

Figure of 7

References:

[1]  Massano, J., Regateiro, F.S., Januario, G., et al., “Oral squamous cell carcinoma: Review of prognostic and predictive factors”, Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 102, 67-76, 2006.
 
[2]  Acha, A., Ruesga, M.T., Rodríguez, M.J., Martínez-Pancorbo, M.A., Aguirre, J.M, “Applications of the oral scraped (exfoliative) cytology in oral cancer and pre cancer”, Med Oral Patol Oral Cir Bucal, 10, 95-102, 2005.
 
[3]  Fedele, S., “Diagnostic aids in the screening of oral cancer”, Head Neck Oncol, 30, 1-5, 2009.
 
[4]  Scully, C., “Oral precancer: prevention and medical approach to management”, Eur J Cancer Oral Oncol, 31, 16-26, 1995.
 
[5]  Schepman, K., Van der Meji, E.H., Smeele, L., Vander Wall I., “Concomitant leukoplakia in patients with oral squamous cell carcinoma”, Oral Dis, 5, 206-209, 1999.
 
[6]  Lee, J.J., Hong, W.K, Hittelman, W.N., Lotan, L.R., Shin, D.M. et al, “Predicting cancer development in oral leukoplakia: ten years of translational research”, Clin Cancer Res, 6, 1702, 2000.
 
[7]  Silverman, S., Gorsky, M., Lozada, F., “Oral leukoplakia and malignant transformation. A follow up study of 257 patients”, Cancer, 53, 563-568, 1984.
 
[8]  Kim, J., M,Adel-el-Naggar, D., Lee, J.S., Corrales, C., Lippman, S.S., Hong, W.K. and Hittleman, W.N., “ Chromosome polysomy and Histological Characteristics in oral premalignant Lesions”, Cancer epidemiology, Biomarkers and Prevention, 10, 319-325, 2001.
 
[9]  Dietrich, T., Reichart, P.A., Scheifele, C. “Clinical risk factors of oral leukoplakia in a representative sample of the US population”, Oral Oncol, 40, 158-63, 2004.
 
[10]  Hollstein, M., Sidransky, D., Vogelstein, B., et al, “p53 mutations in human cancer”, Science, 253, 49-53, 1991.
 
[11]  Bancroft, J.D., Gamble, M., Theory and Practice of Histological Techniques. Sixth Edition: Elsevier Health Sciences. 2008.
 
[12]  Dellis, D., Sternberger, L.A., Mann, R.B. et al., “Immunoperoxidase techniques in diagnostics pathology”, American Journal of clinical pathology, 71, 483-8, 1979.
 
[13]  Raju, B., Mehrotra, R., Oijordsbakken, G. et al., “Expression of p53, CyclinD1 and Ki 67 in pre-malignant and malignant oral lesions: associated with clinic pathological parameters”, Anti cancer, 25, 4699-706, 2005.
 
[14]  Feulgen,. R, Rossenbeck, H., “Mikrosko pisch chemische Nachweeissliner Nukleinsoure vom Typus Thymonucleinsaure und die daranf beruhende elektive Farbung Von Zellkemen in mikroskopischen praparaten”, Hoppe-Seylers Zeitschrift Physiol Chemie, 135, 203-48, 1924.
 
[15]  Millet, J.A., Husain, O.A., Bitensky, L., et al., “Fuelgen–hydrolysis profiles in cells exfoliated from the cervix uteri: a potential aid in diagnosis of malignancy”, J Clin Pathol, 35, 345-49, 1982.
 
[16]  Kumar, V., Rao, N.N., Nair, N.S., “Micronuclei in oral squamous cell carcinoma: A marker of genotoxic damage”, Indian J Dent Res, 11, 101-6, 2000.
 
[17]  Sarto, F., Finotto, S., Giacomelli, L., Mazzotti, D., Tomanin, R., Levis, A.G., “The micronucleus assay in exfoliated cells of the human buccal mucosa”, Mutagenesis, 2, 11-7, 1987.
 
[18]  Squamous Cell Cancer of the Neck–Cambridge University Press, Edited by Robert Herman, University Hospital Leuven, Belgium. 2008.
 
[19]  Napier, S.S., Speight, P.M., “Natural history of potentially malignant oral lesions and conditions: an overview of the literature”, J. Oral Pathol Med, 1, 1-10, 2008.
 
[20]  Taya, Y., “p53 and the RB protein connected by Cdk–inhibitory proteins”, Jikken Fgaku, 13, 17-18, 1995.
 
[21]  Kirsch, D.G., Kastan, M.B., “Tumour suppressor p53: implications for tumour development and prognosis”, J. clin. Oncol,; 16, 3158-3168, 1998.
 
[22]  Sinicrope, F., Ruan, S., Cleary, R., et al., “bcl-2 and p53 oncoprotein during colorectal tumerogenesis”, Cancer Research, 55, 237-41, 1995.
 
[23]  Mazars, R., Pujel, P., Mondiondi, P. et al., “p53 mutations in ovarian cancer, a late event?” , Oncoprotein, 6(9), 1685-1690, 1991.
 
[24]  Kyritisis, A.P., Bondy, M.L,, Hess, K.R. et al., “Prognostic Significance of p53 immunoreactivity in patients with glioma”, Clin Cancer Res, 1, 1617-22, 1995.
 
[25]  Schlüter, C., Duchrow, M., Wohlenberg, C., Becker, M.H., Key, G., Flad, H.D., et al., “The cell proliferation- associated antigen of antibody Ki-67: a very large, ubiquitous nuclear protein with numerous repeated elements, representing a new kind of cell cycle-maintaining proteins”, J Cell Bio, 123, 513-22, 1993.
 
[26]  Risio, M., Lizza, S.C., Ferrari, A., Candeleresi, G.L. and Rossini,F.P., “Immunohistochemical study of epithelial cell proliferation in hyperplastic polyps, adenomas and adenocarcinomas of the large bowel”, Gastroenterology, 94,899-906, 1988.
 
[27]  Rahmanzadeh, R., Hüttmann, G., Gerdes, J., Scholzen, T.,“Chromophore-assisted light inactivation of pKi-67 leads to inhibition of ribosomal RNA synthesis”, Cell Prolif, 40(3), 422-30, 2007.
 
[28]  Steinbeck, R.G., Heselmeyer, K.M., Moberzer, H.B. et al., “The relationship between Proliferating Cell Nuclear Antigen (PCNA), nuclear DNA content and mutant p53 during genesis of cervical carcinoma”, Acta Oncol, 34 (2), 171-6, 1995.
 
[29]  Yamamoto, H., Yamada, N., Asano, G., et al., “Morphological atypis and clinicopathological factors in colorectal adenoma and cancer using nuclear DNA content, p53 and PCNA”, Nippon Geka Gakkai Zasshi,; 95, 763-74, 1994.
 
[30]  Speight, P.M., “Update on Oral Epithelial Dysplasia and Progression to Cancer”, Head Neck Pathol,, 1(1), 61-66, 2007.