Anticancer research · 2008
Aberrant methylation of p16, DLEC1, BLU and E-cadherin gene promoters in nasopharyngeal carcinoma biopsies from Tunisian patients.
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Ayadi Wajdi, Karray-Hakim Héla, Khabir Abdelmajid, Feki Lamia, Charfi Slim, Boudawara Tahia, Ghorbel Abdelmonem, Daoud Jamel, Frikha Mounir, Busson Pierre, Hammami Adnane
Аннотация
BACKGROUND: Aberrant methylation of tumor suppressor gene (TSG) promoters has been extensively investigated in nasopharyngeal carcinomas (NPC) from South East Asia but not from North Africa.
PATIENTS AND METHODS: The methylation status of p16, deleted in lung and esophageal cancer (DLEC1), zinc finger, MYND-type containing 10 (BLU) and E-cadherin gene promoters was investigated in 44 Tunisian NPC biopsies and three NPC xenografts, by methylation-specific PCR (MSP) combined with a quantitative assessment of some of the samples.
RESULTS: The frequencies of aberrant promoter methylation were similar to previous figures reported for Asian series: p16 27/44 (65%), DLEC1 38/44 (86.3%), BLU 15/44 (34.1%) and E-cadherin 35/44 (79.5%). Although in other malignancies, aberrant promoter hypermethylation increases with patient age, it was at the same high frequency in the juvenile and adult forms of Tunisian NPCs. However, there was a strong association between aberrant methylation of E-cadherin promoter and lymph node invasion (p < 0.01). In addition, aberrant methylation of the BLU promoter was significantly correlated with an undifferentiated histological type (p = 0.03).
CONCLUSION: Aberrant methylation of tumor suppressor genes occurs with the same high frequency in NPCs from North Africa as in South East Asia, regardless of patient age.
PATIENTS AND METHODS: The methylation status of p16, deleted in lung and esophageal cancer (DLEC1), zinc finger, MYND-type containing 10 (BLU) and E-cadherin gene promoters was investigated in 44 Tunisian NPC biopsies and three NPC xenografts, by methylation-specific PCR (MSP) combined with a quantitative assessment of some of the samples.
RESULTS: The frequencies of aberrant promoter methylation were similar to previous figures reported for Asian series: p16 27/44 (65%), DLEC1 38/44 (86.3%), BLU 15/44 (34.1%) and E-cadherin 35/44 (79.5%). Although in other malignancies, aberrant promoter hypermethylation increases with patient age, it was at the same high frequency in the juvenile and adult forms of Tunisian NPCs. However, there was a strong association between aberrant methylation of E-cadherin promoter and lymph node invasion (p < 0.01). In addition, aberrant methylation of the BLU promoter was significantly correlated with an undifferentiated histological type (p = 0.03).
CONCLUSION: Aberrant methylation of tumor suppressor genes occurs with the same high frequency in NPCs from North Africa as in South East Asia, regardless of patient age.