Alterations of p16INK4a tumour suppressor gene mucoepidermoid carcinoma of the salivary glands

被引:20
作者
Guo, X. -L.
Sun, S. -Z.
Wang, W. -X.
Wei, F. -C.
Yu, H. -B.
Ma, B. -L.
机构
[1] Shandong Univ, Dept Oral & Maxillofacial Surg, Sch Stomatol, Jinan 250012, Peoples R China
[2] Shandong Univ, Dept Pathol, Sch Stomatol, Jinan 250012, Peoples R China
[3] Shandong Univ, Dept Periodontol, Sch Stomatol, Jinan 250012, Peoples R China
[4] Shandong Univ, Dept Oral & Maxillofacial Surg, Qilu Hosp, Jinan 250012, Peoples R China
关键词
salivary gland; mucoepidermoid carcinoma; p16(INK4a); DNA methylation; mutation; deletion; SQUAMOUS-CELL CARCINOMA; PROMOTER HYPERMETHYLATION; ABERRANT METHYLATION; DNA METHYLATION; CANCER PATIENTS; MULTIPLE GENES; HIGH-FREQUENCY; NECK; HEAD; P16;
D O I
10.1016/j.ijom.2006.11.004
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Mucoepidermoid carcinoma (MEC) is common in the salivary glands, but alterations of the p16(INK4a) tumour suppressor gene are largely unknown. The aim of this study was to analyse p16(INK4a) gene alterations in MEC, and evaluate their significance for carcinogenesis. Thirty-eight salivary glands with MEC and six normal salivary glands were studied for p16(INK4a) alterations. In the MEC-affected group, there were 23.7% (9/38) and 13.2% (5/38) cases of homozygous deletion, and 5.3% (2/38) and 2.6% (1/38) cases of point mutation in p16(INK4a) exon 1 and exon2, respectively. Hypermethylation of the p16(INK4a), gene promoter was found in 13 cases (13/38, 34.2%). Alterations of the p16(INK4a), gene were not found in the normal salivary glands. These findings suggest that the main mechanisms of inactivation of the P16(INK4a), gene in MEC of the salivary glands are promoter hypermethylation and homozygous deletion.
引用
收藏
页码:350 / 353
页数:4
相关论文
共 23 条
[1]   MUCOEPIDERMOID CARCINOMA OF THE SALIVARY-GLANDS - A REAPPRAISAL OF THE INFLUENCE OF TUMOR DIFFERENTIATION ON PROGNOSIS [J].
CLODE, AL ;
FONSECA, I ;
SANTOS, JR ;
SOARES, J .
JOURNAL OF SURGICAL ONCOLOGY, 1991, 46 (02) :100-106
[2]  
Esteller M, 1999, CANCER RES, V59, P67
[3]   Cancer as an epigenetic disease: DNA methylation and chromatin alterations in human tumours [J].
Esteller, M ;
Herman, JG .
JOURNAL OF PATHOLOGY, 2002, 196 (01) :1-7
[4]   Immunohistochemical expression of retinoblastoma pathway proteins in normal salivary glands and in salivary gland tumours [J].
Etges, A ;
Nunes, FD ;
Ribeiro, KCB ;
Araújo, VC .
ORAL ONCOLOGY, 2004, 40 (03) :326-331
[5]   Deletion and methylation of the tumour suppressor gene p16/CDKN2 in primary head and neck squamous cell carcinoma [J].
Gonzalez, MV ;
Pello, MF ;
LopezLarrea, C ;
Suarez, C ;
Menendez, MJ ;
Coto, E .
JOURNAL OF CLINICAL PATHOLOGY, 1997, 50 (06) :509-512
[6]  
GREENE FL, 2002, AJCC CANC STAGING MA, P81
[7]   Mucoepidermoid carcinoma of the salivary glands: Clinicopathologic review of 108 patients treated at the National Cancer Institute of Milan [J].
Marco Guzzo ;
Salvatore Andreola ;
Grazia Sirizzotti ;
Giulio Cantu .
Annals of Surgical Oncology, 2002, 9 (7) :688-695
[8]   Extra-cellular signal-regulated ERK-1/ERK-2 pathway activation in human salivary gland mucoepidermoid carcinoma - Association to aggressive tumor behavior and tumor cell proliferation [J].
Handra-Luca, A ;
Bilal, H ;
Bertrand, JC ;
Fouret, P .
AMERICAN JOURNAL OF PATHOLOGY, 2003, 163 (03) :957-967
[9]   Methylation-specific PCR: A novel PCR assay for methylation status of CpG islands [J].
Herman, JG ;
Graff, JR ;
Myohanen, S ;
Nelkin, BD ;
Baylin, SB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (18) :9821-9826
[10]  
Hsu LS, 2006, ONCOL REP, V15, P507