p53 Polymorphism in Oral Lichen Planus
A comprehensive review
Keywords:
Oral lichen planus (OLP), gene p53, PolymorphismAbstract
Oral lichen planus (OLP) is a chronic relapsing inflammatory disease. It involves T-lymphocyte aggression targeted to the basal layer of the oral mucosa.p53 plays a central role in the prevention of normal cells from the development of the malignant phenotype. Somatic alterations in p53 cause defects in normal p53 function. Wild type p53 plays an important role in repairable damage of the cell due to cellular stresses. Over-expression, as well as polymorphic variants of Mouse double minute 2(MDM2), have effects on p53 disturbances. In addition, degradation of p53 by E6 protein of high-risk human papillomavirus is also suggested as one of the mechanisms which attenuate p53 responses in oral carcinogenesis. Polymorphisms in p53 are anticipated to cause measurable disturbance in p53 function. Polymorphism of the codon 72 on exon 4 of the gene p53 is the first and most commonly known polymorphism of this gene. The presence of p53 has been demonstrated as an early marker of dysplasia in Oral Potentially Malignant Disorders. This review discusses about p53 polymorphism as an early indicator of genetic predisposition to neoplastic transformation in OLP.
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A. Bisso, L. Collavin, and G. Del Sal, “p73 as a pharmaceutical target for cancer therapy,” Current Pharmaceutical Design.2011;11: 578–590.
Abbas AK, Lichtman AH. Cellular and Molecular Immunology. 5th edition. chapter 15. Philadelphia, Pa, USA: WB Saunders; 2004. pp. 345–366.
Acay RR, Felizzola CR, de Araújo N, de Sousa SO. Evaluation of proliferative potential in oral lichen planus and oral lichenoid lesions using immunohistochemical expression of p53 and Ki67. Oral Oncol 2006;42:475‐80.
Gonzalez‐Moles MA, Gil‐Montoya JA, Ruiz‐Avila I, Esteban F, Bascones‐Martinez A. Differences in the expression of p53 protein in oral lichen planus based on the use of monoclonal antibodies DO7 and pAb 240. Oral Oncol 2008;44:496‐503.
Alamsyah, T., Marianthi, D., Hayati, W., & Usrina, N. (2021). Drug user behavior about the development and rehabilitation process in Banda Aceh correctional institution. International Journal of Health & Medical Sciences, 4(1), 88-94. https://doi.org/10.31295/ijhms.v4n1.1348
Arirachakaran P, Chansaengroj J, Lurchachaiwong W, Kanjanabud P, Thongprasom K, Poovorawan Y. Oral lichen planus in thai patients has a low prevalence of human papillomavirus. ISRN Dent 2013.
Azzam GA, Frank AK, Hollstein M, et al. Tissue-specific apoptotic effects of the p53 codon 72 polymorphism in a mouse model. Cell Cycle 2011; 10: 1352–5.
Beckman G, Birgander R, Sjalander A, Saha N, Holmberg PA, Kivela A Beckman L: Is p53 polymorphism maintained by natural selection? Hum Hered 44: 266–270, 1994
Bonafe M, Salvioli S, Barbi C, Mishto M, Trapassi C, Gemelli C et al. p53 codon 72 genotype affects apoptosis by cytosine arabinoside in blood leukocytes. Biochem Biophys Res Commun,2002;299: 539-41.
Bond GL, Hu W, Bond EE, et al. A single nucleotide polymorphism in the MDM2 promoter attenuates the p53 tumour suppressor pathway and accelerates tumor formation in humans. Cell 2004; 119: 591–602.
C. Prives and P. A. Hall, “The P53 pathway,” Journal of Pathology 1999;187:112–126.
Choi S, Myers JN. Molecular pathogenesis of oral squamous cell carcinoma: implications for therapy. J Dent Res 2008; 87: 14–32.
de Villiers EM, Gunst K. Characterization of seven novel human papillomavirus types isolated from cutaneous tissue, but also present in mucosal lesions. J Gen Virol 2009;90:1999‐2004.
Debanth S, Singh PA, Mehrotra R, Singh M, Gupta SC, Pandya S, et al. Human papillomavirus infection and premalignant lesions of the oral
cavity: A cross‐sectional study in Allahabad, North India. Asia Pac J Clin Oncol 2009;5:111‐8.
Dumont P, Leu JI, Della Pietra AC 3rd, George DL, Murphy M. The codon 72 polymorphic variants of p53 have markedly different apoptotic potential. Nat Genet. 2003 Mar;33(3):357-65.
Ebrahimi M, Boldrup L, Coates PJ, Wahlin YB, Bourdon JC, Nylander K. Expression of novel p53 isoforms in oral lichen planus. Oral Oncol 2008;44:156-161.
Field JK, Spandidos DA, Malliri A, Gosney JR, Yiagnisis M, Stell PM. Elevated P53 expression correlates with the history of heavy smoking in squamous cell carcinoma of the head and neck. Br J Cancer 1991;64:573-77.
Freed-Pastor WA, Prives C. Mutant p53: one name, many proteins. Genes Dev 2012; 26: 1268–86.
Ghabanchi J, Fattahi MJ, Mardani M, Tadbir AA, Paydar AA. Polymorphism of tumor protein p53 codon 72 showed no association with oral lichen planus in Shiraz, Iran. J Cra- niofac Surg 2009;20:2168-70.
Girod SC. Tumour suppressor genes and cell proliferation control in the carcinogenesis of the oral mucosa. Quintessenz Verlags.221-23.
González‐Moles MA, Bascones‐Ilundain C, Gil Montoya JA, Ruiz‐Avila I, Delgado‐Rodríguez M, Bascones‐Martínez A, et al. Cell cycle regulating mechanisms in oral lichen planus: Molecular bases in epithelium predisposed to malignant transformation. Arch Oral Biol 2006;51:1093‐103.
Hrstka R, Coates PJ, Vojtesek B. Polymorphisms in p53 and the p53 pathway: roles in cancer susceptibility and response to treatment. J Cell Mol Med 2009; 13: 440–53.
Hu Z, Li C, Chen K, et al. Single nucleotide polymorphisms in selected apoptotic genes and BPDE-induced apoptotic capacity in apparently normal primary lymphocytes: a genotype-phenotype correlation analysis. J Cancer Epidemiol 2008:1-8.
K. H. Vousden, X. Lu, “Live or let die: the cell’s response to p53,” Nature Reviews Cancer 2002;2: 594–604.
Katiyar S, Thelma B K, N.S Murthy, Hedau Suresh, Jain N, Gopal Krishna V et al. Molecular and Cellular Biochemistry.2003; 252: 117–124.
Katiyar S, Thelma BK, Murthy NS, Hedau S, Jain N, Gopalkrishna V. Polymorphism of the p53 codon 72 Arg/Pro and the risk of HPV type 16/18-associated cervical and oral cancer in India. Mol Cell Biochem. 2003;252:117–24.
Khovidhunkit SO, Buajeeb W, Sanguansin S, Poonsawat S, Weerapradist W. Detection of human papillomavirus in oral squamous cell carcinoma, leukoplakia and lichen planus in Thai patients. Asian Pac J Cancer Prev. 2008;4:771-75.
Kim JW, Roh JW, Park NH, Song YS, Kang SB, Lee HP. Polymorphism of TP53 codon 72 and the risk of cervical cancer among Korean women. Am J Obstet Gynecol. 2001;184:55–8.
Korzeniewski N, Spardy N, Duensing A, et al. Genomic instability and cancer: lessons learned from human papillomaviruses. Cancer Lett 2011; 305: 113–22.
Krutchkoff DJ, Eisenberg E. Lichenoid dysplasia: a distinct histopathologic entity. Oral Surg Oral Med Oral Pathol 1985;30: 308-15.
L. Chen and J. Chen, “MDM2-ARF complex regulates p53 sumoylation,” Oncogene 2003;22:5348–5357.
Lodi G, Scully C, Carrozzo M, Griffiths M, Sugerman PB, Thongprasom K. Current controversies in oral lichen planus: report of an international consensus meeting. Part 2. Clinical management and malignant transformation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005; 100(2):164–78.
M. Ebrahimi, K. Nylander, and I. Van Der Waal, “Oral lichen planus and the p53 family: what do we know?,” Journal of Oral Pathology & Medicine.2011; 40: 281–285.
M. Ebrahimi, Y. B. Wahlin, P. J. Coates, A. Wiik, G. Roos, and K. Nylander, “Detection of antibodies against p 63 and p73 isoforms in sera from patients diagnosed with oral lichen planus,” Journal of Oral Pathology and Medicine 2007;36:93–98.
M. S. Rodriguez, J. M. P. Desterro, S. Lain, D. P. Lane, and R. T. Hay, “Multiple C-terminal lysine residues target p53 for ubiquitin-proteasome-mediated degradation,” Molecular and Cellular Biology 2000;20:8458–8467.
M.K.Yoon, J.H.Ha, M.S.Lee, S.W.Chi, “ Structure and apoptotic function of p73,” BMB Reports.2015;48: 81–90.
Meek DW. The p53 response to DNA damage. DNA Repair. 2004;3:1049–56.
Munger K, Werness BA, Dyson N, Phelps WC, Harlow E, Howley PM. Complex formation of human papillomavirus E7 proteins with the retinoblastoma tumour suppressor gene product. EMBO J 1987;8:4099‐105.
Murti PR, Warnakulasuriya KAAS, Johnson NW, Bhonsle RB, Gupta PC, Daftary DK, et al. P53 expression in oral precancer as a marker for malignant potential. J Oral Pathol Med 1998; 27:191-96.
Neville BW, Damn DD, Allen CM, Bouquot JE: Oral and Maxillofacial Pathology. 3rd ed. Elsevier: Saunders company; 2009. p.782-788.
Ogmundsdo ́ttir HM, Hilmarsdo ́ ttir H, A ́stvaldsdo ́ ttir A ́, Jo ́hannsson JH, Holbrook WP. Oral lichen planus has a high rate of TP53 mutations. A study of oral mucosa in Iceland. Eur J Oral Sci 2002; 110: 192–198.
Ogmundsdottir HM, Hilmarsdottir H, Astvaldsdottir A, et al. Oral lichen planus has a high rate of TP53 mutation. A study of oral mucosa in Iceland. Eur J Oral Sci 2003;110:192-198
Partridge M, Costea DE, Huang X. The changing face of p53 in head and neck cancer. Int J Oral Maxillofac Surg 2007; 36: 1123–38.
Partridge M, Gaballah K, Huang X. Molecular markers for diagnosis and prognosis. Cancer Metastasis Rev. 2005;24:71–85
Pim D, Banks L. p53 polymorphic variants at codon 72 exert different effects on cell cycle progression. Int J Cancer 2004;108:196-9.
Pindborg JRP, Smith CJ, van der Waal I. Histological Typing of Cancer and Precancer of the Oral Mucosa. World Health Organization international histological classification of tumours. 2nd ed. Berlin: Springer, 1997.
Pol CA, Ghige SK, Gosavi SR. Role of human papilloma virus‐16 in the pathogenesis of oral lichen planus—An immunohistochemical study. Int Dent J 2015;65:11‐4.
Prabhu SR, Wilson DF. Human papillomavirus and oral disease – Emerging evidence: A review. Aust Dent J 2013;58:2‐10.
R. V. Sionov and Y. Haupt, “The cellular response to p53: the decision between life and death,” Oncogene 1999;18: 6145–6157.
Regezi JA, Sciubba JG, Jordan R; Oral Pathology Clinical Pathologic Correlations. 6th ed. Elsevier: Saunders company; 2012. p.97-102.
S. C. Girod, P. Pfeiffer, J. Ries, and H. D. Pape, “Proliferative activity and loss of function of tumour suppressor genes as ‘biomarkers’ in diagnosis and prognosis of benign and pre-neoplastic oral lesions and oral squamous cell carcinoma,” British Journal of Oral and Maxillofacial Surgery 1998;36:252–260.
Sakamuro D, Sabbatini P, White E, Prendergast GC. The polyproline region of p53 is required to activate apoptosis but not growth arrest. Oncogene. 1997;15:887–98.
Sameera A, Kotikalpudi R, Patel RK, Reddy KK, Prasanna M, Erugula SR. Molecular detection of human papillomavirus DNA in oral lichen planus patients. J Clin Diagn Res 2019;13:Zc20‐4.
Schifter M, Jones AM, Walker DM: Epithelial p53 gene expression and mutational analysis, combined with growth fraction assessment, in oral lichen planus. J Oral Pathol Med 1998; 27: 318–24.
Schliephake H. Prognostic relevance of molecular markers of oral cancer – A review. Int J Oral Maxillofac Surg. 2003;32:233–45.
Storey A, Thom as M, Kalita A, et al. Role of a p53 polymorphism in the development of human papillomavirus-associated cancer. Nature.1998;393:229 –34.
Sugerman PB, Savage NW. Oral lichen planus: cause, diagnosis and management. Aust Dent J 2002; 47:290-297.
Sullivan A, Syed N, Gasco M, Bergamaschi D, Trigiante G, Attard M, et al. Polymorphism in wild-type p53 modulates response to chemotherapy in vitro and in vivo.Oncogene 2004 ;23:3328-37.
Sullivan A, Syed N, Gasco M, Bergamaschi D, Trigiante G, Attard M, et al. Polymorphism in wild-type p53 modulates response to chemotherapy in vitro and in vivo. Oncogene 2004;23:3328–37.
Suryasa, I. W., Rodríguez-Gámez, M., & Koldoris, T. (2021). Get vaccinated when it is your turn and follow the local guidelines. International Journal of Health Sciences, 5(3), x-xv. https://doi.org/10.53730/ijhs.v5n3.2938
Syrjänen S, Lamberg M, Pyrhönen S, et al. Morphological and immunohistochemical evidence suggesting human papillomavirus (HPV) involvement in oral squamous cell carcinogenesis. Int J Oral Surg 1983; 12: 418–24.
T. Buschmann, S. Y. Fuchs, C. G. Lee, Z. Q. Pan, and Z. Ronai, “SUMO-1 modification of Mdm2 prevents its self- ubiquitination and increases Mdm2 ability to ubiquitinate p53,” Cell 2000;101:753–762.
Tabatabaei S H, Sheikhha M H, Karbasi M, Zarmehi S, Hoseinii M. Evaluation of polymorphism of P53 protein codon 72 in oral lichen planus by PCR.Journal of Dental Research, Dental Clinics, Dental Prospects .2018;12(4):246-250.
Talia H, Monie A, Gravitt P, Wu TC. Molecular epidemiology of human papillomavirus. J Formos Med Assoc. 2008;107:198-217.
Tang Y, Zhao W, Chen Y, et al. Acetylation is indispensable for p53 activation. Cell 2008; 133: 612–26.
Valente G, Pagano M, Carrozzo M, Carbone M, Bobba V, Palestro G, et al. Sequential immunohistochemical p53 expression in biopsies of oral lichen planus undergoing malignant evolution. J Oral Pathol Med. 2001;30:135–40.
Van der Meiji EH, van der Waal . Lack of clinicopathological correlation in the diagnosis of oral lichen planus based on the presently available diagnostic criteria and suggestions for modifications. J Oral Pathol Med 2003;32:507–12.
Werness BA, Levine AJ, Howley PM. Association of human papillomavirus types 16 and 18 E6 proteins with p53. Science 1990;248:76‐9.
Whibley C, Pharoah PD, Hollstein M. p53 polymorphisms: cancer implications. Nat Rev Cancer 2009; 9: 95–107.
Williams HK. Molecular pathogenesis of oral squamous carcinoma. J Clin Pathol: Mol Pathol 2000;53:165-72.
Yanatatsaneeji P, Kitkumthorn N, Dhammawipark C, Ra- balert J, Patel V, Mutirangura A. Codon72 polymorphism in the p53 tumour suppressor gene in oral lichen planus lesions in a Thai population. Asian Pac J Cancer Prev 2010;11:1137-41.
Yu H, Huang YJ, Liu Z, et al. Effects of MDM2 pro- moter polymorphisms and p53 codon 72 polymorphism on risk and age at onset of squamous cell carcinoma of the head and neck. Mol Carcinog 2011; 50: 697–706.
Yu H, Huang YJ, Liu Z, et al. Effects of MDM2 promoter polymorphisms and p53 codon 72 polymorphism on risk and age at onset of squamous cell carcinoma of the head and neck. Mol Carcinog 2011; 50: 697–706.
Zhang L, Michelsen C, Cheng X, Zeng T, Priddy R, Rosin MP. Molecular analysis of oral lichen planus. A premalignant lesion? Am J Pathol 1997; 151: 323–7.
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