Detection of p16 promotor hypermethylation in "Maras powder" and tobacco users.

BACKGROUND: A plant powder called "Maras powder" is widely used instead of cigarette smoking in the South-Eastern region of Turkey. It has been confirmed that this powder comprises tobacco Nicotiana rustica L. METHODS: The aim of this study was to assess the effect of Maras powder and cigarette smoking on the P16 promotor hypermethylation. Twenty-two Maras powder users (Group I), 12 cigarette smokers (Group II), and 16 healthy controls who neither smoked nor used Maras powder (Group III) were included in the study. Hypermethylation of the P16 gene was examined using methylation-specific PCR (MSP) method in the blood of the three groups. RESULTS: Aberrant P16 methylation was found in 7 of the 22 (31.8%) in Group I, in 3 of 12 (25%) in Group II, and in 1 of 16 (6.25%) in Group III. CONCLUSION: Maras powder may be as harmful as cigarette smoking, leading to hypermethylation in P16 and warrants detailed studies on this subject.

The effect of maras powder on DNA methylation and micronucleus formation in human buccal tissue.

The plant powder "maras powder" (MP) has been used widely instead of cigarettes in the southeastern region of Turkey. The aim of this study was to assess the impacts of MP and cigarette smoking on the methylation and micronuclei (MN) formation in buccal cells of humans with a comparison to blood lymphocytes. DNA samples from 80 subjects (40 MP users, 20 tobacco smokers, 20 healthy volunteers) were analyzed for their genomic methylation status using Hpa II and Msp I digestions followed by a simple gel electrophoresis and ethidium bromide staining. A densitometric method was developed to measure the methylation in genomic DNA samples and the results were evaluated using a software program designed for this purpose. Buccal epithelial cells were collected from the same groups and examined for MN formation. The results indicated that a general genomic hypomethylation was present in almost all of the samples that were obtained from MP users and tobacco smokers. This hypomethylation was significant in MP users compared to smokers and healthy volunteers. The percentage of cells containing MN was 1.93 in MP users, 0.95 in healthy volunteers, and 1.82 in smokers. The MN frequency was significantly higher in MP users and smokers than in healthy volunteers. There was no statistical difference between smokers and MP users. Evidence indicates that MP usage induces DNA hypomethylation and increase frequency of MN formation.

How the I1307K adenomatous polyposis coli gene variant contributes in the assessment of risk of colorectal cancer, but not stomach cancer, in a Turkish population.

Germline and somatic truncating mutations of the adenomatous polyposis coli gene (APC) are thought to initiate colorectal tumor formation in familial adenomatous polyposis syndrome and sporadic colorectal carcinogenesis, respectively. Recently, an isoleucine-lysine polymorphism at codon 1307 (I1307K) of the APC gene has been identified in 6-7% of the Ashkenazi Jewish population. To assess the risk of this common APC allelic variant in colorectal carcinogenesis, a cohort of unselected Turkish subjects with stomach or colorectal cancer (or both) was analyzed for the APC I1307K polymorphism. Genomic DNA was extracted from patients by obtaining all stomach and colon malign polipose tissues using nuclei lysis methods. Detection of the I1307K mutation was performed using the commercial Pronto APC kit according to the manufacturer's instructions. The APC I1307K allele was identified in 7 of 57 stomach carcinoma patients (12.3%; P > 0.05) and 30 of 56 colon carcinoma patients (53.6%; P < 0.05) using antigen-anticor interaction methods. Comparing the frequencies of the two separate population control groups, the APC I1307K allele is associated with an estimated relative risk of 1.9 for colorectal neoplasia. Furthermore, APC I1307K carriers had greater numbers of adenomas and colorectal cancers per patient than noncarriers. The conclusion is that the APC I1307K variant leads to increased adenoma formation and colorectal cancer. The estimated relative risk for carriers may justify specific clinical screening for Turkish people expected to harbor this allele, and genetic testing in the long term may significantly promote colorectal cancer prevention in this population.