Effects of cigarette smoking across three generations and of perceptions of the smoking-cancer relationship on the cigarette smoking status of Turkish university students.

BACKGROUND: This descriptive and cross-sectional study aimed to investigate effects of cigarette smoking across three generations and perceptions of the smoking-cancer relationship on the cigarette smoking status of Turkish university students. MATERIALS AND METHODS: The study sample comprised of 434 university students studying in different departments of a university. Data were collected using a socio-demographic data collection form and the Decisional Balance Scaleqand evaluated using the Mann-Whitney U test, CHAID and multiple regression analyses. RESULTS: The average age of the students participating in the study is 19.6+.5.0, some 11.3% of the students reporting that they smoked cigarettes. No statistically significant relationship was ascertained between the cigarette smoking statuses of the students based on the cigarette smoking status of their grandparents (p=0.144). but there was a link to that of their parents (p=0.002). The difference between the cigarette smoking ratios of the students based on their perceptions of smoking-cancer relationship was statistically significant (p<0.001). Believing that there is a relationship between smoking and cancer decreased likelihood of cigarette smoking 3.7 fold. Cigarette smoking by grandparents, and believing that there is a relationship between smoking and cancer, and cigarette smoking by parents explained 8.3% of the cigarette smoking status of the students. CONCLUSIONS: While cigarette smoking by grandparents only indirectly influences cigarette smoking by the students, believing that there is a relationship between smoking and cancer, and cigarette smoking by parents are influential variables in determining cigarette smoking by Turkish students.

Systematic reduction of cohesin differentially affects chromosome segregation, condensation, and DNA repair.

Cohesin's complex distribution on chromosomes and its implication in numerous cellular processes makes it an excellent paradigm for studying the relationship between the in vivo concentration of a protein and its in vivo function. Here, we report a method to generate systematic quantized reductions (QR) in the in vivo concentration of any yeast protein. With QR, we generate strains with 13% and 30% of wild-type levels of the limiting subunit of cohesin, Mcd1p/Scc1p/Rad21p. Reducing cohesin levels reveals a preferential binding of cohesin to pericentric regions over cohesin-associated regions (CAR) on chromosome arms. Chromosome condensation, repetitive DNA stability, and DNA repair are compromised by decreasing cohesin levels to 30% of wild-type levels. In contrast, sister-chromatid cohesion and chromosome segregation are unaffected even when cohesin levels are reduced to 13% of wild-type levels. The requirement for different in vivo cohesin concentrations to achieve distinct cohesin functions provides an explanation for how cohesin mutations can specifically lead to adult disorders such as Cornelia de Lange Syndrome and Roberts Syndrome without compromising the cell divisions needed for development and maturation. Our successful application of QR to cohesin suggests that QR is a powerful tool to study other proteins/pathways with multiple functions.

Dissecting the unique role of the retinoblastoma tumor suppressor during cellular senescence.

The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.