Background. Promoter hypermethylation of the SMAD4 gene has been registered
in some cancer types, but in general doesn?t appear to be a frequent event in
carcinogenesis. However, only a few published studies deal with this topic
and not many cancer types have been analyzed. The aim of this study was to
establish SMAD4 gene promoter methylation status in pancreatic and
endometrial cancers. Methods. Patients included in the study (62 subjects)
were diagnosed and surgically treated at the University of Belgrade, Clinical
Center of Serbia. Patients with pancreatic carcinoma (17 subjects) underwent
surgical removal of the pancreatic adenocarcinoma at the First Surgical
Clinic, while the patients with endometrial carcinoma (45 subjects) underwent
hysterectomy with adnexectomy at the Institute for Gynecology and Obstetrics.
Extraction of DNA from fresh tissue samples was performed and the methylation
status of the SMAD4 gene promoter was studied by a previously designed
PCR-based HpaII and MspI restriction enzyme assay. The resulting PCR products
were analyzed by electrophoresis in 2% agarose gels. Results. Neither of the
analyzed samples was found to be hypermethylated. Conclusion. This is the
first report on SMAD4 methylation status in pancreatic and endometrial tumor
specimens, and supports the viewpoint that SMAD4 hypermethylation is not a
common event in malignant tumors. Nevertheless, promoter hypermethylation
remains a candidate mechanism for SMAD4 inactivation in malignant tissue as a
potential cause of decreased or lost SMAD4 expression in certain tumor types,
and should be further investigated in different tumor types and larger
cohorts of patients.
CDH1 Gene Promoter Hypermethylation
