Mechanics behind breast cancer prevention - focus on obesity, exercise and dietary fat.

Cancer prevention is rapidly emerging as a major strategy to reduce cancer mortality. In the field of breast cancer, significant strides have recently been made in the understanding of underlying preventive mechanisms. Currently, three major strategies have been linked to an increase in breast cancer risk: obesity, lack of physical exercise, and high levels of saturated dietary fat. As a result, prevention strategies for breast cancer are usually centered on these lifestyle factors. Unfortunately, there remains controversy regarding epidemiological studies that seek to determine the benefit of these lifestyle changes. We have identified crucial mechanisms that may help clarify these conflicting studies. For example, recent reports with olive oil have demonstrated that it may influence crucial transcription factors and reduce breast tumor aggressiveness by targeting HER2. Similarly, physical exercise reduces sex hormone levels, which may help protect against breast cancer. Obesity promotes tumor cell growth and cell survival through upregulation of leptin and insulin-like growth factors. This review seeks to discuss these underlying mechanisms, and more behind the three major prevention strategies, as a means of understanding how breast cancer can be prevented.

Radiation-induced apoptosis in MOLT-4 cells requires de novo protein synthesis independent of de novo RNA synthesis.

We investigated the effects of inhibition of de novo RNA and protein synthesis in ionizing radiation (IR)-induced apoptosis in the human T cell line MOLT-4. We observed that pretreatment with cycloheximide inhibited IR-induced apoptosis. However, pretreatment with actinomycin D did not inhibit apoptosis induced by IR. These results suggest that apoptosis induced by IR in MOLT-4 cells requires de novo protein synthesis but not de novo RNA synthesis. This finding suggests that the mRNA encoding the proapoptotic protein(s) is stabilized to facilitate translation independent of de novo gene transcription in response to IR. Our results also indicate that translation of the required proapoptotic protein(s) occurs upstream of mitochondrial depolarization and after 2 h post-IR.