Aberrant promoter methylation of PTEN gene among Indian patients with oral squamous cell carcinoma

被引:1
作者
Alyasiri, Nisreen S. [1 ]
Ali, Asgar [1 ]
Kazim, Zakia [1 ]
Gupta, Sunita [2 ]
Mandal, Ashish K. [3 ]
Singh, Ishwar [4 ]
Rizvi, Moshahid A. [1 ]
机构
[1] Jamia Millia Islamia, Genome Biol Lab, Dept Biosci, New Delhi 25, India
[2] Maulana Azad Inst Dent Sci, New Delhi, India
[3] All India Inst Med Sci, Dept Pathol, New Delhi 110029, India
[4] Maulana Azad Med Coll, Dept Otolaryngol Head & Neck Surg, New Delhi, India
关键词
Methylation; OSCC; PTEN; Tumor suppressor gene; PREDICTIVE FACTORS; CANCER; EXPRESSION; ISLAND; BREAST;
D O I
10.5301/JBM.5000030
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Background and aims: Oral cancer is the second most common cancer in men and accounts for 50%-70% of the total cancer mortality in India. PTEN is a tumor suppressor gene that plays a critical role in controlling cell growth and survival. Promoter hypermethylation of the PTEN gene has been reported in many tumors. However, little is known about the association between promoter methylation and oral squamous cell carcinoma (OSCC). Therefore, we aimed to detect the role of PTEN hypermethylation in OSCC patients in the Indian population. Methods: Genomic DNA was isolated from 100 fresh oral tumor specimens and was subjected to bisulfite conversion. Methylation-specific PCR was employed on the converted DNA to investigate the methylation status. Results: Of the total cases examined for PTEN promoter methylation we found that 35% were positive and 65% were negative. When evaluated in connection with tumor differentiation it was found that 82% of poorly differentiated, 24% of moderately differentiated and 32% of well differentiated OSCC samples were methylated. Methylation was further correlated with patient age, sex and tumor grade. Interestingly, we found that patient age and grade of differentiation were significantly associated with PTEN promoter methylation (p=0.05 and 0.0019, respectively) while sex was not (p=0.9). Conclusions: The present study underlines the importance of PTEN hypermethylation among Indian OSCC patients.
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收藏
页码:298 / 302
页数:5
相关论文
共 21 条
[1]   PTEN methylation and expression in glioblastomas [J].
Baeza, N ;
Weller, M ;
Yonekawa, Y ;
Kleihues, P ;
Ohgaki, H .
ACTA NEUROPATHOLOGICA, 2003, 106 (05) :479-485
[2]   Prognostic and predictive factors in oral cancer:: the role of the invasive tumour front [J].
Bànkfalvi, A ;
Piffkò, J .
JOURNAL OF ORAL PATHOLOGY & MEDICINE, 2000, 29 (07) :291-298
[3]   Prognostic and predictive factors in oral squamous cell cancer:: important tools for planning individual therapy? [J].
Bettendorf, O ;
Piffkò, J ;
Bànkfalvi, A .
ORAL ONCOLOGY, 2004, 40 (02) :110-119
[4]   PTEN mutations in gliomas and glioneuronal tumors [J].
Duerr, EM ;
Rollbrocker, B ;
Hayashi, Y ;
Peters, N ;
Meyer-Puttlitz, B ;
Louis, DN ;
Schramm, J ;
Wiestler, OD ;
Parsons, R ;
Eng, C ;
von Deimling, A .
ONCOGENE, 1998, 16 (17) :2259-2264
[5]  
Gale N., 2005, Pathology and genetics of head and neck tumours, P177
[6]  
GONZALEZZULUETA M, 1995, CANCER RES, V55, P4531
[7]  
Kurasawa Y, 2008, ONCOL REP, V19, P1429
[8]   PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer [J].
Li, J ;
Yen, C ;
Liaw, D ;
Podsypanina, K ;
Bose, S ;
Wang, SI ;
Puc, J ;
Miliaresis, C ;
Rodgers, L ;
McCombie, R ;
Bigner, SH ;
Giovanella, BC ;
Ittmann, M ;
Tycko, B ;
Hibshoosh, H ;
Wigler, MH ;
Parsons, R .
SCIENCE, 1997, 275 (5308) :1943-1947
[9]   5' CPG ISLAND METHYLATION IS ASSOCIATED WITH TRANSCRIPTIONAL SILENCING OF THE TUMOR-SUPPRESSOR P16/CDKN2/MTS1 IN HUMAN CANCERS [J].
MERLO, A ;
HERMAN, JG ;
MAO, L ;
LEE, DJ ;
GABRIELSON, E ;
BURGER, PC ;
BAYLIN, SB ;
SIDRANSKY, D .
NATURE MEDICINE, 1995, 1 (07) :686-692
[10]   Altered PTEN expression as a diagnostic marker for the earliest endometrial precancers [J].
Mutter, GL ;
Lin, MC ;
Fitzgerald, JT ;
Kum, JB ;
Baak, JPA ;
Lees, JA ;
Weng, LP ;
Eng, C .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2000, 92 (11) :924-931